Richard G. Petty, MD

Testing for Diabetes in Children

Diabetes mellitus can be a devastating illness, especially when it comes on suddenly in a child or adolescent. In young people it is usually so-called Type 1, or insulin-dependent diabetes, an autoimmune disease in which the immune system attacks the insulin-producing beta cells in the pancreas. The disease can have a major impact on the whole family, and sometimes people forget the way in which it can affect siblings whose needs often need to be subordinated to the needs of the newly diagnosed young person.

And here is an important point: even when it appears suddenly, the disease process may have been going on for some time before the clinical symptoms appear. By the time that blood glucose levels begin to rise, it usually implies that the damage to the insulin-producing cells in the pancreas has reached a critical point, and the chance of recovery is low. Anything that we can do to prevent the disease from progressing to the point of producing symptoms would be immensely helpful, and that starts with early recognition before the pancreatic damage has reached critical.

Although we now understand a great deal about the interplay of genetic, environmental and immunological factors that may lead to the illness, this knowledge has so far not helped us very much. There has been a tremendous need to try and identify the early stages of the disease, but that goal has been elusive.

In a study published in the Journal of Immunology researchers from the University of Queensland's Diamantina Institute for Cancer, Immunology and Metabolic Medicine, are developing a simple test that may predict whether a child will develop Type 1 diabetes. They have identified a cellular pathway known as NF-kappa B that is activated in certain blood cells – monocytes and dendritic cells - of people with Type 1 diabetes.

In healthy people monocytes remain quiescent unless they are activated by an infection or other stressor. Then the NF-kappa B pathway gets activated.

In people with Type 1 diabetes things work the other way round: monocyte NF-kappa B was already activated in the blood, and when exposed to infection the pathway shut down. This tells us that there is a problem of immune control that may cause diabetes to develop in children. It is this monocyte abnormality that will hopefully form the basis of a diagnostic test.

This work is assuming more urgency since there are several trials of diabetes vaccines underway, and if successful, it may become possible to identify and intervene in children at risk of Type 1 diabetes before it occurs.

In addition, understanding why the immune system loses control before the disease starts should open up a number of new options for prevention and treatment.

A Virus Linking Depression, Aging and Heart Disease

We have known for a long time that there are close links between depression, aging and heart disease, but the nature of the link has remained elusive. Most of the smart money has been on inflammation, but there could be other candidates.

New research in the journal Brain, Behavior and Immunity has linked an increase in two inflammatory proteins in the immune system with a latent viral infection and proposes a chain of events that might accelerate cardiovascular disease. It is possible that the same process may be involved in a number of other ailments that can afflict us, as we get older. The findings also suggest that chronic depression may play a key role in initiating the cascade that can lead to the development of coronary artery disease.

It has been known for some time that increased levels of the proinflammatory cytokines, TNF-α and IL-6, predict mortality and morbidity. High levels of each of them are found in the plasma and in atherosclerotic lesions of people with cardiovascular disease.

The levels of IL-6 in the body increase as the immune system ages. Some of the IL-6 is generated by immune cells - macrophages - that go to the site of an infection or injury. Earlier work by the team also showed that increases in psychological stress and depression could substantially raise the levels of IL-6 and TNF-α in the body.

Increased stress and depression can also trigger latent viruses to reactivate and begin reproducing inside cells. The viruses of greatest interest are some herpes viruses such as the Epstein-Barr virus (EBV). We know that up to 90% of the people in North America have been infected by EBV by the time they are adults.

If EBV begins to multiply in cells in the body, it produces a protein called dUTpase that, in turn, can stimulate macrophages to make yet more IL-6.

The researchers developed a model to test these linkages by using endothelial cells that line the inside of veins in umbilical cord tissue. I spent years working with these cells myself, and they provide an excellent substrate for examining vascular responses and the interaction between blood vessels and macrophages when exposed to the virus as well as the dUTpase protein.

As expected, the production of IL-6, as well as TNF-a, were increased just as they would be as part of the inflammatory process in the body. Such chronic incidents of inflammation are integral to the onset of atherosclerosis and an array of other diseases.

This work suggests a new way of thinking about how vascular diseases develop. We carry around these latent herpes viruses in our bodies virtually all our lives and periodically they can hurt us as we age, develop depression or, perhaps a nutritional imbalance.

Taken together with the recent data on the physical effects of loneliness, if you want to live a long and healthy life:

• Watch you mood: depression can kill you
• Stay socially engaged: loneliness can be fatal
• Maintain a balanced diet
• Take some physical exercise every day
• Learn – and practice! – some simple stress management techniques. You can obtain some at RichardGPettyMD.com

Molecules of Loneliness

It is well known that our social environment has a major impact on our health, wellness and longevity. Lonely, socially isolated adults have a higher mortality than those who are socially engaged.

