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  ‘Carbohydrates’ is a term that dates back to the early 18th century, when chemists studied glucose (C6H12O6) and other similar chemicals. They noticed that they could write their chemical formulae as ‘hydrated carbon’—a bunch of carbon atoms (C) joined to a bunch of water molecules. (Glucose would therefore be seen as six C atoms plus six H2O molecules.) Nowadays, we know that some carbohydrates don’t follow this simple formula, but we’re stuck with the name.

  ‘Digestible carbohydrates’ are your regular carbohydrates. The various enzymes in your small intestine will break them down to smaller chemicals, releasing about 16 kJ of energy per gram.

  ‘Indigestible carbohydrates’, the so-called fibre, should really be called ‘partly digestible carbohydrates’, but that’s a big mouthful. They can’t be digested in your small intestine. However the bacteria in your large intestine can partly break them down and get some energy out of them. It’s a win-win situation—both you and the bacteria get energy out of the ‘fibre’. In fact, if you didn’t have the bacteria there, you would get no energy out of the fibre—but because of the bacteria, you get about 8 kJ per gram.

  Energy Tax in Birds

  Human beings are pretty ‘lazy’ when compared to other critters. For example, some tiny Antarctic birds can maintain a high Metabolic Rate for days, even weeks.

  While in Antarctica, Mark Chappell, a biologist from the University of California at Riverside, studied cute little Adelie Penguin (Pygoscelis adeliae) chicks. These baby penguins appeared to be totally lazy—begging food from their parents while sitting perfectly still in the same spot for days at a time. But Chappell discovered that they were actually working very hard.

  If the stomach of an Adelie Penguin chick happens to be empty, the bird is burning up energy three times faster than human beings do. And when they get fed, they double this rate of burning energy again.

  Why do these baby penguins burn up so much energy? Probably because they are the preferred food of a predatory seabird called the skua (or jaeger). These predatory birds see the cute penguin chicks as small, juicy and defenceless food targets. So the baby penguins need to bulk up as quickly as possible so that they will appear more menacing and look as if they could defend themselves against an attacking skua.

  Any sumo wrestler or couch potato can tell you that if you really want to put on some weight, you should eat a lot and do nothing. This is why the penguin chicks just sit in one spot and grow fat and, hopefully, big enough to avoid getting eaten by a predatory seabird.

  Big and Little Calories—Confusing

  I would like to apologise for the fact that calories can be big or little.

  The standard definition for ‘calorie’ in Physics books states that one calorie is the amount of energy needed to heat one gram of water by one degree Celsius. But nutritionists define their ‘calorie’ as being 1000 times bigger than the Physics ‘calorie’—and they use the same spelling for the word ‘calorie’ and don’t even have the Big Calorie spelt with a capital ‘C’.

  Until I realised this, it confused the heck out of me.

  References

  Harris, J. Arthur and Benedict, Francis G., ‘A Biometric Study of Human Basal Metabolism’, Proceedings of the National Academy of Sciences, December 1918, pp 370–373.

  Pearson, Helen, ‘Freaks of nature?’, Nature, 21/28 December 2006, pp 1000, 1001.

  Roan, Shari, ‘Less than zero’, Los Angeles Times, 27 November 2006.

  Secor, Stephen M. and Diamond, Jared, ‘Adaptive responses to feeding’, The Journal of Experimental Biology, 1995, pp 1313–1325.

  Wolke, Robert L., What Einstein Told His Cook, New York: W. W. Norton & Company, 2002, pp 6, 7, 25–27.

  Zaidan, Frederic III and Beaupre, Steven J., ‘Effects of body mass, meal size, fast length, and temperature on specific dynamic action in the timber rattlesnake’, Physical and Biochemical Zoology, April 2003, pp 447–458.

  Near-Death Experience—The Living End

  Most of us have a reasonable idea of what a Near-Death Experience (NDE) is. It’s supposed to happen while you are in the actual process of dying—but if you don’t actually die, you get to talk about the NDE.

