Richard G. Petty, MD

Chronic Fatigue, Epileptic Seizures and Spirituality

Old habits die hard.

I get to hear about a great many medical and psychological problems in people in the public eye. But after 30+ years in medicine, I don’t talk about them. That’s obvious if someone is my patient: everything is completely confidential. But I also will not talk about medical problems in other people, unless they volunteer information.

Many of us have been very concerned over the physical health of the philosopher Ken WIlber.

In August I posted a brief note after he had taken a nasty tumble. I also pointed out that many of his problems with chronic fatigue syndrome could also be re-framed as "Diseases of Discipleship." Based on that, I made some predictions about other possible symptoms.

Ken has now written an extraordinarily important piece, after he suffered from a series of grand mal epileptic seizures at the beginning of December. I had heard about these problems, but would not post anything until Ken did. Even when I saw some really silly comments about the causes of his problems!

There has been speculation for many years now that many shamans had epilepsy or occasional epileptic seizures. There is also an association between one type of epilepsy and hyper-religiosity.

If you have any interest in the deeper meaning of chronic illness, the spiritual path and karma, I urge you to take a few moments to read Ken’s article.

He also mentions a website with more information about the whole Myalgic Encephalomyelitis/Chronic Fatigue complex. I have checked the out, and I agree that this is a most helpful resource.

Get well soon, Ken!

Intestinal Microbes: A Hidden Cause of Obesity

It is no secret that many famous people swear by colonic irrigation. The late Princess Diana used to say that it helped her stay fit and keep her weight steady, though personally I always thought that good genes and regular exercise were the real explanations.

In previous posts I have talked about some of the emerging lines of evidence suggesting that there are at least four previously little recognized causes of obesity:

  1. Stress
  2. Salt intake
  3. Pesticides
  4. Viruses

Following a paper in today’s issue of the journal Nature, it looks as if we shall have to add a fifth: the intestinal microbes that are collectively known as “gut flora.”

We have within us vast communities of microbes that outnumber our own body’s cells by 10 to 1, and may contain 100 times more genes than our own human genome.

We have known for many years that we each contain pounds of these microbes and that they are doing a great deal more than simply sitting there. We have known since the 1950s that many of the microbes are involved in digestion, absorption and immune function. That is one of the reasons why most doctors worry about the unnecessary use of antibiotics: some can knock out the gut flora, sometimes with serious consequences.

It is the first of these – digestion and absorption – that has been attracting attention. Under normal circumstances our bacteria break down many complex molecules like polysaccharides into simple sugars that we absorb and use for energy.

Colleagues from the Washington University School of Medicine in St. Louis have made a remarkable discovery. It seems that the balance of two major families of intestinal bacteria: Firmicutes and Bacteroidetes have a major impact on digestion and obesity. Together these two families constitute 90 per cent of the bacteria in the intestines of humans, and, coincidentally, white mice.

The researchers conducted two parallel studies. In the first they found that as obese people lose weight, the balance between the Firmicutes and the Bacteroidetes changes – the latter increasing in abundance as an overweight person gets slimmer.

The second study used white mice. Here, researchers discovered that the bacteria in the lower intestines of obese white mice were more efficient at extracting calories from complex carbohydrates than the bacteria in the intestines of slimmer mice.

In an earlier study the researchers had shown that the intestines of obese mice had the same depletion of Bacteroidetes as found in the innards of obese humans.

The practical consequence of this finding is immense: it means that if two people are on the same diets and doing the same amount of exercise, one may gain weight and the other stay the same weight. Simply because the person who stayed the same had more Bacteroidetes in his large intestine, extracting fewer calories from the same amount of food. The main reason why his friend gains weight is because he has more Firmicutes and fewer Bacteroidetes.

The researchers suggest that intestinal bacteria could become “biomarkers, mediators and potential therapeutic targets” in the fight against obesity.

