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Posts Tagged ‘allergic reactions’

Calcitonin

Friday, July 31st, 2009

Generic Name
Calcitonin (kal-sih-TOE-nin)
General Information
Calcitonin helps to strengthen bone by adding more calcium to it and slowing the natural process by which bone is broken down. The calcitonin used in this drug is essentially identical to human calcitonin except that it is more potent. It is a synthetic version of the natural calcitonin found in salmon. Calcitonin can increase bone density and reduce the risk of fractures of the vertebrae (bones that comprise the spinal column), which are associated with back pain and loss of height. Calcitonin has been available for years as an injection, but the development of the nasal spray makes the drug easier to use.
Cautions and Warnings
Do not use calcitonin if you are allergic or sensitive to any of its ingredients. Although serious allergic reactions were reported with the injectable form, none have occurred with the nasal spray.
Changes in the tissues lining your nose are possible with longerm use of this product. An initial nasal examination and then peiodic examinations are recommended.
Possible Side Effects
V Most common: stuffy nose, runny nose, and other nasal symptoms; and back pain.
V Less common: joint pain, nosebleed, and headache.
Drug Interactions
None known.
Food Interactions
None known. Usual Dose
Adult: I spray (200 IU) a day. Child: not recommended.
Little is known about the effects of calcitonin overdose or accidental ingestion. Nausea and vomiting have been reported after high doses. Call your local poison control center for more information. Overdose victims should be taken to a hospital emergency room. ALWAYS bring the prescription bottle or container.
Special Information
Alternate nostrils daily when using the nasal spray.
Before you take your first dose, you must activate the pump. Hold the bottle upright and press the two white arms toward the bottle 6 times until a faint spray is emitted. Once this occurs, the pump is activated and ready for use. It is not necessary to reactivate the pump every day.
Store new, unassembled bottles in the refrigerator. Keep the bottle in use at room temperature and discard after 30 days.
If you forget to administer a dose of the nasal spray, do so as soon as you remember. If it is almost time for the next dose, skip the dose you forgot and continue with your regular schedule. Call your doctor if you forget 2 or more doses.
Call your doctor if you develop severe nose irritation or any unusual or intolerable symptom. Follow your doctor’s recommendations regarding calcium and vitamin D supplements. This drug is not intended to replace the need for dietary calcium.
Special Populations
Pregnancy/Breast-feeding: calcitonin does not cross into the fetal circulation, though animal studies have associated the injectable form of the drug with low birth weight. This drug is recommended for use during pregnancy only if its possible benefits outweigh its risks.
It is not known if calcitonin passes into breast milk, though animal studies have shown that it reduces the amount of milk produced. Nursing mothers who must use calcitonin should consider using infant formula.
Seniors: Seniors may use this product without special precaution.

A-Z Principal Drugs (cytarabine - dextran)

Wednesday, June 24th, 2009

cytarabine A cytotoxic agent that prevents cell development by inhibiting the formation of nucleic acid. It is used mainly in the control of acute mycloblastic leukaemia.
Dose: 0.5-3 mg/kg daily by i.v. or s.c. injection. Close haematological control is essential as the drug is a powerful myclodepressant. Other side-effects are those of the cytotoxic drugs, generally, but fever, myalgia and bone pain may also occur. Alexan; Cv cos: r).
Dose:    nig/kg, daily for 10 days, repeated after 4 weeks. Side-effects are severe nausea, bone marrow depression and an influenza-like syndrome. The drug should be handled with care, as it is a tissue irritant. (DTIC).
dactinomycin See actinomycin D.
dalteparin A low-molecular weight heparin given by s.c. injection for pre- and postoperative thrombo-embolic prophylaxis. Dose: 2500 units daily for 5 (lays. (Fragmin). See enoxaprin and tinzaparin.
cytotoxic drugs A term applied to drugs that can kill cancer cells. In practice, many factors influence their therapeutic value. They are rarely selective, and therapeutic doses usually have a toxic effect on sonic normal cells. They may attack cancer cells at different stages of development, as actively dividing cells are more susceptible than resting cells. They may not reach the cancer cells in adequate concentration, or resistance to the drug may develop. The dose may also depend to some extent on the patient’s tolerance of the drug, and combined treatment with two or more drugs may have the advantages of increased potency with reduced toxicity. All cytotoxic drugs, with the exception of bleomycin and vincristine, bring about a depression of the bone marrow, which may be severe, and some degree of hair loss, which is usually reversible. Severe nausea and vomiting are also common, and early use of powerful antiemetics is essential. Many cytotoxic agents are tissue irritants, and with i.v. treatment great care must be taken to avoid extravasation, as severe local tissue damage can occur. See alkylating agents and antimetabolites. See page 122.
clacarbazine A cytotoxic drug that appears to depress purine metabolism and the formation of DNA. It is used mainly in malignant melanoma, and in combination with other agents it is of value in other malignant conditions.
clanazol A derivative of ethisterone that inhibits the release of pituitary gonadotrophins. Used in conditions such as endometriosis and gynaecomastia. Dose: 200-800 ing daily, starting during menstruation. Side-effects are nausea, dizziness, rash, flushing and hair loss. Care is necessary in cardiac, renal or hepatic impairment, and in epilepsy and diabetes. (Danol).
danthron A synthetic anthraquinone laxative used mainly for constipation in the aged, and in drug-induced constipation in the terminally ill. Not suitable for routine use by other patients.
Dose: given in doses of 25–25 mg as codanthramer, and acts within 6-12 hours. the urine may be coloured red.
dantrolene A skeletal muscle relaxant that acts on the muscle fibre, and not at the myoneural junction. The action may be linked with an interference with the movement of calcium ions. It is used in the severe and chronic spastic states that occur after stroke, spinal cord injury, and in multiple sclerosis.
Dose: 21 ing daily initially, increased at weekly intervals up to a maximum of 400 mg daily, as the response is slow and May be inadequate. The side-effects of weakness and Gangue are mild, and often transient, but liver function tests during treatment are essential. Dantrolene is also of value in malignant hyperthermia, a rare but serious complication of anaesthesia, and is given in doses of I mg/kg by i.v. injection as soon as the condition is diagnosed,

dapsone A sulphone compound used in the ti,atnient of leprosy.
Dose: 25-400 mg orally twice weekly and continued for some years. Resistance to dapsone may occur, and combined treatment with clofazimitic and rifarnpicin may lie necessary. Dapsone is sometimes given with pyrimetharnine in chlotoquine-resistaut malaria. Side-effects are nausea, rash, neuropathy and myelodepression.
duration of action. Used in the diagnosis and control of diabetes insipidus, and in the treatment of nocturnal eneuresis. Dose: 10-20pg intranasally once or twice
a day; 1-4 pg daily by injection. IMAM.
desoxymethasone A corticosteroid, for local application in acute inflammatory and allergic skin conditions. Used as oily cream 0.25%. (Stiedex).
daunorubicin See doxorubicin.
debrisoquine An adrenergic neurone blocking agent with the actions, uses and side-effects of guanethidine, except that it is less likely to cause diarrhoea. It is used mainly in resistant hypertension, in association with other drugs. (Declinax).
See page 148 and Table 21.
deflazacort A glucocorticoid with the actions and uses of related drugs, and comparable in activity with prednisolone. Dose: initially in acute conditions up to 120 mg daily; maintenance dose 3-18 mg daily. (Calcort). See hydrocortisone, page 55 and Table 36.
demeclocycline An antibiotic with the actions, uses and side-effects of tetracycline, but more likely to cause photo-allergic reactions.
Dose: 600 mg daily. Used occasionally in hyponatraemia due to overactivity of the antidiuretic hormone. (Ledermycin).
desferrioxamine A chelating agent that combines with iron salts to form a soluble non-toxic complex. Of great value in acute ferrous sulphate poisoning in children. Dose: 2 g immediately by i.m. injection, together with gastric lavage (2 g of desferrioxamine/1) followed by a single oral dose of 10 g. It may also be given by continuous i.v. infusion, 15 mg/kg hourly up to a maximum of 80 mg/kg. It may cause hypotension if the infusion is given too rapidly. It is also useful in the treatment of iron-overload caused by repeated blood transfusions, and for aluminium overload in patients On dialysis. (Desferal).
desflurane An inhalation anaesthetic
similar to CuflUrane. (Suprane).
desmopressin A derivative of vasopressin, with increased potency and longer
dexamethasone A potent synthetic corticosteroid, with reduced salt-retaining properties. Useful in all conditions requiring systemic corticosteroid therapy (except Addison’s disease), including inflammatory and allergic disorders, shock, cerebral oedema and adrenal hyperplasia.
Dose: 0.5-2 mg daily up to a MaXiMUM Of’ 15 mg daily; in shock, 5-20 mg by slow i.v. injection or infusion; in cerebral oedema, 10 ing initially by i.v. injection, followed by 4 mg i.m. 6-hourly. Dexamethasone is also given by infra-articular injection for local inflammation of joints in doses of
0.4-4 mg. It is also used as eye drops (0.1%)
in uveitis, but care is necessary with prolonged treatment as with some patients a ’steroid glaucoma’ may be precipitated. (Decadron). See page M and Table 36.
dexamphetamine sulphate A central nervous system stimulant. It is used in the treatment of narcolepsy and, paradoxically, it is sometimes useful in hyperkinesia in children.
Dose: in narcolepsy, 20-60 mg daily; in hyperkinesia 2.5 mg initially, slowly increased up to a maximunl’of 20 mg daily. Side-effects are insomnia, anorexia and agitation. Dependence and tolerance may occur early. (Dexedrine).
dextran A blood-plasma substitute
obtained from sucrose solutions by bacterial action, and used as solutions of varying molecular weight (dextran 40, 70). Dextran 70 is used as a blood volume expander by i.v. injection in some cases of shock; dextran 40 is used mainly to improve postoperative peripheral circulation, reduce blood viscosity, and to prevent thrombo-embolism. Care must be taken to adjust dose to avoid overloading the circulation. Any blood-matching should be carried out before giving dextran. (Gentran; Macrodex; Rheomacroclex).

A-Z Principal Drugs (co-fluampicil - cyproterone)

Wednesday, June 24th, 2009

co-fluampicil -tablets of flucloxacillin and ampicillin
co-flumactone Tablets of spironolactone and hydrochlorothiazide.
colchicine The alkaloid obtained from meadow saffron. It is used in acute gout. Dose: 500mg every 2 hours until relief is obtained. A total dose of 10mg should not be exceeded, but relief of pain or the onset of vomiting or diarrhoea usually renders full doses unnecessary. It is also used prophylactically in doses ol’500pg 2 or 3 times a day during early treatment with allopurinol, probericcid and sulphiripyrazone. Gire is necessary in the elderly, and in renal impairment. See page 140 and’I'able 17.
corticotrophin The adrenocorticotrophic hormone of the anterior pituitary gland. It stimulates the production of corticosteroid hormones by the adrenal cortex. It is now used mainly as a test of adrenocortical function. See tetracosactrin.
Hydrocortisone.
cortisone one of the corticosteroids secreted by the adrenal cortex. Although it is rapidly absorbed orally, it is inactive until converted in the liver to hydrocortisone. It therefore has the actions, uses and side-effects of hydrocortisone, which is often the preferred corticosteroid. It should be noted that cortisone is of no value for topical application. See hydrocortisone, page 250 and Table 36.
colestipol An exchange resin used in hyperlipidaemia that acts by binding with bile salts in the gut and preventing their reabsorption, and so indirectly lowers the plasma level of cholesterol.
Dose: 10-30g daily. May interfere with the absorption of many drugs. (Colostid). See page 146 and Table 20.
colfoseeril A pulmonary surfactant used in the respiratory distress syndrome of the new-born. (Exosurf). See beractant.
colistin An antibiotic used mainly for bowel sterilization.
Dose: 4.5-9 mega-units daily. In systemic gram-negative infections 2 mega-units 8-hourly by injection have been used, but less toxic antibiotics are now preferred. Colonlycin).
collodion When applied to the skin, it dries to form a flexible film, and is used as a vehicle for the extended local application of drugs such as salicylic acid.
co-phenotrope tablets of diphenoxylate
and atropine. (Lomotil; Tropergen).
co-prenozide Tablets of oxprenolol and cyclopenthiazide. (Trasidex).
co-proxamol Tablets  and paracetamol. (Distalgesic).
corticosteroids Hormones secreted by the cortex of the suprarenal gland. The principal hormone is hydrocortisone but more potent synthetic derivatives such as dexamethasone are also in use.
co-tenidone Tablets of atenolol and chlorthaliclone. (Tenoretic).
co-triamterzide Tablets of hydrochlorothiazide and triannerine. (Diazide).
co-trimoxazole A mixture of trimethoprini and sulpliaiiietlioxazole. Trimethoprim, like the sulphonamides, interferes with the folic acid cycle of bacterial metabolism, but at a different point, and the mixture has an increased antibacterial action. It was once widely used, but is now advised only for Prieunjocystis carinii pneumonia. Occasionally given in acute bronchitis and urinary infections when no other drug is acceptable.
Dose: 120 nig/kf; daily lot- 14 days; 960 ing 12-hourly by i.v. infusion. (Bactrin); Septrin).
coumarins Compounds that depress the formation in the liver of prothrombin and other blood coagulation factors. See warfarin and phenindione.
counter-irritants Substances, also referred to as rubifacients, that, when applied to the skin, produce a mild, local irritation and inflammation, and give symptomatic relief in painful conditions of the muscles and joints. Creams and liniments containing methyl salicylate, turpentine, capsicum resin and menthol are examples of rubifacients.
crisantaspase Asparagine is an aminoacid essential for the development of some malignant cells. Crisantaspase is an enzyme, also known as asparaginase, that breaks down asparagine, and so has an indirect cytotoxic action. It is used to induce remission in acute lymphoblastic leukaemia in children.
Dose: (after pre-treatment with other drugs): 1000 units/kg by slow i.v. injection daily for 10 days. Side-effects include anaphylactic reactions, and skin tests to detect hypersensitivity
are essential before initial and re-treatment. (Erwinase).
crotamiton An ascaricide and antipruritiL. Used by local application as cream or lotion (10%) in the treatment of scabies and itching conditions. (Eurax).
crystal violet A dyestuffwith a selective action against Gram-positive organisms and yeasts. Used as a 0.5% solution for infected skin conditions, and for skin
preparation.
cyanocobalamin The anti-anaemic factor present III liver. It is specific in the treatment of pernicious anaemia and its neurological complications, and of value in some other anaernias due to nutritional deficiencies.
Dose: in pernicious anaemia, I Ing by i.m. injection at monthly intervals. It has been largely replaced by hydroxocobalamin, which has a more prolonged action. (Cytanien). See page 112 and’I'able 3.
cyclizine An antihistamine, used mainly in I ravel sickness and nausea generally. Also useful in vertigo.
Dose: 100-150 mg daily. Side-effects include dryness of the mouth, headache and drowsiness. (%Ialoid).
cyclopenthiazide A thiazide diuretic with the actions, uses and side-effects of bend roll tiazide.
Dose: I mg initially, 250-500mg daily or on alternate days, in the morning, according to need. (Navidrex). See page 148 and Table 21.
cyclopentolate An anticholinergic agent use(] to produce cycloplegia and mydriasis. The action is more rapid and less prolonged than atropine, particularly in children. (Mydrilate).
cyclophosphamide A widely used alkylating
cytotoxic agent, active orally and by injec-
tion. Used in I lodgkin’s disease, chronic
lymphocytic leukaemia and lymphomas. Dose: 100-300 Ing daily, orally or i.v., or 300 mg-1 g weekly. A high fluid intake is necessary, as a metabolite may cause hacm- ( )rrhagic cystitis, and it is sometimes used with mesna to reduce the risk of such cystitis. Nausea and vomiting are common side-effects, as is epilation with high doses. (Endoxana). See page 122 and Table 8.
cyclopropane An inhalation anaesthetic of high potency with which induction and recovery are rapid. It causes some respiratory depression and cardiac irregularities, and its administration requires care. It is used with closed-circuit apparatus as it forms an explosive mixture with air and oxygen. Supplied in orange-coloured cylinders.
cycloserine An antibiotic used in
pulmonary tuberculosis when standard drugs are ineffective. Occasionally used in urinary infections.
Dose: 250-750 mg daily. Side-effects include drowsiness, vertigo and rash. See page 170 and Table 31.
cyclosporin An antibiotic with a powerful inuininosuppressant action. It is used under expert control to prevent graft rejection in organ and bone marrow transplantation, and in the prevention of graft-versus-host disease (GVI-ID). Prolonged therapy over some months may be required. Side-effects may include tremor, gastrointestinal disturbance, hypertrichosis and nephrotoxicity (Neural; Sandinimun).
cyproheptadine A compound with antihistamine and antiserotonin properties. Sonic allergic reactions are due not only to histamine, but also to serotonin, and cyproheptadine is useful in conditions not responding completely to an antihistamine. Dose: 4-20 ing daily. It has been used as an appetile stimulant in doses of 12 mg daily and in refractory migraine. (11criactin). See page 110 and Table 2.
cyproterone An anti-androgen used to reduce libido in sexual deviants. Dose: 50-100 nig daily. It is also used in the palliative treatment of prostatic carcinoma, particularly in advanced cases that have become resistant to other therapy. Dose: 300 mg daily.

