Friday, June 24, 2016

Government should help people in poverty for their better health care. Aleem M A . Hakkim A M. BMJ 2016;353:i3370


A prescription for poverty

BMJ 2016; 353 doi: (Published 20 June 2016)

Cite this as: BMJ 2016;353:i3370

Rapid Response

Re: A prescription for poverty

Government should help people in poverty for their better health care.

Poverty is not an excuse for people to have worst health care.

In Tamilnadu, India, about 70 percent of the population are living in rural areas. The government of Tamilnadu under the leadership of J. Jayalalithaa has provided a free cell phone for every ration card holder in her state.

With that, people anywhere in the state can dial a toll free number 104 and can have free consultation, guidance, and help for any health alignments. If patients are in need of any transport they can get free transport to hospitals by dialing the toll free 108 services.

Poor patients who need any major surgery or medical treatment can have free treatment under the Tamilnadu Chief minister's comprehensive health insurance scheme even in private hospitals in Tamilnadu.

So the government should support the free health care service to people in poverty in rural and urban areas from primary to tertiary care. Health care facilities are for the betterment of poor people 's health.

Competing interests: No competing interests

23 June 2016

M A Aleem


A M Hakkim

ABC Hospital .Apollo Hospital

Annamalainagar Trichy 620018 .Apollo Hospital Trichy 620010. Apollo Clinic Thillainagar Trichy 620018


Friday, June 17, 2016

Gain or Loss To India. Aleem M A. BMJ 2016;353:i3302

FeatureEU Referendum and Health

Why doctors should vote to remain in the EU on 23 June

BMJ 2016; 353 doi: (Published 14 June 2016)

Cite this as: BMJ 2016;353:i3302

Rapid response


Re: Why doctors should vote to remain in the EU on 23 June

Gain or Loss to India

Britain's exit from the European Union may reduce rather than enhance its standing and influence over the world.

As far as India is concerned, the longstanding historical relationships with Britain would be less affected, even if trade declined to some extent.

India has always been more comfortable in dealing with countries individually than as part of a union. India does not see the United Kingdom as a part of the European Union but as a distinct entity because of its history. Some of the most strategic elements in foreign policy cannot be conducted through a union like the EU, but as part of a bilateral relationship.

The existence of a strategic relationship between the UK and India, made up of defence and hi-tech ties, is another element underlying a different approach to British identity.

Overall Britain would somehow regain a unique and strong voice in world affairs once it breaks away from a collective European identity.

Competing interests: No competing interests

17 June 2016

M A Aleem


ABC Hospital

Annamalainagar TRICHY 620018 Tamilnadu India


Monday, June 13, 2016

Lapse of golden Hour. in Trichy The Hindu Readers Mail 14.6.2016

The Hindu Tiruchi 14.6.2016

Readers Mail 

Tamil Nadu

Lapse of golden hour

Updated: June 14, 2016 05:47 IST

Lapse of golden hour

Reaching the critical patients to designated hospital on the Chennai-Tiruchi highway through a detour thanks to the non-availability of inter-junctions just in front of the hospitals has been a matter of concern to the medical fraternity. There are a number of critical care patients who run the risk of losing lives as the life-saving golden hour lapses as ambulances are forced to take long U-turns in both directions on the busy highway (NH-45). At times, the slow-moving traffic adds to woe of patients. The National Highways Authority of India must take steps to provide road intersections in front of the tertiary care hospitals along the highway to ensure that patients were provided timely medical assistance.

Dr. M.A. Aleem,


Sunday, June 12, 2016

Can overcome antimicrobial resistance in developing and underdeveloped countries? Aleem M A . BMJ 2016;353:i3087


What to do about antimicrobial resistance

BMJ 2016; 353 doi: (Published 06 June 2016)

Cite this as: BMJ 2016;353:i3087

Rapid response


Re: What to do about antimicrobial resistance

Can overcome antimicrobial resistance in developing and underdeveloped countries?

Over the counter sales of antibiotics and the irrational use of antmicrobes by the quacks are the most important causes for the development of antibiotic resistance in the developing and underdeveloped countries. Other than this subdosage production of antibiotics by the substandard pharmaceutical companies are also a reason for the development of antimicrobial resistance. Other than this improper usages antibiotics with inadequate dosages for inaquatate period of time are also the reasons for the development of resistance. So the usage of standard appropriate antibiotics with a qualified doctors prescriptions of adequate doses of antibiotics for the guidelines based adequate period of time will be very much useful to prevent antimicrobial abuse and it's resistance.

Competing interests: No competing interests

11 June 2016

M A Aleem


ABC Hospital. Apollo Hospital

Annamalainsgar , Trichy 620018, Tamilnadu India. 6th cross East, Tillainagar, Trichy 620018 Tamilnadu India


Wednesday, June 8, 2016

7 surprising health benefits of Ramadan


20 July 2012


Although three dates are eaten at the start of Iftar every day during Ramadan for spiritual reasons, they also come with the added bonus of multiple health benefits. One of the most important aspects of fasting is getting the right amount of energy, and considering an average serving of dates contains 31 grams of carbohydrates, this is one of the perfect foods to give you a boost. Dates are also a great way of getting some much-needed fibre, which will aid and improve digestion throughout Ramadan. Add to that their high levels of potassium, magnesium and B vitamins, and it quickly becomes apparent that dates are one of the healthiest fruits out there.

Surprising health benefits of Ramadan - dates


Boost your brain

No doubt you’ll be aware of the positive effects fasting can have on your mental wellbeing and spiritual focus, but the brain-boosting powers of Ramadan are even more significant than you might think. A study carried out by scientists in the USA found that the mental focus achieved during Ramadan increases the level of brain-derived neurotrophic factor, which causes the body to produce more brain cells, thus improving brain function. Likewise, a distinct reduction in the amount of the hormone cortisol, produced by the adrenal gland, means that stress levels are greatly reduced both during and after Ramadan.

Ditch bad habits

Because you will be fasting during the day, Ramadan is the perfect time to ditch your bad habits for good. Vices such as smoking and sugary foods should not be indulged during Ramadan, and as you abstain from them your body will gradually acclimatise to their absence, until your addiction is kicked for good. It’s also much easier to quit habits when you do so in a group, which should be easy to find during Ramadan. Fasting’s ability to help you cut out bad habits is so significant that the UK’s National Health Service recommends it as the ideal time to ditch smoking.

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Tuesday, June 7, 2016

Gluten sensitivity as a neurological illness


Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UKCorrespondence to:
 Dr M Hadjivassiliou, Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK;

gluten sensitivity coeliac diseaseneurological illness

From gut to brain

It has taken nearly 2000 years to appreciate that a common dietary protein introduced to the human diet relatively late in evolutionary terms (some 10 000 years ago), can produce human disease not only of the gut but also the skin and the nervous system. The protean neurological manifestations of gluten sensitivity can occur without gut involvement and neurologists must therefore become familiar with the common neurological presentations and means of diagnosis of this disease.


” . . .the stomach being the digestive organ, labours in digestion, when diarrhoea seizes the patient . . .and if in addition, the patient's general system be debilitated by atrophy of the body, the coeliac disease of a chronic nature is formed”.1

This extract is from the book on chronic diseases by Aretaeus the Cappadocian, one of the most distinguished ancient Greek doctors of the first century AD. This chapter, entitled “on the coeliac diathesis”, was the first description of coeliac disease (from the greek word κ⊝ιλιακη meaning abdominal). Aretaeus' books were first published in Latin in 1500 and the new Latin word coeliac was used to translate κ⊝ιλιακη. Coeliac disease (CD) remained obscure until 1887 when Samuel Gee gave a lecture entitledOn the coeliac affection2 at the Hospital for Sick Children, Great Ormond Street, London. In it he acknowledged Areteaus' contribution and went on to give an accurate description of CD based on his own clinical observations.

With clinical manifestations primarily confined to the gastrointestinal tract or attributable to malabsorption, it was logical to assume that the target organ and hence the key to the pathogenesis of this disease was the gut. The first report of neurological manifestations associated with CD was by Carnegie Brown in 1908.3In his book entitled Sprue and its treatment he mentioned two of his patients who developed “peripheral neuritis”. Elders reported the association between “sprue” and ataxia in 1925.4 The validity of these and other such reports before 1960 remains doubtful given that a precise diagnosis of CD was not possible before the introduction of small bowel biopsies.

