Richard G. Petty, MD

Nutrigenetics: A Peak Into the Future

At any given time only about ten percent of you genes are thought to be active. They are switched on and off in response to all kinds of internal and environmental changes. This is particularly true in the metabolic pathways, where gene activation is an essential part of the normal response to dietary changes. We also know that many of us have genetic reasons for varying in our nutritional requirements.

Anybody who has looked into diet and nutrition knows that there is no one approach that works for everyone, and the Holy Grail of weight management is to be able to identify which diet will work for whom.

This goal has just come a little closer with the publication of a report from researchers in Greece, London and Colorado that has been published in the Nutrition Journal.

The paper, “Improved weight management using genetic information to personalize a calorie controlled diet” is available for free download.” The study population consisted of 50 patients who had failed to lose weight. They were offered a nutrigenetic test screening 24 variants in 19 genes involved in metabolism. 43 patients attending the same clinic were selected for comparison using algorithms to match age, sex, frequency of clinical visits and BMI at initial clinic visit. The second group of 43 patients did not receive a nutrigenetic test. BMI reduction at 100 and over 300 days and blood fasting glucose were measured.

The results are very promising. After 300 days of follow-up individuals in the nutrigenetic group were more likely to have maintained some weight loss (73%) than those in the comparison group (32%). Average BMI reduction in the nutrigenetic group was 1.93 kg/m2 (5.6% loss) vs. an average BMI gain of 0.51 kg/m2 (2.2% gain). Among patients with a starting blood fasting glucose of >100 mg/dL, 57% (17/30) of the nutrigenetic group but only 25% (4/16) of the non-tested group had levels reduced to <100 mg/dL after >90 days of weight management therapy.

The paper concludes by saying that the addition of nutrigenetically tailored diets resulted in better compliance, longer-term BMI reduction and improvements in blood glucose levels.

This is a small “proof of concept” study, and the effects are not enormous, but there is easily enough here already to vigorously pursue this genetic approach.

Emotional Eating

A new study from Miriam Hospital's Weight Control and Diabetes Research Center in Providence, Rhode Island, has just been published in the journal Obesity. The research suggests that dieters who tend to eat in response to external factors like parties and celebrations, have fewer problems with their weight loss than those who eat in response to internal factors such as emotions. The study also found that emotional eating was associated with weight regain in people who had successfully lost weight

The researchers analyzed individual's responses to questions in a well-known research tool called the Eating Inventory which is designed to assess three aspects of eating behavior:

1. Cognitive restraint
2. Hunger
3. Disinhibition

The main focus was on the third item, since some previous research has suggested that disinhibition as a whole is an accurate predictor of weight loss.

The disinhibition scale evaluates impulsive eating in response to emotional, cognitive, or social cues.

There were two groups in the study. The first consisted of 286 overweight men and women who were currently participating in a behavioral weight loss program. The second group included 3,345 members of the National Weight Control Registry (NWCR), an ongoing study of adults who have lost at least 30 pounds and kept it off for at least one year. 

The investigators found that the components within the disinhibition scale could be grouped into two distinct factors: external and internal disinhibition.

An example of external disinhibition would be the person who overeats when they are with someone who is also overeating, or the person who just overeats at a party, picnic or celebration.

The person with internal disinhibition eats in response to thoughts and feelings such as loneliness, upset or anxiety.

In both groups internal disinhibition was a significant predictor of weight over time. For participants in the weight loss program, the higher the level of internal disinhibition, the less weight an individual lost over time. The same was true for maintainers in the NWCR: Internal disinhibition predicted weight regain over the first year of registry membership.

Before starting a weight management program it is very helpful to know which group you are in. It provides us with a quick and easy method of tailoring the program to the individual, and tells us where to put our efforts.

More Genes Involved in Obesity

I am impressed by the progress being made by some of my former colleagues who are busily unraveling the complex genetics of obesity.

In a paper in the journal Science a group of British scientists including Chris Ponting of the Medical Research Council Functional Genetics Unit in Oxford and Stephen O'Rahilly’s group at the  University of Cambridge, has made a second breakthrough in twelve months in understanding how a gene triggers weight gain in some individuals. In May we looked at the first piece of work on the gene called “FTO.”

At that time we learned that variations in the FTO gene influence people's risk of becoming obese. This particular gene was of great interest because the genetic variant in FTO that predisposes to obesity is very common in the population.

About half the British population carries a copy of the variant and they are on average 3-4 pounds heaver than those who do not have it. The 16 per cent of the population who carry two copies of the variant and are on average 6-7 pounds heavier. We also learned that carriers of the variant have an increased risk of diabetes. However the function of FTO was completely unknown.

The new paper shows that the FTO gene codes for an enzyme - 2-Oxoglutarate-Dependent Nucleic Acid Demethylase - that can act directly on DNA. This strongly suggests that FTO might have a role in controlling how and when genes are turned on and off.

The investigators also found that FTO is highly expressed in the hypothalamic region of the brain, which has important roles in the control of hunger and satiety. In certain areas of the hypothalamus, the levels of FTO are influenced by feeding and fasting.

This is a remarkable finding. That a gene involved in obesity and diabetes has a direct effect on DNA in specific regions of the brain is very exciting. It suggests that the gene is involved in influencing how well the brain senses hunger and fullness. Small molecules derived from metabolism can modulate the activity of FTO, so we can see a direct link form food to metabolism to DNA in the brain.

The findings raise all kinds of treatment possibilities and also confirm something that I have been teaching for three decades: weight control does not start with a diet. It starts between the ears. Until you have been shown how to re-program your brain, thoughts and emotions, your chance of successfully controlling your weight is, ahem, slim.

He That Enjoys His Portion

Having grown up at a time and in a culture where it was expected that everyone would finish every morsel of food on his plate, it was quite a shock to come to the United States and to be confronted by mountains of food. During my first few months I dutifully consumed everything on my plate and soon noticed the effect on my waistline. But it brought home to me the power of social and cultural factors in eating.

Though each of us is responsible for how much we eat, research suggests that cultural and social norms can make it hard for us to choose appropriate portion sizes. The November 2007 issue of Harvard Women's Health Watch has published an interesting article about the way in which misperceptions about portions can affect calorie intake.

A first point is that many of us tend to treat portions as equivalent to nutritional servings. A serving is a specific quantity of food designated on the basis of nutritional need. However, a portion--the amount you actually get on your plate, in the package, or at the counter--is often much larger. Many of us do not always read the Nutrition Facts label, and may find ourselves eating two or three servings' worth. Studies suggest that we might be satisfied with smaller portions if larger ones were not so easily available. Other research has shown that the more plentiful the food, the more we eat. I know form my own experience that both of those are true.

The Harvard Women's Health Watch offers some advice for “keeping portions in proportion:”

• Train your eye: Measure out servings - not portions - of the food you commonly eat so you know what a single serving looks like
• Change your tableware: Use a smaller bowl or a mug for cereal and a smaller plate at dinner
• Control portions at home: To discourage second helpings, serve food in the kitchen and take it to the table on plates
• Eat at regular intervals throughout the day: Do not wait until you are hungry, since you are then more likely to overindulge at the next meal
• Control portions while eating out: Avoid buffets and salad bars. Instead of a dinner, order a low-fat appetizer and a large salad with dressing on the side

These are all simple and straightforward pieces of advice that will be familiar to anyone working in the weight and metabolism field.

On another occasion I shall give you a few more of my own tips, including “Perimeter shopping”

The Neurology of Eating

Any attempt at weight management that fails to address the whole person is doomed to failure.

It is not enough to diet and exercise, and whatever the truth of manifesting, you cannot think yourself thin. Success demands an approach that integrates every system of your body, mind, social and subtle systems. For many people there is even an important role for integrating their spirituality into a plan for healthy living.

So we need to learn as much as we can about each component. Some fascinating new research has added some important pieces to the puzzle.

Writing in the journal Nature a group of scientists from University College London and King's College London used peptide YY (PYY), a naturally occurring hormone that regulates appetite, to investigate which areas of the brain are involved in controlling food intake.

PYY is released into the bloodstream from the intestine after we eat something. In animals PYY signals the appetite control centers in the hypothalamus and brainstem that food has been eaten. Injections of this hormone have been shown to decrease food intake both in healthy volunteers and in people with obesity.

The hypothalamus and brainstem are ancient regions of the brain involved I te most basic functions. But humans have complex, highly developed brains, and the question was to discover how PYY regulates eating in humans.

The study involved eight normal weight men in a double blind placebo-controlled study. After 14 hours without food the subjects were given an intravenous infusion of either PYY or placebo for 100 minutes. During all this their brains were scanned continuously using functional Magnetic Resonance Imaging (fMRI). Thirty minutes later they were offered an unlimited meal. Each subject was tested twice one week apart, once with PYY and once with the placebo. PYY infusion reduced food consumption in all 8 subjects and on average caused a 25% reduction in the calories eaten.

