1. Decide on a reasonable bedtime for the child. There are no rigid rules for this. It depends on a number of factors, including the number and length of his daytime naps, the amount of sleep the child seems to need at night, the time of awakening in the morning and so on.

2. Establish a set routine that begins 30 minutes before the actual bedtime. Tell the child that it will be bedtime in 30 minutes. Each routine will vary according to child preferences, family routines and so on, but it must be adhered to. A typical routine may involve the child changing into pyjamas, brushing teeth, playing a game with a parent, reading a bedtime story, then saying goodnight to various toys and pets and kissing family members. All of these activities should be quiet so as not to overstimulate the child. Strenuous physical activities are not a good idea.

3. At bedtime, take the child into his bed, tuck him in, say goodnight (Til see you in the morning’), turn off the light (apart from a night light, if the child has one), and leave the room. Some children may like to take a cuddly toy to bed — this is fine.

4. If the child calls out, ignore it. Do not reason in any way. Resist the temptation to call out ‘Go to sleep’. You should not say anything, no matter how desperate the calls and pleas become (and they will become increasingly desperate — young children have an amazing and endless repertoire of wishes and requests designed to tug at the heartstrings of even the most hardened parent).

5. If the child cries, ignore it. The crying may sound as if the child is verydistressed, and persist for a very long time, but the parents must ignore it. To allow the child to cry for a long time and then go in will simply teach him that if he cries for long enough then eventually the crying will be rewarded by the appearance of a parent.

6. If the child comes out of his room take him straight back, without saying a word. Talking to the child or explaining what or why is taken by the child as a form of reinforcement, and will guarantee that the behaviour will continue. It may be necessary to take the child back literally dozens of times initially. Again it is important not to weaken in this resolve — if parents give up in the middle of such an intervention, the child learns that as long as he keeps coming out of the room, sooner or later the parents will weaken and allow him to stay out.

Sometimes a gate can be placed across the bedroom door to prevent the child from leaving the room. This is less frightening for parents and child than locking the door.

7. The next morning, if the child has gone to bed with a minimum of fuss, he should be praised for being ‘such a good/big/grownup boy’. Sometimes a material reward may be given, though there is a danger that the child may come to expect a treat every time.

Sometimes extinction or controlled crying is used for the child who resists going to bed, but this is generally not as successful in this situation as it is for the child who wakes during the night.

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The one experience people worry about is the sensation of their body relaxing. Sometimes people have been so tense for so many years they have forgotten what it is like to feel even slightly relaxed. As their bodies begin to let go of the tension, people become anxious and interpret the sensations as a sign that their worst fears are about to come true. They don’t.

The first stage of meditation can be difficult for beginners. Our thoughts are not used to being ignored and they continually break through and demand attention. As long as we can accept this as normal and let go of them without becoming frustrated, we can move into the second stage of meditation.

As we enter the second stage of meditation we feel the quiet settle over us. Our breathing begins to slow down. Our thoughts are still rising and falling, but our attention is now much more focused on our technique. Everything moves into the background as our quietness grows.

We enter the third stage. Our breathing slows down even further and our body becomes deeply relaxed. We may feel as if we are as light as a feather, or we may feel a comfortable heaviness. We become aware that the continuous stream of thoughts has broken. They now rise slowly and separate from each other. Individually, they quietly rise and fall without us becoming distracted by them. We find our word or mantra becomes distorted. This is what is supposed to happen. Some of us may see brilliant white, black or other swirls of colour. We can use them to take ourselves deeper. Our thoughts drift in and out, slowly and quietly.

We then enter the full meditative state in which there is perfect quietness, an absence of thought, feeling or emotions. Unlike the stages of deep sleep, this state of consciousness is very dynamic. There is full awareness of ‘nothing’, but in that ‘nothing’ is an awareness of ‘every-thing’. In this state there is no technique and no thoughts or feelings-just an all-pervasive quiet. Yet we are aware of everything and in full control. When we think ‘this is wonderful’ the quiet is broken by that thought, but we can return to the quiet simply by returning to our technique.

This is meditation.

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Frequent Waking

Elizabeth is nine months old and I haven’t gotten a full night’s sleep since she was born.

Frequent waking is a problem when a child wakes more than you expect for her developmental level—or more than you can tolerate. This may be once or several times a night.She might never have developed the pattern of sleeping for a long stretch or never learned to get back to sleep after normal nighttime arousals. The problem might be related to difficulty getting to sleep alone. She may have learned to need and expect help from her parents to get back to sleep. Or ne night waking might be stimulated by illness, dreaming, or developmenl disequilibrium. In those cases, she may need to re-learn getting herself back sleep for a long stretch.