The treatment of CD remained empirical until 1940–50 when the Dutch paediatritian Willem Dicke noted the deleterious effect of wheat flour on children with CD.5 Removal of dietary products containing wheat was shown to result in complete resolution of the gastrointestinal symptoms and a resumption of normal health. The introduction of the small bowel biopsy in 1950–60 confirmed the gut as a target organ. The characteristic features of villous atrophy, crypt hyperplasia and increase in intraepithelial lymphocytes with improvement while on gluten-free diet, became the mainstays of the diagnosis of CD. In 1961 Taylor published an immunological study of CD.6 In his paper he commented that “ . . .an obstacle to the acceptance of the immunological theory of causation has been the lack of satisfactory demonstration of antibodies to the protein concerned”. He went on to demonstrate the presence of circulating antibodies against gliadin (antigliadin antibodies), the protein responsible for CD. This provided further evidence that CD was immunologically mediated and that the immune response is not confined to the mucosa of the small bowel. Antigliadin antibodies became a useful screening tool for the diagnosis of CD.

In 1966, Marks et al demonstrated an enteropathy in nine of 12 patients with dermatitis herpetiformis,7 an itchy vesicular skin rash mainly occurring over the extensor aspect of the elbows and knees. The enteropathy had a striking similarity to that seen in CD. It was later shown that the enteropathy and the skin rash were gluten dependent but skin involvement could occur even without histological evidence of gut involvement. This was the first evidence that the gut may not be the sole protagonist in this disease.


In 1966 Cooke published a landmark paper on 16 patients with neurological disorders associated with adult CD.8 This was the first systematic review of the subject after the introduction of diagnostic criteria for CD. Ten of these patients had a severe progressive neuropathy. All patients had gait ataxia and some had limb ataxia. Neuropathological data from postmortem examinations showed extensive perivascular inflammatory changes affecting both the central and peripheral nervous systems. A striking feature was the loss of Purkinje cells with atrophy and gliosis of the cerebellum. All 16 patients had evidence of severe malabsorption as evidenced by anaemia and vitamin deficiencies as well as profound weight loss.

Several case reports followed, primarily based on patients with established CD, often with persisting troublesome gastrointestinal symptoms followed by neurological dysfunction. Data from patients with CD presenting with gastrointestinal symptoms followed up in a gastrointestinal clinic suggest that otherwise unexplained neurological dysfunction is a complication in 6% to 10% of cases.9

A review of all such reports (with biopsy proved CD) from 1964 to date shows that ataxia and peripheral neuropathy are the commonest neurological manifestations seen in patients with established CD (table 1). Less common manifestations include inflammatory myopathies10 and myoclonic ataxia.11 Isolated dementia is uncommon and most cases tend to have additional neurological features (for example, ataxia or neuropathy). Patients with epilepsy associated with occipital calcifications on CT and CD have been described,12 mainly in Italy. Most present with epilepsy in childhood. Such cases are rare in the United Kingdom.

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Table 1

Neurology of coeliac disease (based on a review of 35 papers of single or multiple case reports from 1964 to 2000)


Some studies looking at normal populations have shown that the prevalence of CD is much higher than previously thought13,14 (approximating to 1 in 100). Most of such patients have no gastrointestinal symptoms. In addition, experimental data in patients with gluten sensitivity suggest that there is a range of mucosal abnormalities affecting the small bowel ranging from preinfiltrative (histologically normal) to infiltrative, to hyperplastic to flat destructive (seen in CD), and finally to the irreversible hypoplastic atrophic lesions.15 Increasing the gluten load may result in progression of the severity of the lesion. In those patients where the histology is normal, staining of the T cell subpopulations of the intraepithelium of the small bowel biopsies shows alteration of T cell subpopulations of the intraepithelial lymphocytes (increase of the γ/δ T cells). This finding is said to be a marker of potential CD.16 This procedure is only available in a very few pathology laboratories, rendering its use limited.

Finally, CD has a very strong association with the human lymphocyte antigen (HLA) of the major histocompatibility complex. Ninety per cent of patients with CD have the HLA DQ2; the rest have DQ8.

These advances suggest that gastrointestinal symptoms are absent in most patients with CD, that the definition of gluten sensitivity can no longer be solely based on the presence of an enteropathy and that genetic susceptibility may be an important additional marker for gluten sensitivity. Given the knowledge of these advances and approaching gluten sensitivity from a neurological perspective we set up to address the following question: Does cryptic gluten sensitivity play a part in neurological illness?


Over the past 8 years we have used antigliadin antibodies to screen patients with neurological dysfunction of unknown aetiology. Our original study concluded that gluten sensitivity played an important part in neurological illness.17 The evidence was statistical: Patients with neurological disease of unknown aetiology were found to have a much higher prevalence of circulating antigliadin antibodies (57%) in their blood than either healthy control subjects (12%) or those with neurological disorders of known aetiology (5%). Since then we have identified 131 patients with gluten sensitivity and neurological disorders of unknown aetiology. Table 2 shows the neurological diagnoses we have encountered. Perhaps not surprisingly the commonest manifestations are ataxia (also known as gluten ataxia18) and peripheral neuropathy.19

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Table 2

Neurology of gluten sensitivity


Systematic screening of 143 patients with so-called “idiopathic sporadic ataxia” showed that 41% had gluten sensitivity as defined by the presence of circulating antigliadin antibodies20 (IgG with or without IgA). The prevalence of antigliadin antibodies in 51 patients with familial ataxia did not differ from that found in normal healthy control subjects (13%). The mean age of onset of the ataxia was 54 but we have recently seen three patients with early onset (under 20 years of age) sporadic idiopathic ataxia and gluten sensitivity. Recently four patients have been described with CD presenting as gait disturbance and ataxia in infancy.21 Alhough the ataxia tends to be slowly progressive, in some cases it can take a very rapid course with the development of cerebellar atrophy within a year of the onset of the illness (fig 1). Ataxia and myoclonus is a much less common presentation (only four patients in these series). We have encountered two patients who in addition to ataxia had evidence of chorea but normal genetic testing for Huntington's disease. Gluten ataxia primarily affects the lower limbs and gait. Extrapyramidal or autonomic features are rarely apparent and these features distinguish it from the cerebellar variant of multisystem atrophy (MSA). Screening of patients with clinically probable MSA (cerebellar variant) for the presence of antigliadin antibodies showed the prevalence to be similar to the normal population. Brain MRI usually shows cerebellar atrophy; sometimes with evidence of white matter abnormalities. Up to 40% of patients also have a sensorimotor axonal peripheral neuropathy that can often be subclinical. In a few cases oligoclonal bands are present in the CSF.

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Figure 1

Brain MRI of a patient with gluten ataxia showing rapid onset of cerebellar atrophy over a period of 15 months before the diagnosis of gluten ataxia.


Peripheral neuropathy is the second commonest manifestation of gluten sensitivity. Prospective screening of 101 patients with idiopathic peripheral neuropathy has shown the prevalence of gluten sensitivity to be 40% (unpublished data). The commonest type of peripheral neuropathy we encountered is sensorimotor axonal (26) followed by mononeuropathy multiplex (15), pure motor neuropathy (10), small fibre neuropathy (four) and mixed axonal and demyelinating (two). The neuropathy is usually chronic and of gradual progression. Patients with a pure motor neuropathy may progress to involvement of sensory fibres.


We encountered eight patients with myopathy and gluten sensitivity. Three had an additional neuropathy. Muscle biopsy showed inflammatory changes in five. One patient had evidence of inclusion body myositis. One patient had low concentrations of vitamin D and a predominantly proximal myopathy.

Myelopathy is rare in our series and was only seen in two patients.