Now it gets interesting. The fMRI scans showed that PYY not only targets the primitive parts of our brain that control feeding but it also acts in the corticolimbic brain regions that are involved in the rewarding and pleasurable aspects of eating.

The greatest change in brain activity in response to PYY was within the orbitofrontal cortex (OFC), a region that acts as an integrative center in the brain and is also implicated in reward processing. The change in OFC activity predicted how much food the volunteers subsequently ate. The greater the activation, the less people.

When we are hungry, brain activity within the hypothalamus predicts how much food we should eat. However an infusion of PYY tricks the brain into thinking that it has eaten, and switches on the circuits that control eating. The activity in the orbitofrontal cortex now predicts how much people will eat in the future.

If you have not eaten for a long time, you get full very quickly. It is not that your stomach has shrunk; it is that the production of hormones like PYY has been turned down. When you eat, they are over-produced and switch off more eating. When someone has gastric bypass surgery, their levels of PYY go up and stay up. 

An important aspect of weight management is to retrain and reprogram the mind and body.

This research helps to show us how the approach works.

The Evolving Obesity Pandemic

Here is something that is not too much of a shock. At least it isn’t until you look at the numbers.

People are getting heavier throughout the world, with the possible exception of south and east Asia. These are the conclusions of a one-day global “snapshot:” a single day in 2006 when doctors and nurses in 63 countries across five continents - not even including the United States – found that between half and two-thirds of men and women in were overweight or obese.

The study is being published in the journal Circulation and included 168,159 people. The initial results were published http://eurheartjsupp.oxfordjournals.org/cgi/content/abstract/8/suppl_B/B26 last year in the European Heart Journal, but this new report puts more “flesh” on the original report.

The International Day for the Evaluation of Obesity (IDEA) study looked at two measures of fatness - waist circumference and body mass index or BMI.

A BMI (weight in kg divided by square of height in meters) of 18.5 to 25 is considered healthy. A BMI over 25 is considered overweight and greater than 30 is obese. I shall have something to say about BMI in a moment.

In Eastern Asia 7% were obese, compared with:

• 36% of people in Canada
• 38% of women in Middle Eastern countries
• 40% in South Africa

Canada and South Africa led in the percentage of overweight people, with an average BMI of 29 among both men and women in Canada and 29 among South African women.

In Northern Europe men had an average BMI of 27 and women 26. In other words they were just into the overweight “category.” In southern Europe, the average BMI was 28. In Australia BMI for men was 28 and 27.5 for women. In Latin America the average BMI was just under 28.

Waist circumference was also high - 56% of men and 71% of women carried too much weight around their middle.

The overall frequency of heart disease was 16% in men and 13% in women. In Eastern European men, many of whom still smoke, the rates of heart disease, 27%, and women, 24%. By comparison in Canada the rate of heart disease in women was 8%, and in men 16%.

The rates of diabetes varied across regions. Overall, 13% of men and 11% of women were diagnosed with diabetes.

This means that the rest of the world is catching up with the United States, long considered the country with the worst weight problem.

An estimated two-thirds of Americans are overweight and a third of these are obese. In the US, the lifetime risk of developing diabetes, is also high - 33% for men and 38% for women.

In studies like these, a BMI over 25 is considered to be overweight and greater than 30 is obese. I have commented before about the limitations of using BMI, but it remains a way of getting an overall picture of what is happening in the body.

The findings are deeply worrying.

It is well known that increasing weight, particularly the amount of fat carried inside the abdomen – not the “lovers’ handles!” - increase the risk of coronary artery disease, Type II diabetes and other diseases including some cancers. That point about the “intra-abdominal” fat I all important. For years we have been told that even small increases in weight can do us harm, but that is not completely accurate. It is where the fat is deposited, not only how much we have. It is only when people become extremely obese all over that the risks of many diseases begin to climb.

The moral of the story?

Watch you the size of your abdomen, and stay tuned as I give you more advice about the Whole Person ways to control you weight.

It's Not the Food, It's the Size of the Plate

I grew up in a culture where the aftermath of the Great Depression and the Second World War meant that every child was expected to eat everything on their plates. That created a bit of a problem when I first moved to the United States: my conditioning led me to try and eat every morsel of those huge American portions. Fortunately I quickly noticed the impact on my waistline.

I love simple but practical and important experiments. I have just read about some very nice research from the University of Calgary in Alberta, Canada that fits the bill. It appears that simply using plates and cereal bowls with markers for proper portion sizes can help obese patients with diabetes lose weight. As a result, some can even decrease their use of glucose-controlling medications, according to a report in the Archives of Internal Medicine.

Between 1960 and 2000, the proportion of U.S. adults who were obese increased from 13.4% to 30.9%.  There is clearly an association between type 2 diabetes and obesity although it is not quite as simple as saying that obesity causes diabetes, at least not until the obesity becomes extreme. But we have known for half a century that calorie restriction may improve blood sugar control in diabetics, partially by contributing to weight loss.

The enormous increase in obesity has closely paralleled the explosion of portion sizes of both food and soft drinks.

The researchers conducted a six-month controlled trial of commercially available portion control plates and bowls in 2004. The plates were divided into sections for carbohydrates, proteins, cheese and sauce, with the rest left open for vegetables. The sections approximately totaled an 800-calorie meal for men and a 650-calorie meal for women. The cereal bowl was designed to allow a 200-calorie meal of cereal and milk. The subjects consisted of 130 obese patients with diabetes with an average age 56, half of whom were randomly assigned to use the plate for their largest meal and the bowl when they ate cereal for breakfast. The other half of the participants received usual care, which consisted of dietary assessment and teaching by dieticians.

At the end of the six-months, 122 patients remained in the study. Individuals using the portion-control dishes lost an average of 1.8 percent of their body weight, while those receiving usual care lost an average of 0.1 percent. A significantly larger proportion of those using the dishes - 16.9 percent vs. 4.6 percent - lost at least 5 percent of their body weight.

In addition, at the end of the six months, 26.2% needed a decrease in their diabetes medications compared with 10.8% in the control group.

These results are important: a 5% weight loss has been shown to be clinically significant in terms of decreasing morbidity and mortality associated with obesity-linked disorders.

Simple, straightforward and very practical.

Try it!

Neurological Complications of Gastric Bypass Surgery

Our bodies are highly complex systems. They are not just bags of randomly assorted organs. So tinkering with one part of the system can have an impact in an entirely different part of the body. Many of us have worried for some time about the long-term consequences of gastric bypass surgery for weight loss. We know that some people who have had the surgery develop “substitution addictions.” If they had a real addiction to food before the surgery, after it they may begin to develop an addiction to something else, such as drugs or alcohol.

Now neurologists at the University of Arkansas for Medical Sciences (UAMS) in Little Rock have reported the results of a ten-year study found a link between gastric bypass surgery and several serious neurological conditions.

The study was published online May 22 in the medical journal Neurology and concludes that patients who undergo gastric bypass surgery, also known as bariatric surgery, are at risk for long-term vitamin and mineral deficiencies and as a result may develop a variety of neurological symptoms.

We know that ever more of these operations are being done every year, and so long as people are motivated they are usually successful in reducing weight. But they are not without risk, and we always have to balance that risk against the risk of being morbidly obese. This work is important because it suggests that there is an extra risk about which we previously knew very little.  Many of the complications that patients experience affect the nervous system, and they are often disabling and irreversible.

More than 150 patients who came to the UAMS Neurology Clinic following gastric bypass were included in the report. In 26 of these patients a link between the surgery and their neurological condition was found.

All of the patients involved in the study had previously undergone what is known as the Roux-en-Y gastric bypass procedure in which a small stomach pouch is created by stapling part of the stomach together and bypassing part of the small bowel, resulting in reduced food intake and a decreased ability to absorb the nutrients in food. The interval between surgery and onset of neurological symptoms ranged from 4 weeks to 18 years.

The neurological problems involved many different parts of the nervous system, and the symptoms included confusion, auditory hallucinations, optic neuropathy, weakness and loss of sensation in the legs, and pain in the feet, among other conditions. None of the patients had prior neurological symptoms.

Many of the patients also experienced multiple nutritional abnormalities, especially low serum copper, vitamin B12, vitamin D, iron and calcium.

This study underlines something very important. Many heavy people are actually malnourished, because they eat the wrong things and an excess of fat in the diet can create problems in the absorption of some vitamins and minerals. In addition, surgery like this can cause a form of malabsorption.

It is therefore essential to make sure that people who have this kind of surgery have an adequate long-term intake of vitamin and mineral supplements to prevent these neurological complications. It is important for everyone to know about these potential problems and to be on the lookout for neurological symptoms.

The Integrated Approach to Maintaining a Healthy Weight

Regular readers will have noticed that I have been posting much less than usual over the last couple of months. It is not that I have run out of things to say (!), but I have been working on some new projects that I shall be telling you about fairly soon.