A-Z Principal Drugs (Alprazolam - Aminophylline)

Tuesday, June 23rd, 2009

A-Z Principal Drugs (Alprazolam - Aminophylline)

alprazolam

A benzodiazepine used in the shors-term treatment of anxiety and anxiety with depression.
Dose: 0.75-3 mg daily. Side-effects include dizziness and ataxia. Care is necessary in pulmonary insufficiency. (Xanax). See page H 7 and Table 5.
alprostadil A preparation of prostaglandin li, for i.v. use in maintaining the patency of the ductus arteriosus in neonates with congenital heart lesions requiring surgical correction. The improvement in circulation so obtained permits diagnosis while surgery is being considered.
Dose: 50-100 ng/kg/min i.v. under strict control. Apnoea may occur, usually within an hour of the injection, requiring immediate ventilatory assistance. Bradycardia and hypotension may also occur. (Prostin VR).
alteplase A form of human plasminogen activator with a selective fibrinolytic action on blood-clot-bound plasminogen. It is of value in the early treatment (6 hours) of acute thrombosis, myocardial infarction and pulmonary embolism.
Dose: 10 mg initially by slow i.v. injection; then 90 mg over 3 hours by i.v. infusion. Side-effects are nausea, vomiting and local bleeding. (Actilyse). See streptokinase.
aluminium The powdered metal is used as a skin protective in ileostomy, as Baltimore paste, also known as Compound Aluminium Paste.
aluminium acetate An astringent used as an 8% solution for ear drops in otitis externs. A weak solution (0.65%) is used as a lotion in exudative eczematous states and in suppurative conditions.
aluminium chloride An antiperspirant used in the treatment of axillary hyperhydrosis by the local application of a 20% alcoholic solution. Over-use may cause skin irritation. (Anhydrol; Driclor).
aluminium hydroxide An antacid with a prolonged action.
Dose: as a gel, 7.4-15 ml, or as 500 mg tablets, to be chewed or crushed before swallowing. Best given between meals and at night. May interfere with the absorption of some other drugs. (Aludrox).
alverine An antispasmodic with a local action on intestinal smooth muscle.
Dose: used in irritable bowel syndrome in doses of 60-360 ing daily. (Spasmonal). See page 134 and “Cable 14.
amantadine An antiviral drug thought to act by inhibiting the penetration of the virus into the host cell, and used for the prophylaxis and treatment of influenza. It is also used with levodopa in the treatment of parkinsonism, but it may relieve the rigidity more than the tremor.
Dose: 200 mg daily. Many side-effects are dose-related. (Synimetrel). See page 160 and Table 26.
amethocaine Powerful local anaesthetic, used [or anaesthetic of mucous
membranes 1-2% solution, eve drops 0.25-1 %. As spray for throat before endoscopy, etc, a 0.5% solution may be used. Hypersensitivity and allergic reactions may occur as with other local anaesthetics. Also used as 1% cream for pruritus ,i nd other skin conditions.
amifostine An organic thiophosphoric acid used to reduce neut ropen ia -associated risks of infection after cyclophosphamide and platinum treatment of ovarian cancer. Dose: by i.v. infusion 910 mg/m: daily .10 minutes before chemotherapy.
I lypotension is a side-effect that may limit treatment. (Ethyol).
amikacin A semi-synthetic antibiotic similar in actions and uses to gentamicin, but more resistant to enzyme inactivation. Mainly used in the short-term treatment of serious infections due to Gram-negative, gen tain ici it -resistant organisms.
Dose: 15 ing/kg daily by i.m. injection or i.v. infusion, up to a total treatment dose of 15 g. Side-effects include ototoxicity, drug fever, rash and nausea. Dose should be reduced in renal impairment. (Amikin).
amiloride A potassium-conserving diuretic ,,uh an action on the distal tubule similar to that of spironolactone, although it is not an inhibitor of aldosterone. It is used in
hypertension and heart failure, often with a thiazide diuretic to obtain a more balanced response.
Dose: 5-20 ing daily. Rash is an occasional side effect. See page 148 and Table 2I.
amino acids Certain amino acids are essential for the formation of protein. When oral nutrition is not possible, amino acid preparations may be given by i.v. i ritusion. and such therapy call be extended if necessary to provide total parenteral nutrition by the addition of glucose, electrolytes, fats and vitamins as specially prepared solutions. [it hospitals, a 24-hour supply for total parenteral nutrition can be provided in a single large container and patients may be taught to administer total parenteral nutrition at home. Representative amino-acid products for i.v. infusion are Aminoplex, Perfusin, Synthamin and Varnin.
arninobenzoic acid An absorbent of some of Elie erythema-producing ultra-violet light waves of sunlight. it is present in sonic suit screen preparations.
aminoglutethimide An inhibitor of adrenal steroid and oestrogen biosynthesis. It is used in the control of post-menopausal oestrogen-dependent mammary carcinoma and in the treatment of advanced prostatic carcinoma.
Dose: 250 mg daily, increased, if necessary, to I g daily. Supplementary corticosteroid therapy is essential. Side-effects include drowsiness, rash and drug fever. (()j iineten). See page 122 and Table 8.
aminoglycosides A group of antibiotics that includes amikacin, gentamicin, netilmicin, lobramycin, kanamycin, streptomycin, neomycin and framycetin. They act mainly against Gram-negative bacilli, although they are also active against some Gram-positive organisms. Kanamycin and streptomycin are also active against Mycobacterhan tuberciaosis.'rhe aminoglycosides are not absorbed orally and when injected they are more toxic than most other antibiotics, and in renal impairment care is necessary, as the plasma concentration of the antibiotic may rise to an ototoxic or nephrotoxic level. The toxicity may also be increased by diuretics of the frusemide type. Measurement of plasma levels is essential in high dosage or continued therapy. Gentamicin is the most widely used aminoglycoside for systemic infections, and neomycin and framycetin, being too toxic for systemic use, are of value in skin infections.
may be given by slow i.v. injection. It is not suitable for Liu. administration. Sustained release oral products available cause less gastric disturbance. (Pecram; I'llyllocontin). See page 118 and 'rable 6.
amiodarone An iodine-containing anti-arrhythmic agent of value in all types of paroxysmal tachycardia, especially when the condition is resistant to other drugs. Dose: 600 ing daily for I week; maintenance (lose: 200 ing or less daily. When a rapid response is required, 5 mg/kg may be given by i.v. infusion under cardiac monitoring. it is contraindicated in bradycardia, pregnancy and thyroid disorders, and care is necessary in hepatic impairment. Pulmonary alveolitis, corneal microdeposits and photosensitivity have been reported as side-effects. (Cordarone).
amitriptyline A tricyclic antidepressant similar in action to imipramine, but it also has anxiolytic and sedative properties. Dose: in depression complicated by anxiety, 30-150 mg daily initially; maintenance dose: 20-100 mg daily; sometimes as a single nightly dose to reduce daytime sedation. Lower doses are often adequate in elderly patients. Dose by injection, 40-80 nig daily. Full benefit may not be achieved for some weeks and prolonged therapy may be necessary to avoid relapse. Withdrawal of the drug should be gradual. Atnitriptyline is also used in nocturnal eneuresis in children. Dose: 25-50 mg daily. Side-effects include dryness of the mouth, sedation and cardiac arrhythinias. It is contraindicated in glaucoma, prostatic hypertrophy and after recent myocardial infarction. Mcnti7o];Tryptizol). See page 128 and Table 11.
amlodipine A calcium channel blocking agent used in hypertension and myocardial ischaemia associated with angina.
Dose: 5-10 mg as a single daily (lose. Side-effects are headache, dizziness, flushing and oedema. Care is necessary in renal impair nient. (Istin). See page 148 and Table 21.
ammonium chloride
A mild expectorant present in Ammonia and Ipecacuanha Mixture.
aminophylline A derivative of theophylline with a similar bronchodilater action. It i,, used chiefly in asthma, cardiac oedema and congestive heart failure.
Dose: 300 nig-1.2g orally daily; 5 nig/kg

Accurate Diagnosis

Saturday, May 30th, 2009

The simplest and most certain test for any sensitivity reaction is to expose the person concerned to the substance under suspicion and see what happens. This is known as a

challenge test. With true allergies, challenge tests are powerful tools, but they are also alarmingly close to reality. The risk of provoking a severe reaction requires a very

cautious approach.
By comparison, an indirect test – a roundabout way of seeing how the body responds, such as the skin-prick test (see p. 91) – has the advantage of rarely producing dangerous

reactions. The downside is that indirect tests can be misleading, precisely because they are not like the real-life situation. No indirect test is perfect – there are always

false positives and false negatives (see box on p. 91).
Challenge tests
If you undergo a challenge test with food or an airborne allergen, you will also be given dummy challenges with an innocuous substance which is indistinguishable from the item

being tested. Neither you, nor the tester who is scoring the reaction, should know which is which. This is called a double-blind trial because, to eliminate all possible bias,

both of you are in the dark. (The full name is a ‘double-blind placebo-controlled trial’ – the dummy challenge is also called a ‘placebo challenge’ or ‘control challenge’.)
The double-blind trial is a standard medical procedure and does not imply that the doctors think you are faking symptoms. Psychological forces are powerful things, and just

thinking that you might react to a test can be enough to produce a reaction – the process that generates the symptoms is largely unconscious.
Food challenge
A food challenge – eating the food that is under suspicion – is a key test for food intolerance (see p. 197). It is sometimes used for food allergy and other forms of food

sensitivity too, as a follow-up to skin tests. Some allergists use a food challenge only if the skin test is at odds with actual events reported by the patient. Other allergists

use food challenge more readily, to confirm skin-test results, and to assess the severity of the reaction.
Extreme caution must be exercised with immediate food allergy, because of the considerable risks involved. The test must be done under medical supervision with resuscitation

equipment to hand. A challenge test should never be done for true food allergy without some careful preliminary tests on the face and the lips (see box on p. 23). Even if these

tests produce no reaction, only tiny amounts of the food should be eaten to begin with.
Bronchial challenge
This type of test involves inhalation of an airborne allergen – such as pollen – suspected of causing asthma. Bronchial challenge carries the risk of provoking a severe asthma

attack, and few doctors use it unless there are compelling reasons to do so – such as demonstrating that someone’s asthma is due to an allergen encountered at work.
Skin-prick tests
This is an indirect method of detecting true allergic reactions. It is one of a family of skin tests that use a similar approach. The three different tests in this family are

known as: skin-prick tests or prick tests, puncture tests, and scratch tests.
For the skin-prick test – the technique used in Britain – a small drop of liquid containing an allergen, such as grass pollen, is placed on the arm. The doctor makes a small

prick in the skin, under the drop of liquid, allowing a minuscule amount of the allergen to get into the skin. A positive reaction is recorded if a red bump develops soon

afterwards. For accuracy, the bump must be compared to positive and negative controls (see below).
The puncture method is very similar to the skin-prick test but uses a slightly different technique for breaking the skin. The term prick-puncture test covers both techniques.
With the scratch method, the skin is scratched lightly, and the allergen solution is then applied over the scratch. This method gives less consistent results than prick-puncture

testing.
It is important to include a negative control in the test – a skin-prick test with plain salt water (saline). This should not produce much of a bump – if it does, the skin is

clearly over-reactive and the tests more difficult to assess. The doctor should also include a positive control – a skin-prick test with histamine, the substance that plays a

central role in allergic reactions. This should always produce a bump. If it does not, the skin is decidedly under-reactive, and the tests are invalid.
Taking antihistamines will make the skin under-reactive, and you should stop taking them before the testing, for a period ranging from a day to several weeks – it varies

depending on the particular antihistamine. Ask your doctor for specific instructions about stopping these and other drugs before testing.
Skin tends to be over-reactive to testing in people with dermatographism (see p. 52). Blood tests for specific IgE,
such as RASTs (see p. 92), are needed for anyone who has this condition. Eczema sufferers with a rash over large areas of the body may also require blood tests, if there is too

little clear skin for testing.
Skin-prick tests can produce both false positives and false negatives (see box below). Some allergic diseases will give a lot of false negatives and relatively few false

positives, while for others the reverse is true. The allergen itself influences the rates of misleading reactions: for example, tests for soya allergy are notoriously

unreliable, whereas those for peanut are far more accurate. The age of the person being tested also makes a difference. With all these influences at work, interpreting the test

responses is a real art, and the doctor’s experience counts for a lot.
All sorts of people offer skin-prick tests, including alternative practitioners. Get them done by a qualified doctor, preferably by an allergist, who will know how to make sense

of the reactions.
Note that the purpose of these tests, and of blood tests for specific IgE, is to identify the allergens that are bringing on your symptoms, not to predict how strongly you will

react to those allergens. The tests may give some Indication of the intensity of your reaction, but they cannot be regarded as a good guide to how you will respond to the

allergen in the future.
The safety record of skin-prick tests is very good. Occasionally a systemic reaction (anaphylaxis) occurs with these tests, but there are no records of any deaths. Nevertheless,

if you suffer from severe asthma or have experienced anaphylactic shock in the past, it is advisable for the doctor to have adrenaline and resuscitation equipment available.