We have recently identified a subgroup of patients with gluten sensitivity who complained of episodic severe headache often with transient neurological deficit and extensive white matter abnormalities on MRI.22 Some of them also had ataxia or neuropathy. Their headache resolved with the introduction of a gluten free diet though the MRI abnormalities persisted at least for the short follow up period. We have also found a higher incidence of gluten sensitivity in patients with systemic vasculitis and neurological involvement, perhaps reflecting the autoimmune nature of gluten sensitivity. There is a well known association of CD with other autoimmune diseases23 (for example, diabetes, thyroid disease). This may account for the finding of the presence of antigliadin antibodies in all four of our patients with stiff-person syndrome.

Some researchers think that prolonged exposure to gluten in a gluten sensitive person may be the trigger for the development of other autoimmune disease.23

CONTENTIOUS ISSUES”But antigliadin antibodies lack specificity”

IgG anti-gliadin antibodies have been the best diagnostic marker in the neurological population we have studied. IgG anti-gliadin antibodies have a very high sensitivity for CD but they are said to lack specificity. In the context of a range of mucosal abnormalities and the concept of potential CD, they may be the only available immunological marker for the whole range of gluten sensitivity of which CD is only a part. Further support for our contention comes from our HLA studies. Within the group of patients with neurological disease and gluten sensitivity (defined by the presence of anti-gliadin antibodies) we have found a similar HLA association to that seen in patients with CD: 70% of patients have the HLA DQ2 (30% in the general population), 9% have the HLA DQ8, and the remainder have HLA DQ1. The finding of an additional HLA marker (DQ1) seen in the remaining 20% of our patients may represent an important difference between the genetic susceptibility of patients with neurological presentation to those with gastrointestinal presentation within the range of gluten sensitivity.

”But antigliadin antibodies have been superseded by anti-endomysial and transglutaminase antibodies”

The introduction of more CD specific serological markers such as anti-endomysium and more recently transglutaminase antibodies may have helped in diagnosing CD but their sensitivity as markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity.

“What do I do with a patient with positive anti-gliadin antibody test but normal duodenal biopsy”

Only one third of the patients with neurological disorders associated with gluten sensitivity have villous atrophy on duodenal biopsy. Even some with biochemical markers of malabsorption such as low serum vitamin B12, low red cell folate, or vitamin D concentrations had normal conventional duodenal histology.17 These cases may illustrate the patchy nature of bowel involvement in coeliac disease and the inaccurate interpretation of duodenal biopsies by inexperienced histopathologists. Preliminary data based on staining of the subpopulation of T cells in the small bowel epithelium suggests that these patients have potential CD.24 There are, however, patients where the immunological disorder is primarily directed at the nervous system with little or no damage to the gut. Our practice is to offer a gluten-free diet to these patients unless the HLA genotype is not consistent with susceptibility to gluten intolerance (that is, other than HLA DQ2, DQ8, or DQ1). All patients are followed up and any clinical response is documented.

”But my patient has not responded to a gluten free diet”

Reports in the literature of the effect of the gluten-free diet on neurological dysfunction are conflicting. Almost all patients reported in the literature have the diagnosis of CD before the development of neurological dysfunction. They may represent a different group of patients from those presenting with neurological dysfunction without bowel involvement. Additionally, improvement of gastrointestinal symptoms and improvement of the histological abnormalities on repeat small bowel biopsy often were the measures used to assess the response to the diet. Serological evidence of response (for example, sustained elimination of antigliadin antibodies) has rarely been used as confirmation of strict adherence to the gluten-free diet. Incomplete elimination of gluten from the diet may be enough to abolish gastrointestinal symptoms with recovery of the small bowel mucosa but is insufficient to arrest the state of heightened immunological responsiveness resulting in neuronal injury. There is a group of patients with CD “resistant” to gluten-free diet. This may reflect hypersensitivity to the minute amounts of gluten present in most “gluten-free” products. An analogous situation may exist in cases of gluten ataxia or gluten related neuropathy. The monitoring of neurological improvement in such cases is made difficult by the slow and sometimes incomplete regeneration of the nervous system. In cases of gluten ataxia where the underlying pathology is loss of Purkinje cells, one may only expect the stabilisation of the disease without any definite clinical improvement. This is in marked contrast to the response seen in patients with florid gastrointestinal symptoms who notice almost immediate improvement after the introduction of a gluten-free diet.

“Isn't the neurological damage nutritional?”

Nutrient deficiencies (B12, folate, vitamin D, vitamin E) are rare in this neurological population. Given that two thirds of these patients have no enteropathy this is hardly surprising. The concept of the neurological manifestations being nutritional in origin is now outmoded. Intestinal mucosal damage in coeliac disease is the result of both humoral and T cell mediated inflammation. Such inflammation is not, however, confined to the gut, as activated HLA restricted gliadin specific T cells25 and antigliadin antibodies are found systemically. Antigliadin antibodies are also found in the CSF.26 Postmortem findings from two of our patients with gluten ataxia has shown perivascular cuffing with both CD4 and CD8 cells. This inflammation was primarily seen in the white matter of the cerebellum. There was also marked but patchy Purkinje cell loss. We have also found antibodies against Purkinje cells in patients with gluten ataxia. Our research suggests that IgG antigliadin antibodies cross react with epitopes on Purkinje cells from human cerebellum.27Characterisation of the anti-Purkinje cell antibodies by immunoblotting may provide a useful marker for the diagnosis of gluten ataxia in a manner analogous to the use of antiendomysium antibodies as a marker for coeliac disease or the anti-Yo antibody in paraneoplastic cerebellar degeneration.


Gluten sensitivity is best defined as a state of heightened immunological responsiveness in genetically susceptible people.15 This definition does not imply bowel involvement. That gluten sensitivity is regarded as principally a disease of the small bowel is a historical misconception.28 Gluten sensitivity can be primarily and at times exclusively a neurological disease.29 The absence of an enteropathy should not preclude patients from treatment with a gluten-free diet. Early diagnosis and removal of the trigger factor by the introduction of gluten-free diet is a promising therapeutic intervention. IgG antigliadin antibodies should be part of the routine investigation of all patients with neurological dysfunction of obscure aetiology, particularly patients with ataxia and peripheral neuropathy.


We are currently conducting a trial of the effect of gluten-free diet in patients with gluten ataxia and would welcome referrals of patients with sporadic idiopathic ataxia. We have received funds from SHS International and Ultrapharm Ltd towards a pilot study of the effect of gluten-free diet on patients with neurological dysfunction and gluten sensitivity and a grant from The Friedreich's Ataxia Group for research into the immunological mechanisms of the pathogenesis of gluten ataxia.

From gut to brain


Aretaeus. Liber IV περι κ⊝ιλιακης διαθεσι⊝ς. In: Corpus Medicorum 

Monday, June 6, 2016

Ramadan Fasting Gives Health

In a narration of Abu Nuaim, Prophet Mohammad said, “soomo wa tsahhoo”, which can be translated to mean, “Fast and be healthy.”

Effects on health of fluid restriction during fasting in Ramadan

J B Leiper1, A M Molla2 and A M Molla3

1Department of Biomedical Sciences, University Medical School, Aberdeen University, UK2Department of Paediatrics, Faculty of Medicine, Kuwait University, Kuwait3Faculty of Allied Health Science, Kuwait University, Kuwait

Correspondence: J Leiper, Department of Biomedical Sciences, University Medical School, Foresterhill, Aberdeen AB25 2ZD, UK.

Guarantor: J Leiper.

Contributors: J Leiper reviewed the articles, analyzed the data, drafted and edited the manuscript. All authors were involved in critical revision of the manuscript and approved the final version submitted.


During the 9th month (Ramadan) of the Islamic calendar (Hijra) many millions of adult Muslims all over the world fast during the daylight hours. Since Hijra is a lunar calendar, Ramadan occurs at different times in the seasonal year over a 33-year cycle. Fasting during Ramadan is partial because the abstention from food, fluid, tobacco and caffeine is from sunrise to sunset. Several categories of people are exempt or can postpone the Ramadan fast. The effect on health and well being of the month-long intermittent fast and fluid restriction has been studied in various potentially vulnerable groups in addition to normal healthy individuals in many countries. The majority of the studies have found significant metabolic changes, but few health problems arising from the fast. A reduction in drug compliance was an inherent negative aspect of the fast. Common findings of the studies reviewed were increased irritability and incidences of headaches with sleep deprivation and lassitude prevalent. A small body mass loss is a frequent, but not universal, outcome of Ramadan. During the daylight hours of Ramadan fasting, practising Muslims are undoubtedly dehydrating, but it is not clear whether they are chronically hypohydrated during the month of Ramadan. No detrimental effects on health have as yet been directly attributed to negative water balance at the levels that may be produced during Ramadan.