I find it impressive that some advocates of natural healing had predicted something along these lines in the early days of the 20th century. I am not too keen on colonic irrigation, though I have many colleagues who use it routinely. But there are many other ways of changing your intestinal flora, including probiotics and prebiotics. You may be interested to look back at a few words that I wrote about them in late August.

I would be happy to detail some other evidence-based strategies that we have used for normalizing intestinal flora.

“A man is not rightly conditioned until he is a happy, healthy, and prosperous being; and happiness, health, and prosperity are the result of a harmonious adjustment of the inner with the outer of the man with his surroundings.”
–James Allen (English Author and Mystic, 1864-1912)

“You cannot poison your body into health with drugs, chemo or radiation. “ Health” can only be achieved with healthful living.”

–T.C. Fry (American Writer on Natural Healing and Originator of the Life Science/Natural Hygiene Course, 1926-1996)

Multiple Sclerosis and Vitamin D

I have commented before that the increasing rates of multiple sclerosis as we move away from the equator has lead to speculation that it might have something to do with lack of sunlight and therefore reduced production of vitamin D in the skin.

A lack of vitamin D may also explain the increased rates of both type 1 and type 2 diabetes, as well as cluster headache at higher latitudes.

Vitamin D is not a single vitamin, but is instead a group of fat-soluble prohormones as well as the metabolites and analogues of these substances. There are two major forms of vitamin D: D2 (or ergocalciferol) and D3 or cholecalciferol. Vitamin D3 is produced in skin exposed to sunlight, specifically ultraviolet B radiation. Very few foods are naturally rich in vitamin D, and most vitamin D intake is in the form of fortified products including milk and cereal grains.

It used to be that we all made plenty of Vitamin D simply by being outside in the sun, but our time outside has been steadily falling since the beginning of the Industrial Revolution, and there are the increasing concerns about exposure to sunlight and some skin cancers.

Vitamin D is involved in many critically important chemcial reactions in the body, and Vitamin D receptors are found in cells in most organs in the body, including the brain, heart, skin, gonads, prostate, and breast. Apart from its effects on regulating calcium and phosphorus, Vitamin D is involved in maintaining the integrity of cell membranes and in modulating the immune system. There is some evidence that a modest increase in Vitamin D intake may reduce the risk of colon, breast and ovarian cancers.

There is a risk of overdosing with Vitamin D. The U.S. Dietary Reference Intake
Tolerable Upper Intake Level (UL) of vitamin D for childern and adults
is 50 micrograms/day (2000 IU/day). In adults, a daily intake of 2500
μg/day (100,000 IU) can, over a period of weeks and months, produce toxicity  and, if
taken for years, as little as 50 to 75 μg/day (2000 to 3000 IU) can
produce toxicity.

In this week’s issue of the Journal of the American Medical Association, there is an important report that endorses everything that we have been saying. Researchers from
several prominent institutions in the United States have examined the
hypothesis that higher levels of 25-hydroxyvitamin D are associated
with a lower risk of multiple sclerosis.

The study confirmed the hypothesis: the risk of multiple sclerosis (MS) fell as blood levels of the vitamin rose.

The researchers uncovered 257 cases of MS among more than seven million military personnel who had given blood samples to the US Department of Defense.

Amongst white personnel, there was a 41% decrease in MS risk for every 50 nanomoles per litre increase in 25-hydroxyvitamin D, the key form of the vitamin found in the blood.

Those whose vitamin level was in the top 20% had a 62% lower risk of MS than those whose level was in the bottom 20%.

The researchers found no such association among black and hispanic personnel, but this could be a reflection of the smaller size of these sample groups.

This new research ties in with other work that has shown that Vitamin D supplements can prevent or favourably affect the course of a disease similar to MS in mice, as well as evidence that if you live in the Northern Hemisphere, being born in May is associated with a lower risk of MS than if you were born in the winter. If you are born in May, your mother will probably have been exposed to more sunlight – and therefore have produced more Vitamin D – during the later part of pregnancy when the final development of the nervous system takes place. Or alternatively you may have had a heathy dose of sunlight in the weeks immediately after your birth.