Those with strong allergic reactions to latex may also react badly if they are tested with an allergen that cross-reacts with latex (e.g. cypress pollen), not just when tested

with latex itself. Taking beta-Mockers (see box on p. 150) increases the risk of a life-threatening reaction for anyone in these higher-risk categories.
False positives and false negatives
Apart from challenge tests, none of the tests used for allergy works with 100% accuracy. Most give both false positives and false negatives.
A false positive means that there is a positive test but no actual reaction when the allergen is encountered (e.g. eaten or inhaled). A false negative means that there is a

negative test result despite a genuine reaction (as shown by a challenge test, for example).
A test that gives relatively few false positives has good positive predictive value – in other words, if it suggests you are allergic to something, you probably are.
A test that gives relatively few false negatives has good negative predictive value. If it comes up negative, you are probably not allergic to that allergen.
Some tests for allergic reactions show good positive predictive value but poor negative predictive value, while for other tests the reverse is true.

Allergy and Pregnancy

Tuesday, May 26th, 2009

Few newborns are already capable of mounting an allergic reaction to dust mite. Actual symptoms of allergy may not appear for several months or years, but the essential first

step – making the allergy antibody, IgE, against the mite allergens – seems to have occurred already for some babies.
In situations where IgE does the job it is supposed to do –protecting against worms and other parasites (see p. 13) – this advance programming of the immune system before birth

has definite advantages. A child whose mother is infected with parasites is born with the ability to make IgE against those parasites, even though he or she has had no direct

contact with them before birth. The baby’s immune system has been forewarned of the likely hazards of life in the outside world.
While this is obviously valuable in conditions where parasitic infections are rife, emerging into a carpeted and well-upholstered world with IgE against dust mite already in the

bloodstream is a serious disadvantage, because it can pave the way for rhinitis and asthma. Given the trouble caused by dust-mite allergen, some doctors think that women should

try to reduce their exposure to it during the second half of pregnancy, so that little or none reaches the unborn child. At present it is not known for sure if this can make a

difference to the risk of allergies developing in a child, but it seems plausible.
What is pretty clear, from several previous studies, is that the level of house-dust mite in the home immediately after birth can make a distinct difference as regards the

chance of allergy developing. Minimising a newborn baby’s exposure to dust mite is worthwhile, and the measures needed to achieve this are described on pp. 244-5.
Carrying out these measures will raise the level of dust-mite allergen in the air temporarily, so it makes sense to do the work in the early stages of pregnancy (or – even

better – before conception), rather than expose yourself and the foetus to a tremendous burst of allergen later on in pregnancy. Or, get someone else to do the work, and stay

away while it is done.
There may be other potential allergens which you should try to eliminate from your home before the baby arrives, such as mould allergens (see p. 122).
Pregnancy
First and foremost – don’t smoke while you are pregnant, or afterwards (see box on p. 107). Any other smokers in the household should smoke outdoors.
What about your diet during pregnancy? Certainly you should eat a good balanced diet with plenty of fruit and vegetables. Taking a small supplement of vitamin E, or eating

plenty of sunflower seeds and oil, would be a good idea. Women with a low
intake of vitamin E and antioxidants (see p. 206) during pregnancy run a higher risk of having an allergic child.
Should you also avoid any foods? Food allergens, such as those from cow’s milk, do reach the foetus, passed from the mother’s blood to the baby’s blood via the placenta. And a

few babies are born already capable of making IgE against food allergens. On the basis of these findings, some doctors have suggested that avoiding potentially allergenic foods

(such as eggs, cow’s milk and peanuts) during pregnancy might help to reduce the risk of food allergy. However, evidence from research trials in which pregnant women followed a

restricted diet, and their children were later studied for allergies, does not show any convincing benefit. And in some studies, the women on restricted diets have not gained as

much weight as they should, and the babies have been slightly below average weight at birth. Most doctors now think that dietary restrictions during pregnancy are not worthwhile

– it is more important to eat well and get enough nutrients.
It does seem sensible not to overeat any particular food during pregnancy, although there is no scientific evidence on this point (simply because researchers have not yet looked

for such evidence). In particular, don’t overdo it with milk and milk products. Make sure you get enough calcium, obviously, but don’t force yourself to drink huge amounts of

milk, especially if you have any distaste for it. Talk to your doctor, midwife or health visitor about the possibility of a calcium supplement, if you dislike milk.
Breast-feeding
‘The cornerstone of allergy prevention is breast-feeding,’ according to Dr Erika Isolauri of Tampere University Hospital in Finland.
At one time, this would have been a controversial statement, but there is now a substantial body of scientific evidence to support the ‘breast-is-best’ idea in relation to

allergy prevention. A number of different studies have shown that exclusive breast-feeding, up to at least four months of age, reduces the risk of developing food allergy or

atopic eczema (or both) in the early years of life.
Exclusive means exactly that – no solids at all until after four months (and six months is better), and no supplementary feeds with infant formula, which is made from cow’s

milk, and therefore contains cow’s milk allergens. Unfortunately, it is sometimes far from easy to ensure that formula feeds are not given just after birth, by well-intentioned

nurses on the maternity ward. Given what we now know about the immune system of the newborn, this is the worst possible time to be delivering an onslaught of potentially

allergenic cow’s milk proteins.
Quite apart from the immediate effect of introducing cow’s milk allergens to the baby, a bottle can disrupt the development of a good breast-feeding relationship between mother

and child, and may lead to the early abandonment of breast-feeding.
Why should this happen? Firstly a different technique is needed for sucking on a bottle teat, and your baby may never develop the knack with nipples if given bottles at an early

stage. Secondly, allaying the baby’s hunger with a bottle can also mean that he or she demands less at the next breast-feed – and since the mother’s milk supply is partly

influenced by the level of demand, this can be detrimental. Some experts believe that occasional bottle-feeds can start a downward spiral of ever-diminishing supply from the

mother.
Dr Arne Host of the Department of Paediatrics at Odense University Hospital in Denmark, who has made a special study of breast-feeding, recommends giving a little boiled water

as a supplement during the first 3-4 days of life, if the breast milk supply is inadequate. After that time, the mother’s own supply should increase to meet the needs of her

baby. Introducing bottle-feeds at an early stage can prevent this delicate balance of supply-anddemand from ever being achieved.
Sometimes (though this is rare) despite everything being done just right, a mother’s supply of milk never quite matches her infant’s appetite. When this happens, and the child

concerned is from an allergy-prone family, the breast milk should be supplemented with an ultra-safe formula feed called a hydrolysate (see box on p. 66).
Hydrolysates should also be used for infants at high risk of allergy who, for whatever reason, cannot be breast-fed. Note that there are two categories of hydrolysate –

extensively hydrolysed formula and partially hydrolysed formula. For the purposes of allergy prevention, an extensively hydrolysed formula should always be used because it has

the lowest risk of causing food allergies.
Preparing to breast-feed
Because breast-feeding is natural, many first-time mothers just assume it will come naturally. Sadly, it often doesn’t.
Cracked nipples are a major obstacle. They are the equivalent of chapped hands, and are often caused by the baby not having ‘latched on’ correctly to the nipple. Help from an

expert breast-feeding adviser, right from the start. can avoid this problem.
Because cracked nipples are so sore, breast-feeding can then become a major ordeal rather than a pleasurable experience as it should be. What is more, infectious bacteria can

enter the breast through the cracks in the skin, causing mastitis, which is painful and may require antibiotic treatment: this is not necessarily a good thing for the baby (see

p. 247).
You can minimise the chance of cracked nipples by making the skin on the nipples tougher and more resilient, so that it does
not crack. Start during pregnancy, in about your fourth month. When you have a bath or shower, rub your nipples vigorously with your flannel for a few minutes. After three weeks

of this, graduate to a soft toothbrush, and brush them gently, then more firmly when they feel ready. Progress to a medium, and then a hard toothbrush.
Breast-feeding support groups can be immensely helpful, when you start breast-feeding, or when you feel things are not going right. Some groups have local advisers. all mothers

themselves with first-hand experience of breast-feeding. Having such an adviser with you, watching you breast-feed your new baby and making suggestions, or pointing out where

you are going wrong, can make all the difference. Look for such a group locally, and establish contact with them well before your due date. You may be able to have an adviser

with you at the birth, to help the baby take his or her first feed: this is of enormous value.
Having prepared yourself, you then have to prepare the nursing staff in the hospital where you will give birth, for the fact that you want to breast-feed exclusively. That means

no supplementary feeds from the staff – not even one bottle. The risks of this practice, in sensitising vulnerable babies to cow’s milk, are still not widely known, so you may

need to be persistent and make your feelings very clear. Talk to your midwife about this well before your expected delivery date, and find out what policy the hospital has about

supplementary feeds. Then see the relevant staff at the hospital.
The nurses are most likely to give the baby a bottle because he or she is crying while you are asleep, and they don’t want to wake you. Staff change all the time, so you will

probably need to put a notice on the crib or cot, to be certain that the baby is never bottle-fed while you are sleeping. If this seems ‘over-the-top’, consider the experience

of British researchers investigating allergy prevention who wanted to ensure that a group of newborns were never given supplementary feeds. They put warning stickers on both the

babies’ cots and the mothers’ beds, as well as asking the midwives and mothers to be very vigilant. Despite this effort, several of the babies being studied were given bottles.
Sometimes nurses give a bottle because they believe that the baby is not getting enough milk from the breast. The idea that mothers “don’t have enough milk”, and that this is

quite a common problem, is part of the medical folklore of breastfeeding today. In fact, true milk insufficiency is very rare. Most cases of poor milk supply arise because a

good breastfeeding relationship between mother and child is never established – and supplementary bottle feeds are partly to blame.
It is entirely possible that your milk supply will not be quite adequate in the first few days, but it should increase rapidly. The best thing, if breast- milk supply is

inadequate, is to give boiled water as a supplement during the first 3-4 days of life (see left).
Some preliminary evidence suggests that mastitis may alter the profile of immune cells in the milk, and that this might possibly increase the risk of the child’s own immune

system becoming allergy-prone. A key preventive measure is not to let the breasts become engorged with milk: the build-up of milk can lead on to mastitis. Learning to express

milk (by hand or with a breast pump) will be useful for times when your breasts feel over-full. Talk to a breast-feeding adviser.
Diet during breast-feeding
Pretty much everything you eat works its way into breast milk, though in very tiny amounts.
The food molecules that get through into breast milk can certainly affect babies who are already sensitised to a food. Cow’s milk is the classic example — cow’s milk proteins

get into human milk if the mother consumes any milk, cheese, yoghurt or other milk products. Babies who have already been sensitised to cow’s milk (by a supplementary

bottle-feed, for example, or even in the womb — see p. 241) react badly to the breast milk, unless the mother avoids all dairy products.
What is less certain is whether the traces of allergen in breast milk — cow’s milk allergen or that from any other food — might be capable of starting off allergy or

sensitivity. Are these minute traces enough to sensitise babies with a strong tendency to allergy? If they are, then mothers of high-risk infants might be well advised to avoid

certain allergenic foods while breast-feeding. Some studies do suggest that there is a reduction in food allergy if breast-feeding mothers avoid cow’s milk, eggs, nuts, fish and

soya. But if this restrictive diet makes your life impossible, then it is better to breast-feed your baby and eat what you like, than not to breast-feed at all.
Unfortunately, some babies do get eczema, in spite of being exclusively breast-fed. If this happens with your child, there are a number of steps you can take to deal with the

problem (see box on p. 248).
Treating the gut flora
Taking a probiotic or bacterial replacer (see p. 205) during the later stages of pregnancy, and continuing with this while breast-feeding, may reduce the risk of atopic eczema

in your child.
Weaning — when and how
The key to reducing the allergy risk for babies is to turn that old political jibe ‘too little, too late’ on its head. Research shows that, with weaning, it is ‘too much, too

early’ that increases the chance of allergic reactions developing. Suddenly presenting an infant of three months with a wide variety of solid foods, including potent allergens

such as eggs, peanuts and fish, can increase the likelihood of food allergy and/or eczema developing. Weaning late, with a limited number of safe foods, should be your goal.
At least four months of exclusive breast-feeding, and preferably six months, is now the standard recommendation for allergy prevention, and it is well supported by scientific

evidence.
But how long should breast-feeding continue after weaning begins? There is little concrete evidence here, but there is a strong belief in the medical community that

breast-feeding should go on for several more months, up to or beyond one year of age if possible, allowing the weaning process to be very gradual. The idea is to introduce new

foods one at a time, alongside breast milk.
As well as allowing the baby’s immune system lots of time to adjust to each new food, prolonged breast-feeding may help in another way as well. Recent research shows that breast

milk contains a great many substances which influence the baby’s immune system, nudging it in the right direction — away from any tendency to allergies.
Avoid those expensive little jars of ready-made baby food. Most contain potent allergens such as cow’s milk, wheat or soya. Making your own baby foods is not difficult, and is

the best way to ensure that your child gets only low-risk foods.
Reducing the risk of peanut allergy
Peanut oil, which contains traces of peanut allergen, is an ingredient of some skin creams. Recent research from the United States shows that babies treated with such creams

were seven times more likely to develop peanut allergy later. In the past, concern has focused on traces of peanut allergen that the baby swallows — either in the breast milk

(because the mother has eaten peanuts) or from her nipple cream. What this new research suggests is that peanut allergens absorbed through the baby’s skin are much
more likely to cause sensitisation. Don’t use any skin products if they have ‘Arachis oil’ or ‘Arachis hypogaea’ in the ingredients list — and steer clear of any cream without a

detailed ingredients list. In the same research study, soy formula also emerged as a risk factor: feeding a baby on this doubled the chance of peanut allergy developing later.