Ramadan, intermittent voluntary fasting, fluid restriction, health effects, dehydration


During the religious festival of Ramadan, the majority of adult, practising Muslims refrain from eating, drinking, smoking and sexual relationships during the hours of daylight throughout the lunar month. Since the Islamic calendar is lunar, the start of the Islamic year advances 11 days each year compared with the seasonal year; therefore, Ramadan occurs at different times of the seasonal year over a 33-year cycle (Sakr, 1975; Richards, 1998). This can result in the Ramadan fast being undertaken in markedly different environmental conditions between years in the same country. In addition, the time of sunrise and sunset varies between 12 h at the equator and about 22 h at the 64° of latitude in summertime. For people living in the polar regions, it is recommended, however, that they take the fasting times as those prescribed at Mecca and Medina, or from the nearest temperate zones (Muazzam & Khaleque, 1959; Sakr, 1975;Malhotra et al).

Not only is the eating pattern greatly altered during the Ramadan period, but the amount and type of food eaten during the night may also be significantly different to that usually consumed during the rest of the year. In many cultures, special festival foods that are richer in fat and protein than the usual diet, or that contain large quantities of sugar, are eaten (Sakr, 1975;El Ati et al), while in other countries factors such as poverty ensure that the Ramadan fast results in a reduction in energy intake and a loss of body fat (Angel & Schwartz, 1975; Chandalia et al;Hallack & Nomani, 1988).

The annual Ramadan fast is not obligatory for all Muslims, for there are several categories of healthy people and patients who are exempt (prepubertal children; the insane), or who can postpone the Ramadan fast (the acutely ill; women during menstruation, pregnancy, post-childbirth confinement and lactation; travellers) or who are unable to fast (the chronically ill; the frail elderly), but who are encouraged to feed a needy individual during the month of Ramadan (Sakr, 1975). The list of groups excused, although primarily expressing specific religious beliefs, may also include empirical knowledge on the adverse effects of fasting on health, from a period long before there was a clinical rationale. However, because of local tradition or a variety of personal reasons, many individuals who have the right to be excused decide to observe the fast.

The interaction of these variables involved in the intermittent fast during Ramadan has led to a complex picture, which has led to concern regarding the possibility of an exacerbation of health problems (Prentice et al; Aslam & Healy, 1986; Schmahl et al; Karaagaoglu & Yucecan, 2000; Qaisi, 2001). The observed signs and symptoms may be the result of fasting or dehydration or both. The separation or, much more difficult, the quantification of the effects of the two pathogenic factors is frequently very difficult or impossible. Thus, in this review, all health effects of intermittent fasting and dehydration during Ramadan are systematically listed, especially as such a review is not available and the spectrum of effects may well contain some hitherto unknown effects of intermittent dehydration.

TopPotential health concerns of Ramadan diet restrictions in healthy individualsEnergy balance

Generally, meal frequency is reduced during Ramadan fasting, which it has been found often leads to reduced energy intake and loss of body mass and body fat (Angel & Schwartz, 1975; Hallack & Nomani, 1988). Many researchers have confirmed that lipid, carbohydrate, protein and hormone metabolism changes occur during fasting. Hallack and Nomani (1988), using hypoenergetic diets with different fat and carbohydrate levels, demonstrated that in a group of 16 healthy male subjects energy intake was reduced when subjects were restricted to only two meals per day, although they were allowed to eat as much as they wished at each mealtime. Nevertheless, Frost and Pirani (1987) found that there was a significant increase in energy, fat, carbohydrate and protein intake during Ramadan in the group of Saudi-Arabians they studied. There are many studies that have shown a definite loss of body mass, body fat and/or a decrease in energy intake during the intermittent monthlong fast (Muazzam & Khaleque, 1959; Born et al;Husain et al; Schmahl et al; Sweileh et al; Bigard et al). However, as might be expected from such a diverse variety of cultures and customs, there are as many studies that have shown either no significant loss of body mass (Laajam, 1990;El Ati et al; Afifi, 1997; Ramadan et al;Leiper & Prastowo, 2000) or a slight increase during Ramadan (Frost & Pirani, 1987). In general, any loss in body mass is usually relatively small (Table 1) and it may also be attributed to a decrease of glycogen-bound water stores, extracellular volume contraction secondary to a lower sodium intake, and a moderate degree of hypohydration with little loss of body tissue.

Table 1 - Body mass change during Ramadan.Full table

Psychosomatic alterations

A number of studies have investigated the effect on mood and irritability of individuals during the Ramadan fast. These studies invariably show a decease in subjective feelings of alertness, and an increase in lethargy and irritability during the daytime fast (Afifi, 1997; Kadri et al; Roky et al). Cognitive function has also been shown to be decreased (Ali & Amir, 1989), although this is not a universal finding (Roky et al). Part of this mood change is caused by alterations in normal circadian rhythms, with individuals becoming more active through the evening and night (Taoudi Benchekroun et al), and sleep deprivation (Husain et al;Bogdan et al; Roky et al). However, the effects of restrictions on smoking tobacco, ingesting caffeine and energy and fluid intake must also contribute to this general feeling.

A frequently cited problem of Ramadan fasting is an increased incidence of headaches (Awada & al Jumah, 1999). Examination of 2982 patients who attended clinics in the Kashmir Valley complaining of headaches or cranial neuralgia resulted in a diagnosis of tension headaches in 67% of the cases and migraine in 14%. Irritable-related stress was considered to be the main factor leading to tension headaches, while Ramadan fasting appeared as the prime precipitating factor for migraines (Shah & Nafee, 1999). In the study of Awada and al Jumah (1999)looking at the incidence of headaches in a group of 116 hospital staff in Saudia Arabia, 41% of the 91 respondents who fasted reported having a headache compared to the 8% of those 25 staff who did not fast. Headache frequency increased with duration of the fast and affected mainly those individuals who were normally prone to having headaches. Tension headaches accounted for the majority of cases (78%). The authors suggested that although lack of sleep, hypoglycaemia, and dehydration might have caused some of these incidents, caffeine withdrawal appeared to be the main contributory factor. Another study investigating the effect of the 25 h fast of Yom Kippur identified that of the 211 Israeli hospital staff who fasted, 39% developed headaches while only 7% of 169 staff members who did not fast reported headaches (Mosek & Korczyn, 1995). The number of headache sufferers increased in direct relation to the duration of the fast. Headaches were rated as being mild to moderate in intensity and individuals who were prone to headaches were more likely to develop fasting-induced headaches (66% and 29%, respectively). The investigators in this study considered that caffeine and nicotine withdrawal and oversleeping did not have an influence on headache development in their subjects, but fasting per se was the main contributor to inducing the headaches (Mosek & Korczyn, 1995) but they did not appear to consider the possibility of acute dehydration as a factor.

Accident and emergency cases

An increased number of Muslims attended the Accident and Emergency department of a British hospital during the month of Ramadan compared to similar time periods before and after Ramadan (Langford et al). This finding may be the result of the mood changes (Afifi, 1997; Kadri et al;Roky et al) and decrease in cognitive function (Ali & Amir, 1989) resulting from the alteration in dietary habit during Ramadan. Interestingly, a retrospective examination of all road traffic casualties seen at a local hospital in Al-Ain City, United Arab Emirates, over a 12-month period, found that there was a greater number of injuries during Ramadan than during other months (Bener et al).

Drug compliance

In a group of 750 Ramadan fasting adults in Turkey who were studied by questionnaire, 187 recorded some type of health problem during the fast (Karaagaoglu and Yucecan, 2000). Within this group of people who became ill, 60% were normally taking prescribed drugs and 32% were on diets relating to their health. During Ramadan, 10 and 19% of these two respective groups stopped taking their drugs and did not regularly adhere to their diets. Of 81 Asian Muslim patients questioned, 37 were found to have changed their drug dosage pattern while fasting, 35 had missed doses, eight took their tablets at different times and four took all their medications as one single daily dose after breaking fast in the evening (Aslam & Healy, 1986).

