Richard G. Petty, MD

Curry and Cognition

During a visit to Singapore a couple of years ago, I heard about some interesting research that’s just been published in the American Journal of Epidemiology.

The authors did something fairly simple. They took a group of 1,010 people with no evidence of dementia aged 60-93 years, and correlated their consumption of curry with their cognitive performance. Studies like this are not easy: what if more intelligent people like eating curry to begin with? What if sick people can’t get out to the local curry house? And so on.

But the researchers did this all very carefully: they took into account all the known sociodemographic, health, and behavioral determinants of performance on a simple cognitive test. So they controlled for many of the other factors that can accelerate cognitive decline, like depression, smoking, drinking alcohol, high blood pressure, glucose and lipids.

The result was that people who occasionally or often ate curry had significantly better cognitive function than people who "never, or rarely" ate curry.

Is there any logic to this?

Well in fact there is. Curcumin, from the curry spice, turmeric, has been shown to possess potent antioxidant and antiinflammatory properties and to reduce beta-amyloid and plaque burden in experimental studies. There have been serious suggestions about using active constituents of tumeric to try and prevent the development of Alzheimer’s disease.

This research is all very encouraging. The amount of curcumin used in the experimental studies is similar to the amount ingested by having a couple of curries a week, and now the epidemiological study from Singapore suggest that those couple of curries may have a clinically measurable effect.  That’s not to say that eating curry three times a day is going to be even better.

All things in moderation: too much curry can play havoc with your digestive processes.

And your relationships….

Probiotics: Caveat Emptor

You may well have heard the advice that we all need to keep the bacetria in our intestines healthy. Countless experts have recommended that, as long as we are not lactorse intolerant, we should regularly take some live yoghurt to "re-colonize" our intestines with nice friendly bacteria.

There has just been a briefing in London to warn the public that as many as half of the "probiotic" or "friendly bacteria" products on sale in the United Kingdom could be ineffective and some may even be harmful.

The experts on the panel included Professor Glen Gibson from the University of Reading who is an expert in food microbiology, and recommended sticking to products made by major manufacturers. Too many of the other productsmight not contain the numbers of bacteria advertised, and the icrobes might not survive long enough in the intestines to do much good.

The evidence that probiotics help is still far from settled, as discussed in a recent review. But there are enough reports to think that probiotics may be helpful for irritable bowel syndrome and perhaps inflammatory bowel disease.

An even newer area or interest in the use of "prebiotics:"  short-chain carbohydrates that alter the composition, or metabolism, of the intestinal organisms in a beneficial way.

Make sure that if you are using a product, it comes from a reputable manufacturer, and that it contains at least 10 million bacteria. And as I said in my title, "Caveat Emptor," "Let the buyer beware."

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)

Insulin Resistance, Polycystic Ovarian Syndrome and Sleep Apnea

Polycystic ovarian syndrome (PCOS) is a common endocrine disorder that affects between 5-10% of women in the Western World. It is a leading cause of infertility, and although the underlying cause is still speculative, it is very heavily associated with insulin resistance.

There was an International Consensus Workshop sponsored by the European Society of Human Reproduction and Embryology and the American Society of Reproductive Medicine came up with this set of criteria. PCOS is present if a woman has at least two out of three of:

  1. Oligoovulation and/or anovulation (ovulating only occasionally or not  at all)
  2. Excess androgen (male sex hormone) activity
  3. Polycystic ovaries (which needs a gynecological ultrasonography) and other causes of PCOS are excluded

There is still a great deal of debate about the precise way to define the syndrome. We are currently preparing a scholarly article on the subject and our literature review has included over three thousand papers.

The combination of an excess of the male (androgenic) hormones and insulin resistance can cause an array of symptoms apart form the menstrual disturbances and infertility, including:
Central obesity
Hirsutism, while at the same time experiencing alopecia
Skin flaps and dark patches of skin, usually on the neck or in the armpit
Sleep apnea

It is the last of these that I would like to highlight today.