Good health is one of the most important things we can give our kids,’ says Martha, now in her sixties with two grown-up children.
`When I see how bad my daughter’s asthma is, and how hard her life is sometimes because of it, I do feel bad about the fact that I smoked when I was pregnant. But we just didn’t

know in those days. Even my doctor smoked. No one thought anything of it.
`I stopped when she was little, because it seemed to me that her wheezing got worse whenever I lit up. I’m sure that stopping then was better than nothing. It must have helped.
`In any case, there’s no point feeling guilty about things now - that won’t change anything. But if I’d known what damage it could do, I would have stopped sooner.’ Martha’s

regrets stem from the discoveries made in the past decade about the effects of smoking on allergies. We now know that smoking during pregnancy increases the amount of IgE (the

allergy antibody) in the blood of a newborn baby - an indication that he or she is at an increased risk of developing allergies. After the birth, exposing a child to cigarette

smoke continues to encourage high levels of IgE in the blood, as well as irritating the airways and making asthma more likely to develop.
The research on smoking is just one part of a worldwide research effort, during the past 20-30 years, into the possible causes of the allergy epidemic. That research can help

parents who are themselves atopic (allergy-prone) to reduce the risk of passing their allergy problems on to their children.
Who should be implementing these preventive measures? Firstly, any prospective parents who have allergies themselves, or had them as children. They are at higher risk (compared

to a non-allergic parent) of producing a child who is susceptible to allergies. The risk is especially high if both parents have or have had them at some point in their lives.
Secondly, these preventive measures could be worthwhile for parents who don’t have allergies themselves, but who come from atopic families (families with a tendency to allergy).

If you or your partner have brothers, sisters or parents with allergies, you are more likely than the average person to produce allergic children.
Finally, if you already have one allergic child - even though you and your partner don’t have allergies yourselves, and no one else in the family does - there is a

higher-than-average chance that subsequent children will have allergies. Your allergic child is a sign that the genes for allergy are there.
Given the important role that genes play in allergy (see p. 8), preventive strategies make a lot of sense for parents-to-be with allergies in the family.
Unfortunately, this is a topic which often generates confusion - some people assume that if a trait is genetic, it will inevitably come out in the child, and that nothing can be

done to prevent this happening. Although that is true for some inherited traits, such as metabolic abnormalities (see upper box on p. 75), it is not at all the case for allergy.
Developing allergic disease is not inevitable unless a child has a very big dose of the genes that favour allergy. Only a few children - generally those whose mother and father

are both badly affected by allergies - will come into this category. Even with these very high-risk children, following the measures described here will probably help to reduce

the severity of their allergic problems.
For most children at risk of allergies, even though they have some pro-allergy genes, there has to be an unfavourable environment to actually produce allergic disease.

‘Environment’ here means everything external that affects the child, including diet, air quality, allergens, diseases and medical treatment. Factors occurring before birth, such

as the mother’s lifestyle during pregnancy, are also part of the child’s environment. It is the interplay between genes and environment that will decide whether your child

develops allergies or escapes them.
This interaction is not a simple one, however, and different aspects of the environment operate in different ways. Firstly, there are some environmental factors that work at the

most fundamental level -conspiring with the pro-allergy genes to make the overall tendency to allergy far stronger. These are factors such as cigarette smoking by the mother

during pregnancy, or excessive hygiene during childhood, which influence the fundamental make-up of the child’s immune system. Secondly, there are environmental factors, such as

early exposure to house-dust mite or grass pollen, which can cause trouble by provoking specific allergic reactions. Note that factors like these will not become important

unless the allergic tendency is already there.
Efforts to reduce the risk of allergy operate on both types of factor.
On the one hand, there are measures such as quitting smoking or easing up on hygiene, which tackle the allergic predisposition itself. These measures are, in effect, trying to

make a Western child’s immune system more like the immune system of a child from a poor rural village in the developing world, whose chance of developing allergy is very low

indeed.
On the other hand, there are measures such as reducing dust-mite levels, that try to stop the development of particular allergic reactions.
Obviously, if measures of the first kind could be truly successful, there would be little or no need for measures of the second kind. But this kind of success is very difficult

to achieve in modern Western society. Although we can certainly improve matters a great deal, and lessen the tendency to allergy, the conditions that would completely reverse it

are beyond our reach at present. So both kinds of preventive measure remain necessary.
In reading the pages that follow, it is important to keep things in perspective, and not feel excessively anxious about your child. Do what you can, but don’t feel guilty if you

can’t manage everything that is suggested here. And if you already have a child with allergies, please don’t feel guilty about things that might have contributed to this. Only

hindsight is perfect, and you no doubt did the best you could, given the information you had at the time, and the many other constraints and difficulties that you faced. That is

the best that any of us can do.

Protecting Children Having Allergies

Tuesday, May 26th, 2009

No single factor lies behind the allergy epidemic — the causes are many and various (see p. 20). What this means for parents interested in allergy prevention is that there is no

single measure which will ensure that your children do not develop allergies. Instead there are a great many different things that can be done, each of which reduces the risk to

some extent. The more of these you do, the lower the risk becomes.
Avoiding allergens
Starting before the birth is best, if you want to reduce allergen exposure for your child (see p. 240). But if you have missed the boat with that one, don’t despair – there is

still a lot to be gained by reducing allergen exposure at a later stage.
If you are ridding your home of allergens after the child’s birth, bear in mind that things will get worse before they get better– there will be a temporary surge in airborne

allergen as a result of the clean-up operation, and you will need to protect the child from this. The best strategy is for the child to be away for a few days while the work is

done, especially if you are taking out carpets, furniture or mattresses. Remember to protect yourself as well, if you are allergy-prone (see p. 109).
One of the most important steps you can take to reduce allergen levels is improve the natural ventilation of your home. This lowers the humidity (assuming you don’t live in an

extremely humid climate), which helps combat both moulds and dust mites. Ventilation also flushes out allergens in the air, especially cat, dog and mould allergens. Half the

problem with modern houses is that the airtight seals around doors and windows, introduced to conserve heat and save energy, turn the indoor air into a rich stew of allergens

and irritants.
House-dust mite
Avoiding high levels of house-dust mite in the home is one of the most valuable things you can do to reduce the risk of allergies in your child. Not only is house-dust mite a

powerful allergen in its own right, it may also act as an agent provocateur as far as the immune system is concerned (see p. 12), and may help to initiate allergic reactions to

other potential allergens – such as those from pets or indoor moulds.
Even if you do nothing else to protect your new baby from mite allergen, at least buy a new mattress and pillow for the cot, with ready-fitted allergen-proof covers. Do the same

for the portable crib, if you have one. Choose anti-mite products that are designed for babies and are guaranteed safe – there is a risk of suffocation with some loose covers

sold for older children and adults (see p. 245).
You may want to eliminate house-dust mite from your own bed as well as the baby’s, because there will probably be times when you take the baby into bed with you for a feed or a

cuddle – and times when, as a toddler, he or she just barges in! It is good to know that your child is still breathing air free from dust-mite allergen in these circumstances.
Deal with your own bed as soon as you can. Some doctors believe that lowering your exposure to dust mite during pregnancy may reduce the risk of sensitising your baby before

birth (see p. 241).
When taking anti-mite measures with your own bed, make sure that there is no risk of suffocation to the baby from the allergen-proof materials used. Microporous membranes based

on plastic could, if sucked onto the baby’s face during sleep, cause suffocation. Loose covers on duvets are worrying in this respect. Buy a new duvet with a built-in

allergen-proof cover, for preference, or a duvet that can be laundered at 60°C or above.
All the other measures for combating dust mites, described on pp. 114-17, will help to protect your child. Buy a good anti-allergen vacuum cleaner if you possibly can, and keep

your baby out of the room while vacuuming if you can’t (open the windows too). Make sure the baby only has new soft toys, preferably washable ones (see p. 116).
It is also an excellent idea to reduce dust-mite levels in the carpets and soft furnishings (see p. 117), because children tend to have very close contact with these in their

early years. A crawling baby, motoring enthusiastically around the sitting room floor, is stirring up the stockpile of dust-mite allergen that is found in any carpet, and

inhaling it in full measure. An adult walking around the same room has a far lower exposure, because dust-mite allergen, being relatively heavy, stays near the ground.
The best option is to go for non-carpet flooring, which doesn’t encourage dust mites. Parents tend to worry about the hardness of this, for a baby or toddler. In fact babies are

far more robust than we generally believe, and a hard floor is no problem for a small child who has never known the luxury of carpeting.
If you really hate the idea of your baby having anything other than carpet to play on, the next best option is to get new carpet, so that you start with zero dust mites. You

must then prevent dust-mite numbers from building up too much, by means of good ventilation, or with the use of a powerful dehumidifier (see p. 117).
Although the first year is the most vulnerable time for your baby, you mustn’t let your guard drop too much as time passes. The moment when a toddler moves from a cot to a ‘big

bed’ is sometimes the beginning of allergy symptoms because, after carefully protecting their child from dust mites in infancy, parents then put him or her into a bed with a

used mattress. This sudden exposure to a high dose of
dust-mite allergen can be the start of asthma. Get a new mattress if you can, and put allergen-proof covers on it. Alternatively, put allergen-proof covers on the existing

mattress.
Moulds
Mould spores are another potent allergen, and you should avoid bringing up a vulnerable child in a damp house if you can, because moulds will be growing there in abundance. Some

new research suggests that heavy exposure to mould allergens in childhood makes allergies in general much more likely. Even in a house that is not obviously damp, it is a good

plan to reduce indoor humidity (see p. 119). Carpets and furnishings that are full of mould spores (see p. 122) should be replaced.
Pets
What about pet allergens – should you find another home for your cat or dog when you are expecting a baby? This is a difficult question because the latest research shows that

pets are a double-edged sword as far as allergies are concerned.
A baby with allergic tendencies who is born into a house with a resident cat or dog is more likely to show allergic reactions to cats or dogs some years later. On the other

hand, there is research showing that having a pet in the house reduces the risk of allergies overall, especially for a child with no brothers or sisters. This is probably

because the pet boosts household levels of endotoxin (see p. 21), and generally makes the environment less hygienic for the child, fulfilling the same anti-allergy role as

brothers and sisters would in the early life of a child (see p. 246).
If you are planning to give your child the kind of grubby childhood that seems to protect against allergy (see p. 246), the additional protection provided by a pet is probably

unnecessary. Or, you could view your pet as having both pros and cons, and decide to keep it, while implementing all the other anti-allergy measures described here. If you do

this, ensure that the house is well ventilated (so pet allergens don’t build up to very high levels) and keep the pet out of the child’s bedroom so that he or she is not

breathing huge amounts of pet allergen while asleep. You could also wash the pet regularly (see p. 125) to reduce allergen levels.
If your child begins to show any signs of allergy to the pet, you must then find it another home.
Avoiding irritants
As well as increasing ventilation and eliminating cigarette smoke from the home completely, it may be worth evicting certain specific items that produce irritant gases.
The main ones are:
•    gas cookers (if you can’t afford to switch to an electric cooker, at least improve the ventilation in your kitchen as much as possible)
•    easy-clean plastic wall coverings and flooring
•    materials such as chipboard and MDF, which give off formaldehyde.
The evidence regarding the possible role of these in increasing the risk of allergies and asthma is described on pp. 128-9. In addition, although there is no evidence on this

point, common sense would suggest getting rid of any plastic or lacquered items that have a powerful smell.
Generally speaking, although traffic pollution can act as an irritant, it seems to play a lesser role in causing allergies and asthma than most people imagine. However, it may

sometimes play a part, especially if there are high levels of diesel fumes in the air (see p. 131).
Infections - friend or foe?
A large group of Italian military cadets were recently studied by doctors interested in the causes of allergy. By taking blood samples and testing them for antibodies to common

infections, the doctors could see what diseases the men had been exposed to early in life. At the same time, the young conscripts were assessed for allergies.
Allergies were least frequent among the young men with antibodies against three common infections that are dispersed via food and faeces – Hepatitis A, Toxoplasma gondii and

Helicobacter pylori. Only one in twelve of the cadets in this group had allergies.
Among the men with no antibodies against any of these infections, the rate of allergy was nearly three times as high – one in five of these cadets had allergies.
The doctors who carried out this experiment believe that these three infections are not necessarily important in themselves, but that they identify individuals who were ‘reared

in an environment that provides a higher exposure to many other orofecal or foodborne microbes’. In other words, they grew up in the kind of household where washing your hands

before meals wasn’t considered too important.
This study adds to the growing body of evidence (see p. 21) which shows that an over-clean environment during childhood encourages the development of an allergic disposition.
Those with lower rates of allergy include:
•    children raised on farms with livestock. The more exposure the children have to farm animals, the less the likelihood of them developing allergies.
•    children from homes with high levels of bacterial endotoxin in the household dust (see p. 21)
•    children who have fewer baths, and wash their hands less often (see p. 21)
•    children with brothers and sisters, especially those with older siblings. Some of the protection here may be due to the impact of the mother’s hormones and immune system

on the foetus in the womb: these effects change with successive pregnancies. But close contact with older siblings, and thus exposure to more microbes, probably plays a part.
•    children who go into kindergarten, nursery school or day care with other children at an early age – this is only valuable for children without brothers and sisters
•    children with pets at home – the benefits are much more pronounced for children without brothers and sisters.
The Italian study is especially important because, for the first time, it gives detailed information about the kinds of infections that make a difference in allergy prevention.

The military cadets were also checked for antibodies to measles, mumps, rubella, chickenpox and herpes. None of these infections gives protection against allergies – only

infections carried in food and faeces do.
Exactly what practical use you make of these discoveries is up to you. For most of us, the importance of hygiene was so firmly instilled during our own childhood that it is

quite hard to suddenly become more relaxed about it. But do let your children play in the garden, if you have one, and don’t worry so much about how dirty they get. Encourage

them to do some gardening – medical researchers believe that harmless bacteria in the soil may be particularly important in educating the immune system away from allergies (see

p. 21). Let them play with pets, as long as the animals are not carrying harmful parasitic worms (talk to your vet about whether pets should be treated for parasites). Ease up

or, hand-washing and, if this is your first baby, make sure he or she plays with other children as early in life as possible.
A few chest infections do seem to increase the risk of asthma, notably Respiratory Syncytial Virus (RSV). If this Infects babies, it provokes an IgE-reaction (see box on p. 12)

which may encourage the development of allergies. Unfortunately, there is very little you can do to protect your child from this common virus, but it makes sense not to take the

baby to a hospital for unnecessary trips (visiting relatives, for example) because RSV infections are often picked up in hospital.
Taking care with antibiotics
The possible role of antibiotics in making allergies more likely to develop is an exceedingly controversial topic. Before making any practical decisions in this respect, you

must consult your doctor. Never go against your doctor’s advice, if he or she thinks that antibiotics are necessary.
Several different studies have now produced evidence of a link between antibiotic use before the age of one or two, and the later development of allergies, asthma or both. The

best of these studies was carried out by doctors in Oxford, who followed 1900 children up to the age of sixteen. Among children at risk of allergy (because their mothers had

allergies) taking antibiotics before the age of two was linked with an increase in the rate of allergy from 32% to 54%. The more courses of antibiotics a child received, the

greater the risk.
The type of infection for which the drugs were prescribed was not important, as far as the risk of allergy was concerned, but the type of antibiotic did make a difference.