  During an NDE you might hear strange noises and have feelings of blissful peace and joy sweeping over you. You might then float out of your body, seeing it from above, and head towards a tunnel. You enter the tunnel. At the far end of the tunnel is a bright light. As you get close to the light, you are met by someone already dead, who tells you that this is not yet your time, and regretfully, you are plunged back to our prosaic planet with the rest of the Great Unwashed. In fact, this rather complex hallucination comes from your own Personal Theatre of the Mind.

  In a nutshell, it is commonly believed that the NDE happens only to those who are dying and that it is proof of an afterlife—but neither belief is correct.

  History of NDE

  In 1926, Sir William Barrett, a Fellow of the Royal Society, published a slim volume on deathbed visions, in which the survivors described to him the basic elements of the NDE.

  However, the NDE became very popular in 1975, with the publication of Raymond Moody’s bestselling book, Life after Life, which recounts the anecdotes of over 50 survivors. At first, there was some resistance to the concept of the NDE, but with further research, it was found to be surprisingly common.

  Over the years, researchers have gathered some statistics.

  About 60% of people have a positive NDE experience and about 30% are separated from their body. About 23% enter a dark tunnel, about 16% see a light in the tunnel, while 10% actually enter it.

  Stay away from the light

  A Near-Death Experience (NDE) is supposed to happen while you are in the actual process of dying—but if your don’t actually die, you get to talk about your NDE.

  Who Has an NDE?

  About 10–20% of survivors of heart attacks report having an NDE. Similar figures come from survivors of electrocution, coma, attempted suicide, near-drowning, massive shock due to blood loss, bacterial infection and anaphylactic shock.

  As you can see, NDEs can happen under many circumstances. And there doesn’t seem to be any common factor.

  NDE Without Death?

  You don’t have to be dying to have an NDE.

  Near-Death Experiences can happen even when you are not close to dying (despite the ‘D’ in NDE). For example, the training of combat fighter pilots can involve high G-forces in a centrifuge, which forces the blood away from the brain to the feet—leading to unconsciousness. Dr James A. Whittery, former chief aeromedical scientist for the US Naval Air Warfare Center, gathered data on some 1200 pilots, more than 200 of whom experienced NDEs. The typical pathway involves a greying of the vision, followed by total blackout and vivid dreams. Some 20% of pilots who blackout in this centrifuge training later report classic NDEs with the out-of-body experience.

  And to further separate the NDE from death, look at hospital situations where patients report an NDE. Half of them would have survived without any medical intervention—in other words, they were nowhere near death. And yet they had classical NDEs.

  Consciousness

  We still don’t know exactly what causes an NDE, simply because the brain is so fiendishly complicated—as is the whole concept of consciousness. Consciousness begins with knowledge about the world both outside and inside our skin.

  The brain receives information from our primary senses, i.e. vision, sound, taste, smell and touch. Skin sensors add information on temperature, pain and pressure, while sensors in the ear provide information about balance and orientation. Other sensors in the joints, tendons, muscles and bones tell the brain where our limbs are located.

  All of these bits of information, and many more as well, flow into our brain like many rivers into a sea, to give us the strange perception that we call ‘consciousness’.

  Cause of NDE

  As a result, there are dozens of theories about what causes an NDE. These include bizarre electrical
activity in parts of the brain; endorphins in the brain stem; as-yet-undiscovered hypothetical chemicals in the brain such as endopsychosin; intrusion of our normal REM dream sleep into our consciousness and stimulation of the vagal nerve. All of these theories have some elements of fact to back them up and are probably all involved in varying amounts, depending on the person having the NDE.

  But recently, Dr Olaf Blanke, a neurologist at the École Polytechnique Fédérale de Lausanne in Switzerland, was able to consistently duplicate some of the elements of the NDE in the laboratory. He stimulated, with electricity, a part of the brain called the left angular gyrus. Patients immediately reported the impression of a shadowy person lurking behind them, parallel to them. And when he stimulated the right angular gyrus, they reported that they left their physical body and could look down on it from above—the classic out-of-body experience.

