Monthly Archives: April 2009


Dental caries, or tooth decay, is caused by an accumulation of plaque deposits on the teeth. Plaque is a colourless mixture of saliva, food particles and bacteria. The bacteria act on starchy and sugary foods to produce lactic acid, which in turn acts on the surfaces of the teeth. Once the enamel is penetrated, the decaying process eventually leads to toothache.

It is impossible to prevent plaque forming, and the use of plaque disclosing tablets will reveal the amount of plaque present on your teeth. The best prevention is reducing the intake of refined sugars and effective oral hygiene, including brushing and flossing. There is also some evidence that vegetarians suffer less from dental caries than the rest of the population.

Toothbrushes should be replaced every three to four months and should not be too hard. Teeth should preferably be brushed after every meal. If this is not possible, rinse the mouth thoroughly with water. Brushing after breakfast and before going to bed is recommended as a minimum to prevent plaque building up.

Brushing technique involves brushing down on upper teeth and up on lower teeth. Brushing should commence at the gums and move to the outer edges of the teeth. Make sure you brush the backs of both upper and lower teeth. Scrub the teeth thoroughly for three minutes.

Flossing is also an important aspect of dental hygiene. Floss is a thin thread which can be purchased from the chemist either waxed or unwaxed. Flossing enables you to remove food particles which have lodged in areas inaccessible to a toothbrush. The floss should be strung tightly between the index fingers, inserted between the teeth and moved up and down to a point just under the tissue of the gum. Flossing massages the gums and improves circulation.



Before we try to answer this question, it is important to concede up front that researchers do not know for sure how any antidepressants work. But we have a strong suspicion that most anti-depressants work by affecting the way nerve signals are conducted from one nerve cell (neurone) to another. The brain consists of millions of neurones, which communicate with one another at synapses, points at which they are in close proximity but do not actually touch. Neural signals pass along the transmitting neurone in the form of electrical impulses until they reach the synapse, where they are converted to chemical signals that stimulate the receiving neurone, where they are once again converted into electrical signals. Normal transmission of electrical signals along neuronal pathways is necessary for the proper maintenance of all brain-regulated functions, including the control of mood, sleep, eating, thinking and other basic processes that are disrupted in depression.

The chemical transmission of the signal at the synapse involves the release of specific nerve chemical messengers or neurotransmitters, which are housed in little pockets or vesicles in the transmitting neurone, into the synaptic cleft, where they act on specific receptors on the surface of the receiving neurone. After they have communicated their chemical messages, the neurotransmitters are taken back up into the transmitting neurone again, where they are broken down by an enzyme called monoamine oxidase or MAO. This reuptake of released neurotransmitters is handled by special transporter proteins attached to the surface of the transmitting neurone. The transporter proteins for the neurotransmitters involved in synaptic transmission have been the focus of considerable attention, because most commonly used anti-depressants inhibit the reuptake of neurotransmitters by these proteins, a step that is thought to be the initial action that sets in motion a cascade of effects ultimately responsible for reversing the symptoms of depression.

Different neurones use different types of neurotransmitters to conduct their messages. Those neurotransmitters that have been most intensively studied are serotonin, norepinephrine and dopamine. One of the major ways in which anti-depressants differ from one another stems from the relative potency with which they inhibit the reuptake of these different neurotransmitters. These differences affect their side-effect profiles and, probably, their therapeutic effects as well. Older anti-depressants were rather unselective in their effects, affecting many different types of receptors. For this reason they caused several undesirable side-effects. When the newer family of anti-depressants including the enormously popular Prozac” and Lustrar’ were introduced, their major attraction was that they selectively affected serotonin reuptake without affecting other neurotransmitters to anywhere near the same degree: hence their generic name, selective serotonin reuptake inhibitors (SSRIs). Another anti-depressant commonly used in the US, bupropion or Wellbutrin, is thought to act more selectively on dopamine and norepinephrine. Most of these studies, incidentally, have been conducted on ground-up extracts of rat brains, though the results are believed to be applicable to the intact human brain as well.