Broad-spectrum antibiotics, which kill a wide range of bacteria, were more risky –suggesting that the depletion of friendly bacteria in the gut (see p. 204) could be responsible

for increasing the allergy risk. Penicillins seemed less likely to promote allergies than erythromycin or cephalosporins.
This research is not widely known, as yet. And because there is a widespread assumption that giving an antibiotic can do no harm, even if it is unnecessary, antibiotics are

sometimes prescribed when they serve no purpose. In particular, antibiotics are often given for virus infections, especially in childhood, despite the fact that antibiotics are

of no value whatever against viruses. Research shows that doctors are sometimes responding to pressure from anxious parents when they prescribe antibiotics – it is difficult for

some parents to accept that a virus infection cannot easily be treated and just has to ‘run its course’. (Although there are drugs that combat viruses, these are expensive and

produce unpleasant side effects – they are reserved for very serious virus infections such as hepatitis.)
Obviously. when a child needs antibiotics to deal with a serious infection there can be no question about giving them. This is why you should always follow your doctor’s advice.

But it is also worth asking the doctor the following questions before giving antibiotics to your child:
•    are you sure that this is a bacterial infection, and not a virus infection?
•    would it be possible to do tests and check that it is a bacterial infection, before prescribing antibiotics?
•    what is the chance of the child overcoming the infection without antibiotics?
•    would it be dangerous to wait and see if the infection clears up naturally?
Vaccination
The same Oxford research team that investigated antibiotics (see left) also looked at the question of vaccination and allergy. They found a link between vaccination for

pertussis (whooping cough) and increases in asthma, eczema and hayfever. However the increases were not large, and a study from Sweden found that whooping cough vaccination did

not have any effect on rates of allergy and asthma. And researchers in Ethiopia have found that whooping cough vaccination actually reduces the risk of allergy in their country.
This is clearly a complex issue. The contradictory results from different parts of the world suggest that the ‘big picture’ is what counts here – the overall combination of

childhood infections, antibiotic treatment and exposure to harmless bacteria such as those in the soil or from animals. Depending on this big picture, vaccination against

whooping cough may push the allergy risk one way or the other.
There are many other arguments both for and against vaccination and, given our current state of ignorance about the possible effect on allergy, these other considerations are

probably more relevant. Discuss the matter in detail with your doctor before making a decision.

Doctors in Japan recently tried a very simple experiment in allergy prevention. They chose babies suffering from atopic eczema who were allergic to foods, but not allergic to

house-dust mite. Dividing the babies into two groups, the doctors put special allergen-proof covers, designed to protect against house-dust mite (see p. 115), on the mattresses

of all the babies in the first group. Babies in the second group were given ordinary cotton covers.
When the babies were one year old, they were tested again for allergy to house-dust mite. Two out of three children in the second group now gave a positive skin test to

house-dust mite.
By comparison, only one in three of the children from the first group gave a positive skin test. In other words, using the anti-allergy covers for these high-risk children had

cut by half the number who developed an allergic reaction to dust mite.
As this experiment shows, even if a child has already developed allergies, it is not too late to bring protective measures into play. Indeed, an allergy problem in infancy, such

as atopic eczema, can be seen as a warning sign to parents, telling them that they should reduce the child’s exposure to allergens as much as possible.
As well as reducing dust-mite levels, you should minimise your child’s exposure to moulds at home by limiting indoor humidity (see p. 119) and cleaning up any existing mould

growth (see pp. 122-3). This will lessen the chance of mould allergy developing.
Try to avoid staying, even temporarily, in any house that is damp or has old carpets and mattresses. When you are moving house, or carrying out any kind of renovation work,

remember that this will stir up a lot of dust-mite and mould allergens. Protect your child by arranging for a stay away from home.
This pro-active approach should not just apply to airborne
allergens, but also to food, in the opinion of some experts. They
suggest that any child with a true allergy to cow’s milk or egg
should not be given peanuts, tree nuts, fish or shellfish until three
years of age, to avoid sensitisation to these potent food allergens.
Pets are a more difficult issue, with both pros and cons as
regards allergy-prone children (see p. 245). If you decide to keep
your cat or dog, always ventilate the house well, and wash the animal regularly if you can (see p. 125). Be alert for your child developing an allergic reaction to your pet –

don’t turn a blind eye to the symptoms, as parents sometimes do because they are reluctant to accept that the child has become allergic to the family’s much-loved pet. If your

child does develop an allergy to the pet, the best option is to find the animal another home as quickly as possible (see p. 124).
Breast-fed babies with atopic eczema
Although breast-feeding is a good way of protecting children against atopic eczema, it is no guarantee. Sometimes babies become sensitised to food, in spite of being breast-fed,

and then they may react to traces of that same food, eaten by the mother and coming through in her breast milk.
Skin-prick tests (see p. 91) may help to identify the foods responsible for the eczema. Otherwise, a simple elimination diet by the mother, as used for colic (see p. 203), may

pinpoint the offending food. Keeping that food out of the mother’s diet will often clear the baby’s eczema.
Sometimes a breast-fed child’s eczema remains severe, despite the elimination of suspect foods from the mother’s diet. In this case, what should be done? New research from Or

Erika Isolauri – a staunch advocate of breast-feeding – suggests that the best option at this point is to stop breast-feeding promptly. Her research team found that breast-fed

children with persistent eczema had a slower growth rate. If these babies are switched to hypoallergenic formula – either an extensively hydrolysed formula or an artificial

amino-acid formula (see box on p.66) – their eczema symptoms usually subside, and their growth picks up.
Is vaccination safe for those with allergies?
The influenza vaccine and a few others (e.g. yellow fever) are grown in eggs and are not usually given to people with egg allergy. Measles vaccine is grown in cells taken from

eggs and may contain a minute trace of egg allergen, but only those who are extremely sensitive will react: there should be resuscitation equipment available for children who

have had anaphylactic reactions to egg and for those with severe asthma as well as egg allergy. Some vaccines come in vials with latex seals that are designed to be pierced by

the needle of the syringe. A different method should be used for latex-allergic patients. Smallpox vaccine (for bio-terrorism threats) is dangerous for children with atopic

eczema.
Never too late?
The role of modern ultra-clean lifestyles in promoting allergies is now well established (see p. 21). If your child already has allergies, it may seem as if these discoveries

have come too late to help —but that is not the case. Some research suggests that the battle for supremacy between Th1 and Th2 cells (see p. 11) — the unseen power struggle

which decides whether a child will be allergy-prone — is not really settled until some time between the ages of five and seven years. So there is still some potential for

intervening right up to this age. Some studies have suggested that the immune system can be pushed away from an allergic disposition at an even later age, right into adulthood,

by exposure to endotoxin, a bacterial product found around livestock and in `lived-in’ homes.
Several research groups are working on vaccination strategies (for example, using extracts of soil bacteria) that might also be able to achieve this. The initial results are

promising and they suggest that these vaccines can even help adults with allergies. Unfortunately, such treatments will not be available for many years. In the meantime, you can

probably reduce your child’s chance of developing new allergies, and perhaps make the existing ones less severe, by easing up on hygiene (see p. 246).
Fresh air and exercise
With the boom in watching TV and videos, and playing on computer games, some modern children hardly go outdoors at all. As far as allergies and asthma are concerned, there are

two big disadvantages to being a juvenile couch potato. For a start, the couch is also home to dust mites in their millions, and secondly the child is not running about and

using his or her lungs to the full. Airways that are never stretched (because the child never gets out of breath) lose their youthful flexibility in time. Once this has

happened, the airways can never be stretched to their full capacity. Some doctors believe that this may make asthma more likely to develop, or help to make it more severe once

it has developed. Inactivity also encourages obesity, which increases the risk of asthma developing.
Getting outside and running around, or engaging in other vigorous exercise, should be encouraged for any child with allergies. Obviously, you should balance this against the

need to protect the child from pollution peaks and (if your child has hayfever) pollen peaks. Children with exercise-induced asthma should use their reliever inhalers to allow

them to take exercise (see p. 41).
Keep the air at home free from irritants such as nitrogen dioxide (see p. 128), formaldehyde, air fresheners, paint, polish and strong-smelling cleaning fluids. These may

encourage new allergies to develop, and can make existing asthma worse.
Medical treatments
Antihistamines may have a preventive role in very young children with allergies. A study of one- to two-year-olds with atopic eczema found that the antihistamine cetirizine,

taken daily for 18 months, halved the chances of the children developing asthma later.
The children who benefited in this study were those with several risk factors for becoming asthmatic. They had moderate to severe atopic eczema, at least one close relative with

allergies, and allergic sensitisation to pollen or house-dust mite, as shown by skin-prick tests (see p. 91).
The cetirizine was taken at fairly low doses and had no bad effects on the children in this study. What is more, it seemed to benefit their skin as well as reducing the risk of

asthma: those taking the drug had less need of high-strength steroid creams. There is some controversy about the validity of these results, so few children with atopic eczema

are receiving antihistamines at present.
No one yet knows if other antihistamines might have the same effect as claimed for cetirizine. Ketotifen, which is an atypical antihistamine (see p. 159), may do so.
Immunotherapy may also have a protective effect. One study, involving children suffering from nasal allergies, found that those given immunotherapy were less likely to develop

asthma (see p. 165). Another study shows that immunotherapy for children with mite allergy halves the risk of their developing new allergic reactions to other allergens.

Allergy: Avoiding Milk and Lactose

Tuesday, May 26th, 2009

Avoiding Milk and Lactose
Fruit lassi
There are two quite distinct reasons for avoiding milk: either to avoid milk proteins or to avoid

lactose, the sugar found in milk. It is important not to confuse these two because the details of the

avoidance diet required are different. Only a few people need to avoid both milk proteins and lactose.
Diarrhoea and wind in response to drinking milk, but few other symptoms, usually indicates a reaction

to lactose — but a reaction to milk proteins could be an alternative explanation. If it is a reaction

to lactose, this may be due to either primary lactase deficiency or secondary lactase deficiency — your

doctor can order tests to make an exact diagnosis (see p. 79). Note that a bout of diarrhoea, however

caused, often produces a temporary lactose intolerance (secondary lactase deficiency).
Any symptoms other than (or in addition to) diarrhoea and wind strongly suggest a reaction to milk

proteins. This might be a true allergy, another type of immune reaction to milk (see pp. 72-3), or an

idiopathic intolerance reaction (see pp. 76-7). In theory, skin tests should identify true allergic

reactions to milk proteins. Unfortunately, skin tests are not infallible, and it is possible to have a

genuine allergy or other immune reaction to milk proteins, but give negative skin tests. This is

especially common with babies (see p. 65 and p. 69). There are no accurate tests that can confirm

intolerance reactions to milk proteins.
It is possible to have sensitivity to both milk proteins and lactose.
If tests do not give you a definitive answer, you may have to try both types of diet and see which one

works. Remember that lactose intolerance may be only temporary.
Avoiding milk proteins
If you have a sensitivity reaction to cow’s milk proteins, then you need to avoid:
•    milk and all milk-based drinks, including lactose-reduced milk (if you need to avoid lactose as

well, drops and tablets to reduce lactose — see Using lactase replacers, p. 183 — are safe and could be

used with a tolerated milk, e.g. goat’s milk)
•    cream, yoghurt, creme fraiche
•    all kinds of cheese, cottage cheese and cream cheese (some people may be able to tolerate

Norwegian brown cheese, called Gjetost, which is made with milk whey)
•    white sauce, bechamel sauce and other creamy sauces
•    custard, rice pudding and other milk-based puddings
•    almost all home-made cakes, biscuits, cookies, pancakes and pastry
•    some bread, rolls, waffles
•    almost all chocolate
•    casein, casemate, and lactalbumin in packaged foods (see p. 173); you may be able to tolerate

whey but experiment cautiously.
Unless your sensitivity is fairly mild, you will also need to avoid:
•    butter, except clarified butter (ghee)
•    most kinds of margarine (they generally contain milk derivatives, but
some are milk-free — health-food shops are a good source of these).
As long as you do not have a severe allergy to milk, you should be able to tolerate clarified butter.

Make this by melting butter over a low heat, pouring it into a glass jar, and leaving it to cool in the

refrigerator. The milk proteins will settle to the bottom, and be visible as whitish granules — only

eat the clear butter above this level.
Alternatively, put olive oil into a wide-necked container and place in the freezer. It will solidify,

and can be used as a spread in place of butter.
A few of those with cow’s-milk allergy can tolerate sheep’s milk, and possibly (but less commonly)

goat’s milk. However, most people must avoid these as well. (There are also rare individuals who are

allergic to goat’s and sheep’s milk but not to cow’s milk.) Ass’s milk, if you can get it, is tolerated

by most with cow’s-milk allergy. There are many substitutes for cow’s milk now available, such as soya

milk, almond milk, rice milk and hazelnut milk. Try a health-food shop for these. All can be used in

place of ordinary milk when cooking.
Margarine or clarified butter can be used in recipes that call for butter. Soya yoghurt and cream make

reasonable substitutes for ordinary yoghurt and cream.
Avoiding lactose
If you have lactose intolerance, you must avoid:
•    milk and all milk-based drinks, unless lactose-reduced
•    cream, creme fraiche
•    most kinds of yoghurt, especially mild yoghurt. A very strong, acidic yoghurt may contain

little lactose. The bacteria that make yoghurt turn lactose into lactic acid, so the more acidic it is,

the less lactose it contains.
•    cottage cheese and Norwegian brown cheese, or Gjetost. Other kinds of cheese are usually so low

in lactose that they are tolerated. Only those people with extreme lactose intolerance need to avoid

all cheeses.
•    white and bechamel sauce, custard, rice and other milk-based puddings
•    almost all home-made cakes, since milk is generally used for baking. Items cooked with butter

but not milk, such as biscuits, cookies and pastry, are usually tolerated, as is butter itself, and all

margarine.
•    lactose in medicines. Lactose powder is used in many tablets and capsules, just to bulk out the

drugs. The amount used can be sufficient to evoke symptoms in some people with lactase deficiency.