There has been a lot of speculation about the factors involved, and there is a fascinating study published in the current issue of the journal Genome Biology.   

Researchers from UCLA identified a distinct pattern of gene expression in the white blood cells of people who experience chronically high levels of loneliness. The findings suggest that feelings of social isolation are linked to alterations in the activity of some of the genes that drive inflammation providing a molecular framework for understanding why social factors are linked to an increased risk of heart disease, viral infections and cancer.

Lonely people suffer from higher mortality than people who are not, and the debate has been whether that risk is a result of reduced social resources, or whether it is biological.

In this study the researchers used DNA microarrays to survey the activity of all known human genes in white blood cells from 14 individuals in the Chicago Health, Aging, and Social Relations Study. Six participants scored in the top 15% of the UCLA Loneliness Scale, a widely used measure of loneliness that was developed in the 1970s; the others scored in the bottom 15%. The researchers found 209 gene transcripts that were differentially expressed between the two groups, with 78 being over-expressed and 131 under-expressed. Genes over-expressed in lonely individuals included many involved in immune system activation and inflammation. At the same time, several other key gene sets were under-expressed, including those involved in antiviral responses and antibody production.

The first author on the study s Steve Cole, an associate professor of medicine in the division of Hematology-Oncology at the David Geffen School of Medicine, and a member of the UCLA Cousins Center for Psychoneuroimmunology, and he had this to say:

"What this study shows is that the biological impact of social isolation reaches down into some of our most basic internal processes the activity of our genes.
We found that changes in immune cell gene expression were specifically linked to the subjective experience of social distance. The differences we observed were independent of other known risk factors, such as health status, age, weight, and medication use. The changes were even independent of the objective size of a person's social network."

“We found that what counts at the level of gene expression is not how many people you know, it's how many you feel really close to over time.”

This study was supported by the National Institutes of Health, the Mind, Body, Brain and Health Initiative of the John D and Catherine T MacArthur Foundation, the Norman Cousins Center at UCLA, the John Templeton Foundation, and the James B Pendelton Charitable Trust.

Although small, this is remarkable and shows how much nature not only abhors a vacuum, but also dislikes isolation. We are social animals and anything that gets in the way of that will likely lead to a very poor outcome.

It is fitting that Norman Cousins, for whom the UCLA center is named, had this to say:
“The eternal quest of the individual human being is to shatter his loneliness.”

“The most terrible poverty is loneliness and the feeling of being unloved.”
-Mother Teresa of Calcutta (Albanian-born Indian Nun, Humanitarian and, in 1979, Winner of the Nobel Peace Prize, 1910-1997)

The Curse of Crystal Meth

I have the dubious distinction of living in a part of the United States with one of the highest rates of methamphetamine abuse in the country. Around here most of the first time users are teenage girls who are trying to lose weight.

In the last few years the spread of methamphetamine abuse across the United States has been as rapid as it has been alarming. Until about six years ago, methamphetamine use was seen mostly in the western and rural United States. Then it jumped over the Mississippi and continued its demonic march to the sea and Georgia has been hit like a ton of bricks.

Not only can crystal met ravage the brains of users, they can get a wide range of physical problems including inflammatory and immune problems throughout the body.

Methamphetamine abuse has now expanded rapidly throughout the rest of the country and across different ethnic groups. According to the 2005 National Survey on Drug Use and Health it is estimated that 10.4 million Americans ages 12 or older have used methamphetamine at least once in their lifetimes for non-medical reasons.

There is a new and important study from the Scripps Institute that has shown that long-term methamphetamine use changes circulating proteins in drug users, causing aberrant immune responses. As a result, increased levels of pro-inflammatory cytokines - proteins that are involved in immune responses - may initiate a previously unrecognized molecular mechanism for the development of cardiovascular disorders including vasculitis, an inflammation of the blood vessels.

It appears that methamphetamine can add sugars (a.k.a. “glycate”) proteins. The researchers found that the immune system responds dramatically to this methamphetamine-induced glycation, which may lead to vascular inflammation. There was a direct relationship between methamphetamine intake and the level of circulating antibodies in animal models. This immune response, coupled with antibodies binding to methamphetamine, might make the drug less biologically available leading to an increased need for higher and higher doses, a problem found among chronic methamphetamine users.

