This page contains summaries of health related news which we think may be of interest to readers of this website. Hopefully the contents will serve to inform and to pique your interest in health matters. Eventually we hope you will be empowered to take more control of various health issues which impact you and your family.
The content of this page is changed weekly, usually on a Monday. Any comments or suggestions related to this news feature are welcome. So, read on …
Archive for September, 2007

Snoring & obstructive sleep apnoea

September 24th, 2007

Sleeping in the same room as someone who snores loudly can be difficult and disruptive. (Snoring is the sound of turbulent air moving through the back of the mouth, nose and throat.) The partner who is disturbed by the snoring may feel that the snorer is having a good nights sleep. However, that might well be far from the truth.

Someone who snores may well be suffering from obstructive sleep apnoea (OSA). These individuals typically snore loudly during sleep. The snoring is interrupted with periods of silence due to a cessation of breathing (called apnoea). This arrest of respiration is followed by a gasp and the resumption of breathing. Although these individuals appear to be asleep throughout the night, they have a restless sleep and, during the day, they are plagued by excessive daytime sleepiness. In dramatic cases, someone with severe OSA can fall asleep for brief periods during conversations with others at social gatherings! One of the treatment methods for OSA is to use continuous positive airway pressure (CPAP) ventilation during sleep. This involves going to sleep wearing a face mask with a tube attached to a machine that blows pressurized air into the mask and through the airway to keep it open. The most serious consequence of prolonged severe OSA is the development of increased arterial pressure in the lungs which is transmitted back to the right heart. Prolonged raised right heart pressure then leads to congestive heart failure, called cor pulmonale. In some patients with severe heart failure, heart transplantation may be the only solution!

The Toronto Rehabilitation Institute studied 164 patients with heart failure to determine if there was a difference in the death rate between patients with mild to no sleep apnoea (M-NSA) and patients with untreated moderate to severe OSA (J Am Coll Cardiol 2007; 49: 1625 – 1631). The researchers found that the death rate in the untreated OSA patients was twice that in the M-NSA patients. In another study from the University of Toronto, the researchers studied patients with central sleep apnoea (CSA) and heart failure who were treated with CPAP. (CSA is a form of OSA; Circulation 2007 115: 3173 – 3180) They found two distinct groups of patients – one group of patients whose CPAP did reduce the apnoea-hypopnoea index to < 15 events / hour of sleep (CPAP-CSA suppressed) and another group whose CPAP did not reduce the index to < 15 (CPAP-CSA unsuppressed). The CPAP-CSA suppressed patients experienced a greater increase in the left ventricular ejection fraction at 3 months (which means better heart function) and significantly better transplant-free survival than the unsuppressed patients.

It is important to realize that not everyone who snores has OSA. However, there is one group of ‘healthy’ individuals which is more at risk of developing OSA – obese individuals! In this millennium, obesity is a major problem in every corner of the globe. According to old Chinese beliefs, being obese is a sign of prosperity. If prosperity means increased risk of developing type II diabetes, heart problems, high blood pressure, arthritis, certain types of cancer and OSA, I’d rather forgo prosperity and stick with a lean healthy body. If you are obese and suffer from excessive daytime sleepiness, you might want to consult your doctor to rule out the diagnosis of OSA. In the meantime, lose some weight, you might get to live longer in order to enjoy whatever prosperity is left.

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Extra butter flavoured microwave popcorn

September 17th, 2007

An evening at the cinema is incomplete without the popcorn and soft drink. With the advent of DVD movies and DVD movie rental shops, more and more people are watching movies at home. With microwave technology you can now make your own fresh popcorn in the kitchen. Put one packet of extra butter flavoured microwave popcorn into the microwave, set it on high for 3 minutes and voila! You have a big bowl of perfectly made popcorn with its rich buttery smell wafting into the living room! If you do this on a regular basis, you might just like to know that that lovely buttery smell may be a potential health hazard.

A news article by Associated Press on 5th September reported that a lung specialist at Denver’s National Jewish Medical and Research Center has written to the federal agencies informing them that they may have the first case of a consumer who developed severe lung disease from the fumes of microwaving popcorn. The man consumed several bags of extra butter flavoured microwave popcorn every day for several years. He progressively developed coughing and shortness of breath over the years. When he was told to stop using microwave popcorn, his condition seemed to stabilise.