It is most likely that the Vitamin D helps by modulating the immune system and suppressing autoimmune reactions caused by specialised T helper 1 cells attacking myelin, the insulating material that sheathes most nerves. It is these attacks that are thought by most experts to play a key role in the development of MS.

If confirmed, the finding suggests that many cases of MS could be prevented or its severity reduced by increasing our levels of Vitamin D.

The data also confirm a point that we have made before: we should not be aiming to "boost" our immune systems, but to "modulate" them.

If you see an advertisement for some potion that is supposed to boost your immune system to help you ward off colds, the flu or something more serious, be suspicious: if the seller does not know the  difference between boosting and modulating, it would be best to move on.

Another Reason Why Breast Is Usually Best

Last month we looked at some of the extraordinary benefits of breast feeding.

There is an interesting paper in this month’s issue of the journal Pediatrics.

Approximately 19 percent of children are prone to the chronic and recurrent ear infections collectively known as otitis media. These infections can cause deafness and thereefore interfere with the development of language and lead to learning difficulties. We have known for many years that there can be a genetic predisposition to otitis media, but there has been little research to try and pinpoint the specific genes involved. There is also a complex relationship between genes, specific infectious agents and environmental factors such as exposure to cigarette smoke and breast-feeding.

The new research from the University of Texas Medical Branch at Galveston examined genetic samples taken from 505 children in Texas and Kentucky, about 60 percent of whom were classified as "otitis media susceptible" because they had:

  • Suffered an ear infection before the age of 6 months
  • Or undergone three or more episodes of acute otitis media within a six-month period
  • Or four or more episodes within a 12-month period
  • Or had six or more episodes by age 6.
  • Or had required drainage tubes to reduce recurrent or persistent ear infections

The researchers looked for small genetic variations called "single-nucleotide polymorphisms," – or SNPs – in three important genes that produce inflammatory signaling molecules for the immune system.

Two genes known known to generate the immune proteins known as tumor necrosis factor-alpha (TNF-alpha) and  interleukin 6 (IL-6). SNPs in each individual gene were enough to create an increased risk for childhood ear infections, and simultaneous SNPs in both genes increased the risk even further. These particular genetic variations cause a greater production of inflammatory signaling molecules and reduce the effectiveness of the immune system.

But here is the fascinating thing: the researchers found that the genetic effect could be counteracted by breast-feeding, which is well known to increase immune resistance.

We have here another fine example of how a healthy practice can overcome a genetic predisposition to illness. Remember what I have said many times before: Biology is not destiny.

On the hand another environmental factor – exposure to cigarette smoke – increased vulnerability to otitis media in children with the TNF-alpha gene variation. Cigarette smoke exposure alone was not enough to increase the risk for ear infections. 

Genes, Environment and the Brain

We recently looked at the worrying suggestion that environmental toxins could, in susceptible individuals, be contributing to the apparent increase in autism over the last three decades.

There is increasing evidence that there are complex genetic and environmental interactions that contribute to abnormal aging and neurodegenerative disorders like Alzheimer’s, Parkinson’s and Huntington’s diseases.

A new study from Duke University Medical Center in Durham, North Carolina, has done more to dissect this interaction. They collected information on 1136 consecutive patients who presented to the Joseph and Kathleen Bryan Alzheimer Disease Research Center. They showed possible significant contributions of toxic environmental and occupational exposures to pathological aging in 21% of the patients, and interactions of these exposures with common genetic polymorphisms that affect cell injury and inflammation. They found a series of genes that could partially account for differences in the type of cognitive problems that people experience, the age at which they developed them as well as the rate of progression.