  Living End

  At some stage in the future, we might know enough about the brain to fully understand the Near-Death Experience. But right now, we know two facts about the NDE. First, you don’t have to be dying to have one. Second, the NDE neither proves nor disproves the existence of an afterlife.

  OBE = Out-of-Body Experience

  In an Out-of-Body Experience (OBE), a person sees their body and the world from a location outside their regular physical body. They feel that they are awake, even while looking down at their sleeping body.

  These experiences are surprisingly common. If you look at people who have had at least one OBE in their whole life, the statistics range from 8% in Iceland to over 50% in ‘special’ groups such as marijuana users. The experience usually lasts for less than a minute.

  References

  Blackmore, Susan, ‘Near-death experiences: in or out of the body?’, Skeptical Inquirer, 1991, Vol 16, pp 34–45.

  Blakeslee, Sandra, ‘Out-of-body experience? Your brain is to blame’, The New York Times, 3 October 2006.

  Blanke, Olaf, et al., ‘Induction of an illusory shadow person’, Nature, 21 September 2006, p 287.

  Fox, Douglas, ‘Light at the end of the tunnel’, New Scientist, 14 October 2006, pp 48–51.

  Nelson, Kevin R., et al., ‘Does the arousal system contribute to near death experience?’, Neurology, April 2004, pp 1003–1009.

  van Lommel, Pim, et al., ‘Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands’, The Lancet, 15 December 2001, pp 2039–2045.

  Leprosy, Limbs and Lies

  I was recently rereading a favourite article, ‘A short history of leprosy in postage stamps’, when I suddenly wondered what the average person thought leprosy was. I asked a random passer-by (okay, my daughter) and she said something along the lines of ‘their hands and legs fall off, and sometimes even their heads’. I’m sure that she meant their noses rather than their heads. However, like many of us, she believed that leprosy caused bits of your body to fall off—but this is not true.

  History of Leprosy

  The word ‘leprosy’ comes from the ancient Greek words lepros meaning ‘a scale’ and lepein meaning ‘to peel’.

  Leprosy has afflicted human beings for many centuries. It existed in ancient China, India and Egypt as far back as 6000 BC.

  It was probably introduced into Europe by Alexander the Great around the 4th century BC. It later reappeared in Europe with the returning legions of Pompey into Italy after the war with King Mithridates of Pontus in the 1st century BC. There is evidence of leprosy in Great Britain and France as far back as 500 AD. The Vikings then apparently carried it back to Scandinavia from Great Britain. (By 1230 AD there were 250 leper hospitals, or leprosaria, in England alone.) The incidence of leprosy in Europe peaked in the 14th century. At this stage, there were about 300 leprosaria across northern Europe. To warn uninfected people to keep their distance lepers had to carry a warning bell. However, they were allowed to gain comfort from their religion. For this reason small, round ‘leper holes’ were made in the walls of many churches, so that they could at least see a church service—but from the outside.

  Although already on the decline in Europe, leprosy was brought to the New World by explorers in the 16th century. It was later introduced to Australia and the Pacific Islands. In fact, between 1920 and 1929, 35% of the entire population of Nauru was infected with this disease.

  In Western Australia during the 1930s, Aboriginal lepers were confined above the 25th parallel, which became known as the ‘Leper Line’. They were sometimes kept in chains while waiting for a ship to transport them to the Commonwealth Leper Station in Darwin. Once they arrived, they were crammed into very small compounds or shelters, often left open to the weather. However, white patients with leprosy were sent to the far more salubrious Wooroloo Sanitorium (an infectious diseases hospital) near Perth. The white lepers lived in small comfortable rooms (with fireplaces) near the sea, where the food was excellent and the staff cleaned for them.

  In the past lepers were expected to live in isolated leper colonies. Such colonies still exist today in India, the Philippines and Vietnam.