Occupational heat stress

One study highlighted the detrimental effect that the Ramadan fast could have on Muslim labourers carrying out light-to-moderate physical work in an industrial setting (Schmahl et al). In all, 32 males, mainly of Turkish origin, working in a chemical factory in Germany were studied during Ramadan in June 1983, when the daylight lasted for 18 h daily. These workers lost an average of 3.6 kg of body mass during the month of intermittent fasting and several of their biochemical parameters suggested that they were significantly hypohydrated. Five of these labours had such severe health problems that they had to interrupt their observance of Ramadan because they could not continue working and fasting.


A reduction in energy or fluid intake by the pregnant mother may produce detrimental effects on foetal growth. Evidence of increased metabolic stress in pregnant women undergoing the Ramadan fast has been recorded in two studies (Prentice et al;Malhotra et al). Women in late pregnancy showed the phenomenon of 'accelerated starvation' during Ramadan, characterized by low serum levels of glucose and alanine, and especially high levels of free fatty acids and beta-hydroxybutyrate. The additional metabolic stress of Ramadan fasting in pregnancy and during lactation has the potential to cause retardation of foetal (Tyson et al; Prentice et al; Picciano, 1996) and neonatal growth and development, respectively (Prentice et al; Heird, 1996). In Saudi Arabia, the ratio of low-birthweight babies born during the festival months of Ramadan and Hajj was significantly higher than in the non-festival months (Opaneye et al). This contrasts with the finding of Cross et al (1990), who could find no obvious effect of Ramadan fasting on the mean birth weight or prevalence of low-birthweight babies at full term in a cohort of 13 ,351 deliveries that occurred between 1964 and 1984 in a British hospital.

In several countries, fasting by breastfeeding mothers of infants is common during Ramadan (Prentice et al; Ertem et al). A Turkish study that surveyed 129 breastfeeding mothers of infants aged 6 months or younger from an impoverished city area found that 28 mothers considered that the volume of breast milk they produced was reduced during the Ramadan fast and 30 mothers increased the amount of solid supplements they gave their children during Ramadan (Ertem et al). In 10 lactating Gambian women, the total breast milk output during Ramadan was not different from that during a comparable period before or after Ramadan. However, fasting caused changes in milk osmolality, and lactose and potassium concentrations indicative of a marked disturbance of milk synthesis (Prentice et al). Both authors concluded that child health care providers should find religious and culturally appropriate methods to combat the possible unfavourable effects of intermittent fasting for infants and children.

TopPotential health concerns of Ramadan diet restrictions in patientsDiabetes

Owing to the relationship between fasting and hypoglycaemia, diabetics who undertake Ramadan fasting have been considered as a highly vulnerable group. Several clinical studies have examined the effect of the daytime fast on hypoglycaemic control of non-insulin-dependent diabetics (NIDD).

In one large study, 365 Ramadan fasting diabetic Moroccans were compared with 177 nonfasting patients (Belkhadir et al). At the end of Ramadan, there were no significant differences between the nonfasting and fasting groups, respectively, in serum fructosamine concentration (4.00 and 3.81 mmol/l), total glycated haemoglobin level (14.7 and 13.3%) or the number of reported hypoglycaemic events (11 and 13). Body mass tended to increase over the period of Ramadan (0.5 and 0.75 kg, respectively), while serum creatinine levels increased, inferring that overall the subjects were hypohydrated at the end of Ramadan.

Several other studies have shown stable or a slight improvement in fasting blood sugar during the Ramadan fast (Mafauzy et al; Katibi et al). Other studies have proposed that improvement in glycaemic control can only be detected in patients who show a decrease in body mass caused by the intermittent Ramadan fast (Ch'ng et al; Laajam, 1990). While the general consensus from the clinical studies undertaken appears to be that most established NIDD patients can cope with the intermittent fasting during Ramadan, medical practitioners must make their patients aware of the potential hazards involved and should consider the use of longer acting drugs during fasting (Garcia-Bunuel, 1989). At least one report, however, has cautioned against Ramadan fasting for any diabetics, because they identified several diabetic patients, some of whom were insulin-dependent, who lost diabetic control due to the change in dietary habits and omission of drugs during Ramadan (Tang & Rolfe, 1989).

Acute coronary heart disease

There appears to be no obvious increase in acute coronary heart disease events associated with Ramadan (Temizhan et al), although there is one anecdotal remark from Sudan pointing to a noticeable increase of angina pectoris during Ramadan (Gumaa et al). However, a few claims have been made that the fast of Ramadan has several benefits in reducing the likelihood of cardiovascular disease. Ramadan fasting has been shown to increase HDL cholesterol, while either lowering LDL cholesterol (Adlouni et al) or not affecting the levels of other cholesterol fractions (Maislos et al). Some of the apolipoprotein fractions associated with diminished risk of atherogenesis have also been shown to increase during Ramadan fasting (Adlouni et al).

Peptic ulcer complications

In a retrospective clinical study in Turkey, a slight but significantly increased rate of peptic ulcer complications was observed during Ramadan, compared with an equivalent period before Ramadan (Donderici et al).


In a western region of Saudi Arabia, an area with a high prevalence of urolithiasis, the effect of climatic changes, Ramadan fasting and pilgrimage festival on the occurrence of urinary stone colic in males was evaluated retrospectively (Al-Hadramy, 1997). There was a strong positive correlation between environmental temperature and the rate of urinary stone colic, but there was no significant change related to Ramadan or the Hajj.

Renal transplant patients

Daytime dehydration will induce a degree of stress on the concentrating ability of the kidneys. A group of 43 renal transplant patients, whose kidney function was assessed as being stable, demonstrated excellent concentration ability after a daylong Ramadan fast. A mean (range) urine osmolality of 826 (729–1000), mosm/kg at the end of the fast was similar to the mean 873 mosm/kg urine osmolality produced by a group of healthy, age-matched controls who had fasted for the same time (Rashed et al). In a similar study carried out in Saudi Arabia, 17 kidney transplant patients with normal functional ability and six with impaired but stable renal function were examined 1 week before, weekly during, and 1 week after the Ramadan fast (Abdalla et al). Urinary and serum biochemistry and haematocrit showed no significant changes. The authors concluded that it was safe for most Muslim renal patients to undertake the Ramadan fast 1 year after kidney transplantation. However, given the deteriorating effect of chronic hypohydration on renal function in animals with impaired renal function (Bouby & Fernandes, 2003), the number of transplanted patients with impaired but stable renal function is probably too small to draw definite conclusions.

TopPotential health concerns of intermittent dehydration and chronic hypohydration

In normal life, total body water content is subject to minor fluctuations throughout the day, but the water content of adults normally remains relatively constant on a daily basis. Body water is unavoidably lost to the environment as urine, in faeces and as respiratory and insensible transcutaneous water losses. Water may also be lost as sweat if body temperature is raised above that which can be maintained by non sweating mechanisms. Fluid intake occurs in the form of food and drinks, with the sensation of thirst underpinning drinking behaviour (Fitzsimons, 1972). Individuals usually ingest more fluid than they require to match obligatory water losses and the excess water intake is excreted by the kidneys as dilute urine. Drinking tends to be associated with eating and, in situations where access to food is restricted, fluid intake is often voluntarily reduced (Brown, 1947; de Castro, 1988). In situations where normal drinking and eating habits are altered, individuals may ingest significantly less fluid than usual, as they become more reliant on stimuli relating to actual body water deficit (Fitzsimons, 1972). The sensation of thirst in man may not be sufficient to induce drinking up to hypohydration levels equivalent to 2% of the body mass (Greenleaf, 1992) and in some situations to a 5% body mass loss (Brown, 1947).