There has also been something else that I had not planned to talk about until a conversation that I had a couple of days ago. I mentioned in passing that I had noticed that my weight had crept up a bit over the last couple of years, but that I had identified the reasons, corrected it, and lost twenty pounds over the last eight weeks. I was immediately surrounded by people wanting to know the secret. Well it’s no secret. It is a series of techniques that I, and people that I have trained, have used with thousands of people over the last thirty years. Then I realized that this secret had somehow not got as much coverage or publicity as it should have.

The other day I was talking to someone who has had some legitimate concerns about her weight for over ten years. She has tried every fad diet going, and has spent a fortune on books, tapes and courses. All to no avail.

I asked her, “Why do you keep falling for these fad diets? They are the nutritional equivalent of get-rich-quick schemes!”

“But there must be an answer somewhere,” she replied.

Well, she was half right: there is an Answer that is based on impeccable scientific research, and has been validated with tens of thousands of people. But it is not a fancy diet, supplement or exercise plan.

The first point is that we never recommend, “dieting” to get healthy. You get healthy so that your body can keep you do the work that it was designed to do. And that includes keeping you at your ideal weight.

Humans participate in multiple relationships, from our cells to our soul, and from the smallest atoms to the largest galaxies: we are connected to all of them. Weight problems invariably imply an imbalance in one or more of these relationships. We are more than physical bodies. We are also psychological, social and spiritual beings who are engaged in these multiple relationships. And the quality of these relationships is essential to our well bring.

The approach that we have used for three decades is very precise and consists of two parts.

First is the Plan: a series of steps that involve the re-integrations of your body with your mind, your relationships, the subtle systems of your body and your spirituality. Part Two consists of a series of “Rescues and Re-starts.” Anybody who has ever tried a weight management program knows that it is easy to fall off the wagon. There are times when things happen. You are tempted to miss an exercise session or to eat something that your body does not need. The beginner’s mistake is to respond by feeling bad, becoming disheartened or having someone reprimand you. Those are all a waste of energy. The smart thing is to have a series of sixty-second strategies that rescue you and start you on the Plan.

The first step is to treat you body so that you are ready to achieve and maintain a healthy weight. Remember the “hidden” causes of weight gain:

• Stress
• Salt
• Pesticides
• Viruses
• Intestinal bacteria

It can he hard to rid ourselves of all of these, but we can certainly reduce the effect that they have on us.

There may be other physical factors that contribute to weight problems. One that has recently attracted some publicity has been the idea that some people have a “leaky gut” – and increase in intestinal permeability - that allows them to absorb toxins that should stay out of the circulation. I have a friend and colleague who, starting in the early 1980s, did a ton of research on intestinal permeability in illnesses like alcoholism, celiac disease, inflammatory bowel disease, arthritis and schizophrenia. I also did a study of intestinal permeability in migraine, which was negative. There certainly are ways in which intestinal permeability can be increased: alcohol, allergies and some drugs will do it. But so far the evidence that increased intestinal permeability is a common cause of weight problems or other symptoms is not good. That could always change: that is what science is all about: testing falsifiable hypotheses and changing models, practice and recommendations if the evidence changes.

After attending to the physical side of weight maintenance, we go on to recommend some simple psychological work. As I said at the beginning, if your brain thinks that you are trying to kill yourself by starving to death, it will sabotage you: millions of years of evolution have designed you to stay alive and to put on weight whenever possible. So we it is essential to understand and work with those psychological mechanisms from the very beginning.

But it is not enough to simply change your thinking: much of your behavior is driven by unconscious, preconscious and subconscious “thoughts.” We also have several sets of emotional systems that drive our behavior. What’s more, there are separate sets of habits and automatic behaviors that we need to identify and deal with. We also have to deal with the effects of certain foods on your moods and perceptions: countless eating plans have failed because nobody considered that a person might be sensitive or allergic to some foods, or that changes in diet can have a big impact on the way in which our brains function. When we work with all of them the results start to come in very quickly.

We also have to deal with the social aspects of weight: have you been stigmatized because of weight? Have you been sabotaged by people around you, or family members? Do you or your family use meal times to socialize? Do you constantly eat out? There are a huge number of social issues that can mess with healthy eating. Ignore them, and it will be nearly impossible to achieve your aims.

We then also work on any disorganization or blockages in the subtle systems of the body, as well as the spiritual aspects of health and wellness.

It may sound odd to talk about spirituality when considering weight management and health, but they are inseparable.

It is only after we have done all of those things that we look at the precise composition of your diet, tailored to your age and gender. Just as important as what you eat, is when you eat. The way in which you exercise, stretch, breath and sleep can be as important as what and when you eat, and each has to be carefully tailored to the individual.

On a future occasion I shall explain exactly how your can work with each of the five systems of you body – Physical, Psychological, Social, Subtle and Spiritual – to create and maintain vibrant health and a radiance that at the moment you can only dream about.

That’s a promise!

“I don't eat junk foods, and I don't think junk thoughts.”
--Peace Pilgrim (a.k.a. Mildred Norman, American Peace Activist, 1908-1981)

“He that takes medicine and neglects diet, wastes the skill of the physician.”
--Chinese Proverb

“Give the body the attention it deserves, but not more. When you cultivate the attitude that you are the body, the body will demand from you more food, more variety in food, more attention to appearance and physical comfort.”
--Sathya Sai Baba (Indian Spiritual Teacher, c.1926-)

Diets Make You Fat

Most people who have tried dieting know a sad truth: they do not usually work for very long. Our bodies are designed to form and retain fat stores and millions of years of evolution have created sophisticated and elegant systems to thwart any attempt at self-starvation. That is the real reason why most quick fix promises are doomed to failure. As day follows night, every time that a scientist somewhere publishes another piece of the obesity puzzle, a flurry of articles and books will follow, claiming that they have The Answer, never realizing that there are several hundred interlocking pieces to the puzzle.

Yet more research  has confirmed that diets rarely help. A group of investigators from UCLA published their findings in the April issue of American Psychologist,  the journal of the American Psychological Association. 

Traci Mann and her co-authors have conducted the most comprehensive and rigorous analysis of diet studies that I have ever seen. They analyzed 31 long-term studies in which people were followed for two to five years. What they found clearly mirrors clinical experience. Most people can initially lose 5 to 10 percent of their weight on any number of diets: low carb; low fat; high protein or pretty much anything else. But then the weight comes back: in the majority of people they regained all the weight plus more. Sustained weight loss was found only in a small minority of participants, while complete weight regain was found in the majority.

Their conclusion: diets do not lead to sustained weight loss or health benefits for the majority of people. And since people who regain weight usually have the “bounce” where they regain with interest, most people would have been better off not going on the diet at all. This is important: aggressive dieting can be dangerous to the body. It has been suggested that repeatedly losing and gaining weight is linked to cardiovascular disease, stroke, diabetes and altered immune function. So if people had not dieted, their weight would be pretty much the same and their bodies would not have suffered the wear and tear from losing weight and gaining it all back.

Over the years, many diet studies have looked good, but the results have often been skewed by a number of factors. For example, in some studies participants self-reported their weight by phone or mail rather than having an objective weight measurement. Many studies also had very low follow-up rates: eight of the studies had follow-up rates lower than 50 percent.

Traci Mann, the lead investigator was asked, “If dieting doesn't work, what does?”

"Eating in moderation is a good idea for everybody, and so is regular exercise," Mann said. "That is not what we looked at in this study. Exercise may well be the key factor leading to sustained weight loss. Studies consistently find that people who reported the most exercise also had the most weight loss."

Happily there ARE genuine solutions to the problems of weight, but they do not begin with a diet. They begin with a totally new understanding of how our bodies operate, how to deal with the psychological and social barriers to health and how to activate the natural abilities of the body balance and heal itself.

I am going to talk about those a little more in the next post.

“I've been on a diet for two weeks and all I've lost is fourteen days.”
--Totie Fields (American Comedian, 1930-1978)

“The Diet Mentality has come about because there is agreement in our society that the only way to lose weight is by dieting. But dieting produces absolutely no permanent, positive results. In fact, it makes you feel worse about yourself and probably does more damage than good to your health.”
--Bob Schwartz (American Health Expert and Author)

“Gluttony is the source of all our infirmities and the fountain of all our diseases. As a lamp is choked by a superabundance of oil, and a fire extinguished by excess of fuel, so is the natural health of the body destroyed by intemperate diet.”
--Robert Burton (English Cleric and Writer, 1577-1640)

Motivational Interviewing and Exercise

Researchers from Germany have re-visited the interesting topic of the association between aerobic exercise and psychiatric disorders, and presented their work in a poster (NR20) at the 2007 Annual Meeting of the American Psychiatric Association in San Diego, California, this morning.
There is good evidence that exercise can help people with depressive and some other psychiatric disorders. Unfortunately, like everyone else, people with psychiatric problems have trouble in developing regular exercise habits or staying with the program. The mood problem itself may stop them, or the physical pain that so often accompanies depression.