The researchers targeted three genes in particular – apolipoprotein E, alpha-1-antitrypsin and the hemochromatosis gene. All three are expressed in the liver and in macrophages: cells that play a critical role in immune responses, inflammation and the body’s response to stress and infections. The first two genes are particularly involved in the metabolism of lipids and the third in the balance of iron and trace minerals. This ties in with another observation. Many chronic illnesses are associated with anemia. It is now thought that this also is a defensive reaction. Not to chronic illness, but to the problem that was far more common during evolution, and that was infection. The liver pulls iron out of the circulation so that bacteria cannot use it for their own growth. This is one of a number of adaptive responses that I discuss in the book and CD series, Healing, Meaning and Purpose.

But it was also clear form this new study that genes were not the only factor. I have spoken before about the small number of strategies that can dramatically reduce our risk of developing Alzheimer’s disease. The authors of this study agree about the importance of factoring in environmental factors including, alcohol use, nutritional deficiencies and sleep and mood disorders, all of which can have an impact on cognition.

This study is yet another step toward clarifying the role of genes, inflammation and cell injury in the development of degenerative changes in the brain.

While pharmacologists can use this information to help devise new ways to protect your brain, you can use it immediately. There is a range of behavioral and dietary strategies that can reduce the burden of inflammation in the body. I shall write about some of them in articles and an eBook in the near future.

We do not know whether these strategies can reduce the risk of Alzheimer’s and Parkinson’s diseases, but there are some intriguing suggestions that they can.

Multiple Sclerosis and Stem Cells

If you have been reading my recent posts about multiple sclerosis (MS), you may be interested in an useful resource from the New York Academy of Sciences.

I have the privilege of being a member of the Academy and I’ve been impressed by its increasing efforts to educate the general public. There are regular "eBriefings" that are well written and succinct.

This one on stem cells and MS is timely and encouraging. It is also a good jumping off point if you want to follow up on some of the issues.

The existence of stem cells in the central nervous system has already raised some intriguing possibilities for treatments based on activating and directing them in the brain. The second idea, of dismantling the diseases immune system and replacing it with a new clean one, is not science fiction but part of a concerted effort to reprogram the body.

This is precisley the kind of approach that we advocate when we use "Information Medicine," designed to correct faulty information that produces faulty DNA and ultimately faulty proteins and organs.

Chloroquine, Insulin and Inflammation

Your humble reporter was fascinated to read about some new research using the anti-malarial agent chloroquine as a potential treatment for the insulin resistance syndrome.

I have a personal reason for being interested. Hypoglycemia (low blood glucose) is an occasional feature of treatment with chloroquine and in 1980 a study first indicated that chloroquine might slow the break down of insulin by the liver. In the early 1980s there were a flurry of papers indicating that chloroquine did some subtle things to insulin and insulin receptors in many tissues. So we came up with the idea of measuring its effects in humans. There was a memorable occasion on which I was doing an outpatient clinic with an intravenous line in my arm. (English doctors are well known for doing experiments on themselves: I had a professor in medical school who said that you should never do to a patient what you haven’t had done to yourself. I shall leave it to you, gentle reader, to wonder if I’ve tried everything….).

So there I am doing my clinic when, around 11AM I begin to feel really strange: my glucose level was almost unrecordable and my insulin level was off the chart. Nothing that couldn’t be solved with a large dollop of sugar, but it made me very sympathetic to people who get hypoglycemic from their regular treatments.