Waking for Feeding

I give him a bottle and he goes right back to sleep, but I wonder if he real needs it. Some infants simply sleep through the expected feeding time, others continue waking long after what seems developmentally appropriate. This chi never learns the pattern of sleeping a long stretch. He requires food to satisfy “learned hunger” or requires sucking and comforting to get back to sleep.

Difficulty Getting to Sleep

After the third glass of water, I’m ready to scream! She is afraid of the monsters in her closet. This problem can affect all ages. Bedtime is drawn out and battles get worse and worse. Parents cajole, threaten, and bribe, and then they wonder how things got so out of control. There can be many reasons for this, including fears separation anxiety, and simply not having learned the skill of getting to sleeep on one’s own.

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Diarrhoea due to malabsorption can often be corrected by a special diet and medications to help the bowel break down and absorb fats. If the malabsorption is due to blockage of the tubes running from the liver or pancreas to the bowel, it may be possible to correct this surgically. Just because it is possible does not necessarily mean it is best. Check the likely costs and benefits carefully.

Whether or not the cause of your diarrhoea is being tackled, you should take something to control it in the meantime. Anti-diarrhoea drugs work by slowing down the bowel muscle ^nd/or making the motions more solid. Chemical names of some good ones include kaolin, pectin, codeine phosphate, aluminium hydroxide, loperamide hydrochloride and diphenoxylate hydrochloride. It should be possible to improve diarrhoea greatly within less than a day with these drugs. If anti-diarrhoea treatment is not offered to you while the cause of your diarrhoea is being looked for or treated, ask for it.

It is important to make sure that you don’t get dehydrated while you have diarrhoea. If it is severe or accompanied by nausea and vomiting, you might need intravenous fluids until it is brought under control.

If you have malabsorption, you could become deficient in certain vitamins (such as vitamins A, D and K) and minerals (such as calcium). Make sure your doctor checks these. You may need to take extra of some things, either by mouth or in injection form.

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Diet has always been a controversial factor in studying gout. Purines are the chemicals which readily break down to form uric acid, so food high in purine should be avoided. These include anchovies, liver, tongue, kidneys and sweetbreads.

Alcohol also has been controversial. It is now established that beer tends to precipitate an acute attack, as does red wine — but whisky appears to be free of blame.

An injury to the joint or the stress of an operation or acute infection may bring on an attack. Penicillin, aspirin, some diuretics (used for blood pressure or heart trouble and which remove fluid from the body) may all raise the uric acid levels.

In psoriasis, or some blood disorders like leukaemia where there is a rapid breakdown of cells, an excess of uric acid may result.

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What is required to prevent the upsets in a woman’s emotional and sexual function following hysterectomy is better pre-operative preparation.

Every woman is entitled to a full explanation of what is wrong with her and what the doctor intends to do about it.

Following hysterectomy, the ovaries may not continue functioning beyond six months or so and so many women experience the symptoms associated with the menopause, including depression, hot flushes, headaches, tiredness, a dry vagina and often pain on intercourse.

There is no doubt that giving oestrogen to a menopausal woman will relieve most of these symptoms.

The big difficulty has been that prolonged treatment with oestrogen carries a considerable risk of causing cancer of the body of the womb. This risk is increased some five to seven times in those taking oestrogen beyond six months.

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A meal containing carbohydrate must be eaten about two hours before strenuous exercise, such as a race, allowing time for the food to leave the stomach and reach the small intestine. You may experience nausea and stomach cramps if you eat too close to the race, e.g. less than an hour beforehand.

The problem is that by allowing a gap of about two hours, the carbohydrate in most foods would have been burnt as fuel well before the race begins. The small intestine would be empty and no longer acting as a reservoir of carbohydrate. There is one other possibility. What if you could package the carbohydrate in such a way as to make it be released more slowly from the small intestine during the event?

What is needed is a food that is so slowly digested that it remains in the small intestine for hours after consumption. Only some foods have their carbohydrate packaged in such a way as to make it slowly digested and absorbed and gradually released from the small intestine.

In the same way that certain drugs have been formulated as lente (the Italian word for slowly) or ‘slow-release’ compounds so that the drug’s action is evenly maintained throughout the day, it is possible to do this with the carbohydrate in food, too.