223 people were screened at the time of admission to hospital and 82 decided to participate. That is a disappointing but unsurprising rate of participation. The patients were offered a three-month running/walking program that they could continue after discharge. They all had weekly meetings that included exercise-related psychoeducation, stretching and 40-50 minutes of aerobic exercise.

In addition the experimental group received brief interventions using motivational interviewing, a specific technique to foster changes in behavior. Motivational interviewing is a client-centered non-judgmental and non-confrontational appraoch to change that attempts to increase peoples' awareness of the potential problems caused, consequences experienced and risks faced as a result of the behavior in question. Alternatively, therapists help clients to try and envision a better future and to become increasingly motivated to achieve it. These strategies seeks to help clients think differently about their behavior and ultimately to consider what might be gained through change.

In people who had the motivational interviewing, the completer rate was 78%, compared with 33% in the control group who just had the psychoeducation, stretching and exercise.

The patients’ initial self-assessments concerning the importance and efficacy of regular exercise for their individual recovery did not predict compliance.

This confirms that motivational interviewing is highly effect in helping people with mental illness initiate and continue with a regular exercise program.

This new research adds to a body of evidence that has shown that motivational interviewing can be helpful in the treatment of obesity, weight management in women with type 2 diabetes, exercise in women with fibromyalgia, quality of life in people with chronic heart failure and physical exercise in long-term cancer survivors.

It may also be very helpful in people who need to exercise yet have no psychiatric problems: any of us!

Researchers from Germany have re-visited the interesting topic of the association between aerobic exercise and psychiatric disorders, and presented their work in a poster (NR20) at the 2007 Annual Meeting of the American Psychiatric Association in San Diego, California, this morning.
There is good evidence that exercise can help people with depressive and some other psychiatric disorders. Unfortunately, like everyone else, people with psychiatric problems have trouble in developing regular exercise habits or staying with the program. The mood problem itself may stop them, or the physical pain that so often accompanies depression.

223 people were screened at the time of admission to hospital and 82 decided to participate. That is a disappointing but unsurprising rate of participation. The patients were offered a three-month running/walking program that they could continue after discharge. They all had weekly meetings that included exercise-related psychoeducation, stretching and 40-50 minutes of aerobic exercise.

In addition the experimental group received brief interventions using motivational interviewing, a specific technique to foster changes in behavior. Motivational interviewing is a client-centered non-judgmental and non-confrontational appraoch to change that attempts to increase peoples' awareness of the potential problems caused, consequences experienced and risks faced as a result of the behavior in question. Alternatively, therapists help clients to try and envision a better future and to become increasingly motivated to achieve it. These strategies seeks to help clients think differently about their behavior and ultimately to consider what might be gained through change.

In people who had the motivational interviewing, the completer rate was 78%, compared with 33% in the control group who just had the psychoeducation, stretching and exercise.

The patients’ initial self-assessments concerning the importance and efficacy of regular exercise for their individual recovery did not predict compliance.

This confirms that motivational interviewing is highly effect in helping people with mental illness initiate and continue with a regular exercise program.

This new research adds to a body of evidence that has shown that motivational interviewing can be helpful in the treatment of obesity, weight management in women with type 2 diabetes, exercise in women with fibromyalgia, quality of life in people with chronic heart failure and physical exercise in long-term cancer survivors.

It may also be very helpful in people who need to exercise yet have no psychiatric problems: any of us!

Insulin, Intestinal Metabolism and Arteriosclerosis

Here is some research that provides further evidence of the links between systems of the body.

Diets high in sugar and fats can cause chronic elevations of insulin. High levels of insulin are a key feature of insulin resistance, a metabolic problem that affects at least a third of people living in the Western world and is also growing extremely rapidly in much of the developing world. Insulin resistance may be caused by a diet or genetics, or most commonly a combination of the two. It is known that insulin resistance can lead to the development of diabetes and arterial disease. The question has been how?

Almost forty years ago it was first suggested that insulin itself might be the problem. Not only is insulin involved in metabolism, it is also a potent growth factor for some of the smooth muscle cells found in the wall of major blood vessels. There has also been a suspicion that some of the metabolic effects of insulin increase the risk of arteriosclerosis by actions in the liver and intestines.

In research published in the journal Atherosclerosis, nutritional scientists at the University of Alberta have found a connection between high insulin levels and dysfunction of intestinal lipid metabolism. The finding provides critical support for the notion that impaired intestinal metabolic function plays a critical role in the development of cardiovascular disease.

Using a type of obese rat, the researchers found that excessive insulin slows the removal of chylomicrons from the blood stream following a fatty meal. Chylomicrons transport dietary fat from the intestine to the rest of the body.

Excessive amounts of insulin appear to alter the dynamics of the walls of blood vessels, allowing chylomicrons and cholesterol to build up in them. Over time this build up may creates blockages in the flow of blood.

It is good to see research that is re-examining the role of chylomicrons in vascular disease. Interest in them began to wane about twenty years ago, and since then most of the research and most of the screening recommendations have been based on cholesterol. Most doctors have been taught that cardiovascular disease is connected to increased levels of low-density lipoprotein (LDL) cholesterol, which is derived from the liver. However, fifty per cent of cardiovascular disease events occur in the presence of normal LDL-cholesterol levels. That is one of the reasons why many experts in metabolism have been saying for years that we must not forget the contribution of triglyceride and chylomicrons. This research confirms that we were right.

Although there are no accepted guidelines on this, people at risk of developing cardiovascular disease should not only have their LDL-cholesterol and HDL-cholesterol levels checked, but should also have the level of chylomicrons measured.

Technically it is not a difficult thing to do, although not all laboratories are able to do it. If chylomicron levels are high, it is an extra incentive to reduce fat consumption, and there are new medicine being tested that may help reduce chylomicron levels.

This research provides yet more evidence about the importance of the intestine in general health and disease. I constantly have people telling me that certain diets, colonic irrigation or probiotics may improve intestinal health and therefore general health and well-being. They may be correct. But what we really need is research to discover if there are viable ways of improving intestinal health that can prevent disease onset and progression.

Half the Population Has Genes to Make Them Fat

I have talked a bit about my skepticism concerning the genetic contribution to obesity, insulin resistance and diabetes.

I was fascinated to see a huge fifteen year study that has just been published in the journal Science. I felt a touch of pride: back when the earth was new, I helped train more than one of the authors.

The study involved over 42,000 people and found an association with body mass index at every age [from seven to 70] in populations throughout the UK and Europe.

Unlike previous work, it shows a very common genetic link with mild obesity rather than a rare genetic link with extreme obesity.

There were 42 scientists in the group and they found that if people carry one copy of a variant in a gene called FTO, as does half of the general population, it will lead to a gain in weight of 2.6lb or put just over half an inch on their waists and raise their risk of being obese by one third. People with two copies of this variant in the FTO gene, which is the case in one in six of the population, then they will gain almost 7lb more than those who lack the variation and are at a 70 per cent higher risk of obesity.

The researchers then tested a further 37,000 people from Bristol, Dundee and Exeter as well as a number of other regions in Britain, Italy and Finland. In every case the same variant in the FTO gene - which is mostly present in the brain and pancreas, among other key tissues - was associated with type 2 diabetes and obesity.

They also showed that in children, this particular FTO variant was associated with increased body weight.

We hope that in the future, once we have found additional obesity genes, it may be possible to offer advice based on a person's genetic make-up. We all know that folk are eating more and doing less exercise, but some people gain more weight than others. Similarly two people on the same diet and exercise plan lose different amounts of weight. There are undoubtedly some unrecognized factors in weight gain, but genes remain in the mix.

Never be disheartened if your first attempt at diet and exercise is not crowned with success: they are only two of a dozen factors that play into weight control.

Do not fall into the fatalistic trap of thinking that biology is destiny.

We are talking about a factor that may modulate the way in which we control out weight.

As promised, I shall soon be publishing a book detailing specific methods for dealing with whichever ones are important in your life.

Your future lies in your hands: not in a string of chemicals.

 

A Pill for Every Ill?

Many of us have been becoming more and more worried by the idea that if we don’t like something, then we should take a pill, rather than trying to get to grips with the causes.

Can’t sleep? Take this pill. {Ahem, but why not try sleep hygiene first?)

Shy? No, you’re not allowed to be shy, you have social phobia, take this medicine.

Don’t like the size of your tummy? Don’t exercise; we have just the pill for you!

Not only does this approach undermine our responsibility and autonomy, it also minimizes the suffering of people with real clinical problems. When every headache gets labeled a “migraine” and every cold gets turned into “’flu,” it is easy to lose patience, empathy and understanding for people who are really suffering with the genuine article.