Sometimes Nature does our experiments for us: we did a lot of work on diabetes because it is associated with high rates of vascular disease. So understanding the mechanisms by which diabetes does that may help illuminate some of the cellular disturbances underlying arteriosclerosis in general. We are also interested in the few illnesses in which a single disturbed gene may lead to a definable set of signs and symptoms. There is a rare illness known as ataxia telangiectasia in which sufferers have a high risk of developing some cancers particularly lymphomas and leukemia. People with the illness are very sensitive to ionizing radiation, have a specific type of immune deficiency, degeneration of parts of the brain related to muscle function and coordination and they age prematurely. More than ten years ago it was discovered that a single gene – ataxia-telangiectasia mutated (ATM) gene – was responsible for the illness. The gene is responsible for producing a protein that recognizes damage to DNA. It now seems that ATM may also be linked to metabolic and cardiovascular diseases. It does this by inhibiting a protein called JNK, a stress kinase involved in inflammation with related effects in insulin resistance and atherosclerosis. So to everyone’s surprise a gene that can cause a rare disease can also cause insulin resistance.

In the November issue of Cell Metabolism, researchers at Washington University School of Medicine in St. Louis and St. Jude Children’s Research Hospital in Memphis, Tennessee report that a small dose of chloroquine eased many symptoms of metabolic syndrome in mice, reducing blood pressure, decreasing hardening and narrowing of the arteries and improving blood sugar tolerance. The results suggest we may only need very low and perhaps infrequent doses of chloroquine to achieve similar effects in humans. Both insulin and chloroquine activate the ATM gene.

This adds to the data that some of the metabolic dysfunctions triggered by obesity may be linked to the inflammatory responses that go wrong in autoimmune disorders like arthritis and systemic lupus erythematosus.

And an older treatment for rheumatoid and lupus just happens to be chloroquine.

Chloroquine itself has some side effects, but this is important information that will help us design more effective and carefully targeted holistic treatments for both metabolic disturbances and inflammatory conditions. All in all, very good news indeed.

Multiple Sclerosis

Multiple sclerosis (MS) can be a horrible illness that does not respect age or class. Neil Cavuto, Captain Beefheart and Montel Williams are just three well-known people who have said that they have the illness. Here is a list of many other sufferers.

MS is a chronic, inflammatory disease that affects the central nervous system (CNS). MS can cause a wide variety of symptoms, including changes in sensation, visual problems, muscle weakness, depression, difficulties with coordination and speech, severe fatigue, and pain. The classic pathology is what is known as demyelination (loss of the myelin that insulates nerve cells). Since myelin is white, the lesions are typically fuond in the white matter of the CNS.

The cause remains unknown, though I shall have more to say about some of the MS theories. Amongst the candidates have been autoimmunity, slow viruses, myelinic enzymes and polio vaccination.

Most people begin to experience symptoms between 20 and 40 years old, and rarely after 50. The onset is usually insidious, though every now and then someone starts with sudden onset of a catastrophic neurological or visual problem. Symptoms are usually vague and the diagnosis is often missed in the early stages. Females are affected slightly more than males. MS seems to be a disease of temperate latitudes in both the Northern or Southern hemispheres and is rarely seen in equatorial regions. This association with latitude has fueled some of the viral theories as well as ideas to do with the impact of decreasing sunlight on vitamin D and cell membrane function.

One of the things that makes the disease such a great masquerader is that it is typically marked by apparently random exacerbations and remissions. As the disease progresses, the remissions become less complete and permanent deficit more apparent.

There is an enormous research literature on MS: over 35,000 papers at last count. But there have been some recent highlights.

There has recently been a major breakthrough in discovering the mechanism by which myelin forms. The finding from the Keck School of Medicine of the University of Southern California and the Institut de Recherches Cliniques de Montreal in Canada, could have a major impact on the treatment of multiple sclerosis and demyelination as a result of spinal cord injuries.

Jonah Chan and his colleagues showed that a protein, Par-3, is at the base of the myelination process. This protein becomes localized to one side of the myelin-forming cells that are known as Schwann cells, upon contact with the axon that is to be myelinated. Par-3 acts like a kind of molecular scaffold to set-up an "organizing centre" that brings together the key proteins essential for myelination, in particular a receptor for a molecule that is secreted by the neurons.