The resulting glycated proteins are called advanced glycation end products (AGEs) that modify the function of proteins and are associated with a number of diseases including diabetes and Alzheimer's disease.

Methamphetamine-AGE proteins not only increased antibody production, but also were strong enough to overcome the drug's natural immunosuppressive qualities. Furthermore, a wide range of cytokines directly linked to AGE exposure were increased in rats that self-administered methamphetamine.

The study also showed that even limited daily access to the drug was enough to produce an over-expression of vascular endothelial growth factor which is a potent signaling cytokine involved in angiogenesis and vasodilatation.

If you know anyone tempted to dice with this vile toxin, ask them to have a look here. 

T'ai Chi Ch'uan and Shingles

Shingles can be a particularly nasty problem, and treatment can be tough. It should be called herpes zoster, and it is caused by re-activation of varicella zoster virus (VZV) that causes chickenpox.

A new study  from the Norman Cousins Center for Psychoneuroimmunology at UCLA, has shown that t’ai chi therapy can stimulate the immune system of patients with shingles to levels comparable to those achieved using a vaccine against VZV.

It was a controlled trial in which the researchers randomized 112 healthy adults aged 59 to 86, who had a history of varicella infection, to Tai Chi Chih (TCC, a simplified, standardized form of tai chi) or health education (HE) for 25 weeks. After 16 weeks of intervention, subjects were vaccinated against VZV. The results of blood tests showed that TCC alone increased immunity against VZV by an amount comparable to that induced by varicella vaccine in the HE group.

It was interesting that the effects of the two were additive; TCC, together with varicella vaccine, produced a substantially higher level of immunity against VZV than vaccine alone, raising it to levels usually observed in adults 30 years younger.

The tai chi group also showed significant improvements in scores for physical functioning, bodily pain, vitality, and mental health.

Regular readers will recall another report from this research group, indicating that TCC reduced the activity of the sympathetic nervous system. The two studies both show that there is something special going on: the practice does not only calm the mind and body, it also regulates parts of the body that are normally beyond voluntary control.

There are clearly plenty of reasons for taking up t’ai chi, though now we shall have to see whether other forms of t’ai chi can achieve the same results.

T’ai Chi Ch’uan and Diabetic Health

Regular readers will know that I am a great fan of t’ai chi ch’uan and qigong. I have been recommending them to people for years and even taught it for a while.

I have also been very interested in metabolic problems, particularly insulin resistance and diabetes.

So I was intrigued to see a study  from Taiwan that was just sent to me.

The trial involved thirty-two people with type 2 diabetes mellitus who participated in three hour-long tai chi sessions once a week for 12 weeks. The conclusions were that practicing t’ai chi might help improve one component of immune function and also improve the control of blood glucose.

The researchers found statistically significant reductions in levels of glycosylated (glycated) hemoglobin in the blood of participants, indicating improved long-term blood glucose control. Glycosylated hemoglobin or HbA1c reflects the average blood glucose over the last 8-12 weeks, implying that the improvement must have been quite swift.

They also found increased numbers of regulatory and killer T cells. This may be important: people with diabetes are at considerably increased risk of getting infections.

It is even more impressive that the study was published in the journal Diabetes Care, that is known for its exacting standards.

If you or a loved one has diabetes, you may want to think about taking up t'ai chi.

Good luck!

Sleep Deprivation

When I was a young doctor we used to work absurdly long hours: for more than three years I worked every other night and every other weekend. It was not uncommon to be on your feet for three at a time. It is a wonder that we didn’t die or make more mistakes.

We know that sleep deprivation is not healthy, but we are only now beginning to find out just how damaging it can be. One of the biggest problems is that sleep deprivation interferes with the normal functioning of the immune system.

I saw an interesting paper (NR619) at the 2007 Annual Meeting of the American Psychiatric Association in San Diego last month.

A team from Korea took sixteen healthy volunteers and made them stay awake for 48 hours. They found that even this relatively short period of sleep deprivation produced some impressive effects on the body and the mind:

• Thyroid hormone levels rose
• The speed and accuracy of reaction times fell
• Blood glucose and protein levels rose, and there were disturbances in several liver function tests
• White blood counts increased
• There was a slight fall in immunoglobulin levels

We already know that insufficient sleep is associated with insulin resistance and weight gain, and it is likely that these are mediated by a rise in inflammatory mediators in the blood.

It is remarkable how quickly the effects occur.

And how pleased I am that young doctors no longer have to tolerate those incredibly long shifts.

Some things have changed for the better!