Here is a fine example of an announcement that has doubtless caught the attention of headline writers around the world. Researchers from the Medical Research Council's Human Reproduction Unit in Edinburgh in Scotland are reported to be working on a pill that would simultaneously boost a woman’s libido while at the same time reducing her appetite for food.

So what is this all about? Professor Robert Millar leads the Edinburgh team that has been looking at the properties type 2 gonadotropin-releasing hormone (GnRH), one of the hormones responsible for the release of sex hormones.

When it was given to monkeys, they displayed mating behavior such as tongue-flicking and eyebrow-raising to the males. When it was given female musk shrews, they displayed their feelings via "rump presentation and tail wagging.” These are two interesting visual images.

The thing is this. The tongue-flicking, eyebrow-raising tail wagers also ate around a third less food than they normally would. So now the search is on to find a pharmaceutical company that would like to make some kind of GnRH pill that would, presumably, produce libidinous skinny women.

Not only is this a frightful type of reductionism, but it raises all kinds of ethical issues.

The researchers in Edinburgh have been turning out a substantial body of very respectable data over the years, and this story looks very much like something that has been embellished.

Few people believe that eating or human sexuality are reducible to single chemicals in the brain. Low libido is a common problem, but it is usually a sign of stress, fatigue or relationship problems, rather than a chemical imbalance in the brain. And what, when and how we eat is an extraordinarily complex issue that is as much psychological and social as it is chemical. Stimulating the libido of someone in a lousy relationship is unlikely to lead to peace and harmony.

The whole concept also returns to the question of “what is normal?” when it comes to food, size or sex.

Insulin Resistance in the Brain and What It Means for Dieters

Most people have been taught that increasing weight is the cause of insulin resistance, which in turn may cause an array of different health problems. That is only half true: insulin resistance may contribute to the development of obesity, and once we start gaining abdominal fat then that may indeed contribute to insulin resistance. So a vicious circle is established in which insulin resistance helps cause obesity, which in turn causes more insulin resistance.

Another thing that we have been taught for half a century that the brain is an insulin-insensitive tissue. What that means is that the uptake and use of glucose by the brain is not affected by circulating levels of glucose and insulin. That has always seemed a bit strange, because insulin is very important in cognition. Some experts believe that disturbances of insulin and closely related hormone – insulin like growth factor 1 (IGF-1) are involved in the pathogenesis of Alzheimer’s disease. 

When someone is insulin resistant, they have high circulating levels of insulin, and an obvious question is whether these high insulin levels may interfere with the normal functions of the brain. This is not a new idea. It has been known for many years that high levels of triglycerides, that may be a marker for insulin resistance, may be associated with cognitive impairment in people with type 2 diabetes.

Now colleagues in London have found that people who have peripheral insulin resistance also have brain insulin resistance especially in two brain regions  - the ventral striatum and prefrontal cortex – that are involved in appetite and reward.

It looks as if one of the reasons why people with insulin resistance become obese is that the normal link between the control of food intake and energy balance is broken.

This is yet more evidence that a simple diet will not work in the long term. If the problem is metabolic and involves damage to the mechanisms that control eating, the only way to help is to use a combined approach that deals not only with the composition of the diet, but the precise time when people should eat, and the psychological and social barriers that are left over from millions of years of evolution. I outline a comprehensive and highly successful weight management technique in Healing, Meaning and Purpose. Over the last few months I have had an enormous number of requests to expand that material into another book, and in between writing this blog, I am hard at work on completing a full account of exactly what we do to help people manage their weight.

Race and Diabetes

It’s another one of those, “Everyone knows that…” facts. For forty years we have all been taught that some ethnic groups are at higher risk of developing insulin resistance and type 2 diabetes mellitus. So now “everyone knows that” African Americans, Native Americans and people from the Indian sub-continent are all genetically predisposed to these medical maladies.

Now it looks as if "everyone" might have been wrong.

James Neel first proposed the theory of the "thrifty genotype" in 1962. He suggested that cycles of feast and famine early in human history created a gene that helps the body use scarce nutrients - a gene that leads to obesity and diabetes in sedentary modern populations with ready and continuous access to food.

Several months ago I pointed out some of the problems with the thrifty genotype theory, and why many of us have become more convinced about the concept of the “thrifty phenotype.” I have many friends, colleagues and former trainees who have dedicated themselves to hunting for diabetes genes. As early as the mid-1980s I was worried that they were going to vanish down a rabbit hole.

It seemed illogical that a gene or genes could “explain” an illness that was, until recently, very rare. It would have to be a gene that was somehow switched on and off by diet or some other environmental factors. It is certainly possible but seemed implausible, given that there are dozens of genes designed to control food intake and metabolism. But my friends the gene jockeys had the louder voice, and it was good for them to see what they could find. Now, twenty years later, more than 250 genes have been studied as possible causes of type 2 diabetes, but together these genes explain less than 1 percent of diabetes prevalence worldwide.

There is an interesting piece of research published in the journal Perspectives in Biology and Medicine by a team of researchers from the United States and Australia, that supports what I was saying. The study was co-authored by UC Irvine anthropologist Michael Montoya, an anthropologist at the University of California at Irvine, together with an epidemiologist and population geneticist. Together they analyzed existing genetic studies published across a variety of disciplines. The team found no evidence to support the thrifty genotype theory.

They also found that in most existing studies of the suspected genes that contribute to diabetes in ethnic minorities, researchers had failed to control for the potential impact of social and environmental factors. If those factors are taken into account, other factors - such as poverty, housing segregation or poor diet - were stronger indicators of diabetes than genes.

As Montoya said,

"Our study challenges the presumption that Native American, Mexican American, African American, Australian Aborigine, or other indigenous groups are genetically prone to diabetes because the evidence demonstrates that higher rates of diabetes across population groups can be explained by non-genetic factors alone. Our study shows that by focusing on genes, researchers miss the more significant and alterable environmental causes of diabetes."

One of Montoya’s co-authors, Stephanie Malia Fullerton, a population geneticist and bioethicist at the University of Washington added,

"When it comes to diabetes, we're finding that genes are no more important for ethnic minorities than for anyone else."

This new critique of genetic and ethnic studies will need to be replicated, and it is a little bit of a surprise that such important work was published in Perspectives rather than one of the journals dedicated to epidemiology.

I have no inside knowledge about why the study was published where it was. But it often happens that it can be very difficult to get new research published if it contradicts the mainstream. There have been examples of experts squashing data that contradicts their own, but it is uncommon. Most of the time the difficulty in getting revolutionary new data published is not because of some conspiracy, but because any kind of evidence, particularly if it is radically different, attracts the most concentrated scrutiny by independent reviewers.

If this new data analysis is confirmed, it is going to mean a radical re-think about the ways in which we screen, manage and advise people from different ethnic groups.

It also confirms something that I've said a hundred times: Biology is Not Destiny.

Pesticides, Weight Gain and Insulin Resistance

On this blog and in Healing, Meaning and Purpose, I have talked about some of the less well recognized contributors to obesity, including:

1. Stress
2. Salt
3. Viruses
4. Pesticides
5. Intestinal bacteria

There is some new evidence from Korea published in the journal Diabetes Care, supporting the possible contribution of pesticides to insulin resistance.

People with high levels of persistent organic pollutants (POPs) in their blood were more likely to develop insulin resistance, which may lead to type 2 diabetes. Insulin resistance may also lead to obesity, hypertension and an array of other diseases. It is well recognized that increasing amounts of intra-abdominal fat may increase insulin resistance. It is less well known that this obesity is part of a viscous circle, with insulin resistance being associated with elevated insulin levels that may cause fat to be laid down throughout the body. Once the fat is laid down in the abdomen, it can break down, releasing fatty acids and triglycerides that in turn affect the breakdown of insulin by the liver and the release of insulin by the pancreas.

Previous research by the same group found a link between POPs and type 2 diabetes. This study confirms that background exposure to some POPs, chemicals such as organochlorine pesticides and polychlorinated biphenyls (PCBs), is also associated with insulin resistance among people who do not yet have diabetes.

The researchers also found that the association between organochlorine pesticides and insulin resistance became stronger as people got fatter. However, among people who had very low concentrations of pesticides in their blood, the researchers found little association between waist size and insulin resistance.

Some studies have suggested an association between background exposure to POPs and a variety of adverse health effects in humans and wildlife. POPs can be particularly problematic because they persist for long periods of time in the environment, accumulate up the food chain, and can travel great distances through the air and water. Therefore, even people and animals that live nowhere near a place where POPs are being applied often show high levels of these chemicals in their bloodstream.

An international treaty banning a dozen of the world's most dangerous POPs has helped reduce exposures, but many harmful chemicals remain in use and even those that have been banned may linger in our environment for years to come. For example, chlordane was banned two decades ago in the United States but continues to be present at high levels in our food supply.

The researchers concluded that some POPs "may be involved in the pathogenesis of insulin resistance." They advise urgent prospective studies among those who have background exposure to POPs, which mostly comes from eating fatty animal foods. Since obesity may increase the toxicity of POPs, controlling weight could also help to reduce the impacts of these molecules.