The researchers found that when they disrupted this organizing centre, cells could not form myelin normally. Importantly, their discovery demonstrates that Schwann cells need to become polarized so that they know which side is in contact with the axon to initiate wrapping and to bring essential molecules to this critical interface.

These studies open up some new possibilities that should help to identify other components that are recruited at the organizing center set-up by Par-3. In multiple sclerosis, or after injury, Schwann cells can re-myelinate axons of the central nervous system to some degree. Therefore, these experiments bring about the possibility that manipulating the Par-3 pathway might allow for more efficient re-myelination of damaged or diseased nerves.

In a separate study researchers from the Virginia Commonwealth University researchers have identified a unique mechanism of action of a new drug that shows great promise for the treatment of MS.

The researchers reported the unique action of FTY720, or Fingolimod, an immunosuppressant drug that was already known to affect the functioning of the immune system by preventing the egress of white blood cells from the lymph nodes into the blood. The article was published in Blood: The Journal of the American Society of Hematology, that appeared online on Sept. 28.

In this study, the research team found that FTY720 also inhibited the activity of a key enzyme called cPLA2, which is necessary for the production of inflammatory mediators, known as eicosanoids. Eicosanoids drive inflammatory disorders such as asthma and multiple sclerosis.

The inhibition of cPLA2 would shut down the entire inflammatory pathway, possibly without the side-effects caused by medications such as Vioxx, that have been withdrawn from the pharmaceutical market.

FTY720, is a drug developed by Novartis, has shown considerable therapeutic effects in a recent small, placebo-controlled clinical trial involving patients with relapsing multiple sclerosis. The study was published in the September 2006 issue of the New England Journal of Medicine by an international research team.

I could easily select a dozen more important papers published in the last year, but I am particularly interested in basic research that teaches us something new, and treatments that could fit into a comprehensive Integrated plan of treatment.

I am going to post more about the causes of this illness as well as less orthodox approaches to help the physical, psychological, social, subtle and spiritual aaspects of these illnesses.

Tourette’s Syndrome

No surprise here, but I was just sitting on a plane.


When I heard people sniggering.

Why? A young man in his thirties was walking along trying to find his seat. As he did so he was constantly grunting, saying partially intelligible words and jerking. As a clinician it was immediately obvious that he almost certainly had Tourette’s syndrome, a developmental disorder of the brain in which people have involuntary, stereotyped, repetitive motor and phonic tics. Some people with the disorder exclaim obscene words or socially inappropriate and derogatory remarks, which together are known as coprolalia.

The illness was originally named for Georges Albert Édouard Brutus Gilles de la Tourette, (1859–1904), a French physician and neurologist, who published an account of nine patients with the now classic clinical features in 1885.

You may not often see someone with this problem, but it is good to know what it is, and that it is an illness that can cause great distress.

We have recently made some interesting discoveries about Tourette’s syndrome.

  1. It is an illness involving the dopamine systems in the basal ganglia of the brain together with some regions of the midbrain and some very specific linked regions of the cerebral cortex, cerebellum and limbic system.
  2. In adults with Tourette’s syndrome, the prefrontal cortex is a little smaller than normal, and the corpus callosum linking the hemispheres is larger than expected. These findings correlate with problems in the way in which people transfer information between the hemispheres and modulate attention.
  3. Very recent evidence has shown us that there are small hyper-intense lesions in the deep regions of the brain in people with Tourette’s, obsessive-compulsive disorder and attention deficit disorder. These three problems seem to have a number of biological links and two or more may co-exist in the same person. In children and adolescents with Tourette’s, the tics tend to get better over time but obsessive-compulsive disorder symptoms become more severe and persistent as they get older.
  4. There is important evidence that in some people, Tourette’s is linked to a post-infectious autoimmune disorder, and many have antibodies directed against neurons in the brain.
  5. There is also a link between Tourette’s and having low iron stores. Low iron stores are common in people with many chronic inflammatory illnesses. Iron is crucially important in the development of key regions of the brain. We do not have any viable evidence that giving people iron supplements will reduce the severity of Tourette’s, but it is something that needs to be examined in a formal study.