A Promising New Treatment for Lupus Kidney Disease

Systemic lupus erythematosus (SLE) is an out-of-control, malignant attack on the body by its own immune system. It can be a horrible illness that may affect virtually every organ of the body. One of the worst things is that it can lead to renal (kidney) failure. Until now, the treatments of SLE have been either symptomatic or "disease-modifying." The second is what we really want: to prevent the illness from progressing. But it has been very difficult to do that, and I have seen some real tragedies in my career.

We now have a new approach that highlights a new approach to illness in general. Students are usually taught that there are diagnostic tests for illnesses like SLE or prostate cancer. The idea of using the tests for treatment is fairly new. So one of the proteins that goes up in prostate cancer becomes the target for treatment.

But what about SLE?

SLE is a chronic inflammatory disease in which the body produces antibodies against the nuclear components of its own cells. The most worrying are  antibodies to double-stranded DNA (dsDNA). These antibodies can be triggered by  genetics, environmental  factors like sunlight and some drugs.

The antibodies attack the body’s cells and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but most often damages the heart, joints, skin, lungs, blood vessels, liver, kidneys and nervous system.

La Jolla Pharmaceutical Company just announced positive interim antibody results from its ongoing double-blind, placebo-controlled randomized Phase 3 trials of Riquent(R) (abetimus sodium). This is a drug candidate for SLE. Analyses of interim antibody data indicate that patients treated with 900 mg or 300 mg per week doses of Riquent had greater reductions in dsDNA antibodies than patients treated with 100 mg per week or placebo. The results showed a significant dose response when comparing all Riquent-treated patients to placebo-treated patients (p < 0.0001), and each Riquent dose group to the placebo dose group (p < 0.0015 for 100 mg, p < 0.0001 for 300 mg and 900 mg).

For people not used to looking at statistics, these are impressive data.

Clearly other analysts feel the same way: the price of the company's shares went up 40% on the announcement.

We shall keep an eye on the development of this new medicine to see if it fulfills this early promise. At this moment the data are very exciting.

Here Comes the Sun: To Screen or Not To Screen?

I have been worried to see some people - all, I think, without scientific training - proclaiming that there is no need to protect ourselves against the sun because there is no evidence that sulight causes any health problems.

Ultraviolet radiation (UVR) from the sun has been part of the environment since the first cells began to form. When we discuss the effects of UVR on human health and the environment, the range of UV wavelengths is often subdivided into:

• UVA (400–315 nm), also called Long Wave or "blacklight"
• UVB (315–280 nm), also called Medium Wave
• UVC (< 280 nm) also called Short Wave or "germicidal”

The key questions are these:
Can sunlight cause health problems?
Do the benefits of sunlight outweigh their risks?”

UVB is required for the conversion of 7-deoxycholesterol to vitamin D, (the sunshine vitamin!) which is critically important in the maintenance of healthy bones, although there may also be another mechanism by which vitamin D is generated in the body. As we have seen research is making clear that vitamin D has other potential roles in the maintenance of human health. Low levels of vitamin D have been linked to:

• Rickets
• Osteomalacia
• Osteoporosis
• Maintaining the integrity of cell membranes
• Type 2 diabetes mellitus
• Schizophrenia
• Multiple sclerosis
• Pre-eclampsia (hypertension and accompanying problems during the late stages of pregnancy)
• Some types of cancer
• Fibromyalgia-like pains
• Immune deficiency: Africa Americans do not generate enough of a protein needed to ward off tuberculosis. Why? Because the protein needs vitamin D to be activated, and dark skin is inefficient at absorbing and converting UVR. It may also be that we see epidemics of colds and flu in the winter because that is when we have low levels of vitamin D, which allows the viruses to overwhelm our immune defenses.

This does not necessarily mean that taking extra vitamin D will ward off all of these problems.

In the days before the Industrial Revolution, unless we lived in the frozen North, we had no trouble in getting the amount of vitamin D that we needed. In most of the United States, during the summer months, 10-15 minutes outdoors at midday will generate around 10,000 international units (IU’s) of vitamin D in an average fair-skinned person. This is far in excess of the government’s dietary recommendations of 200 IU’s/day in people up to age 50, 400 IU’s up to age 70 and 600 IU’s in people over 70. Not surprisingly many experts – me included – believe and have provided evidence that these daily requirements are much too low. (Have a look at the comments here.)

Of course many of us do not spend much time outside and don’t take in as much in the way of vitamin D containing foods - such as milk and salmon – as we should. I’ve seen evidence to suggest that we in Atlanta are probably at the Northernmost point in the United States were we could hope to get enough sunshine and therefore vitamin D from modest winter exposure to the sun.