A new study by Dr. Esra Tasali and her colleagues from the University of Chicago has found that in women with PCOS, sleep apnea is, as expected, associated with high fasting insulin levels. Sleep apnea might worsen the metabolic consequences of insulin resistance.

Regular readers may recall that I highlighted the association between insomnia, insulin resistance, weight and diabetes a couple of months ago. Here we have yet more confirmation of this link.

Not getting enough sleep – for any reason – can play havoc with your metabolism. It seems that in women with PCOS, it’s really easy for a vicious circle to become established:
Insulin resistance -> weight gain -> sleep apnea -> insomnia -> more insulin resistance -> more weight gain and so on.

It is important for everyone to know about this association, because chances are that you know someone with PCOS and/or sleep apnea.

How Many Angels Can Dance on the Head of a Needle? Moving Beyond the Metabolic Syndrome

I have written a great deal both on this blog and in scholarly articles, about insulin resistance and the insulin resistance and metabolic syndromes.

You will have noticed that I’ve always used the term insulin resistance syndrome.

This is not a matter of semantics. For years now I’ve been worried about the splitting that’s been going on in the field: we currently have six sets of definitions of the metabolic syndrome. And apart from the fun of going to all those conferences in exotic parts of the world, you have to ask what’s been achieved by these ever more divisive attempts to “define” the medical consequences of insulin resistance.

The American Diabetes Association has begun to promote the concept of “cardiometabolic risk.” The Association has established a national Cardiometabolic Risk Initiative (CMRI) to stress the association between diabetes, heart disease and stroke. The idea of introducing this umbrella term is to help people better understand and manage all diabetes and cardiovascular risk factors, and to side-step some of the controversy surrounding the definition of insulin resistance or metabolic syndrome and which cluster of variables are in and out.

A new Cardiometabolic Risk (CMR) Calculator to help us evaluate an individual’s risk of diabetes or vascular disease should be available by the end of the year.
The formula already includes factors such as:
1.    Body mass index
2.    Waist circumference ratio
3.    Fasting plasma glucose
4.    HDL-cholesterol
5.    LDL-cholesterol
6.    Triglycerides
7.    Apolipoprotein B
8.    Blood pressure
9.    C-reactive protein
10.  Age
11.  Sex
12.  Race/ethnic origin
13.  Family history
14.  Tobacco use

Part of the reason for this new initiative is the discovery that pre-diabetes, or impaired fasting glucose, where plasma glucose levels are 100-125 mg/dl, is associated with a high prevalence of cardiovascular disease risk factors such as obesity, hypertension and dyslipidemias.

The person who first proposed the insulin resistance syndrome, a.k.a. syndrome X, a.k.a. metabolic syndrome, is Gerald Reaven who first recognized the syndrome in a landmark paper in 1988. He recently gave a lecture entitled; “Insulin Resistance Versus Metabolic Syndrome: Different Names, Different Concepts, Different Goals.” I am in complete agreement with his basic proposition, which is that insulin resistance explains the clustering of all of the components that make up the metabolic syndrome. So Gerry’s position is that there’s no point in trying to make a diagnosis of metabolic syndrome: everything is due to insulin resistance.

So instead of wasting time and resources in trying to diagnose metabolic syndrome, it is much better to understand the pathophysiology: what is going on at the molecular level, how these processes produce risk factors, and whether we can predict others. We should identify and treat each of the underlying processes and the complications of insulin resistance. If we are going to have a syndrome, it should be called insulin resistance syndrome.

And let’s stop these academic debates and get on with the job at hand: there is a 600% variation in peoples’ ability to have insulin transport glucose into cells. More than half the US population is destined to develop at least some degree of insulin resistance, so we need to look for better ways to identify people who have it, and to apply the principles of integrated medicine to keeping them healthy.