People have typically been treated with antipsychotic medicines such as risperidone that block dopamine receptors in the brain, and they can certainly help. A more recent approach is to use medicines like aripiprazole that modulate dopamine activity in the brain. A recent study done by some colleagues in the United Kingdom have confirmed that aripiprazole seems to be very helpful in about half of patients with Tourette’s, though neurological side effects do sometimes occur.

There has recently been a lot of interest in Habit Reversal Therapy: a behavioral treatment for tics. The therapy takes a lot of time and effort, but it is very interesting that behavior therapy can help with a neurological illness.

There is no published data on the use of Integrated Medicine in the treatment of people with Tourette’s, but many experts have reported that some patients have been helped with homeopathy and acupuncture.

That guy in the next seat who is cursing may not just be mean and uncouth. He may be suffering.

But maybe not for much longer.

We are getting very close. Not just to discovering the physical basis of the illness, but perhaps its meaning and purpose as well.

New discoveries are coming thick and fast, and I shall keep posting about those that will help individuals and illuminate the principles of Integrated Medicine.

Handedness and Immunity

In 1982, one of my mentors, the late Norman Geschwind, and two colleagues – Al Galaburda and Peter Behan – proposed an extraordinary hypothesis. It was that the levels of testosterone to which a baby is exposed before birth influence the development of both the cerebral and immune systems. According to this theory, high levels of testosterone result in greater incidences of left-handedness, deviations from the standard distribution of cerebral functions and increased autoimmune dysfunction. If the theory is right, then male brains should mature later than female brains, and the left hemisphere should mature later than the right.

It is certainly true that if a boy gets a head injury or infection involving the brain, he is less likely to recover than would a girl, and boys are far more likely to have some types of neurodevelopmental problems like dyslexia.

For a while it seemed as if there was also a strong association between left-handedness and certain types of allergy, and also with inflammatory bowel disease. This association with immunity also seemed to be present in mice: those who had left paw preference had more reactive immune systems, and they were thought to be more likely to produce auto-antibodies, suggesting that the central nervous system was involved in the genesis of some autoimmune diseases. Over the years the data has become less clear-cut, but the idea of an association between anomalous cerebral asymmetry and autoimmune disease never completely went away.

Recent data has again found an association between inflammatory bowel disease and laterality. And left-handers really do have more autoimmune disease.

The Geschwind-Galaburda hypothesis proposes that there should be a four-way association among neurodevelopmental disorders, special talents, non-right handedness, and immune disorders. In a huge study of 11,578 children, less than 1% had all four.

So where does this leave us?

The original theory was half right:

  1. There is indeed a link between testosterone and early brain development
  2. People who are left-handed or have a strong tendency toward left-handedness do seem to be at slightly increased risk of several autoimmune conditions
  3. People who are left-handed or have a strong tendency toward left-handedness may have a slightly increased risk of high blood pressure, asthma and migraine
  4. People who are left-handed or have mixed handedness are more likely to excel in certain disciplines: creative arts, music, computer programming and mathematics. What we don’t know is whether people with these special skills are more likely to have autoimmune diseases
  5. Amongst very successful tennis players,  there are far more left-handers than would be predicted by chance. This supports the idea that support the notion that left-handed people have neurological advantages in performing certain tasks, such as visuospatial visuomotor cognitive tasks.

I was reminded of the way in which Nature seems to like to balance things out a bit: with some notable and famous exceptions, many successful athletes have not done so well academically and many academics would be unlikely to survive on the plains of Africa. Only some of these differences can be explained in terms of early direction and encouragement in school or while growing up: it seems that most of us cannot hope to become the kind of superman that Nietzsche used to dream about.

Perhaps it’s a way of stopping us from getting too full of ourselves.

logo logo logo logo logo logo