It shouldn’t come as a surprise to learn that nature originally provided carbohydrate in a slow-release form or as lente carbohydrate. Starch and sugars in raw, unprocessed foods are packaged in a cell matrix surrounded by fibre and only gradually broken down by the enzymes of the gastrointestinal tract. In the days of hunter-gatherers, when early humans literally ran for their lives from predatory animals, slow-release carbohydrate gave them the ultimate survival advantage. Before the introduction of horses, American Indians ran for miles rounding up bison and herding them over the cliffs to their death. The traditional foods of these people provided a slow-release source of glucose for the exercising muscle.

Fortunately, there are still some foods in our modern diet that remain slowly digested and absorbed. These foods have a G.I. factor less than 55. They include all kinds of pasta, barley, whole grains, porridge, All-Bran and some varieties of rice, and bread made with softened whole grains. They also include many foods made with lentils, chick peas, couscous and barley. The traditional Mediterranean diet was high in legumes, which have exceptionally low G.I. factors.

Low G.I. foods have been proven by Australian researchers to extend endurance when eaten alone one to two hours before prolonged strenuous exercise. When a pre-event meal of lentils (low G.I. factor) was compared with one of potatoes (high G.I. factor), cyclists were able to continue cycling at high intensity (65 per cent of their maximum) for 20 minutes longer when the meal was lentils. Their blood sugar and insulin levels were significantly higher at the end of exercise, indicating that carbohydrate was still being absorbed from the small intestine even after 90 minutes of strenuous exercise.

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It has been known for some time that substances must exist in the blood which signal the state of energy stores to the brain so that hunger can be turned on and off. In the early 1950s, a mechanism called an ‘appestat’ was hypothesised to operate like a thermostat in ‘switching off hunger after a certain level of food intake. This was further supported in the 1960s and 1970s by some ingenious research carried out by Dr Douglas Coleman at the Jackson Laboratory in Maine with two inbred strains of obese mice (called ‘db’ for diabetes and ‘ob’ for obese). Coleman joined these mice with normal lean mice (a process called ‘parabiosis’) so they both had the same circulatory system. In doing so, strange things happened.

When a normal mouse was joined with a ‘db’ strain mouse, the lean mouse actually starved to death—even in the presence of abundant food. This suggested that the ‘db’ strain had an over-supply of some substance in the blood to tell it to stop eating, but that this wasn’t working in the ‘db’ mouse. When an ‘ob’ and a ‘db’ mouse were joined, the ‘ob’ mouse died from starvation, but the ‘db’ mouse increased its weight by over-eating. Again, this suggests that the ‘db’ mouse was over-supplying a ‘switch off substance which was not working with it, but which worked excessively well with the ‘ob’ mouse. Finally, when a normal mouse was joined with an ‘ob’ mouse, the ‘ob’ mouse lost weight and became normal. All this suggested that normal mice have a normal amount of a substance which the ‘ob’ mouse does not have, and which the ‘db’ mouse has too much of, but which has no effect (i.e. does not reach a receptor) in the ‘db’ mouse.

Dr Jeremy Friedman and his team from Rockefeller University in New York then isolated a gene which codes for the production of a protein from fat cells, which tells the brain when satiation has been reached. The protein has since been identified, synthesised and injected into obese mice and found to reduce their body weight The substance has been called ‘leptin’ (after the Greek word ‘leptos’ meaning ‘thin’), and the race is now on to develop drugs which may be useful in human obesity. Most scientists, however, warn that the discovery is not likely to be as simple a remedy as some have claimed, and that much more work still needs to be done.

There are likely to be few, if any, human equivalents of the ob or db mice which have major single gene abnormalities. In humans, there may however, be gene variations which result in some people being less able than others to switch off their appetite. Genetic influences in human obesity are indicated by some simple factors such as:

• Presence of lifetime or long term obesity in one or both parents. Studies have shown that the chances of being obese are around 80 per cent if both parents are obese, 40 per cent if one parent is obese and only 7 per cent if neither parent is obese.

• Presence of obesity since childhood. Genetically influenced obesity is usually manifest early in life, particularly before or around adolescence. For this reason someone who has always had a problem, particularly if the problem is also in the immediate family, is more likely to be genetically influenced.

• Presence of type I obesity. Abdominal obesity, particularly in men, is generally regarded as being environmentally determined. Ovoid-shaped fatness, together with the factors mentioned above, may suggest genotypical influences.

Although the factors mentioned above provide no certainty about genetic influence, they may give some indications that fat loss is likely to be a more difficult proposition in an individual who is genetically predisposed to fatness and that efforts to prevent fat gain may need to be lifelong; therefore, this person needs long term goals which are realistic. Special attention may also need to be given to hunger and behavioural cues and to maintenance of body weight after slimming.

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