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Cannabinoid Receptors and Cardiovascular Risk Factors

Clinicians throughout the world are looking forward to being able to use a new medicine for obesity called rimonabant, which will be marketed as Acomplia by Sanofi-Aventis. It was launched in the United Kingdom yesterday, after being given official European Union marketing approval last week. We do not expect to get it in the United States until sometime in 2007, assuming that the FDA gives it approval. The medicine is not cheap, but interestingly there is also some data to suggest that it may help some people stop smoking.

So why the interest? The original idea for the compound was based on the observation that many people become very hungry if they use cannabis and specific cannabinoid receptors were found in the brain that are responsible for many of the actions of the drug.

A recent and important study involving a two-year investigation of 3045 obese or overweight individuals was published in the Journal of the American Medical Association. It indicated that treatment with 20 mg/day of rimonabant plus diet for 2 years promoted modest but sustained reductions in weight and waist circumference and favorable changes in metabolic and cardiac risk factors.

Only about half of the people in the study completed it, so we must interpret the data cautiously. The idea of using a pill to manage weight is appealing as a weight-loss aid for some patients. But as I have pointed out before, the control of weight is highly complex, and it is highly unlikely that a pill will be successful on its own. What are needed are long-term, comprehensive lifestyle changes, together with careful attention to the psychological and subtle aspects of weight control.

We have had a great many requests to publish our own comprehensive weight management strategy – The Atlanta Approach – that we have been using with great success for almost two decades. If there is interest in me doing so, I shall put our notes together into a downloadable eBook.

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Insulin Resistance, Insulin Resistance Syndrome and Race

I often hear clinicians say that they are not too clear about the differences between insulin resistance and insulin resistance syndrome. Let me define them, and then tell you why they are so important, and why everyone needs to be informed about them.

First, insulin is a hormone produced primarily in the cells of the Islets of Langerhans in the pancreas. It has over 500 functions in the human body, but its main actions are on the regulation of the metabolism of carbohydrates and fats. Insulin enables glucose – one of the major sources of energy – to move into many of the cells in the body. Insulin is also involved in the conversion of glucose to glycogen. These two actions lower the blood glucose level.

Insulin resistance is defined as an impaired biological response to insulin. It is a condition in which many of the cells of the body – mainly in the liver, fat and muscle – become resistant to the effects of insulin. The normal responses to a given amount of insulin are reduced. As a result, higher levels of insulin are needed in order for insulin to have its effects. There are many potential causes of insulin resistance: genetic; an increase in intra-abdominal fat; smoking cigarettes; being of low birth weight; and there are some prescription medicines that can cause insulin resistance. Insulin resistance is one of the underlying causes of type 2 (maturity onset) diabetes mellitus, as well as an array of other illnesses including polycystic ovarian syndrome. Most studies have suggested that around a third of people living in the United States and Western Europe have insulin resistance, and there are marked ethnic differences.

The insulin resistance syndrome has several other names: Metabolic syndrome; (Metabolic) Syndrome X; Dysmetabolic syndrome; Reaven’s syndrome; multiple metabolic syndrome. There are several sets of criteria for defining the insulin resistance syndrome. In the USA it is usually defined as the presence of 3 or more of the following:
1. Abdominal obesity (Waist circumference >40 inches in men; >35 inches in women
2. Glucose intolerance (fasting glucose ≥110 mg/dL)
3. Elevated blood pressure ≥130/85 mmHg
4. Triglycerides >150 mg/dL
5. Low HDL (Men: <40 mg/dL; women: <50 mg/dL)

There is a constant debate in the medical literature about whether insulin resistance syndrome is an illness, and what should be included in it. It is important, because it appears to predict the development of diabetes and coronary artery disease, and between 20 and 25% of the population of the Western world has it. So what normally happens is that a person develops insulin resistance, which eventually evolves into the insulin resistance syndrome, before diabetes and heart disease appears. There can be as long as twelve years between the development of insulin resistance, and the diagnosis of diabetes, and we have very good evidence that lifestyle changes can dramatically reduce the risk of moving from insulin resistance to the insulin resistance syndrome and diabetes.