Given the central role that inhibition of the reuptake of neurotransmitters appears to play in the action of other anti-depressants, it was logical to study whether St John’s Wort might have such effects as well, and that is precisely what Walter E Miiller and colleagues in Frankfurt, Germany set out to study. What they found is that an extract of St John’s Wort is capable of inhibiting the reuptake of all three neurotransmitters mentioned above: serotonin, norepinephrine and dopamine. Curiously, St John’s Wort appears to inhibit the reuptake of these neurotransmitters in a manner different from that encountered with other antidepressants. These are exciting findings to a psycho-pharmacologist such as myself because they have implications both in terms of the type of anti-depressant response and the profile of side-effects one might expect to encounter when using St John’s Wort.

I have often treated depressed patients with a selective serotonin reuptake inhibitor such as Prozac or Lustral and have observed only a partial response or an initial response that later fades. In such situations I have found that the addition of an antidepressant which acts primarily on norepinephrine transmission, such as bupropion or desipramine, will nicely complement the serotonergic drug and take care of the remaining depressive symptoms. I have treated some patients with such medication combinations for years without observing any loss of effectiveness.

As far as side-effects are concerned, the newer SSRIs appear to cause the most bothersome sexual side-effects in some people, whereas the older anti-depressants, which affected both serotonin and norepinephrine systems, appear to cause fewer problems in this regard. The balanced profile of neurotransmitter reuptake inhibition observed by Miiller and colleagues may explain why many people appear to experience fewer sexual side-effects on St John’s Wort than they do on the SSRIs.

Another important question that Miiller and his colleagues tackled was whether St John’s Wort has any significant effects on inhibiting the enzyme monoamine oxidase (MAO). An earlier report had suggested that it did have such activity, though this was not corroborated in a subsequent study As I mentioned above, MAO is responsible for breaking down neurotransmitters after they have been taken back up into the transmitting neurone at the synapse. If this enzyme is inhibited, the concentrations of these neurotransmitters would increase in the synapse, which is believed to be the way in which a group of anti-depressants, the MAO-inhibitors (or MAOIs), exert their anti-depressant effects. A major problem with these drugs, however, is that they inhibit MAO elsewhere in the body, most importantly in the bowel where the enzyme is normally responsible for detoxifying chemicals contained in ordinary foods such as yellow cheese and red wine. As a consequence, if someone on an MAO-inhibitor should eat one of these prohibited foods, a serious toxic reaction can result, with marked and sometimes dangerous elevation of blood pressure. In addition, there is a potential for dangerous interactions between MAO-inhibitors and other drugs, such as the SSRIs. If St John’s Wort were indeed an MAO-inhibitor of any potency, this would seriously limit its usefulness. The good news is that Miiller and colleagues found that St John’s Wort is not an MAO-inhibitor to any significant degree, which means that there are no food restrictions for anyone on the herbal anti-depressant and no concern on this basis about combining it with most other anti-depressants, such as the SSRIs. Just as with other anti-depressants, however, you should not take St John’s Wort if you are also taking an MAO-inhibitor.

One aspect of the mode of action of anti-depressants that needs to be explained is why it generally takes anti-depressants, including St John’s Wort, several weeks to have their effects. The effects on reuptake of neurotransmitters seen following administration of most anti-depressants are immediate and are therefore unlikely to be a complete explanation of clinical effects that take weeks to unfold. Current thinking is that the effects of antidepressants on the reuptake of neurotransmitters may be just the first in a cascade of biochemical steps necessary for reversing the symptoms of depression. Certain brain changes following the administration of anti-depressants have been found to occur a few weeks after treatment is started, after a time lag very similar to that required for the anti-depressants’ clinical effects to kick in. Researchers have suggested that these other brain changes may play a role in the mode of action of anti-depressants. Interestingly, Miiller and colleagues have found that delayed brain changes similar to those seen with other anti-depressant treatments also occur in rats a few weeks after they have been given St John’s Wort. This is another piece of biochemical evidence linking the effects of the herbal anti-depressant to those of conventional synthetic ones. It is not only in ground-up extracts of rat brains that St John’s Wort has been found to resemble other anti-depressants, but also in live rat models of depression, where the herbal anti-depressant increases an animal’s resistance to a variety of stresses just as is seen with its synthetic counterparts.