Recent data has suggested that if you spend no time at all in the sun, then you may need as much as 4,000 IU’s of vitamin D/day, though that figure has not yet been widely accepted.

Exposure to UVR, whether of solar or artificial origin, also carries potential risks to human health. UVR is a known carcinogen and excessive exposure, at least to the solar radiation in sunlight, increases the risk of cancer of the lip, basal cell, and squamous cell carcinoma of the skin and melanoma, particularly in fair-skinned populations. There is also evidence that solar UVR increases risk of several diseases of the eye, including cortical cataract, some conjunctival neoplasms, and perhaps also melanoma of the eye.

We have good data for the existence of a threshold amount of UV-B exposure that may lead to the formation of cataracts. The amount needed to cause cataracts depends in part on the amount of pigment in the eye, so albino rats get cataracts with much lower exposures to UV-B.

So what to do?

Sunlight has a definite benefit in preventing or treating many clinical problems and it is no surprise that after 3000 millennia we are adapted to make use of the sun’s largesse. What is less easy to understand is why an excess of sunlight can cause so many problems, unless it is our hairlessness and environmental change that has lead to a loss of the ozone layer.

Some years ago it was suggested that sunscreens may themselves cause skin cancer, but the data has shown that to be false. Indeed modern sunscreens almost certainly reduce melanoma risk.
So how do we balance the positive and negative effects of sunlight? A recent review precisely reflects my own thinking:

• We need some sunlight
• Depending on where you live, you need only a few minutes each day
• Sunscreens confer protection on the skin without blocking all the health benefits
• If you have a medical reason for avoiding sunlight, then your health care provider should measure your vitamin D status.

 

Toxoplasmosis and Behavior

Last August I wrote an article about some extraordinary new evidence implicating Toxoplasma gondii in some psychological and psychiatric illnesses. Latent infection with Toxoplasma gondii is amongst the most prevalent of human infections and it had been generally assumed that it is asymptomatic unless there is congenital transmission or reactivation because a person has an immune system that has become depressed or compromised. That assumption is being completely re-evaluated. 

The article generated some extremely interesting correspondence and some spirited discussions.

Here is a very insightful letter from a physician:

Dear Dr. Petty,

I thought about the concept of psychological illness caused by a virus or other organism. I was wondering what would be the mode of dispersion of such a virus. Upper respiratory tract infections, skin and gastrointestinal infections spread by cough, by touch and hand to mouth respectively. How would such a brain virus or protozoal organism promote itself? Of course it could be by the above methods but it seems that there should some way that the specific disease process is connected to a behavior that helps it to spread itself. 

Then I got to thinking; diseases have learned physical ways to disseminate themselves, I wonder if a disease could change behavior to promote it's own dissemination and survival? I imagine that if that were true, people with the flu would be sociable, people with infectious diarrhea would be sociable and hungry, people with AIDS would have increased libido. I haven't yet seen any data for this. Although I've always felt that there was one disease that did alter behavior in a way that is conducive to disseminating itself, and that is rabies. The host goes from being docile, to seeing all others as the enemy. He then attacks them, bites them and thus passes on the organism. A true mind altering virus, although it's psychology works better with animals than with people. Do you think that there are other diseases that spread purely by behavior, that cause the host to seek out the next host and not just pass the disease from one to another just due to proximity?

This was my response:

What great questions!

And believe it or not, there's quite a lot of empirical research on these very topics.

There is a whole textbook on the behavioral effects of parasites edited by Janice Moore entitled  Parasites and the Behavior of Animals. Here's an interesting one: rats and mice are hard wired to avoid cats. Millions of years of programming have ensured that Tom's very presence would send Jerry packing. Cats carry Toxoplasma gondii and if mice or rats become infected with it, usually by eating cat poop, they lose their fear of felines. So now Tom can have lunch at his leisure.

I've also talked about the way in which people with creativity and schizotypal personality disorder (i.e. carriers of genetic risk) tend to be promiscuous, while people with schizophrenia have fewer children. Both groups tend to get more sexually transmitted diseases than the general population. It would be tempting to think that toxoplasmosis can be spread that way, however there's a 32-year old study in German that showed that Toxoplasma was not transmitted by intercourse. However, cytomegalovirus, a common partner to Toxoplasma may be. And both modulate dopamine activity in the regions of the brain involved in salience.

I have done a very detailed literature search encompassing papers written in all the languages that I can read, and have not been able to find any clear evidence of behavior change induced by HIV, influenza or infectious diarrhea: what interesting and important questions to research.