It has become quite well-known that people of African and Asian Indian heritage are at increased risk of developing insulin resistance, and some of the sequelae of insulin resistance: insulin resistance syndrome, diabetes mellitus, hypertension and gout. These may in turn lead to increased rates of myocardial infarction and strokes. A study presented last Monday at ENDO 2006, the annual meeting of the Endocrine Society in Boston helps further clarify some of these ethnic differences. Researchers analyzed data from the Insulin Resistance Atherosclerosis Study (IRAS), designed to assess relationships between insulin resistance and cardiovascular disease in a large multi-ethnic population.

The investigators divided data from female IRAS participants into different groups based on body mass index (BMI), a measure of body fat based on height and weight. A BMI of less than 25 is usually considered "normal." The analysis revealed that 47 percent of black women of normal weight had insulin resistance, compared to less than 20 percent of the Hispanic or White women. Both insulin resistance and the likelihood of developing type 2 diabetes increase as obesity increases. It had long been suspected that there was an independent effect of race, but this study not only shows that race alone may influence insulin resistance, but that we may therefore need to change the definition of obesity in women of African heritage.

The news reports on this important finding failed to mention that previous research has found something very similar in Asians from India, China and Japan. Each of these ethnic groups may develop insulin resistance, insulin resistance syndrome and diabetes without being obese, though obesity dramatically increases their risks of running into trouble.

It is relatively simple and inexpensive to measure insulin resistance, and many metabolic experts, including your humble reporter, have, for more than a decade, been measuring it in high-risk individuals. Clearly we cannot do anything much about an ethnic or genetic risk, but we can alter the way in which the body responds to that risk. If a person is insulin resistant, diet, exercise, specific nutritional and herbal interventions and occasionally medications, may all reduce the risk of developing diabetes and heart disease.

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The Genetics of Eating

The BBC has just run a story about the latest installment of some fascinating work being done by Professor Jane Wardle, of Cancer Research UK’s health behavior unit.

Two years ago she published data on genetic predispositions to unhealthy eating behaviors. This new study involved more than 200 pairs of same-sex twins, about half of whom half were identical, so sharing all their genes. Based on questions given to the childrens’ mothers, it now appears that a taste for high protein foods like meat and fish are largely inherited. By contrast, a liing for vegetables and sweets are less likely to be fixed and more a reflection of the menu provided by parents. Interestingly, girls were found to be more likely to enjoy vegetables than were boys.

It’s not clear why there should be this separation: genetic predisposition toward protein eating and environmental toward vegetables and sweet things. The researchers though that it might have something to do with variety of choices of vegetables and little choice in types of proteins.

I think, though, that this all makes good sense from an evolutionary prespective. We are going to be exposed to different fruits, vegetables and sweet things throughout the year and particularly as our ancestors migrated. Copying what foods to eat would make sense. The trouble arises when the availability of food throws the system off.

In Healing, Meaning and Purpose, I point out that as recently as ten thousand years ago, is someone wanted something sweet, it would mean sucking a sweet vegetable or risking a raid on a beehive. Oh how things have changed! In 1905 The average annual intake of refined sugar was 60 pounds per person, up from 7 pounds per person in 1805. (It is estimated to be an average of about 150 pounds for each person in the United States in 2005. A twenty-fold increase in just 200 years.)

This research indicates that parents could have a profound impact on their children’s dietary preferences – and help steer them toward healthy options. That being said, there are so many children who develop all manner of likes and dislikes for no readily apparent reason. We have recently been taking a great deal of interest in the oversensitivity to taste and texture of food in many girls with attention deficit disorder. I shall write more about that soon.

But the research also reinforces what I have said so many times: genes are important, but biology is not destiny. There are millions of vegetarians who presumably still have those meat-liking genes on board.

“Give me the children until they are seven and anyone may have them afterward.”
–St. Francis Xavier (Spanish Jesuit Missionary and Co-Founder, in 1534, of the Jesuit Order, 1506-1552)

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Add Years to Your Life and Life to Your Years: The Power of Small Changes.