Intermittent dehydration

During the daylight hours of Ramadan fasting, practising Muslims are undoubtedly dehydrating at a rate that is determined by the loss of body water minus the amount of metabolic water that is produced over this period. Acute changes in total body water are best characterized by repeated measurements of body mass. However, with small losses in body mass over a long period, any other changes in body composition may bias the calculation. Moreover, changes in functional water volume may be more important clinically than gross differences in total body water (Kampmann et al).

Water deprivation is functionally characterized by maximum urine concentration. In 20 Malaysian Muslims, urine was collected before, during and after Ramadan fasting each in the morning (0800–1200), afternoon (1200–1600) and overnight (1600–0800) (Cheah et al). The authors found that Ramadan fasting did not affect the overnight urine volume (values not given in the paper) or osmolality (means: 649–781 mosm/kg), indicating that the subjects were probably not subjected to severe water deprivation. Over the morning and afternoon collection periods, however, urine volume, sodium, potassium and total solute excretion were lower, and urinary osmolality was higher during Ramadan than either before or after Ramadan. During Ramadan, the osmolality of the urine samples collected in the afternoon were very high (means: 849–937 mosm/kg), indicating effective water conservation (Shirreffs, 2003) both by maximum urinary concentration and a decreased obligatory urine output. In 16 Sudanese Muslims, daytime urine volume and total daytime urinary sodium excretion were decreased during Ramadan fasting (Mustafa et al). Daytime urine osmolality tended to increase progressively throughout the month of intermittent fasting. At the end of the month of Ramadan, daytime urine osmolality was in the range of maximum urine osmolality and the osmolality of the urine voided overnight was also markedly elevated for the first time, indicating an additional stress due to water deprivation on this day. The mean urine osmolality of spontaneous urine samples from 15 Tunisian Muslims was already very high before (881 mosm/kg) and after (898 mosm/kg) Ramadan fasting hinting at a normal restricted daily fluid intake (Zebidi et al). During Ramadan, urine osmolality was even higher (1023 and 920 mosm/kg) 90 min before breaking their fast.

Several alternatives have been used to give estimates of hydration status of individuals (Shirreffs, 2003). In 12 Muslims fasting for 12–14 h, there was a significant increase in haematocrit (+11%), serum albumin (+4%) and serum creatinine (+12%), indicating hypohydration due to water deprivation (Born et al). Similar findings were observed in 15 fasting Tunisian Muslims, who also showed an average increase in serum urea of 23% (Zebidi et al), and in a group of fasting British Muslims who also demonstrated increases in serum sodium and chloride (Sweileh et al). In Kuwait, a significant increase in serum osmolality, sodium and bicarbonate was observed only in a group of fasting Muslims with sedentary lifestyles, but not in a comparable group of physically active Muslims (Ramadan et al). The authors of that study assumed that the likely higher fluid turnover of the active group allowed more precise regulation of the body fluids than that of the sedentary group (Ramadan et al).

The use of the stable isotopes oxygen-18 or deuterium oxide as tracers for water has meant that a simple and reliable assessment of daily water turnover (ie the volume of water entering and leaving the body daily) can be made in free-living individuals (Leiper et al). However, the correlation between daily water turnover and hypohydration resulting from a deficit of the balance of total or functional water volume is limited. Decreases in daily total fluid intake (in the form of beverages, preformed water in food and the water of oxidation of the diet) or increases in water losses if not adequately corrected obviously lead to dehydration. Estimates of the normal daily water turnover greatly differ in individuals in the countries where studies have been carried out to investigate the effects of Ramadan fasting on fluid balance. The average daily water turnover rate is approximately 2–3 l in healthy humans living normally in temperate environmental conditions (Leiper et al). Augmenting the daily fluid intake will speed the rate of water turnover as urine volume increases (Leiper et al), while exercise of sufficient intensity and duration will promote faster water turnover even in a cool ambient conditions (Leiper et al), and exposure to a hot environment can also accelerate sweating and raise the rate of water turnover (Brown, 1947). In most situations where water turnover rate is altered, the total body water content is usually conserved. In a recent study using an isotopic tracer technique in Malaysian Muslims (Leiper & Prastowo, 2000), it was demonstrated that total body water content was conserved during Ramadan although daily water turnover was reduced (Table 2). The decrease in water turnover in this study appeared to be due to a reduction in recorded fluid intake, but euhydration was maintained by a drop in nonrenal losses (Leiper & Prastowo, 2000). The daily mean (range) water turnover rates of 5.2 (3.2–9.0) l have been recorded in a group of Gambian women carrying out heavy agricultural work for more than 7 h in hot ambient conditions (Singh et al). Others have shown, however, that water turnover in hot desert conditions can be similar to that occurring in cooler environments if individuals are relatively inactive and they seek shade (Brown, 1947).

Table 2 - Fluid balance parameters measured during weekly periods before, during and after Ramadan.Full table

Most Muslims with a predominantly sedentary occupation have few problems or relevant clinical symptoms connected with Ramadan fasting. Physiologic studies show, however, that Ramadan fasting leads to impairment in muscular performance and to a decrease in orthostatic tolerance (Bigard et al). In those Muslims with psychosomatic complaints or headaches during Ramadan, intermittent dehydration may be a more important pathogenic factor than intermittent energy restriction. However, if fasting is extended (eg up to 18 h) on a daily basis and work is physically demanding, or has to carried out in a hot environment, complaints of tiredness, dizziness and nausea may become so predominant that both fasting and working have to stop to allow the individual to recover (Schmahl et al).

Chronic hypohydration

An actual decrease in total body water content is the most reliable measure of hypohydration and this can now be accurately and safely determined in humans using stable isotopes of water (Schoeller, 1996). For example, in the study by Leiper and Prastowo (2000)using deuterium oxide as a water tracer, it was demonstrated that total body water content was conserved during Ramadan although daily water turnover was reduced (Table 2). Theoretically, a cumulative negative water balance of more than 3% of total body water is indicative of hypohydration. To our knowledge, there are no valid data of total daily water intake and output of Muslims during Ramadan fasting in the literature. In an early study (Muazzam & Khaleque, 1959), a body mass loss over the month of Ramadan of 1.4 kg was reported and this loss was equated with a drop in 24 h urinary volume during this period. However, the mean urinary output only dropped from 1.4 l/d before Ramadan to 1.2 l/d during Ramadan, and this lower excretion rate was established by day 10 of the fast before there was any sign of body mass loss. There was no change in haemoglobin levels or of pulse rate seen throughout the study. A group of Sudanese Muslims showed signs that their hydration status was progressively stressed during Ramadan; at the end of the fasting month, the mean daytime urine osmolality was about maximum, however the urine passed through the night was fairly dilute. This suggests that there was compensation for daytime dehydration by increased drinking during the night, which prevented the individuals from becoming chronically dehydrated. A similar observation was made in Malaysian Muslims, who before, during and after Ramadan showed a relatively similar overnight urine osmolality that was well below the renal concentration maximum (Cheah et al). In one study observing a group of Tunisian Muslims, however, the daytime mean urine osmolality collected before and after Ramadan was already in the range of maximal renal concentration ability (Zebidi et al). Fasting during Ramadan led to a further increase in daytime urine osmolality. In this instance, chronic hypohydration during Ramadan appears to be a possibility, but as the osmolality of the overnight urine was not measured this hypothesis cannot be verified (Zebidi et al).