  Leprosy rates in Australia are only about one case per million, with higher rates in indigenous Australians and immigrants from countries where the disease still exists. Worldwide, leprosy is endemic in Angola, Brazil, Central African Republic, Democratic Republic of Congo, India, Madagascar, Mozambique, Nepal and the United Republic of Tanzania. There are also instances of leprosy in parts of the USA.

  Leprosy and Stamps

  Many countries have released stamps relating to leprosy.

  In 1948, Cuba celebrated the International Leprosy Conference when the disease was first given its modern classification. In 1964, Belgium released a stamp for World Leprosy Day. In 1973, the centenary of Hansen’s discovery of the bacterium, more than a dozen countries commemorated his work with stamps.

  In 1971, Fiji released a stamp when it closed its old leper hospital. This is the first and probably the only stamp relating to leprosy that has been released by any British administration.

  Leprosy is now known as Hansen’s Disease

  Leprosy is now called Hansen’s Disease after Armauer Hansen, the Norwegian who in 1873 discovered the bacterium (Mycoacterium leprae) that caused Leprosy.

  Christianity and Leprosy

  St Francis of Assisi (1181-1226 AD) took special interest in caring for lepers. Around the late 1200s, many Christian Knights formed various Orders to care for the unwell, including lepers. One of the first of these was the Order of the Hospital of St John of Jerusalem.

  In 1873, a Belgian priest called Father Damien set up a leper colony on the Hawaiian island of Molokai. He contracted the disease in 1884 and died of it in 1889.

  Cause of Leprosy

  Leprosy is now called Hansen’s Disease, named after Armauer Hansen, the Norwegian who in 1873 discovered Mycobacterium leprae, the bacterium that caused it. In fact, it was the very first bacterium to be discovered that caused a human disease.

  There is a reason why it was discovered in Norway. Although leprosy was in general decline throughout most of Europe, it was endemic (two cases per 1000 population) in Norway. At the time, Norway was a deprived and neglected colony of Denmark and along the Norwegian west coast in winter there was massive overcrowding, thanks to the poor housing conditions.

  Spread of Leprosy

  It turns out that leprosy is not as highly contagious as was once thought. In fact, most people who are exposed to the bacterium will never get the disease. While it is still not exactly clear how the disease is contracted, it is thought to be spread from human to human by respiratory droplets. It is probably not spread through intact skin but possibly through broken skin.

  After exposure it can take a long time to develop leprosy, even up to 50 years. The average incubation period is about 5–10 years.

  Pathology of Leprosy—Overview

  Leprosy affects the skin, the nerves and the lining of the upper respiratory tract.

  Think about it as a two-stage disease. First,
the bacteria attack you and, in return, your immune system responds. Second, you lose the motor and sensation functions of your nerves.

  It then gets more complicated. Leprosy affects people differently, depending on their genetic make-up.

  In fact, genetic make-up is so important to leprosy that 90–95% people who are exposed to the disease never become infected. Only 5–10% of people are susceptible to leprosy. Some of those saintly missionary types were susceptible and some were not—but they didn’t know it at the time.

  If left untreated, leprosy can cause collapse of the nose, clawed hands, dropped feet and bending and shortening of the fingers and toes. It can also cause blindness.

  Pathology of Leprosy—Details

  If your immune system responds vigorously, you will suffer a mild version of the disease—the paucibacillary (or tuberculoid) type.

  With this type of leprosy your skin is less affected. Because your own cells crowd in around the invading bacteria in an attempt to seal them off, small nodules (or tubercules) appear in the skin. The robust reaction of the immune system involves the full thickness of the skin around the nodule, including the sweat glands and the nerves. This results in a firm, dry spot on the skin where there is no sensation of temperature, and very importantly for the myth, no sensation of touch. The immune system response is a doubleedged sword. It stops the bacteria from spreading rapidly but also causes damage to the local tissues. Usually, the disease progresses slowly and irreversibly, although this type of leprosy will sometimes spontaneously disappear as your immune system overcomes it.