Certain asthma inhalers also contain lactose (see p. 162), and a small amount may be swallowed. The

lactose from inhalers will affect you only if you have severe lactase deficiency.
Soya-based products, and all other nut- or grain-based milk substitutes, are lactose-free. Sheep’s

milk, goat’s milk and other animal milks (including human breast milk) all contain lactose.
Using lactase replacers
Many people with lactose intolerance are able to eat a more varied diet by using lactase replacers.

These provide a temporary supply of the missing enzyme, lactase (see p. 79), which helps out by

digesting the lactose in milky foods. Lactase replacers must be taken at the same time as the milky

food, and are only effective for that one meal. The more lactose there is in the meal or snack, the

more of the lactase replacer you need – trial and error is the only way of working out how much you

need for a particular food. There are a number of different brands of lactase replacer now available,

and it is worth trying out several. Some people find that they are sensitive to an added ingredient in

some brands. Sources of lactase replacers include health-food shops and specialist suppliers – these

can be located through the Internet (see p. 255).
Savoury white sauce
Savoury white sauce is the base of many dishes. Here the flavour of the wine and stock goes well with

chicken, vegetables or fish.
PREPARATION TIME: 7-8 minutes MAKES: approx. 600ml (1 pint)
50g (13/4oz) milk-free baking margarine 50g (1314oz) plain flour
200ml (7fl oz) dry cider or dry white wine 400ml (14f1 oz) vegetable or chicken stock 1 bay leaf, salt

and pepper
Melt the margarine in a small saucepan and stir in the flour. Cook, stirring, over a low heat for
1 minute then stir in the cider or wine, followed by the stock. Add the bay leaf and simmer, stirring

occasionally, for 5 minutes until thickened. Season to taste.
Variations. add approx. 6 tbsp finely chopped herbs, e.g. parsley, chives, tarragon or chervil; or add

English or French mustard; or add lemon juice.
Sweet white sauce
PREPARATION TIME: 5 minutes MAKES: approx. 300ml (’/?pint)
2 tbsp cornflour
25g (1 oz) caster sugar
300ml (V2 pint) apple or white grape juice 4 tbsp soya cream
25g (1oz) milk-free margarine
In a saucepan, mix the cornflour and sugar with a little of the juice to give a smooth paste then

gradually stir in the rest of the juice and bring to a simmer over a low heat. Simmer for 1-2 minutes

until thickened, stirring all the time. Finally, add the soya cream and margarine.
Variations: melt in 1008 (3-/2oz) or more of milk-free chocolate; or add rum or brandy to taste; or add

4-6 pieces finely chopped stem ginger together with 1-2 tbsp of their syrup.
Pancakes
Soya milk has a slightly thicker consistency than cow’s milk and therefore more is used in this pancake

recipe than would be needed in a traditional one.
PREPARATION TIME: 25 minutes MAKES: approx. 16 small pancakes
150g (5V2oz) plain flour, sieved 2 large eggs
pinch salt
450ml (16f1 oz) soya milk
oil or milk-free margarine for frying To serve:
lemon juice and caster sugar or golden syrup
Combine the flour, eggs, salt and soya milk in a liquidiser until smooth. Alternatively place the

flour, eggs and salt in a bowl and slowly whisk in the soya milk to form a thin batter.
Heat approx.1 tsp oil or margarine in an 18cm (7in) non-stick frying pan and swirl until hot. Pour in

sufficient batter to just cover the base of the pan and cook until golden. Turn and cook on the other

side until golden.
Serve with lemon juice and caster sugar or with golden syrup.
Apple and frangipane tart
An alternative to a milk-based custard tart. The combination of apple and almond is delicious. Serve

freshly baked. It can also be eaten cold, but if possible, warm it a
little before serving.
PREPARATION TIME: 30 minutes COOKING TIME: 1-11/4 hours MAKES: 8 servings
Pastry:
175g (6oz) plain flour, sieved
1008 (3 V2oz) milk-free baking margarine, softened
25g (1 oz) caster sugar
Filling:
50g (13/4oz) milk-free sunflower margarine 1008 (3112oz) ground almonds
100g (3112oz) plus 1 tbsp caster sugar 2 egg yolks
2 tbsp dark rum, brandy or orange juice 2 large dessert apples
4 tbsp apricot jam
Work the flour, margarine and sugar together with 1 tbsp cold water to make a soft dough. Roll out and

use to line a deep 20cm (8in) fluted flan tin. Chill this while you prepare the filling.
Preheat the oven to 190′C/375′F/gas mark 5. Beat together the margarine, ground almonds, 100g (3Y2oz)

caster sugar, egg yolks and rum. Peel, core and roughly chop one apple and stir into the mixture.

Spread this in the pastry case. Core and thinly slice the remaining apple and arrange the slices on

top. Sprinkle with the remaining sugar and bake for 1-1′/’4 hours until risen and golden. Cool slightly

then brush the surface with the apricot jam (warm this gently in a saucepan first).
Coconut rice pudding with mango
This pudding is based on a Thai recipe. The rice pudding will become thicker the longer it cooks and

also as it cools. Make sure the mango is ripe.
COOKING TIME: 30-40 minutes MAKES: 6 servings
175g (6oz) pudding rice, rinsed 50-75g (131-2314oz) sugar
1 litre (13/4 pints) carton rice milk 400ml (14f1 oz) coconut milk To serve:
1 extra-large ripe mango, peeled and diced
toasted coconut shreds
Place the rice in a large saucepan with 50g (13/4oz) of the sugar and the rice milk and coconut milk.

Bring to a simmer, stirring. Simmer gently for 30-40 minutes, stirring occasionally, until the rice is

cooked and the milk absorbed. Add the extra sugar if wished. Serve warm or cold, topped with mango and

toasted coconut.
Baked strawberry creams with strawberry sauce
The riper the strawberries the better, to give intensity to both the creams and the sauce.
PREPARATION TIME: 30 minutes COOKING TIME: 20-25 minutes MAKES: 6
1008 (3112oz) caster sugar
4 tbsp Muscat wine
1 tsp lemon juice
350g (12oz) strawberries, hulled and sliced
4 large eggs, beaten Sauce:
225g (Boz) strawberries, hulled and chopped
2 tbsp icing sugar 2 tbsp Muscat wine To serve:
a few whole strawberries
Preheat the oven to 1 70′C/325′F/gas mark 3. Set six 1 50ml (Y4 pint) ramekins in a small roasting tin.

If you plan to unmould the creams, oil the ramekins lightly.
Place the sugar, wine, lemon juice and strawberries in a saucepan and heat gently to dissolve the

sugar. Bring to the boil and cook, uncovered, for 5 minutes. Cool slightly then puree in a liquidiser

and whisk into the beaten eggs. Pass through a sieve then pour into the ramekin dishes.
Pour hot water from a kettle around the ramekins and cook in the centre of the oven for 20-25 minutes

until lightly set.
Remove the dishes from the tin and allow to cool. Chill, if wished.
Combine all the sauce ingredients and liquidise until smooth. Pass through a fine sieve.
Serve the creams in the ramekins with a little sauce poured on top and decorated with a whole

strawberry, or carefully unmould, pour a little sauce over, then decorate with a whole strawberry.
Variation: oil the ramekins. Dissolve 100g (31/2oz) caster sugar in 4 tbsp water in a small saucepan

over gentle heat, then cook to a rich caramel without stirring. Pour a little caramel into each oiled

ramekin then continue as above. Pour the wine for the sauce into the pan used to make the caramel and

warm gently to dissolve any leftover caramel, then continue with the sauce as above.
Frozen vanilla dessert
This is a cross between a sorbet and an ice cream.
PREPARATION TIME: 30 minutes, plus freezing MAKES: 4-6 servings
1 vanilla pod, split
150g (51/2oz) caster sugar 500g carton soya yoghurt
Place the vanilla pod and sugar in a saucepan with 300ml (1/2 pint) water. Dissolve over gentle heat

then bring to a simmer and simmer for 20 minutes. Leave to cool then remove the pod, scraping all the

seeds from it and returning them to the syrup. Beat in the soya yoghurt and freeze.
You will get the best texture by using an ice-cream machine. Alternatively, freeze in a plastic

container then remove from the freezer and beat the mixture well until smooth (you can do this in a

food processor). Return to the freezer. Repeat this process once or twice.
Baked strawberry cream with strawberry sauce
Variations: add 100g (31/2oz) melted plain chocolate; or add 2 tbsp instant espresso coffee dissolved

in 2 tbsp hot water. Alternatively, dissolve 100g (3/2oz) caster sugar over a gentle heat in a small

saucepan until it turns to a rich caramel; then add 100g (31/2oz) unblanched almonds and stir with a

metal spoon until they start to pop. Transfer to an oiled tray and leave to set. Crush roughly and add

to the basic mixture.
Fruit lassi
This refreshing Indian drink can also be made with frozen fruit, in which case don’t use iced water –

cold will do.
PREPARATION TIME: 10 minutes
MAKES: approx. 1.35 litres (21/4 pints)
500g carton soya yoghurt
50-75g (1314-231aoz) sugar
225g (8oz) berries such as raspberries, strawberries, blackberries or blueberries or the equivalent

weight of chopped fruit such as mango, peach or papaya
600ml (1 pint) iced water
Place all the ingredients in a liquidiser and blend until smooth.
Frozen vanilla desert
Banana and strawberry shake
A special treat for a child who cannot have milk.
PREPARATION TIME: 5 minutes MAKES: 600ml (I pint)
2 large, very ripe bananas
150g (5112oz) strawberries
1112 tbsp olive oil
a little nutmeg or other spice, if liked 200ml (7fl oz) water
Peel the bananas and roughly chop the fruit. Combine all the ingredients in a blender until very

smooth. Serve immediately, or cover tightly and store in the refrigerator.
Variations: use a nectarine or a skinned peach instead of strawberries; use coconut milk (available in

tins) instead of olive oil, and the flesh of a small mango, or half a large mango, instead of

strawberries.

Alternative Ways of Allergy Treatment

Sunday, May 24th, 2009

When Leonard Noon reported his first tentative experiments with immunotherapy for hayfever, in 1911 (see p. 164), he believed that pollen contained a toxin. Most people were

‘immune’ to this toxin, he said, in the same way that people might be immune to measles or diphtheria, but hayfever sufferers lacked this immunity. Noon thought that his

steadily increasing doses of pollen, injected just under the skin, were inducing immunity to the pollen toxin, in the same way that a smallpox vaccine could induce immunity to

smallpox.
Noon’s theory was all wrong, as we now know, but the important thing was that the treatment seemed to work. In fact it transformed the lives of some patients, especially those

who were very severely affected by hayfever. One spoke of a ‘marvellous cure’, another of going for walks to kick my old enemy the hay’.
So doctors kept using Noon’s treatment, and in time — when it became clear that Noon’s theory was flawed — medical researchers began trying to figure out how the injections

really worked.
Surprisingly, they have still not succeeded, even though a great deal is now known about the changes that can occur in people undergoing immunotherapy. Despite a wealth of

detailed knowledge (see p. 166), it remains impossible to say exactly how conventional immunotherapy reduces allergic reactions. Surprising discoveries about the effects of

conventional immunotherapy are being made all the time.
New methods of immunotherapy are still being devised today, and there are three different approaches being taken.
Firstly, there are doctors experimenting with modifications of the technique devised by Noon. For example, instead of injecting the allergen extract, some doctors are giving it

to their patients in capsule form. to be swallowed. Others are giving it as a liquid, to be placed under the tongue and held there for a few minutes, then swallowed (see p.

169). Sound scientific trials show that both these methods work well, at least with some allergens.
There are also experiments with speeded-up immunotherapy
(see p. 166), called ultrarush techniques — at the outset, injections are given at hourly intervals, or even more frequently (in hospital, of course, where severe reactions can

be dealt with immediately). Doctors have found that they can induce a remarkably rapid tolerance of the allergen in this way.
The second approach is to apply modern medical knowledge about allergic reactions and so develop entirely new methods of immunotherapy (see p. 168-9). Such research involves

working out, from first principles, novel ways of modifying the immune response in general, or the reaction to one allergen in particular.
This theory-led approach is certainly successful for classical allergies such as hayfever and perennial allergic rhinitis, where there is a good understanding of the basic

mechanism (i.e. the malfunctions of the immune system that produce the disease). But for those diseases where the underlying mechanism is only partially understood, such as

atopic eczema, this approach is not necessarily the best one. And for diseases such as food intolerance, where the cause of the illness remains largely unknown, it is a complete

non-starter.
The third type of approach is to devise a technique by trial and error, and then puzzle out the ‘how’ question later. This is the same sort of path as Noon originally took, and

some believe that this kind of pragmatic experimental approach — practising a method which seems to be effective, even though it’s a mystery how it works — is as valid now as it

was in 1911. Others disagree.
210 complementary therapies The two most widely used methods that have been developed in this way are Provocation-Neutralisation and Enzyme- Potentiated Desensitisation.

Although these techniques are practised by doctors with a conventional medical training, they remain ‘outside the pale’ as far as orthodox medicine is concerned. The

controversies that surround them are discussed below.
Enzyme- Potentiated Desensitisation (EPD)
This technique has been developed by a British doctor, Dr Len McEwen, who began work on it in the 1960s. It is now practised in many parts of the world, as well as Britain,

including the United States, Germany and Italy.
EPD is used for a far wider range of problems than conventional immunotherapy, being given to people with food intolerance and chemical intolerance, as well as to those with

true allergies. This — along with the fact that it is unclear how it works —contributes to the controversies that surround it, because these conditions do not have the same

basic causes.
Dr McEwen began with the observation that, when immune cells are aroused during inflammation — whether caused by allergy or some other stimulus — they release large amounts of

an enzyme called beta-glucuronidase. This enzyme increases the immune response to the allergen or antigen that provoked the inflammation.
Dr McEwen experimented with injecting beta-glucuronidase into the skin, along with very small amounts of allergen, believing that in such circumstances the enzyme might have the

opposite effect, and reduce the immune reaction to the allergen. Eventually he discovered a combination of enzyme and allergen which seemed to have the desired effect.
EPD has been tested, in a rigorous scientific manner, and the results suggest that it can work for hayfever and asthma, as well as for childhood migraine and hyperactivity in

children when these are triggered by foods.
In one trial with hayfever patients, researchers measured the levels of anti-pollen IgE following EPD treatment, and it did not rise during the pollen season as it normally does

in those with hayfever. This kind of finding is impressive because it is unlikely to be due to placebo effect. Not all studies have produced positive results, however.
In addition, doctors using EPD claim that it is very effective for patients with allergies who have not done well on the standard course of immunotherapy injections (see p.