In separate research involving mice, Frederick vom Saal from the University of Missouri in Columbia, Missouri has studied the effects of a different class of endocrine-disrupting chemicals, including bisphenol-A (BPA). Not long ago, BPA made news in San Francisco, where there was a lot of controversy over an ordinance that seeks to ban its use in children's products. vom Saal's most recent work was presented at the 2007 Annual Meeting of the American Association for the Advancement of Science (AAAS). He found that endocrine-disrupting chemicals cause mice to be born at very low birth weights and then very rapidly gain abnormally large amounts of weight: they could more than double their body weight in just seven days. Vom Saal followed the mice as they got older and found that these mice were obese throughout their lives. He said studies of low-birth-weight children have shown a similar overcompensation after birth resulting in lifelong obesity.

(Regular readers might remember the concept of the thrifty phenotype, and see how this research ties in with that concept). More research must be done to determine which chemicals cause this metabolic effect. According to vom Saal, there are approximately 55,000 manmade chemicals in the world, and 1,000 of those might fall into the category of endocrine disrupting. These chemicals are found in common products, from plastic bottles and containers to pesticides and electronics.

These chemicals are so pervasive that it is difficult to avoid them, and there is scant evidence that "detoxification" helps clear them. That being said, and depsite the lack of evidence, we recommend certified organic produce and regular mild detoxification programs, together with nutritional support and  tapping therapies.

Twelve Tips to Reduce Your Risk of Colorectal Cancer

Colon cancer, or, more accurately colorectal cancer, includes cancerous growths in the colon, rectum and appendix. It is the third most common form of cancer and the second leading cause of death among cancers in the Western world. Colorectal cancer surpasses breast and prostate cancers as a leading cause of cancer deaths in both men and women.

And the key point is that with early screening and a few simple dietary modifications, you can dramatically reduce your risk of getting it.

These are the 12 Tips to Slash Your Risk of Colorectal Cancer

1. Receive regular colorectal cancer screenings beginning at age 50 if you are at normal risk
2. If you are at higher risk due to a personal or family history of colorectal cancer, other cancers or inflammatory bowel disease have a discussion with your health care provider about screenings before age 50
3. Eat between 25 and 30 grams of fiber each day from fruits, vegetables, whole grain breads and cereals, nuts, and beans
4. Eat a low-fat diet: colorectal cancer has been associated with diets high in saturated fat, particularly fat from red meat
5. Eat foods with folate, such as leafy green vegetables
6. Try to drink at least 80 fluid ounces of pure water a day unless you have a medical reason for not doing so
   
7. Drink alcohol in moderation: 2 units of alcohol or less each day
8. If you smoke, here is another good reason for quitting. Alcohol and tobacco in combination are linked to colorectal cancer and other gastrointestinal cancers
9. Exercise for at least 20 minutes three to four days a week. Moderate exercise such as walking, gardening or climbing stairs may help reduce your risk
10. If you get any persistent symptoms such as blood in the stool, a change in bowel habits, weight loss, narrower-than-usual stools, abdominal pains or other gastrointestinal complaints, it is essential to report them to your health care provider
11. Maintain a healthy weight. Obesity may increase the risk of colorectal cancer
12. Maintain a good intake of calcium and vitamin D:  this combination has been shown to reduce the risk of colorectal cancer

For more information, I recommend visiting the Web site of the American Cancer Society.

I keep their details in the "Resources" section on the left hand side of this blog.

Medication-induced Weight Gain

It is not really a surprise that medicines that are designed to have effects on emotion might also have other effects. After all, emotion originally evolved as an outgrowth of the sympathetic nervous system, which, as every student of biology knows, is involved in the "Four F's:"

• Fear
• Fight
• Flight
• Sexual activity

So if powerful medicines influence emotion, they will likely also influence one or more of these.

Cocaine and amphetamine lead to a loss of appetite for food, though I am told that marijuana makes people hungry. I do not, of course, know that from personal experience.

Many antipsychotics, mood stabilizers and antidepressants cause weight gain by an array of different mechanisms.

New research published by colleagues from Johns Hopkins has done a lot to clarify the role of histamine in the appetite problems that often occur with antipsychotics.

You may be interested in reading more here.

The conclusion? Histamine has a major role to play in antipsychotic-induced appetite increase.

But it is not the only factor in the weight gain, insulin resistance and diabetes problems that seem to bedevil some of these medicines.

Before the book comes out, I shall write some more about the ways in which the Atlanta Approach successfully - and uniquely - deals with all of those problems.

Aging and Exercise

It is a common observation that it becomes more difficult to do a lot of exercise as we get older, and the biceps no longer bulge quite as much after an hour in the gym. We have to exercise harder to get the same results.

Metabolism slows down as well, and for years it has been assumed that those events are linked: we slow our metabolism and find exercise harder because we gradually lose muscle mass.

But new research shows that it isn’t quite so simple, and the results should encourage any of us over forty to stay in the gym.

A new study published in the journal Cell Metabolism will likely help our understanding of that difficulty, as well as unlocking another of the secrets of type 2 diabetes.

As we become older, we hide more fat in our muscles and livers, and this fat has been linked to the age-related rise in insulin resistance that may go on to cause type 2 diabetes and hypertension.

A research team from the Howard Hughes Medical Institute based at Yale University School of Medicine compared the skeletal muscle of rats aged three-month-old and two-year-olds.

They found that an enzyme called AMP-activated protein kinase (AMPK) slowed down its activity in the older animals. AMPK's role in skeletal muscle is to stimulate the body to burn off fat and to provide fuel for the cells. It does this by producing mitochondria – the power packs of the cell. So AMPK activity in our skeletal muscle does at least three things: it stimulates glucose uptake, increases fat oxidation and promotes the production of new mitochondria.

It has been known for some time that the skeletal muscles of marathon runners have a much greater mitochondrial content and a greater capacity to burn fat. This is probably linked to high levels of AMPK activity.

The animals were exposed to a chemicals that produce that produce acute or chronic stimulation of AMPK. They were also exercised and some were fed more food, each of which should stimulate the production of new mitochondria.

The researchers found that the older rats had lower AMPK activity than the younger animals. In addition, the muscle of young rats who did more exercise had double the normal AMPK activity while in older rats this effect was severely blunted.

The message is this: as we age it is not muscle mass but enzyme activity that falls first. We have to work harder when trying to maintain the same benefits from exercise as we did when we were young.

We know that loss of skeletal muscle mass and function as we age is a major problem that has a significant effect on quality of life of older people. If this study is confirmed in humans it would have enormous implications. In the older rats, the AMPK activity was almost gone, implying that no amount of exercise would bring those muscles back. But it would be good to know if we can work out some other methods for bringing those enzymes back to life.

Although the paper doesn’t mention it, there is also some evidence that AMPK activity may be important in controlling feeding behavior in the hypothalamus at the base of the brain and the “stress hormone” norepinephrine plays a critical role in the way in which exercise stimulates AMPK. As we get older we usually find that our tempers are less fiery and part of the reason for that is that we produce less norepinephrine.

Start exercising early in life, and never get out of the habit. For if you do, you might lose that AMPK activity forever.

“Wholesome physical exercise reconstitutes energy, stemming the aging process, making the body light and firm, while safeguarding against fatigue and inducing cheerfulness.”
--Sushruta Samhita (Indian Surgeon who wrote the book the Sushruta Samhita, c. 6th Century B.C.E.)

“Exercise is the chief source of improvement in our faculties.”
--Hugh Blair (Scottish Presbyterian Minister and Writer, 1718-1800)

“It is exercise alone that supports the spirits, and keeps the mind in vigor.”
Marcus Tullius Cicero (Roman Political Figure and Orator, c.106-43 B.C.E.)

Juices, Cardiovascular Disease and Cancer

There was an important study that came out a few months ago in the International Journal of Food Science and Nutrition.

Investigators from Dundee in Scotland decided to look at the health benefits of fresh fruit juice. While it is widely accepted that fruit and vegetables lower the risk of some cancers and of most cardiovascular diseases, the role of pure fruit and vegetable juices has never been clear. In fact many textbooks have said that 100 percent juices play a less significant role in reducing risk for both cancer and cardiovascular disease than whole fruits and vegetables since they contain less fiber, and it had been assumed that it was the fiber that was the key to their value.

The researchers analyzed a variety of studies that looked at risk reduction attributed to the effects of both fiber and antioxidants. They found that the positive impact offered by fruits and vegetables is derived not from just the fiber but also from antioxidants which are present in both juice and the whole fruit and vegetables. Juices are comparable in their ability to reduce cancer and cardiovascular risk compared to their whole fruit/vegetable counterparts.

This research  goes a long way in demonstrating that fruit and vegetable juices may play an important role in reducing the risk of various diseases.