In previous sections, we have looked at the basic concept of clinical ecology and at the different stages and symptoms which environmentally caused disease can engender. In this section, I shall explain in more detail some of the techniques which advocates of this new approach have devised to cope with the ecologic disaster of the twentieth century.

The first problem is one of diagnosis. Conventional medicine recognizes the fact that millions of people are chronically ill and that it can offer little for their arthritis, or migraine, or fatigue, or depression but chemically derived pills. Patients with a welter of confusing symptoms are often treated contemptuously, because the underlying cause of their many illnesses goes unnoticed. By its very nature, the etiology of environmentally caused chronic disease is hidden: this is “nature’s medical coverup.” The first job of the clinical ecologist is to cut through the confusion and demonstrate the underlying causes with convincing tests.

Over a period of about fifty years, clinical ecologists have worked out procedures which differ from those used by conventional doctors. Even the history-taking interview is different. I practice “poker-faced medicine,” in that I do not pass judgment on a patient’s symptoms upon first hearing them, no matter how bizarre they may seem. Many such symptoms later turn out to have significance in the patient’s medical history. A chemical questionnaire, which is included in Chapter 19, evolved through many editions and helps reveal a patient’s susceptibility. The reader can take this test himself and get a preliminary idea of his own degree of sensitivity to chemicals.

Treatment by the methods of clinical ecology is safe, inexpensive, and effective. It is based, primarily, on avoidance of those environmental agents which cause trouble. The Rotary Diversified Diet (described in Chap. 18) works well for all types of food allergies and can help those who wish to diagnose their food allergies, as well as those who wish to avoid their development.

The treatment of chemical susceptibility is also largely based on avoidance. A number of simple and inexpensive procedures are described which can help protect the many people who suffer unknowingly from chemical-related problems.

Taken together, the chapters in this section can help any reader to become more aware of his own highly personalized reaction to common foods and chemicals and to begin to take simple steps to deal with a growing problem.



When kidney failure progresses to the point where urinary waste products accumulate in the bloodstream, either dialysis or a kidney transplant is required. At different times, both may be needed by the same patient. During the first year, for instance, rather than accepting the first available kidney, which may not match well with the recipient’s tissues, it may be safer to continue dialysis until a kidney which matches well becomes available.

However, the record of the hospital where dialysis is being given should be taken into account. For instance, according to Medical World News (22#25:16), the success of dialysis (as measured by the percentage of patients surviving one year), varies from hospital to hospital by as much as from 55 to 85 percent.

After the first year, the success of dialysis falls so dramatically that a transplant then offers a much better chance of survival, even with a kidney that does not closely match the host’s tissues. Three-year transplant survival can vary between 65 and 85 percent, depending on how well the tissues match.




Symptoms in boys: burning during urination; discharge from penis

Symptoms in girls: vaginal discharge, abdominal pain.

Gonorrhea in girls often shows no symptoms.

Home care: Gonorrhea must be diagnosed and treated by a doctor.

The best preventive measure is to provide your children with appropriate and adequate sex education.


-    Be aware that venereal (sexually transmitted) gonorrhea is being seen with increasing frequency among sexually active teenagers and younger children.

-    Sexually abused children may contract this disease.

-    A mother who has gonorrhea can transmit the disease to her baby as the child passes through the birth canal during delivery.

-    A girl with gonorrhea may show no symptoms and the infection may go undetected and untreated, with serious consequences including sterility (inability to bear children).

-    Some doctors recommend that sexually active girls be tested for gonorrhea at the time of routine school or annual medical checkups.

Gonorrhea is an infection caused by a specific gonococcus germ, which is usually sexually transmitted.