Butter flavouring contains a compound called diacetyl. Diacetyl is also used in other flavouring industries. The first report linking obstructive lung disease with the microwave popcorn industry was in May 2000. An occupational medicine physician contacted the Missouri Department of Health and Senior Services (MoDHSS) to report the occurrence of fixed obstructive lung disease in 8 former workers of a microwave popcorn factory. At the factory, soybean oil, salt and flavourings are mixed into a large heated tank in a process that produces visible dust, aerosols and vapours with a strong buttery odour. The authorities analysed the patients according to their work proximity to the mixing tank: mixing workers who had direct contact with the tank; microwave-packaging workers who worked 5 – 30 metres from the tank and workers in other areas > 30 metres from the tank. All the cases involved workers who had direct contact with the tank or worked within 30 metres of the tank. (To read the report by MoDHSS go here)

In August 2004 the California Department of Health Services (CDHS) and Division of Occupational Safety and Health (Cal/OSHA) received the first report of a case of bronchiolitis obliterans in a flavour-manufacturing worker in California. In April 2006 a second case in a flavour-manufacturing worker from another company was reported. Neither worker was employed in the microwave-popcorn industry but both worked in a flavour-manufacturing industry which produced artificial butter flavouring and other flavours such as cherry, almond, praline, jalapeno and orange. Both workers had handled pure diacetyl and other additional chemicals. Since April 2006 five additional cases have been discovered; all were working in the flavouring industry. All seven cases occurred in individuals without any known pre-existing lung problems. (To read the report by CDHS go here)

At present, safe occupational exposure levels for diacetyl and many other flavouring chemicals have not been established. Only guidelines are available to employers on how to implement measures to minimize exposure at the work place. As for those of us who love making microwave popcorn at home, I would suggest you make sure the kitchen is well ventilated before you press the start button on your microwave. When you take the popcorn out of the microwave just resist that long, deep breath! You can still enjoy the popcorn in front of the TV.

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Food additives & children behaviour

September 10th, 2007

Parents of very active children sometimes wonder if they have a hyperactive child on their hands. Indeed they might secretly fear that the child could be suffering from attention-deficit hyperactivity disorder (ADHD) which is the most common cognitive and behavioural disorder diagnosed among school children. Children with ADHD have problems maintaining attention and in problem solving. They are also hyperactive and have difficulty withholding incorrect responses. It is estimated that the prevalence of ADHD in children is 4 – 5%. This can persist into adulthood and the ADHD prevalence in adults is thought to be 4%. While a substantial proportion of the cause of ADHD is genetic, published studies have also shown that many environmental risk factors and potential gene-environment interactions may increase the risk of the disorder. ADHD is probably at the extreme end of a spectrum of very active children. Not infrequently, parents may well have noticed that their children have periods of being agitated and unable to concentrate on tasks. However, these do not occur daily and there is no real fixed pattern. Is this ADHD or is there an alternative explanation?

A group of researchers from Southampton University carried out a double blind, cross-over study on 3-year-old and 8 / 9-year-old children in the community to see if intake of artificial food colour and additives (AFCA) affected childhood behaviour (The Lancet 2007 September; Epub DOI:10.1016/S0140-6736(07)61306-3). They studied one hundred and fifty three 3-year-old and one hundred and forty four 8 / 9-year-old children. They were challenged with 3 types of juice drink: Mix A and B both contained sodium benzoate (E211) and one of two AFCA mixes. The third drink was a placebo mix. The children were monitored and a global hyperactivity aggregate (GHA) score was obtained. The 8 / 9-year-old children also had a computerized test of attention. The study showed that when the 3-year-old children had consumed more than 85% of the juice, their behaviour was adversely affected by Mix A but not by Mix B, when compared to placebo mix. The adverse effect of Mix A on the 3-year-old children was greater than that seen in the 8 / 9-year-old children. However, in the 8 / 9-year-old children, their behaviour was adversely affected by both Mix A and B. (The additives used were E102, E110, E122, E124 and E129.) 

Since the 1920s, we have been deliberating whether food and the environment can affect human behaviour or not. While the argument cannot be settled by this study alone, it probably has given some succour to parents with children who become hyperactive ‘out of the blue’. With some detective work, these parents may well be able to tease out what food or drinks might cause the hyperactive episodes. To me the study raises another interesting point. An agent (such as colourings, preservatives), when taken in sufficient quantity, may have no effect on a child at the age of 5, but when consumed at the age of 13 makes him jump about like a monkey. Furthermore, among children of a similar age, the additive(s) can give rise to a range of responses.

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