We do have some more data confirming the effects of Toxoplasma infections on the behavior of rats: they become less anxious and therefore do not respond to environmental threats as quickly as uninfected rodents. An antipsychotic medication (haloperidol), a mood stabilizer (valproic acid) and two chemotherapeutic agents - pyrimethamine or Dapsone – have all been shown to prevent the development of Toxoplasma-induced behavioral change.

Another recent study from the Departments of Parasitology, Microbiology and Zoology, Charles University, the Centre of Reproductive Medicine and GynCentrum, in the Czech Republic also speaks to the significance of latent Toxoplasma infections: the presence of the parasite in the blood of pregnant women increases their chance of giving birth to boys. The increased survival of male embryos in infected women may be explained by Toxoplasmosis infections modulating and suppressing the immune system.

If Toxoplasma plays a part in the development of some psychiatric illnesses, yet a high proportion of the population carries it without any problems, one obvious question is what activates it? Environmental stress might, perhaps, cause the Toxoplasma to become reactivated and play a part in the development of specific psychiatric symptoms.

This story is continuing to develop and I am going to watch it closely. If it is confirmed, it could open up some brand new avenues for helping treat and perhaps even prevent some types of psychiatric illness.

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.

Again.

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.

Peripheral Neuropathy

Treating peripheral neuropathy can be one of the toughest problems facing a clinician. Peripheral neuropathy simply means disease affecting the peripheral nerves.

There are a great many cause of peripheral neuropathy. This is just a partial list to give you an idea of the things that a clinician has to think about before starting treatment:

1. Metabolic illnesses: Diabetes mellitus; porphyria; chronic renal failure; amyloidosis and disturbances in circulating proteins
2. Vitamin deficiencies: Vitamins, B1, B3, B6 and B12
3. Drugs and chemicals: Alcohol; Heavy metals like arsenic, lead and mercury; organic pesticides; several drugs used in cancer chemotherapy; isoniazid; nitrofurantoin
4. Infections: Lyme disease; Herpes zoster (shingles); Diphtheria; Brucellosis; Leprosy; Tetanus; Botulism
5. Malignant illnesses
6. Inflammatory and autoimmune illnesses: Rheumatoid arthritis; Systemic lupus erythematosus; Polyarteritis nodosa; Sarcoidosis; Guillain-Barre syndrome; Celiac disease
   
7. Physical injury: Trauma, stretching and compression of nerves, which can include things like carpal tunnel syndrome.
8. Congenital illnesses

Many causes of peripheral neuropathy, particularly diabetes, may also damage the autonomic nervous system that controls the heart, blood pressure, swallowing, intestinal and bladder function.

Neuropathic symptoms typically start in the feet, because the nerves running down there are longer and more vulnerable than the ones going to the hands.
The most common symptoms are:

1. Numbness
2. Tingling
3. Abnormal sensations called dysesthesias
4. A characteristic form of pain, called neuropathic pain or neuralgia: people usually describe it as “pins and needles,” a steady burning sensation or “electric shocks.” These pains can be difficult to describe: typically pains, like stubbing your toe or stepping on something sharp, are transmitted through pain fibers. Neuropathy also involves other neurological pathways, so that the brain receives impressions that it cannot process.

There has been a revolution in out understanding of neuropathic pain in recent years. It is now considered to be a disease rather than a symptom. Normal pain is designed to protect you: you put your foot on a hot plate and you pull it away immediately. Neuropathic pain is different: it is non-protective and it persists and therefore behaves like a disease.

Multiple different classes of medications have been shown to be effective in some people with neuropathic pain, though most are not approved for use by the Food and Drug Administration:

1. Lidocaine patches and creams
2. Capsaicin creams
3. Opioid analgesics
4. Tricyclic antidepressants
5. Serotonin-norepinephrine reuptake inhibitors (SNRIs)
6. Anticonvulsants: Carbamazepine; gabapentin; pregabalin

Earlier this week, data presented at the European Federation of IASP (International Association for the Study of Pain) Chapters (EFIC) indicated that an innovative combination of painkillers might hold the key to unlocking the severe and relatively untreatable pain of peripheral neuropathy.

Dr Magdi Hanna, Director of Pain Clinical Research Hub at King's College Hospital in London, has been studying the combination of the strong opioid oxycodone (OxyContin) with gabapentin (neurontin) in over 300 patients with severe diabetic neuropathy. This combination demonstrated a significant 33% improvement on top of the best pain relief achievable using the maximum tolerated dose of gabapentin as monotherapy. The study was part funded by one of the medicine manufacturers.

This study is good news, but even in this study there were a great many people who were not helped. In another blog item, I’m going to talk about some of the unorthodox approaches that have helped some people.