In the days before antibiotics, infants born to mothers who had gonorrhea commonly developed gonorrhea infections of the eyes, which caused blindness. Now antibiotics and the required Credes treatment (placing silver nitrate solution into the eyes of all newborns) have almost eliminated this previously common cause of blindness.

Today, venereal (sexually transmitted) gonorrhea in adolescent and younger boys and girls is being seen with increasing and alarming frequency. One of the dangers of genital gonorrhea is that often a girl who has gonorrhea will show no symptoms; therefore, the infection may not be detected and treat. Serious consequences, including sterility, may result from untreated gonorrhea in females.

Another disease, caused by gonococcus bacteria, is now being recognized in adolescents and even in younger children who have been sexually abused. It causes sore throat and anal infection, with or without fever. Ordinary throat cultures done for sore throats do not grow the gonococcus germ, which leads to the false conclusion that this infection is viral and that no antibiotic need be prescribed.



Bile acid sequestrants

Drag names and brand names: Cholestyramine (Questran Lite), colestipol (Colestid Granules).

How do bile acid sequestrants work? They bind with cholesterol containing bile acids in the intestines, and are then removed in bowel motions. These drugs typically lower LDL cholesterol by 10-20%. Sometimes a bile acid sequestrant is given with a statin drag in order to lower cholesterol levels more efficiently. Together, these two drags can lower LDL cholesterol by approximately 40%. Triglycerides are not lowered by bile acid sequestrants. These drags usually come as powders and are mixed with water or juice and consumed once or twice daily with meals.

Side effects of bile acid sequestrants: These drags reduce your ability to absorb other medications you take. They also inhibit the absorption of the fat soluble vitamins A, E, D and K, therefore long term use of bile acid sequestrants usually requires vitamin supplementation. Antacids impair the effectiveness of bile acid sequestrants, therefore the two drags should not be taken together. The most common side effects of these medications are digestive upsets such as gas, nausea, bloating and constipation.

Cholesterol absorption inhibitors

Drug name and brand name: Ezetimibe (Ezetrol).

How do cholesterol absorption inhibitors work? This is a new class of drugs which was first approved by the US FDA in late 2002. Ezetimibe inhibits the intestinal absorption of cholesterol found in bile and the diet. When given by itself, ezetimibe reduces LDL cholesterol by 18-20%. It is often given with a statin, especially in people who get side effects from high doses of statins. Ezetimibe can increase HDL cholesterol, but the way it does this is not yet known. It has no effect on the absorption of triglycerides, bile acids, fatty acids and fat soluble vitamins. This drug is taken in tablet form once daily.

Side effects of cholesterol absorption inhibitors: So far studies have shown that side effects in people taking ezetimibe were no greater than those taking a placebo. It is generally well tolerated if taken on its own.



Doctors are divided over the importance of stress in infertility and yet stud-have shown that it can affect a man’s fertility to the point where not only the count is reduced but also the quality of the sperm, with abnormal sperm and decreased motility.

Stress can also affect a man’s hormone balance, lowering his levels of testosterone and luteinising hormone.

The release of the stress hormone prolactin in response to a crisis can affect a woman’s ability to conceive and in extreme cases can stop her ovulating. It seems to be nature’s way of protecting women from getting pregnant at a time when they would find it hard to cope. Women going through a bereavement or other kind of trauma for instance can stop having periods altogether.

Couples trying for a baby often experience high levels of stress, particularly if medical intervention is required. The longer it takes, of course, the more anxious you may become – and the more chance there is of stress inhibiting your fertility. A number of studies show that if a woman becomes totally obsessed with having a baby she may release eggs which are not mature enough to be fertilised.

There are many anecdotes concerning couples who have given up fertility investigations, put their names down for adoption, and then found themselves pregnant. One lady I saw gave up work to have a baby and got so bored that she decided to find another job and then got pregnant. Other women may find that the stress of the job they are doing may be affecting their fertility. We are all so different and what affects one person may not trouble another – ‘one man’s meat is another man’s poison’.