In a remarkable study in Gambian women, four dehydrating factors were combined (Prentice et al). This study was undertaken primarily to look at the effect of the fast on lactating mothers' milk output, but several indicators of hydration status were also measured. The study involved 10 Gambian mothers who were breastfeeding their infants and 10 nonlactating women from the same area, all of whom continued to carry out their normal strenuous agricultural work for approximately 7 h each day in conditions of high thermal stress during the Ramadan fast. Although the authors state that there was a gradual reduction in body mass over the entire study period, total body water content of the lactating mothers was at least conserved, and may have been slightly increased, during Ramadan (Table 3). The body water content on the nonlactating group was only measured during Ramadan (Table 3), but the values are quite similar to that of the lactating group, suggesting that none of the subjects in this study underwent chronic hypohydration during Ramadan. The body mass loss of the subjects during Ramadan was not reported, but the authors considered that the majority of the loss was due to reductions in adipose tissue, as a consequence of a decrease in energy intake. The daily mean water turnover rate of the non lactating women in this study was 4.4 l/d, which was only measured during Ramadan, and appears to be slightly slower than the median (range) 5.2 (3.2–9.0) l/d that Singh et al (1989) determined in a similar group of Gambian women carrying out much the same heavy agricultural work in comparable environmental conditions. The daily mean water turnover in the lactating mothers in this study was over 6 l/d before and during Ramadan (Table 3), while the mean urine output was almost 1 l/d (Table 4). Both the lactating and nonlactating women undertaking the intermittent fast of Ramadan developed a distinct acute dehydration before breaking the fast each day (Prentice et al). This was characterized by a body mass loss of 2.5 and 2.0 kg, respectively and an estimated 7.6 and 6.2% loss of total body water, respectively. There were also significantly increased levels of serum osmolality, sodium and uric acid, and high urine osmolalities in both groups. However, the osmolality of the morning urine collections were relatively low, indicating that no chronic hypohydration developed in either fasting group. Obviously, some individuals would develop a greater degree of acute intermittent dehydration, while it would be less for others. The authors of this study did not discuss any of the possible health effects of acute intermittent dehydration, except that it interfered with the normal process of breast-milk synthesis and secretion (Prentice et al).

Table 3 - Mean values for fluid balance parameters in lactating (Lact) and nonlactating (NL) women measured over a 24 h period before, during and after Ramadan.Full table

Table 4 - Mean values for 24 h urine parameters in lactating (Lact) and non-lactating (NL) Gambian women before, during and after Ramadan.Full table

Every year, millions of Muslims undergo Ramadan fasting all over the world in very different circumstances, resulting in some cases in additional dehydration stress. No detrimental effects on health have as yet been directly attributed to intermittent negative water balance at the levels that may be produced during Ramadan. However, epidemiological research is still sparse in this field, and it will be extremely interesting to see if the traditional exemptions from Ramadan fasting have also a modern scientific basis.