Parkinson’s Disease, Allergies and Inflammation

The symptoms of Parkinson’s disease have been reported throughout history, but it was first described in the modern era by the great Scottish neurologist James Parkinson in 1817. Even after all these years, we still do not know all that much about what causes it. There’s an interesting study in the August issue of the journal Neurology, which is the official publication of the American Academy of Neurology.

Investigators from the Mayo Clinic used what is known as a case-control design (196 cases and 196 matched controls). What they found was that people who suffered from hay fever or allergic rhinitis, are 2.9 times more likely to develop Parkinson’s disease over a 20-year period.

The researchers did not find any association with autoimmune illnesses such as lupus, rheumatoid arthritis, pernicious anemia or vitiligo. They also did not find any association with asthma.

In addition, people who developed Parkinson’s disease used anti-inflammatory agents less frequently than controls, although this result was not statistically significant. The results may support the hypothesis that there is an inflammatory component in the causation of Parkinson’s disease.

You may ask, “Why on earth would anyone even look at a link like this?” The answer is that there have been previous reports of an association between the use of non-steroidal anti-inflammatories and lower rates of Parkinson’s disease in men but not in women and Alzheimer’s diseases.

This study does not suggest that hay fever causes Parkinson’s disease: it provides evidence for an association between the two. Parkinson’s is probably a group of illnesses with different causes. However, if chronic inflammation around the upper airways could produce inflammation in the brain, we might have a whole new way of preventing a degenerative brain disease.

In a future posting I’ll talk about some natural methods for reducing the burden of inflammation in your body.

How Does Fiber Help You?

Unless you’ve been living on Mars (!), you will doubtless have heard of the advantages of increasing the amount of fiber in your diet. A high-fiber diet reduces your risk of colon cancer, constipation, hemorrhoids hypercholesterolemia and insulin resistance syndrome.

We have always wanted to know how fiber does so many magical things at once, and now we may an answer. In a paper published in the open-access Public Library of Science Biology today, by a group from one our local institutions – the Medical College of Georgia in Augusta – collaborating with a researcher from Josai University, Sakado, Saitama in Japan.

The epithelial cells lining the intestine have a life span measured in 1-5 days. They spend their short life times working to process enormous amounts of food residue on its way past. It is this layer of cells that acts as the barrier between the body and items floating past on the inside of the intestine.

Long before it became the topic of some popular books are over-enthusiastic magazine articles, we became very interested in the idea of the “Leaky gut:” the concept that some illnesses are a result of breakdown of the normal integrity of this protective barrier. Over 20 years ago, a friend and colleague at Northwick Park Hospital - Ingvar Bjarnason - did some pioneering work on this important issue. Several recent studies have indicated that a breakdown of this barrier may be involved in several childhood illnesses including allergies and asthma. There is also some early information suggesting that “leaky gut” may be involved in some autoimmune processes involving the intestine. Both zinc supplementation and oats may prevent gut leakiness under certain very specific circumstances.

When the epithelial cells in the gut wall encounter indigestible fibrous foods, the outer covering of the cell ruptures, releasing a coating of cell-protecting mucus. In a matter of seconds, the cell begins to repair itself, in the process releasing yet more of the beneficial mucus. Not only does it lubricate, but also it may keep some carcinogens and allergens out of your system.

The constant buffeting of the cells causes mild damage that increases the level of lubricating mucus. Injury at the cellular level promotes the health of the gastrointestinal tract as a whole.

Here we see a basic principle of nature: many of the same things that apply in the cells of the body apply equally in the life of someone trying to achieve success. Without the buffeting, the cells of the intestine could not produce the mucus on which your life depends.

Without some occasional adversity, you will find it more difficult to grow as a human being.

“Storms make oaks take deeper root.”
-- George Herbert (English Religious Poet, 1593-1633)

“He who knows no hardships will know no hardihood. He who faces no calamity will need no courage. Mysterious though it is, the characteristics in human nature which we love best grow in a soil with a strong mixture of troubles.”
--Harry Emerson Fosdick (American Clergyman, Writer and Broadcaster, 1878-1969)

Lupus Question

I had a very nice letter from a gentleman who posed the following question, which I have slightly edited in order to maintain confidentiality:

"A friend of mine, a 36 year old female has been diagnosed with Lupus.Healing by her doctors is not an option. Treatment yes. That's not good enough. Any recommendations on how to heal it, who to see, what to read?"