A study published in the American Journal of Medicine in September found that consuming a variety of 100 percent fruit and vegetable juices was associated with a reduced risk for Alzheimer's disease. Japanese American individuals who drank three or more servings of fruit and vegetable juices per week had a 76 percent lower risk of developing Alzheimer's disease than those who drank juice less than once per week. That finding seemed robust, even taking into account other potential variables. So I think that we may be able to add juices to our strategies for reducing the risk of developing Alzheimer's disease as we get older.

There is another point of importance. Some of the fad diets claim that fruit juices should be avoided at all costs, since they can cause the release of insulin, and insulin is bad. Those proclamations have usually come from people with a limited background in biochemistry or metabolism. The research shows that they were not correct. The key is balance, and as part of a comprehensive nutritional approach, juicing can be very helpful.

And a final point: careful use of juices has long been one of the "secret" components of our system of weight management.

“Drinking freshly made juices and eating enough whole foods to provide adequate fiber is a sensible approach to a healthful diet.”
--Jay Kordich (American Health Expert, Author and Lecturer, 1921-)

“If people would only stop putting into their bodies the things that are creating their physical problems, and eat a predominantly raw vegetarian diet, along with raw vegetable juices, almost all physical problems would soon disappear from the face of the earth!”
--Reverend George M. Malkmus
 (American Minister and Originator of the Hallelujah Diet, 1934-)

Mindless Eating

One of the keys to any successful weight management strategy is awareness:

1. Awareness of our bodies
2. Awareness of our bodies' needs
3. Awareness of what we are doing physically
4. Awareness of what we are eating
5. Awareness of the impact of food on our bodies and our minds
6. Awareness of the content and consequences of our diets
7. Awareness of our eating on other people
8. Awareness of our food choices on animals and our physical and emotional environment
9. Awareness of the things that drive us to eat even if we are not hungry
10. Awareness of the spiritual consequences of eating

I have looked at hundreds of books on diet, health and nutrition and it constantly astonishes me that hardly any of them address this central component, not just of weight management, but of life management. There is some fine exceptions: one is a new book by Brian Wansink called Mindless Eating, that does a good job of discussing some of these problems of awareness about eating.

The author is a practicing researcher and Professor at Cornell, and he has an interesting paper in the current issue of the Journal of Marketing Research. Part of his thesis is that “low fat” nutrition labels may lead to the over-consumption of nutrient-poor and calorie-rich snack foods. 

I was pleased to see the experimental data, which exactly confirms my observations. After nearly thirty years of working with people with weight challenges, one of the more common problems is that some people have been brain washed into thinking that if it says “low fat” on the label, you can eat as much as you want. The trouble is that if you know how to read labels, some of the low fat foods are also low health foods. The authors of the paper make some good suggestions for changing policy to help rectify the situation.

When it comes to what we eat, part of the problem is that most of us are so comfortable with the status quo that we rarely notice much that is going on inside or around us.

A fish only becomes aware that it lives in water once it’s dragged up on shore!

And we only realize our own potential for growth and change when we become aware of the dynamic, interconnected beauty and complexity of a world that lies just beyond the reach of our senses. Growing our awareness of food, nutrition and eating can be a transformative experience. I have known some spiritual teachers who would not accept heavy people as students, saying that if they could not even control their weight, then how could they control their minds or any energies that might be released from meditation, qigong, yoga and the like?

Although I understand what they are saying, I respectfully disagree. As I have discussed many times, there are physical as well as psychological, social, subtle and spiritual reasons for having trouble with weight, and I don’t think that these are grounds for excluding people from learning these practices. For today I urge you to spend a few minutes working on your own “Ten Awarenesses” about food and nutrition. It could be the best thing that you do for yourself all year.



“Neither the body with its senses nor the mind with its thoughts is the ultimate being that I am. The body acts and the mind moves, but behind them is the thought-free Awareness, the Knowing Principle.”
--Paul Brunton (English Spiritual Teacher and Author, 1898-1981)

“The voyage of discovery lies not in finding new landscapes, but in having new eyes.”
--Marcel Proust (French Novelist, 1871-1922)

Do Healthy Foods Taste Bad?

There is a valuable study in the Journal of Marketing, which I must confess is not normally on my overloaded reading list. At least it wasn’t until I discovered an astonishing number of articles that are highly relevant to our basic themes of Health, Integrated Medicine, Meaning and Purpose.

We are all constantly puzzled by the way in which so many people seem to enjoy unhealthy foods. This is a matter of enormous importance: countries like China and India are now getting fattest the fastest, partly because of their peoples’ craving for Western junk food, coupled, in many cases, with a metabolic inability to process the food in the same way that most Europeans do.

Well, according to this study, foods that we think are healthy taste worse. This is the "unhealthy = tasty intuition." In one of the experiments, test subjects were offered a mango lassi, an Indian yogurt drink that has the consistency of a thick milkshake. Those who were told that the lassi was "unhealthy" liked the drink significantly more than those who were told the drink was "healthy.”

When I was a young student one of my teachers told me that patients always believe that if something tastes foul then it must be doing them some good. A lesson that I had learned from my grandmother when still a small child. By the age of five I already knew that any rash or snivel would mean having to take some pungent and disgusting potion: some secret recipe that had been in the family for generations. Even then I wondered how it was that so many family members had lived to great ages. It didn’t seem possible.

This research fits in with the teachings of my grandmother and my professor. People assume an inverse relationship between tastiness and healthiness. In the study people believed that what they were consuming was unhealthy, they guessed that it would taste better, be more enjoyable to eat and that they would be more likely to choose it in a test.

This is important research and has a number of practical implications for helping people to adopt more healthy eating patterns.

This reminded me of a salutary lesson. Some years ago I spent a very happy year doing a part time course in wine tasting. Fascinating topic taught by Masters of Wine who said that they could tell incredible things about a wine after the smallest taste. A couple of years ago such claims were put to the test in Bordeaux in France, which is, of course, famous for its wines. In the first experiment 54 acknowledged wine experts were asked to give their impressions of two glasses of wine: one white and one red. The wines were actually the same white wine, one of which had been tinted red with an odorless food coloring. But here it gets interesting: the experts described the "red" wine in language typically used to describe red wines. For instance one said tat the colored wine had a “flavor of crushed red fruit.” Not a single one noticed it was actually a white wine.

In a second experiment an inexpensive wine was presented to the experts in two different bottles, one fancy and one plain. The experts gave the two bottles completely different evaluations. The experimenters described their results in terms of the interaction between vision of colors and odor determination. But we can also interpret the data in terms of expectation and perspective. If we expect something to taste good it tends to do so. Yes of course you can get a nasty surprise, but there is a powerful subjective component in how we interpret sensations.

I strongly suggest that you analyze your own reactions to food. Do you believe that healthy foods have to taste awful?

This may be an important key to changing your own eating patterns.

"Life expectancy would grow by leaps and bounds if green vegetables smelled as good as bacon.”
--“Doug Larson”



“As for food, half of my friends have dug their graves with their teeth.”
--Chauncey M. Depew (American Politician and, from 1899-1911, Senator from New York, 1834-1928)

“To lengthen thy life, lessen thy meals.”
--Benjamin Franklin (American Author, Inventor and Diplomat, 1706-1790)

“If you have formed the habit of checking on every new diet that comes along, you will find that, mercifully, they all blur together, leaving you with only one definite piece of information: french-fried potatoes are out.”
-- Jean Collins Kerr


(American Author and Playwright, 1923-2003_

Common Misconceptions About "Weight Loss" Supplements

My recent comments about chromium, the penalties handed down over false weight loss claims and my inability to find  any support for an apparent claim concerning probiotics and  weight gain, have lead to a flurry of questions and helpful responses.

By far the most common has been surprise. Most people assumed that:

1. These dietary supplements are regulated and that:
2. They are therefore safe and
3. They have had to demonstrate that they are effective

In fact all of those three assumptions are wrong.

I have just found a most helpful article that you can download for free.

Last October at the 2006 Annual Scientific Meeting of NAASO - the Obesity Society - the results of a collaborative research program by the University of Connecticut's Center for Survey Research & Analysis (CSRA) in Stamford, Connecticut and the University of Pennsylvania's Center for Weight Loss and Eating Disorders in Philadelphia were presented. GlaxoSmithKline (GSK) Consumer Healthcare funded the study.

Findings from this first national survey on the safety and regulation of dietary supplements for weight loss include:

• 65% believing that weight-loss products are tested for safety
• 63% believing that weight-loss products are tested for effectiveness
• 54% believing that weight-loss products are approved by the FDA
• 64% believing that manufacturers are required to include warnings about side effects
• 50% of African Americans and 49% of Hispanics were more likely than Whites of European origin (36%) to believe supplements are safer than OTC or prescription weight-loss drugs

Congressman John Dingell from Michigan has indicated that the new Congress will be re-visiting the issue of the FDA's regulation of some of these supplements.