TopReferencesAbdalla AH, Shaheen FA, Rassoul Z, Owada AK, Popovich WF, Mousa DH, al-Hawas F, al-Sulaiman MH & al-Khader AA (1998): Effect of Ramadan fasting on Moslem kidney transplant recipients.Am. J. Nephrol. 18, 101–104. | PubMedAdlouni A, Ghalim N, Benslimane A, Lecerf JM & Saile R (1997): Fasting during Ramadan induces a marked increase in high-density lipoprotein cholesterol and decrease in low-density lipoprotein cholesterol. Ann Nutr. Metabol. 41, 242–249.Adlouni A, Ghalim N, Saile R, Had N, Parra HJ & Benslimane A (1998): Beneficial effect on serum apo AI, apo B and Lp AI levels of Ramadan fasting.Clin. Chim. Acta 271, 179–189.Afifi ZE (1997): Daily practices, study performance and health during the Ramadan fast. J. R. Soc. Health 117, 231–235.Al-Hadramy MS (1997): Seasonal variations of urinary stone colic in Arabia. J. Pak. Med. Assoc.47, 281–284.Ali MR & Amir T (1989): Effects of fasting on visual flicker fusion. Percep. Motor Skills 69, 627–631.Angel JF & Schwartz NE (1975): Metabolic changes resulting from decreased meal frequency in adult male Muslims during the Ramadan fast.Nutr. Rep. Int. 11, 29–38.Aslam M & Healy M (1986): Compliance and drug therapy in fasting Moslem patients. J. Clin. Hosp. Pharm. 11, 1–5.Awada A & al Jumah M (1999): The first-of-Ramadan headache. Headache 39, 490–493.Belkhadir J, el Ghomari H, Klocker N, Mikou A, Nasciri M & Sabri M (1993): Muslims with non-insulin dependent diabetes fasting during Ramadan: treatment with glibenclamide. Br. Med. J. 307, 292–295.Bener A, Absood GH, Achan NV & Sankaran-Kutty M (1992): Road traffic injuries in Al-Ain City, United Arab Emirates. J. R. Soc. Health 112, 273–276.Bigard AX, Boussif M, Chalabi H & Guezennec CY (1998): Alterations in muscle performance and orthostatic tolerance during Ramadan. Aviat. Space Environ. Med. 69, 341–346. | PubMed | ISI | ChemPortBogdan A, Bouchareb B & Touitou Y (2001): Ramadan fasting alters endocrine and neuroendocrine circadian patterns. Meal time as a synchronizer in humans. Life Sci. 68, 1607–1615.Born M, Elmadfa I & Schmahl FW (1979): Auswirkungen eines periodischen Flüssigkeits- und Nahrungsentzuges. Muench. med. Wschr.121, 1569–1572.Bouby N & Fernandes S (2003): Mild dehydration, vasopressin and the kidney: animal and human studies. Eur. J. Clin. Nutr.. in press.Brown AH (1947): Fluid intake in the desert. InPhysiology of Man in the Desert. ed. EF Adolph et al, pp 110–114. New York: Interscience Publishers.Chandalia HB, Bhargaua A & Kataria V (1987): Dietary pattern during Ramadan fasting and its effects on the metabolic control of diabetes. Pract. Diabetes 4, 287–289.Cheah H, Ch'ng SL, Husain R & Duncan NT (1990): Effects of fasting during Ramadan on urinary excretion in Malaysian Muslims. Br. J. Nutr. 63, 329–337.Ch'ng Sl, Cheah SH, Husain R & Duncan MT (1989): Effect of alteration of eating pattern on serum frutosamine: total protein ratio and glucose level. Ann. Acad. Med. Singapore 18, 326–327.Cross JH, Eminson J & Wharton BA (1990): Ramadan and birth weight at full term in Asian Moslem pregnant women in Birmingham. Arch. Dis. Child. 65, 1053–1056. | PubMedde Castro JM (1988): A microregulatory analysis of spontaneous fluid intake by humans: evidence that the amount of liquid ingested and its timing is mainly governed by feeding. Physiol. Behav. 43, 705–714.Donderici O, Temizhan A, Kucukbas T & Eskioglu E (1994): Effect of Ramadan on peptic ulcer complications. Scand. J. Gastroenterol. 29, 603–606.El Ati J, Beji C & Danguir J (1995): Increased fat oxidation during Ramadan fasting in healthy women: an adaptive mechanism for body-weight maintenance. Am. J. Clin. Nutr. 62, 302–307.Ertem IO, Kaynak G, Kaynak C, Ulukol B & Gulnar SB (2001): Attitudes and practices of breastfeeding mothers regarding fasting in Ramadan. Care Health Dev. 27, 545–554.Fedail SS, Murphy D, Salih SY, Bolton CH & Harvey RF (1982): Changes in certain blood constituents during Ramadan. Am. J. Clin. Nutr. 36, 350–353. | PubMed | ISI | ChemPortFitzsimons JT (1972): Thirst. Physiol. Rev. 52, 468–561. | PubMed | ISI | ChemPortFrost G & Pirani S (1987): Meal frequency and nutritional intake during Ramadan: a pilot study.Hum. Nutr. Appl. Nutr. 41, 47–50. | PubMed | ChemPortGarcia-Bunuel L (1989): Clinical problems during the fast of Ramadan. Lancet 1, 1396 (letter).Greenleaf JE (1992): Problem: thirst, drinking behavior, and involuntary dehydration. Med. Sci. Sports Exerc. 24, 645–656. | PubMed | ISI | ChemPortGumaa KA, Mustafe KY, Mahmoud NA & Gader AMA (1978): The effects of fasting in Ramadan: serum uric acid and lipid concentration. Br. J. Nutr.40, 573–581. | PubMedHallack MH & Nomani MZ (1988): Body weight loss and changes in blood lipid levels in normal men on hypocaloric diets during Ramadan fasting. Am. J. Clin. Nutr. 48, 1197–1210. | PubMed | ISI | ChemPortHeird WC (1996): Nutritional requirements during infancy. In Present Knowledge in Nutrition. 7th Edition, eds. EE Ziegler & LJ Filer, pp 38–39. Washington: ILSI Press.Husain R, Duncan MT, Cheah SH & Ch'ng SL (1987): Effects of fasting in Ramadan on tropical Asiatic Moslems. Br. J. Nutr. 58, 41–48. | PubMedKadri N, Tilane A, El Batal M, Taltit Y, Tahiri SM & Moussaoui D (2000): Irritability during the month of Ramadan. Psychosom. Med. 62, 280–285.Kampmann B, Manz F & Kalkowsky B (2003): "Voluntary dehydration": Loss of body mass and total body water, but almost no change of functional water volume. In Quality of Work and Products in Enterprise of the Future. eds H Strasser, K Kluth, H Rausch & H Bubb, pp 235–238. Publisher:Stuttgart: Ergonomia.Karaagaoglu N & Yucecan S (2000): Some behavioural changes observed among fasting subjects, their nutritional habits and energy expenditure in Ramadan. Int. J. Food Sci. Nutr. 51, 125–134.Katibi IA, Akande AA, Bojuwoye BJ & Okesina AB (2001): Blood sugar among fasting Muslims with type 2 diabetes mellitus in Ilorin. Nig. J. Med. 10, 132–134.Laajam MA (1990): Ramadan fasting and non-insulin-dependent diabetes: effect on metabolic control. East Afr. Med. J. 67, 732–736.Langford EJ, Ishaque MA, Fothergill J & Touguet R (1994): The effect of the fast of Ramadan on accident and emergency attendences. J. R. Soc Health 87, 517–518.Leiper JB, Carnie A & Maughan RJ (1996): Water turnover rates in sedentary and exercising middle aged men. Br. J. Sports Med. 30, 24–26.Leiper JB, Pitsiladis Y & Maughan RJ (2001): Comparison of water turnover rates in men undertaking prolonged cycling exercise and sedentary men. Int. J. Sports Med. 22, 181–185.Leiper JB & Prastowo S-M (2000): Effect of fasting during Ramadan on water turnover in men living in the tropics. J. Physiol. 528, 43 (abstract).Mafauzy M, Mohammed WB, Anum MY, Zulkifli A & Ruhani AH (1990): A study of the fasting diabetic patients during the month of Ramadan.Med. J. Malaysia 45, 14–17.Maislos M, Khamaysi N, Assali A, Abou-Rabiah Y, Zvili I & Shany S (1993): Marked increase in plasma high-density-lipoprotein cholesterol after prolonged fasting during Ramadan. Am. J. Clin. Nutr. 57, 640–642.Malhotra A, Scott PH, Scott J, Gee H & Wharton BA (1989): Metabolic changes in Asian Muslim pregnant mothers observing the Ramadan fast in Britain. Br. J. Nutr. 61, 663–672. | PubMedMosek A & Korczyn AD (1995): Yom Kippur headache. Neurology 45, 1953–1955.Muazzam MG & Khaleque KA (1959): Effect of fasting in Ramadhan. J. Trop. Med. Hyg. 62, 292–294.Mustafa KY, Mahmoud NA, Gumaa KA & Gader AM (1978): The effects of fasting in Ramadan. 2. Fluid and electrolyte balance. Br. J. Nutr. 40, 583–589.Opaneye AA, Villegas DD & Azeim AA (1990): Islamic festivals and low birth weight infants. J. R. Soc. Health 110, 1060–1007.Picciano MF (1996): Pregnancy and lactation. InPresent Knowledge in Nutrition. 7th edition, eds EE Ziegler and LJ Filer, pp 38–39. Washington: ILSI Press.Prentice AM, Lamb WH, Prentice A & Coward WA (1984): The effect of water abstention on milk synthesis in lactating women. Clin. Sci. 66, 291–298.Prentice AM, Prentice A, Lamb WH, Lunn PG & Austin S (1983): Metabolic consequences of fasting during Ramadan in pregnant and lactating women. Hum. Nutr. Clin. Nutr. 37C, 283–294.Qaisi VG (2001): Increasing awareness of health concerns during Ramadan. J. Am. Pharm. Assoc.41, 511.Ramadan J, Telahoun G, Al-Zaid NS & Barac-Nieto M (1999): Response to exercise, fluid, and energy balances during Ramadan in sedentary and active males. Nutrition 15, 735–739.Rashed AH, Siddiqui SA & Adu Romeh SH (1989): Clinical problems during fast of Ramadan. Lancet1, 1396 (letter).Richards EG (1998): Mapping Time: The Calendar and its History. pp 231–235. Oxford: Oxford University Press.Roky R, Chapotot F, Hakkou F, Benchekroun MT & Buguet A (2001): Sleep during Ramadan intermittent fasting. J. Sleep Res. 10, 319–327.Roky R, Iraki L, HajKhlifa R, Lakhdar Ghazal N & Hakkou F (2000): Daytime alertness, mood, psychomotor performances, and oral temperature during Ramadan intermittent fasting. Ann. Nutr. Metab. 44, 101–107.Sakr AH (1975): Fasting in Islam. J. Am. Diet. Assoc. 67, 17–21.Schmahl FW, Metzler B, Born M & Elmadfa I (1988): Ramadan, Gesundheitsgefährdung während des Fastenmonats. Dt. Ärztebl. 85, B-842–B-844.Schoeller DA (1996): Hydrometery. In Human Body Composition. eds AF Roche, SB Heymsfield & TG Lohman, pp 25–43. Champaign, IL: Human Kinetics.Shah PA & Nafee A (1999): Clinical profile of headache and cranial neuralgias. J. Assoc. Physic. India 4, 107–107.Shirreffs SM (2003): Markers of hydration status.Eur. J. Clin. Nutr. in press.Singh J, Prentice AM, Diaz E, Coward WA, Ashford J, Sawyer M & Whitehead RG (1989): Energy expenditure of Gambian women during peak agricultural activity measured by the double-labelled water method. Br. J. Nutr. 62, 315–329. | Article | PubMed | ChemPortSweileh N, Schnitzler A, Hunter GR & Davis B (1992): Body composition and energy metabolism in resting and exercising Muslims during Ramadan fast. J. Sports Med. Phys. Fitness 72, 156–163.Tang C & Rolfe M (1989): Clinical problems during fast of Ramadan. Lancet 1, 1396 (letter).Taoudi Benchekroun M, Roky R, Toufiq J, Benaji B & Hakkou F (1999): Epidemiological study: chronotype and daytime sleepiness before and during Ramadan. Therapie 54, 567–572.Temizhan A, Donderici O, Ouz D & Demirbas B (1999): Is there any effect of Ramadan fasting on acute coronary heart disease events? Int. J. Cardiol. 70, 149–153. | Article | PubMed | ISI | ChemPortTyson JE, Austin K, Farinholt J & Fieldler J (1976): Endocrine-metabolic response to acute starvation in human gestation. Am. J. Obstet. Gynecol. 125, 1073–1084.Zebidi A, Rached S, Dhidah M, Sadraoui M, Tabka Z, Dogui M, Sfar H, Chaieb M & Chaieb A (1990): The effect of Ramadan fasting on some plasmatic and urinary parameters. Tunisie Med. 68, 367–372.

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Friday, June 3, 2016

Shoes and bags need disinfection to prevent Zika infected mosquito transmission. Aleem M A. Hakkim A M: BMJ 2016;353:i2899


Call to cancel 2016 Olympics because of Zika risk is not backed by WHO guidance

BMJ 2016 ; 353 doi: (Published 20 May 2016)

Cite this as: BMJ 2016;353:i2899

Rapid response

Re: Call to cancel 2016 Olympics because of Zika risk is not backed by WHO guidance

Shoes and bags need disinfection to prevent Zika infected mosquito transmission

Zika viral spread during the Olympics in Brazil is not a threat to conductig the events in its capital. But precautions should be taken by participants in preventing the spread and acquiring of Zika viral infection. To prevent mosquito transmission to their home towns all the shoes and bags should be disinfected before depature and on arrival.
Competing interests: No competing interests
03 June 2016
MA Aleem
AM Hakkim
ABC Hospital Trichy. Apollo Hospital Ttichy . Dhanalakshmi Srinivasan Medical college and Hospital Perambalur
No 1 Annamalainagar Trichy 620018 Tamilnadu India