Many couples find that they conceive on holiday when they are relaxed and have forgotten about all their domestic worries. Infertility is clearly a multi-factorial problem, which is why this book looks at all the possibilities, not only the physical aspects (such as hormones and nutrition) but also the psychological and emotional side.



At least two million Americans have glaucoma, the second leading cause of preventable vision loss after diabetes. The disease – a result of extra pressure on the optic nerve from improperly draining eye fluid – isn’t curable, but it’s treatable, often with pressure-reducing eye drops.

In other words, you don’t have to go blind if you get glaucoma. But some people do.

“There’s no excuse for vision loss from glaucoma other than personal neglect,” insists Richard Bensinger, M.D., a spokesman for the American Academy of Ophthalmologists in Seattle. “Either you never got your eyes checked or your physician didn’t nag you hard enough to follow the medical regimen.”

Why should you have to be nagged into not going blind? According to Dr. Bensinger, it’s not just the mild inconvenience of an eye drop routine but also the lack of immediate payoff. “We don’t have to encourage people with arthritis because they’re hurting, and when they take their medicine, the pain goes away,” he says. “But with glaucoma the results seem like nothing. You don’t see any better or feel any better after you take the drops.”

There’s a similar reluctance about eye checkups, even though if you catch glaucoma in the bud via an eye-pressure test, you keep most of your sight. “The problem is that garden-variety glaucoma doesn’t have any symptoms,” Dr. Bensinger says.

So don’t wait till it’s too late. Dr. Bensinger recommends that you get your eyes examined every five years from age 25 to 50, and every two years after that. And you should have your eyes checked more often if there is a history of glaucoma in your family.

And please, take your medicine.



The DSM-HI-R (Diagnostic and Statistical Manual of Mental Disorders) is more than just a psychiatric cookbook. No mere list of diagnostic criteria can describe the many ways a mental disorder affects people, while diagnosing by symptoms alone will not fully explain a condition. To enhance its usefulness, the manual describes some of the other features of anorexia nervosa.

For example, it notes the different ways weight loss can occur. One woman might rely on reduced food intake alone. Another might reduce intake but exercise excessively as well. Others use self-induced vomiting or laxatives or diuretics. The manual thus acknowledges that bulimia and anorexia may indeed coexist.

The compulsion to exercise is very common in anorexia. Even doctors a century ago recognized the symptom.

Many anorexics feel they have to run everywhere, that walking is just a missed opportunity to burn off more calories. Parents often tell me that their anorexic daughter “never stands still” or that she “always runs up the stairs” or that she “pedals her exercise bike until after midnight.”

Anorexics aren’t driven to exercise because they want to be physically fit. They simply want to burn off energy (and thus weight) in any way possible. Excessive exercise may also trigger some pleasurable changes in brain chemistry, producing effects such as the “runner’s high” that many joggers report. Thus anorexics may exercise to experience a neurochemical “reward.”

Besides exercise, other weight-loss methods include use of laxatives to stimulate bowel movements or diuretics to decrease water in the body. Anorexics frequently resort to such tricks to speed up the removal of food from the body.

The results can be disastrous. Many patients-some of whom use between thirty and a hundred laxative tablets a day-report cramps and abdominal pain. What’s more, the body, robbed of its ability to regulate elimination on its own, can become dependent on a laxative. I find that weaning patients from laxatives is one of the hardest tasks in treating eating disorders.

Laxatives and diuretics can produce severe dehydration and electrolyte imbalance. Electrolytes are chemicals such as sodium and potassium that help transmit electrical signals within the body. An insufficient supply of electrolytes puts tissues and organs, particularly the heart, at risk of failure. Patients who abuse laxatives and diuretics risk problems with their hearts and other organs, problems that in some cases lead to death. Ironically, laxatives don’t even help that much. A laxative abuser loses no more than 10 percent of available calories through this method, and most of the weight loss is merely “water weight” anyway, as I mentioned earlier.

Of course, the problem with starving yourself is that you’re always hungry. No matter how carefully you defend yourself against food, sooner or later you will have to eat something or die. Because the hunger can be overwhelming, eating even small amounts can trigger a binge.