164). This fits in with other studies suggesting that the immune changes brought about by EPD are fundamentally different from those induced by traditional immunotherapy.
Patients with true food allergy have been given EPD, and while it does not enable them to eat their culprit food, it does
seem to reduce their reaction to accidental exposures.
Doctors in the Netherlands are using EPD as a treatment for people with Chronic Fatigue Syndrome (CFS), and report that it helps about 50% of patients.
One point in favour of EPD is that it uses very small amounts of allergen, and is therefore very safe — anaphylaxis has never occurred with this technique.
Provocation-Neutralisation
‘After following conventional methods [of immunotherapy] for thirteen years, I heard Carleton H. Lee deliver a paper on provocative testing in 1965, at a meeting of the American

College of Allergists in Chicago. I was naturally sceptical, but tried his suggestions when I returned to my office. The results can only be described as astounding. Many

patients with unresolved allergic problems responded markedly and rapidly. Many with resistant asthma or perennial allergic rhinitis improved greatly or cleared completely when

food injection therapy was added to their inhalant injection therapy.’ So wrote Dr Joseph B. Miller — a distinguished allergist and paediatrician, and a Professor of Medicine at

the University of Alabama, in 1972.
The technique which he learned from Carleton H. Lee was controversial then and, although Miller developed it with great care and precision during the years that followed, it

remains controversial now.
There are two elements in provocation - neutralisation: testing and treatment. Both are used for a wide range of problems — not just classical allergic diseases, but also food

intolerance and chemical intolerance. As with EPD (see left), this is one of the controversial aspects of the technique.
Although provocation-neutralisation involves an injection technique that looks, superficially, very much like conventional immunotherapy (see p. 164), there are several

important differences. Firstly, the allergen extract used (in the case of true allergies) is a very dilute extract, so that far less of the allergen is injected than in

conventional immunotherapy. Likewise, in the case of food intolerance and chemical intolerance, the extracts of the offending substance are used in highly dilute form.
Secondly, the idea of the neutralising dose — which is the central plank of provocation-neutralisation — is quite different from anything in conventional immunotherapy. Broadly

speaking, the conventional technique (see pp. 165-6) works by slowly reeducating the immune system with a gradually increasing dose of the allergen. Only after a succession of

injections does the immune system start to behave differently on encountering the allergen. By contrast, in provocation-neutralisation treatment, the neutralising dose is

claimed to have an instantaneous and direct effect on the body, ‘turning off’ symptoms that have already begun. This is the neutralisation aspect of the technique. The doctors

who practise this technique do not claim to know how the neutralising dose might work.
According to the theory of provocation-neutralisation, the strength of the extract that acts as a neutralising dose is specific for a particular allergen and a particular

person. It can only be worked out by a rather slow procedure involving a series of injections. These are intradermal injections – they place the allergen extract in the skin, at

a slightly deeper level than a skin-prick test. (For treatment, rather than testing, subcutaneous injections are used – these go deeper than intradermal injections, placing the

allergen extract just underneath the skin. Neither hurts very much.)
Ideally, the neutralising dose should be decided on by measuring the size of the wheal (a raised area of skin around the injection site), and whether it grows, stays the same

size, or disappears. The doctor or nurse carrying out the procedure can, in theory, work out the neutralising dose just by careful examination of the skin wheals.
However, it is part of the tradition of provocation-neutralisation techniques that verbal feedback from the patient is also taken into account – so if the patient says that an

injection has turned off the symptoms, that reinforces the belief that the neutralising dose has been found.
The problem with this aspect of provocation-neutralisation is that expectations, and the power of suggestion, can become involved. So if the doctor or nurse says ‘you may find

that this next injection makes the symptoms go away’, that is often exactly what happens – because the forces of placebo effect (see p. 233) come into play. Unfortunately,

verbal interactions such as this are a key aspect of the provocation-neutralisation procedure in many clinics.
Just the same hazard besets provocation - neutralisation if it is used to test for the existence of allergy or intolerance, because it is quite common for practitioners to tell

patients which allergen (or other offending substance) is being injected and to ask if any symptoms are provoked by the injection. This is not good practice – if someone expects

to react to a particular substance, they are quite likely to produce symptoms through purely psychological mechanisms (see pp. 232-3).
Quite apart from this, the question of allergy testing with provocation-neutralisation techniques is contentious, because the pioneers of the technique, such as Professor

Miller, never advocated using provocation - neutralisation in this way. Using it as a routine test for sensitivity reactions was a later development, and there are many doctors

today who, while they practise provocation-neutralisation as a treatment, say that it does not work well as a test for sensitivity reactions. While they agree that injecting a

dose
which is either stronger or weaker than the neutralising dose may provoke actual symptoms (this is the provocation aspect of the technique) they don’t think the reaction is

reliable enough to form the basis of a test for allergies. Nor do they think that using skin-wheal measurements alone (i.e. silent testing) turns the technique into an accurate

test for allergies. That is not what the provocation-neutralisation technique was designed for – it is about treatment, not testing.
The evidence from research
Recent research from the Nova Scotia Environmental Health Centre in Canada confirms that testing by provocation injections is not reliable. The subjects in this study were all

suffering fr= multiple chemical intolerance, a condition which – for one reasor or another – makes patients liable to develop symptoms at an,, time. No less than 70% of these

patients experienced symptoms in response to a dummy injection which contained none of the offending substance. Indeed, 15% of patients also produced a skin wheal in response to

some of the dummy injections, confirming that even this reaction may be subject to the power of suggestion (see pp. 232-3).
Looking just at the patients who did not react to the placebo injection (i.e. those least susceptible to suggestion) the test still did not yield any reliable result – a person

might react to one injection with a particular substance, but fail to react to a subsequent injection with the same substance. The authors concluded that their patients were ‘in

a state of heightened sensitivity as the result of the chronic irritation by various environmental components and other external and internal stressors’. In this state of

sensitivity. patients are so close to the brink all the time that the smallest thing can trigger symptoms. So the apparent reactions to the test injections were actually

determined by other factors – some psychological factors (including a psychological response to the prick of the needle) and some external ones, such as exposure to smells or

very small amounts of airborne chemicals.
Another recent research study, carried out by scientists at the University of California, confirmed the finding of the Nova Scotia team as regards testing. Although this study

did not set out to look at the use of the neutralising dose for treatment, some of the patients were given neutralising doses during the testing process and the researchers

observed that ‘in most cases a single neutralising injection relieved the symptoms’. This casual observation clearly needs to be confirmed by more rigorous testing. Oddly

enough, despite this positive observation about the neutralising doses, the overall conclusion of the researchers was to completely dismiss all aspects of

provocation-neutralisation as ‘the result of suggestion and chance’. This conclusion has been widely publicised in the United States as part of a general campaign against

provocation-neutralisation and doctors who practise it.
Other researchers have looked at treatment with neutralising doses, using stringent scientific methods (a double-blind placebo-controlled trial — see p. 90), and found that they

do work. In one such trial, patients with asthma. and allergies to dogs or cats, were treated with injections of the neutralising dose. They showed a reduction in the

sensitivity of their airways, as measured by objective tests. In another experiment, patients with perennial allergic rhinitis and an allergy to house-dust mite were studied,

and the neutralising dose was given as drops of allergen extract placed under the tongue (sublingual drops) – an alternative to injections. The blockage of the nose, as measured

by scientific tests, was reduced by the neutralising dose.
A great many more trials of this kind would be required to convince most doctors that provocation-neutralisation works.
Furthermore, the recent study from California – which observed a number of practitioners of provocation-neutralisation at work with their patients — showed that these

practitioners need to be a lot more rigorous and objective in their approach. However, the fact that provocation-neutralisation is often practised badly does not necessarily

mean that the basic technique is without any value. There are a great many level-headed doctors and patients who, while initially very sceptical about

provocation-neutralisation, have found it surprisingly effective – just as Professor Miller did back in 1965.
Deciding for yourself
So is provocation-neutralisation an option that is worth trying for your condition?
As regards testing, the answer is probably ‘no’. The most reliable tests are skin-prick tests or FAST blood tests for true allergies (see pp. 91-2), an elimination diet for food

intolerance (see p. 194), and avoidance followed by re-exposure (a challenge test) for chemical intolerance.
As regards treatment for true allergies, conventional immunotherapy has been far more thoroughly tested and, if you can get it (not easy in Britain — see p. 164), is probably a

better bet. It is definitely the best treatment for allergy to insect stings.
The major advantage that provocation-neutralisation has over conventional immunotherapy, in the case of true allergies, is that it is far safer. Because such small amounts of

allergen are used, anaphylactic reactions (see p. 58) don’t occur.
When it comes to treatment for food intolerance, complete avoidance of the problem food(s), for a period of a year or two, is usually a very effective treatment (see p. 77).

Other forms of treatment are only needed for people who find that they have
intolerance to a great many different foods (on the basis of an elimination diet, not kinesiology, blood tests and the like — see p. 93) and cannot devise an adequate diet from

the foods they are able to eat. For such people, provocation-neutralisation may be worth a try. Many patients feel that they have gained considerable help from this treatment.

They report suffering fewer symptoms and being able to return to a more nutritionally balanced diet.
In the case of chemical intolerance, the first line of treatment should be to avoid the substances concerned as far as possible, eat a good balanced diet, and take a vitamin and

mineral supplement if nutritional deficiencies are suspected. Treating any underlying hyperventilation (see pp. 226-9) can also help considerably. Only if there are persistent

symptoms, and you are sure these are not due to psychological causes, might provocation-neutralisation be worth a try. Some people with chemical intolerance do find it is

helpful, but whether this is a real effect, or simply placebo, remains uncertain.
If you decide to give provocation-neutralisation a try, find a practitioner who has good medical qualifications, who seems objective and sensible in their approach, and who

doesn’t make implausible claims for the technique. Take note of what other treatments the practitioner offers, and whether these seem rational or not – this is often a good

guide to the care and objectivity with which provocation - neutralisation is carried out.
Ask the doctor how he or she assesses the neutralising dose. and avoid anyone who does not use the traditional method of a series of injections combined with wheal measurement.

When the neutralising dose is being assessed, say that you would like it to be done ’single-blind’ – that is, you don’t want to be told anything about what is being injected.

Reporting how you feel to the doctor or nurse during the assessment is fine, but only mention really significant symptoms, or a very definite clearance of the symptoms, if this

occurs. These precautions will help you to be sure that you are getting something which is of genuine benefit, rather than just a very expensive form of placebo treatment.
I always wanted to be a doctor, and I enjoyed
medical school immensely, but once I became a
ell GP, I no longer felt quite so sure about what I was doing. It seemed clear to me that there were a lot of people coming to my surgery who I couldn’t do much for. And there

were others who, while I could treat their obvious medical problems with some success, remained distressed and were not coping well with life. Once I became a senior partner in

this practice, I experimented with having a counsellor come in for one session a week, and then an osteopath for the bad backs. It was popular with the patients, and I saw some

people improve enormously. Now we have stress-management classes too, and one of my colleagues has trained in acupuncture, which he uses for selected patients. We also use

elimination diets for patients with a lot of long-term problems like migraine. Overall, I think of it in terms of having more tools at our disposal - being able to tackle things

from a different angle when standard medicine isn’t hitting the spot.’
Geoffrey, a GP in the north of England, is typical of the reconciliation that is now beginning to occur between conventional medicine and alternative medicine. But he also has

plenty of criticisms to make of the alternative scene. ‘The idea that alternative medicine is “holistic” while conventional medicine isn’t, really raises my hackles. Most GPs

could be magnificently holistic if they had an hour with each patient as alternative therapists usually do. We have just 15 minutes, on average, and we have to pack a lot into

that - including our basic duty to eliminate the possibility of serious organic disease such as cancer. Time pressure is everything now, and it has squeezed the humanity out of

medicine, to a very large extent. But the potential for a holistic approach is there - most doctors have a tremendous store of wisdom and life
experience at their disposal, which could form the basis of a holistic approach to treatment if only there were more time to spend with each patient.’
It is in search of a more unhurried and all-embracing approach to treatment that many people turn to alternative medicine. Frequently, what they get out of the therapy has less

to do with the actual methods used, and still less with the theories behind those methods, but everything to do with spending a quiet hour with someone supportive and caring who

listens to all the complex concerns that surround any illness, gives reassurance or advice, or just offers a `safe space’ in which to talk about life’s difficulties.
Other people turn to alternative therapies due to a more serious disillusionment with orthodox medicine. When patients with inscrutable medical problems -such as persistent

unexplained diarrhoea, joint pain or chronic urticaria - are given a succession of different diagnoses by different doctors, they often lose faith entirely in modern medicine

and reject orthodox treatment in favour of alternatives. This is a great mistake. Modern medicine isn’t perfect, but that is only to be expected, because it is not a fixed body

of knowledge but a process - a continuing journey of questioning, investigation, discovery and improvement. Scientific medicine has come a tremendously long way from the state

of ignorance that prevailed two centuries ago, and it will undoubtedly go farther.
Conventional medicine has a great deal going for it - ask anyone over 50, with severe life-long asthma, what they think of treatment now compared to treatment in the 1950s or

early 1960s. You will hear a hymn of praise to the improvements in both drugs and drug delivery systems. Asthma is just one example -conventional medicine has a lot to offer for

all the classical allergic diseases. Alternative medicine should always be regarded as an adjunct to conventional treatment, not a replacement. That is why many doctors prefer

the term complementary medicine.
A third reason for using alternative medicine is a more philosophical one, a need to understand illness in some larger sense, often part of a general search for meaning in life.

Some types of alternative treatment attempt to offer metaphysical reasons for allergy -rather than the mundane explanations of antibodies and immune cells that are given in this

book - and this can be attractive to some people. There is no harm in this approach, which can prompt you to make a critical review of your life, look at unresolved emotional

issues, or reassess choices that are making you unhappy.
But not all illness, or worsening symptoms, can be explained by emotional causes, and the rigid belief that every illness must have a meaning can be damaging. It easily

degenerates into the wholesale psychologisation of illness, the kind of blame-the-victim mentality which can attribute hayfever to ‘Emotional congestion; fear of the calendar; a

belief in persecution; guilt’ and asthma in babies to ‘Fear of life; not wanting to be here’. Both these diagnoses are taken from the best-selling You
can Heal your Life by Louise Hay, which is very influential among some alternative therapists. This compulsive psychologisation of illness can be profoundly damaging, and if

your complementary therapist is preoccupied by ideas of this kind, you could find yourself on a very long guilt trip indeed.
Apart from the psychological aspects of alternative medicine, there is the question of whether it actually works in a practical sense - whether it provides more than just

emotional support and placebo effect (the benefit that comes from any treatment which you believe in). This is always the central question for scientific medicine in relation to

its own treatments,
and conventional doctors naturally apply the same criteria to alternative medicine. Most of this chapter is concerned with trying to answer that question.
Unfortunately, there are so many different kinds of alternative therapy available today that it is impossible to cover all of them in this book. To complicate matters further,

many complementary therapists now practise two or more different techniques, mixing them to
produce their own unique cocktail of diagnosis and treatment. This eclectic approach can span a remarkable range - you may find a therapist doing distinctly whacky stuff such as

iridology (looking at the eye to diagnose all illness - it has been tested and definitely doesn’t work), combined with something perfectly rational such as an elimination diet.