I want to tell you about a mind bogglingly important study that many professionals have known about, but somehow hasn’t popped up on most people’s radar. The story  was broken by the BBC last month. It is about an exceptionally important study that has been running in Norfolk, in Eastern England, as well as other parts of Europe since 1992. The British section is directed by Professor Kay-Tee Khaw who is Professor of Clinical Gerontology at the Department of Public Health and Primary Care at the University of Cambridge. The main focus of the Clinical Gerontology Unit is the maintenance of health in aging populations, with a particular emphasis on the combined role of lifestyle, environmental and genetic factors in chronic diseases.

The UK arm of the study has been following 25,663 men and women aged between 45 and 79 years old, looking at their diet, environment, lifestyle and health. The latest results from the study have confirmed several things that we already suspected: 1. Eating five portions of fruit and vegetables a day can give you the life expectancy of someone three years younger.
2. Not smoking turns back the clock by four to five years.
3. Even increasing exercise by a moderate amount can increase your life expectancy by three years. But the amount of exercise someone would need to do to achieve that depends on their job. A sedentary office worker would need to do one hour of exercise, such as swimming or jogging every day. By contrast, a person with a moderately active job, such as a hairdresser, would need to take 30 minutes of exercise a day. Here’s some more good news: People with very active jobs, including nurses and bricklayers, do not need to do any extra exercise – as their work is strenuous enough.

I think that just about anyone can take those baby steps toward a longer and healthier life

There’s an old Yugoslavian Proverb:
“Grain by grain a loaf, stone by stone, a castle.”

That seems about right!

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Attention Deficit Disorder, Allergies and Membranes

There has been a long-running debate about the relationship – if any – between allergies and attention deficit disorder (ADD).

As long ago as 1991 a paper seemed to indicate that there were higher rates of hyperactivity in the parents of children with allergies as well as increased rates of allergies in children with ADD. Recently a study from New York seemed to show higher rates of allergic rhinitis in children with ADD. The problem with all this is that we are looking at two common problems and trying to sort out a genuine connection can be tricky.

I started thinking about this problem again, after a recent report that some children had symptoms of hyperactivity, inattention, attention-deficit/hyperactivity disorder, and excessive daytime sleepiness as a result of sleep-disordered breathing. But what was remarkable was the number who improved after they had their tonsils taken out. The tonsils are one of the first lines of defense in the immune system, which is why they so often become enlarged with infections, or for that matter in any kind of immunological reaction. Now I’m not much of one to take out tonsils unless there’s a really good reason, but it is certainly an important observation for anyone who has a child with behavioral or cognitive difficulties: he or she may not be sleeping properly.

I have seen quite a number of people who had physical and psychological problems, including headaches, depression and attentional problems, who turned out to have either allergies or environmental sensitivities, and when those were addressed, the symptoms resolved. I have also seen some people who followed the notoriously difficult Feingold diet with some success, even though the research doesn’t seem to be very supportive of elimination diets. And I’ve seen just as many people who got no relief at all from elimination diets.

I have just done a detailed literature review on the topics of allergy and attention, and I don’t think that we have enough evidence to suggest that everybody with attention deficit needs to see an allergist. But what this highlights is that not all people with attentional problems or hyperactivity have ADD. They may have attentional problems because of sleep disturbance, depression, anxiety, obsessive compulsive disorder and a range of other problems.

There is some exciting research indicating that one of the problems in many cases of ADD is a disturbance in the normal functioning of cell membranes. If that is correct, it may be that there are disturbances in the membranes of both neurons in the brain and membranes of cells in the immune system. That link is not entirely proven. But it has received further credence by the finding that some children and adults with ADD seem to show improvements of both attention and immune function when they take omega-3 fatty acids. I have recently been hearing some encouraging reports from people who have used the Omega-3 Formula made by Omegabrite (And no, I have no link with the company!)

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