For people with these disorders, eating anything, especially when it leads to a binge, represents loss of control. Vomiting restores control-at least until the next urge to eat comes along.

About half of all anorexics practice self-induced vomiting. I’ll have more to say about the physiological impact of vomiting in the discussion about bulimia in the next chapter.

By acknowledging these weight-loss practices, the DSM-III-R recognizes the differences between anorexics who attempt to starve themselves exclusively through reduced food intake (restricting anorexics) and those who reduce weight by extraordinary means (bulimic anorexics).

The manual goes on to describe some of the other common features of anorexia nervosa-for example, the “magic power” that food has over its victims.

Once I discovered that a patient named Debbie had stuffed whole packages of cookies, cheese, fruit, and candy into her underwear drawer in her hospital room. When I asked whether she was preparing for an eating binge, she replied, “Oh, no. I’m not going to eat that stuff. I just keep it there to show myself how much control I have over it. The more food I can lay my hands on, the greater the temptation to eat. And the more I can hold out and not eat, the stronger I feel.”

Like Debbie, many anorexics exhibit peculiar behavior connected to food. They imbue food with enormous, almost supernatural force. Some prepare elaborate meals for their families, but eat nothing themselves. Or they toy with the food on their plate, poking it around with their forks, and finally throwing the whole meal away.

Anorexics see their starvation not as a defect, but as something that makes them special. “Look at me,” they seem to say. “See how much control I have over my body.” Almost every one of my patients, at one time or another in the course of her illness, will feel something to the effect that “Not everyone can do this.”

Because they deny the problem, anorexics feel that therapy, or any attempt to intervene, constitutes a deadly threat, a plot to rob them of their “specialness.” Needless to say, such an attitude makes my job as their doctor much more difficult..



Marlene Dropp was so out of shape that she couldn’t even walk around the block. Seven years later, at age 51, she walked a marathon.

A veteran dieter, Marlene had struggled with her weight all of her life. Sometimes she’d lose a few pounds, but they would always come back.

Then one day, as she looked in the mirror, Marlene realized how much she disliked the image that she saw. “I was a frumpy 200-pound matron,” says the mother of four. “My dress had stripes, a frilly collar, and fluffy sleeves, like something my mother would have worn. I couldn’t fit into more fashionable clothes. That’s when I started feeling like a blimp.”

That’s also when she decided to do something about it. Because of her weight, Marlene had always felt too self-conscious exercise in public. But this time, she was determined.

So one beautiful morning in 1989, with her husband at home to watch the kids, Marlene decided on impulse to take a walk around her Hibbing, Minnesota, neighborhood. To her surprise, she arrived home energized. “That’s when I decided to make walking part of my daily routine,” she says.

Immediately, Marlene set a goal for herself. She wanted to advance from walking around the block to walking 5 miles a day. Her neighborhood is laid out in half-mile circles, so she just kept adding circles to her route. Within 2 months, she achieved her goal. So she set her sights on a new objective: She wanted to cover a mile in 13 minutes. A year later, she could do it with ease.

Within 2 years of starting her exercise program and making some changes in her eating habits—primarily avoiding fats and sweets—Marlene lost 50 pounds. As she got faster, she began entering racewalking competitions—milers, 2-milers, and 5Ks. In 1996, she celebrated her 51st birthday by entering a marathon. She completed the 26-mile course in less than 6 hours.

Even though she continues to compete, Marlene credits those daily walks around the block with jump-starting her weight-loss efforts. Today, at age 55, she maintains a healthy weight of 150 pounds.


Follow the 10 percent rule. Just as Rome wasn’t built in a day, neither is an exercise program. Whatever activity you choose—walking, running, cycling, swimming, or something else—start slow and easy. Gradually build to

your desired duration and intensity A good rule of thumb is to increase your level of activity by 10 percent a week. So if you’re able to walk for 10 minutes your first time out, stay at that level for 1 week. Then add 1 minute—10 percent—to your workout the next week. Continue until you’re walking for 30 minutes a day.