It is always difficult for a health care practitioner to make precise recommendations about an individual whom they have not seen. That’s why we get so frustrated by some of the people who sell “cure alls” on their websites or infomercials. And when they are challenged say “but I’m not a doctor.” In which case, why are you giving advice??

Let me first say something about lupus. Systemic lupus erythematosus (SLE) is one of the so-called non-organ specific autoimmune diseases. What that means is that it can attack virtually any organ that has a DNA “command center.” And immune complexes can attack the skin, joints, kidneys, lymph nodes and so on. The autoimmune diseases show us how unwise it is for folk to advise us to “boost” our immune systems. SLE is an example of an overly boosted immune system. We should aim to balance our immune systems.

There is a lot of evidence that SLE has been becoming more common in recent years. Though we always have to be careful when we are told that an illness is becoming more common. That apparent increase may also be accounted for by other factors:

1. More physicians may be becoming familiar with the illness: I saw this happen some years ago after I published an account of the first British case of a very rare type of headache. Within months, several other cases had been found. In each case doctors wrote to me saying that they had been treating the sufferer without success for many years, but after my report, understood what the problem had been, and, following my rules, had cured their patients.
2. Diagnostic tests are becoming more sensitive, so more cases are turning up.
3. Specialists are very good at changing the diagnostic criteria for an illness, or the level at which treatment is required: the “when is a difference a disease?” issue. Skeptics are forever saying that the only reason for doing so is so that drug companies can sell more drugs. But that’s a real misunderstanding: it’s actually the other way round. We change criteria once we have evidence that treatment may do some good. A good example is blood pressure. The levels at which we recommend treatment have been falling in recent years, because we now know that even minor hypertension can increase the risk of heart disease. Or diabetes mellitus, where the diagnostic blood sugar levels have been reduced for this reason: even small elevations of blood glucose increase the chance of damage to some blood vessels. It’s not the glucose itself that’s the problem, but the consequences of an elevated glucose level.

The reason for this preamble is this: if SLE is becoming more common, it is difficult to explain using conventional medical models. Some years ago, there was a report that more than half of all sufferers carried an organism called mycoplasma, and that this might be the cause of the illness. Nobody was ever able to replicate that finding, so the idea of an infectious cause is firmly on the back burner.

So let’s look at the illness from the perspective of physical, psychological, social, subtle and spiritual factors, for all come into play in someone dealing with SLE. The key to treatment is to have a healing synergy between all of the interlinked aspects of our lives.

On the physical front, conventional medicines have a great deal to offer, but as you said, for treatment rather than cure. They are also used to help protect organs against damage. One potential reason for the increase in the prevalence of SLE, is that there is a close link between the amount of fat in the abdomen and the production of some classes of inflammatory mediators. So question one: does the sufferer have an excess of intra-abdominal fat? If yes, diet and much gentle exercise as the illness will allow. What kind of a diet? Balanced, and following the principles which I outlined in the final part of the Healing, Meaning and Purpose.

There have been countless reports of people with SLE and other forms of inflammatory arthritis, especially rheumatoid, having food sensitivities particularly to dairy or to alfalfa. The research base is weak, but it is always worth exploring. There has been growing interest in the use of DHEA and foods high in omega-3 fatty acids. Some people have also reported some benefit from Vitamins C and E, and selenium. The treating physician can help with doses. There are also some herbal and homeopathic remedies that may be helpful. I quite like The Arthritis Bible by Craig Weatherby and Leonid Gordin as an overview of some of these approaches.

Next is psychological. Sunlight, stress, fatigue and lack of sleep can all make the condition worse, and I would urge the person to follow some of the plans that I outline on the CDs and in the book. An awful lot of people suffer from illnesses like this as a consequence of psychological factors. So it is a really good idea to use the approaches to see if there are any emotional, cognitive or relationship problems which have triggered or are perpetuating the autoimmune process.

Next is the subtle systems that underlie the physical and psychological. These may need to be re-programmed using acupuncture, or Reiki, or Thought Field therapy, or even high potency homeopathic remedies.

Finally the spiritual. I cannot over-emphasize the importance of this in all our lives. Again, I have made some suggestions in the program. It would not be right for me to tell others what or how to practice, but keeping in touch with, and strengthening the contact with your spiritual essence provides a wellspring of healing energy and support.

There is a final point that I would like to make. Not all illnesses can be made to disappear, and sometimes our focus has to change to one of helping the individual understand, learn from and coexist with the illness.

Who to see? Any health care professional that will respect all five domains, and help the individual to help themselves.

Now, back to you: does that help?

+ Are there others out there who would like to share their experiences?

Technorati tags  Lupus  Thought Field Therapy  Healing