(The elimination diet might be presented as a ‘detox diet’, but it is actually being used to detect food intolerances.)
With new forms of therapy springing up all over the place, a healthy scepticism is a distinct asset for the consumer. Be sceptical about any diagnostic test or treatment that is

only being practised by one person in the country, or in the world - when doctors hit on something that works, they want other doctors to try it out. World exclusives in

medicine are usually suspect.
Avoid any practitioner who tells you to stop using your drugs without your doctor’s consent. Likewise, avoid those with a messianic gleam in their eye, an evident disregard for

logic or reasonable discussion, or an amazing cure that fixes everything from acne to AIDS. Very few of those who sell bogus cures and phoney diagnostic tests are complete

rogues. Most are nice people who are quite genuinely convinced that they have indeed found the answer to people’s problems. The powers of placebo effect (see p. 233) can sustain

such a conviction for a very long time.

Allergens and Irritants at Work

Sunday, May 24th, 2009

Allergens and irritants at work
Some workplaces have very high concentrations of allergens in the air, especially if proper safety procedures are not being followed. Occupational allergies can begin with symptoms in the nose, such as sneezing, blockage or constant streaming (allergic rhinitis). You may also suffer with itchy or watery eyes (conjunctivitis), a cough, sweating and a feverish feeling. Alternatively, direct contact with the allergen can produce a skin rash (dermatitis) or itchiness and swelling (contact urticaria/nettle rash and angioedema).
If you work somewhere with an allergy risk (see pp. 133-4), be vigilant for such symptoms and see your doctor immediately. These symptoms can be the forerunners of occupational asthma, which is a serious and potentially irreversible problem. Some allergens, such as latex, can even produce anaphylactic shock (a life-threatening allergic collapse).
Skin-prick tests (see p. 91) can show if you have an allergy to a substance encountered at work.
Acting promptly gives you the best possible chance of recovery and is vital if you have occupational asthma. Only if exposure to the allergen stops promptly do you have a good chance of shaking off the asthma. See your doctor as soon as possible and ask for a referral to a chest specialist, so that a definite diagnosis can be made. This is essential if you are going to make a claim for compensation.
Far too many people with occupational asthma are just sent off with an inhaler when they first see their doctor. By delaying the moment when work is identified as the source of the problem, and the exposure to the allergen is stopped, drug treatment can turn occupational asthma into a disabling lifelong problem. Although drugs can be helpful in speeding your recovery once exposure to the allergen
Latex allergy
Sensitisation to latex usually occurs at work (see pp. 133-4), or as a result of having many surgical operations. But latex allergy sometimes occurs in allergy-prone people even though they don’t work in a high-risk job and haven’t had many operations. Some doctors think that if a child with severe allergies needs surgery, this should be done in latex-free conditions, even though the child has no allergy to latex, because of the risk that the operation will sensitise.
Latex can cause either contact dermatitis (see p. 55) or a Type I allergy, whose symptoms can include urticaria, asthma and anaphylaxis. Latex allergy often goes undiagnosed. Once sensitised, you may react to balloons, elastic bands, condoms and household gloves. Latex in the air,
due to powdered latex gloves being used, can be a hazard for someone who is highly sensitive, as can latex traces in food (see box on p. 175). Medical treatment may be problematic (see p. 98 and box on p. 249). Cross-reactions to certain foods can occur (see p. 15 and p. 51).
For those avoiding latex, there are non-latex gloves (see p. 57), and non-latex condoms. Immunotherapy (see pp. 164-9) may be useful in severe cases: it can reduce sensitivity and eliminate cross-reactions to foods.
Other hazards
This article (pp. 132-5) deals mainly with allergens at work, that is, substances which provoke classical allergies (Type I reactions). In addition, there are skin irritants and antigens in workplaces which can provoke contact dermatitis (see p. 56) or contact urticaria (see p.50).
Some of the most dangerous workplace substances are those that bring on asthma but are not allergens. These are usually called low-molecular-weight asthmagens. The most notorious of these are platinum salts, isocyanates (used in cement, in the manufacture of foam, plastics and varnishes, and for spray-painting cars, aeroplanes and boats), colophony (used as a solder in electronics), glutaraldehyde (used in hospitals for sterilisation procedures), and persulphate (used in hairdressing). Powerful respiratory equipment, supplying air from outside the area (see p. 135) is needed if you work with some of these substances, e.g. isocyanates for spray-painting cars.
has ended, they should not be seen as a way of allowing you to go on working with the offending allergen or asthmagen.
If it seems plausible that your allergies or your asthma are related to your work, your doctor should be able to give you a sickness certificate, so that you can have some time away from the workplace, to see if you recover. The medical service at your workplace may be better at diagnosing occupational asthma than your own doctor, but be cautious. In some workplaces they do operate as they should and offer genuinely confidential treatment. But there have also been cases of information being passed to the management, and workers with the early signs of occupational allergies and/or asthma being dismissed on a pretext, or made redundant, to avoid a possible compensation claim. Most occupational health services claim to be independent, but they actually have to earn the trust of the workforce. Before you make any move, ask your colleagues for their views, especially those who have worked there for many years.
Choosing a job
If you have any tendency to allergies, or come from an allergy-prone family, you should be very choosy about where you work. Try to avoid workplaces where there is heavy exposure to allergens, especially airborne allergens which can provoke asthma:
• Bakeries and flour mills, where the allergens concerned may be wheat proteins in the flour, or enzymes added to the flour mix. These allergies can take years to begin.
• Other food-processing works, particularly those dealing with tea, soyabeans, other beans (e.g. gram flour), shellfish and fish (especially if automated gutting machines are used without adequate ventilation). Food preparation and sandwich-making can cause contact urticaria, if there is prolonged contact with a particular foodstuff (e.g. tomatoes).
• Farms, docks and cotton mills – or any other workplace generating dust from plant products. On farms, it is the dust from grain and hay that is often responsible, although mould spores (see p. 121) can also be the culprit. Allergies to mites (found in hay, grain and flour) sometimes occur and eczema is the most common symptom – often called simply ‘grain itch’.
• Saw mills and joineries, because of the wood dust, especially that from hardwoods and from red cedar (Thuja plicata).
• Paper recycling plants, if there is a lot of paper dust in the air.
• Detergent and pharmaceutical factories handling enzymes – these are added to ‘biological’ washing powders and are potential allergens. The risks are less these days, as the enzymes are in granule form rather than powder.
• Factories processing natural products such as psyllium or ispaghula, which are used as laxatives. Anyone who has been sensitised should avoid taking medicines containing the offending substance in the future, because these can sometimes provoke a dangerous anaphylactic reaction.
• Hospitals, clinics and dental surgeries, mainly due to latex rubber, used in gloves and equipment. Although nursing staff and surgeons are most susceptible, other staff including hospital administrative workers can occasionally be affected. Fears about the spread of the HIV virus has led to a huge increase in the use of latex gloves in medicine and dentistry, and a consequent epidemic of latex allergy. The main problem is with powdered latex gloves, which release 15,000 times as much allergen into the air as unpowdered gloves. Unpowdered, low-allergen gloves greatly reduce the risk of latex allergy developing, and non-latex gloves are even better. There are moves to ban the import of powdered latex gloves into Britain. They are already being phased out in hospitals and other medical facilities, but progress is slow in some areas.
• Other workplaces where powdered latex gloves are used, including
Making the workplace safe for everyone
Note that these choices about employment are for the individual employees to make for their own protection - an employer cannot refuse to take anyone on because they have allergies or come from an atopic (allergy-prone) family.
The reasoning behind this is that the workplace should be safe for everyone, as far as possible. As many as one in three of the population may be susceptible to allergies, and it is clearly wrong to bar all such people from major industries. Current thinking, in most countries, is that the focus should be on getting allergens and asthmagens out of the air, not keeping the more vulnerable workers out of the workplace.
hairdressers, dental surgeries, pathology laboratories and police stations. Construction workers wearing rubber gloves are also at risk. Someone who has been sensitised by powdered latex gloves may then react to other items (see box on p.132). Those severely affected can have great problems in daily life and with medical treatment, so anyone with a strong tendency to allergy should strenuously avoid becoming sensitised.
• Factories making or using rubber items may also expose workers to the risk of latex allergy. Anything made by the ‘dipping method’ (e.g. balloons, condoms, elastic bands and gloves) is highly allergenic. Moulded rubber items, such as tyres, are much less of a problem. Neoprene and other synthetic rubber items are not allergenic.
• Chiropody and podiatry clinics, where there is a risk of allergic reactions to the fungus that causes athlete’s foot. It is inhaled on skin flakes from the patients’ feet.
• Laboratories and other workplaces where animals are kept. In the case of mice, rats and other rodents, the allergen is found in the animals’ urine, and becomes airborne as the urine dries. Insects and spiders (e.g, those reared for biological pest control), are also allergenic due to small airborne particles from their bodies. Those working closely with bees (either honeybees or bumblebees, now reared for pollinating glasshouse crops) are liable to be stung frequently, and this can lead to sting allergy (see pp. 60-61).
• Hairdressing salons, where many different items are used that are potentially allergenic, including latex gloves (see above), permanent-wave solutions and henna. The risks of contact dermatitis are also high (see p. 55).
• Greenhouses, where the enclosed conditions can lead to high levels of allergens from plants, moulds and insect pests. There may also be exposure to pesticide sprays or their residues, which can greatly aggravate any underlying tendency to allergies.
If you have ever suffered from atopic eczema, work situations that can bring on contact dermatitis should also be avoided (see p. 55).
Taking a risky job
If circumstances force you to take a job with an allergy risk, observe all the safety procedures that are in place, and where you have the option of turning on extractor fans, wearing protective gear, or simply opening doors and windows, always do so. If the safety procedures seem inadequate, talk to your trade union Safety Representative, or the local Health and Safety Executive which can run a check on safety procedures in your workplace. This will be presented to the employer as a routine check, so they need never know that a member of the workforce has contacted the HSE.
Whatever you do, if you are in a risky job, don’t smoke. At a salmon processing plant in Scotland, 40% of the smokers developed allergies (resulting in asthma) to the fish allergens in the spray from the fish-gutting machine. Non-smokers - who formed the overwhelming majority of the workers - were not affected at all. In United States cotton mills, smokers are affected by levels of cotton dust in the air that are legally defined as ’safe’, while nonsmokers remain unaffected.
Passive smoking at work is also an important issue. A recent US study showed that non-smokers were more likely to develop asthma if they worked alongside a smoker. Your employer has a duty to provide you with clean air. This includes ensuring that other employees do not impose their cigarette smoke on you.
Respiratory equipment
Where respiratory equipment is needed, your employer must provide this, and it must be the right equipment for the job. It should be inspected, tested, cleaned and repaired after each use, and filters should be replaced regularly. All this is your employer’s responsibility, but check that it is being done, and always look the mask over before you put it on.
Two different types of respiratory equipment are currently in use:
• Those that give you a supply of air from outside the work area, either from a compressed-air cylinder, or via an air-hose (airline) supplied with fresh air. In Britain these are called breathing apparatus.
• Those that use the surrounding air but filter it to remove allergens and asthmagens. In Britain these are called respirators. (In some countries this term describes any kind of respiratory equipment.) Ordinary respirators may pose problems for some asthmatics because they cannot breathe in strongly enough to draw sufficient air through the filter. Powered respirators can be the answer: they have a battery-powered unit to help with pulling in the air.
There are government regulations concerning the type of equipment required for each type of allergen and asthmagen. Large companies generally follow these regulations, but small businesses, such as local sawmills, joineries and car-repainting workshops, may not even know about them.
Any respiratory equipment that has a face mask must form a tight seal with your face. Facial hair will prevent this, and so will stubble, so shave carefully. Faces vary enormously in shape, and if your face mask does not fit, ask for a different type of mask or a different type of respiratory equipment. Persist until you get one that’s right for you.
Carry out a ‘fit check’ each and every time you wear the mask. For example, with respirators, you can check the fit by covering the air intake completely with your hand and breathing in sharply: if the mask fits properly, it should collapse onto your face, and remain stuck to your face for several seconds. Look at the manufacturer’s instruction booklet as there may be a specific fit check recommended for the equipment you are using.
If there is any difficulty in breathing through the respiratory equipment, the replaceable filter cartridge or the equipment itself should be replaced. You should also take action immediately if you can smell the substance being handled – but never rely on this as a danger sign, because an extremely small amount, way beyond the detection capacity of the human nose, may be very damaging indeed to your health.
Keep your mask on throughout the work period. If you find this impossible, talk to your employer or
line manager about getting a different kind of respiratory equipment – a powered device, for example, that assists the inflow of air.
No form of respiratory equipment provides complete protection against allergens and asthmagens: there is always the chance of some small amount getting through. This is why respiratory equipment should not be used by those who have already developed occupational asthma but want to stay in their job.
Those who really cannot change jobs (e.g, farmers) are sometimes able to use a powered respirator helmet, which allows them to go on working despite the allergen. But this is not an ideal solution from a purely health point of view. Farmers can also improve matters, where moulds are the source of allergens, by keeping all harvested crops dry and thoroughly ventilated.
A lasting problem
As long as you catch the problem early, and are no longer anywhere near the allergen, your symptoms should disappear completely, but remember that you may still be highly sensitive to the allergen, even years afterwards. For a year or two at least, avoid contact with it again, even in tiny amounts. If someone else in your family works at the same place, they may bring home traces of the allergen on their clothes and hair: ask them to leave their workclothes outside the house and shower on arriving home.
With occupational allergies to airborne food particles, it is possible that the affected individual will later react to the same food when eaten. Experiment very cautiously, especially if the allergen is fish or shellfish.
The allergy may persist long after the job has ended. In one case, doctors found that a woman who had developed ‘baker’s asthma’, while working briefly in a bakery when young, was still allergic to the enzyme additive in bread 20 years later. She suffered an asthma attack whenever she ate bread.