That would probably be wise.

Though as a very firm advocate for health freedom, I always worry when new regulations are proposed, simply because they sometimes lead to the baby being ejected with the bath water.

I shall continue to watch this developing story and to let you know how things develop.

Chromium

When talking about chromium we’re not talking about that stuff that gets applied to metals to make them shiny.

For more than 20 years I've been interested and intrigued by its role in metabolism. This month's issue of Harvard Men's Health Watch highlights some of the research indicating possible links between chromium deficiency and diabetes, high cholesterol, heart disease and weight management.

The journal is only available for subscribers, but let me summarize some of the data for you.

Chromium exists in many forms and not all are either absorbed or biologically active. Antacids, phytates found in grains and tannins found in tea may all lower the absorption of chromium.

A point that always comes up when we discuss supplements is that some people will feel that recommended daily allowances are too low and that using larger - sometimes vast - amounts will achieve additional biological effects. There is some evidence that very large amounts of chromium may damage cells in tissue culture but very little evidence for chromium toxicity in humans. People probably vary greatly in their tolerance to chromium.

1. Diabetes: Chromium has attracted most interest because of its action on the binding of insulin to at least one of the insulin receptors. Insulin is more effective if chromium is present. Chromium also has a positive influence on one of the glucose transporters in cultured fat cells. The effects of chromium on glucose and insulin seems to vary in different species. So it is difficult to extrapolate from an animal study to humans. In people with both the major types of diabetes, the consensus seems to be that chromium supplements containing 200-1,000 mcg chromium as chromium picolinate a day have been found to improve blood glucose control. Chromium picolinate is the most efficacious form of chromium supplementation. There is a small pilot study that found that in women with polycystic ovarian syndrome, a low dosage of chromium picolinate improved glucose tolerance, but did not help with the hormonal or ovulatory disturbances. This has just been confirmed in a study using a higher dosage (1,000 mcg/day). Based on a detailed review of the literature, the United States Food and Drug Administration (FDA) has determined that chromium - at least chromium picolinate - does not reduce the risk that you might develop insulin resistance or diabetes and the American Diabetes Association agrees that the benefit of chromium supplements has not been conclusively demonstrated.
2. Cholesterol: Chromium deficient rats develop high cholesterol levels. But the evidence that chromium supplementation helps cholesterol levels in humans is thin. Chromium may also help people with diabetes to lower their cholesterol levels. The published evidence indicates that any beneficial effects of chromium on cholesterol is much smaller than the effects of diet and exercise.
3. Coronary artery disease: There is a study suggesting a correlation between chromium levels and the risk of having a heart attack, with lower levels being associated with higher heart attack risk. That does not, of course, necessarily mean that taking chromium supplements will reduce the risk of a heart attack.
4. Weight management: Despite all the advertisements, chromium supplements have not been shown to be effective in producing sustained weight loss.

There remains a possibility that some other form of chromium may be more effective on some of these parameters. There has recently been some interest in a product called Diachrome, that contains chromium and biotin. There have been several very interesting presentations about it at international meetings, but we need to see if the results pass peer review and replication.

A diet containing plenty of whole grains, nuts, broccoli, and green beans, should provide you with enough chromium. Chances are that taking a supplement will not cause harm and may perhaps help if you are at high risk of diabetes. But the evidence is still controversial.

I know of several other studies that are underway, and I shall report them to you as they appear.

But for now, when it comes to buying supplements, this is another one of those times that I say, "Caveat emptor!"

The Ape Diet

The BBC is carrying an article today about an experiment done for a television program in the United Kingdom.

Nine volunteers aged 36 to 49 set up home in a tented enclosure at Paignton Zoo, Devon, right next door to the ape house.

They were then put on what was essentially a vegan diet for a week followed by a vegan and fish diet for five days. They didn't call it a vegan diet, choosing the more catchy name of an Evo Diet. The nutritionist who designed the eating plan was inspired by the diet consumed by apes in the wild.

She devised a three-day rotating menu of fruit, vegetables, nuts and honey. The prescribed menu was designed to be safe to eat raw; to meet adult human daily nutritional requirements; and it provided 2,300 calories - between the 2,000 recommended for women and 2,500 for men.

They typically ate 5kgs {Yes, ELEVEN POUNDS (!)} or 2,300 calories of fruit, vegetables, nuts and honey.

On a 3-day rota, they typically ate broccoli, carrots, radishes, cabbage, tomatoes, watercress, strawberries, apricots, bananas, mangoes, melons, figs, plums, oranges and hazelnuts.

Volunteers could also drink water. In the second week, standard portions of cooked oily fish were introduced. The idea was that this was to simulate the diet of a hunter gatherer.

Although this is really a mock experiment, it was a shame that they added the fish in the second week: it would have been nice to have seen the impact of just twelve days on a vegan diet.

Even so, the results were remarkable. The average cholesterol of the group fell by 23%, they lost an average of just under ten pounds and average blood pressures fell from 140/83 to 122/76.

I don't find any of this at all surprising: I've done countless experimental diets on healthy volunteers, on patients and I've also tested them all on myself.

Eating the kind of diet to which we adapted over hundreds of millenia obviously makes good sense. And is far more likely to be successful than the latest fad diet based on some highly unnatural approach. The trouble with this experiment was that it actually did not simulate our ancestral diet: some - but not all - people do much better if they "eat with the seasons:" eating summer fruits in the summer, winter vegetables in the winter and so on. From what we know from the fossil record, it appears that our ancestors became omnivorous a very long time ago, and fish may have been a relatively recent addition to our diet.

Apart from those nit picky theoretical objections, the main problem with this diet is practical: it can be hard to carry around eleven pounds of fruit and vegetables. I've done it as part of an experiment, so I know that it is doable: it depends on how much you want to take control of your body.

There are, of course, loads of supplements for sale that claim to give you all the goodies packed into those eleven pounds of food, but in one convenient little pill. The trouble is that natural foods contain many other nutrients, not all of which have yet been identified. The bulk and the fiber are also important components of your diet.

The second problem is psychological: in Healing, Meaning and Purpose we spend a whole chapter/CD on methods for maintaining motivation and overcoming the psychological, social, subtle and even spiritual problems that often prevent us from looking after our bodies.

“As houses well stored with provisions are likely to be full of mice, so the bodies of those who eat much are full of diseases.”
--Diogenes (a.k.a. Diogenes Laertius, a.k.a. Diogenes the Cynic, Greek Philosopher and Founder of the Cynic School, c.412-323 B.C.E.)

“To become vegetarian is to step into the stream which leads to nirvana.”
--Buddha (a.k.a. “The Awakened”, a.k.a. Siddhartha Gautama, Indian Religious Figure and Founder of Buddhism, c.563 B.C.E. – c.483 B.C.E.)

“It's bizarre that the produce manager is more important to my children's health than the pediatrician.”
--Meryl Streep (American Emmy and Oscar-winning Actress, 1949-)

Dogs, Diet Pills and Healthy Eating

Pfizer Animal Health announced today that the Food and Drug Administration (FDA) has approved Slentrol(TM) (dirlotapide) for the safe and effective management of canine obesity, making it the first and only veterinary-approved obesity drug for dogs in the United States.

Because of our intense interest in metabolism, we have been tracking the rise in canine obesity since 2001. Wild dogs do not get fat, but under-exercised canines given the wrong food rapidly do. Many owners think that they are too busy to exercise them and many neighborhoods either have no side walks or are simply not safe for a walk. Having just received multiple bags and boxes of food, I can also attest to something else: we often equate food with love - without being aware of the potential adverse health consequences.

According to 2002 data from the American Veterinary Medical Association 40 percent of dogs - around 17 million - are considered overweight (5 percent to 20 percent over ideal weight) or obese (20 percent or more over ideal weight).

Depending on the species, our canine friends get many of the same problems that we associate with overweight in humans: arthritis, heart disease, respiratory conditions and some cancers. Obesity can also worsen the signs associated with pre-existing diseases such as osteoarthritis. In addition, obesity can affect a dog's quality of life by making exercise and play more difficult or even impossible.

The medicine is, quite rightly, designed to be used with a diet and exercise plan.

This new medicine does appear to be a real advance, and its mode of action very interesting. Indeed I am at this moment looking at a dog who might benefit!

But I also notice that a number of news outlets have reproduced the Pfizer press release verbatim, and presented it as a news item.

What Pfizer said is 100% accurate, but when the media reporduce something without comment I worry that this is an example of "fake news."

It is interesting to me that this story was released two days after the release of a report from researchers at the University of Alberta Hospital that has just been published in the Lancet.

Their conclusion? That we need better data on the long-term effects of anti-obesity drugs before more widespread use of the therapies. We need to know not just if a medicine leads to weight loss, but whether it leads to clinical benefit. We saw this with the recent tragedy with the medicine torcetrapib. This was a medicine designed to increase levels of HDL-( "good") cholesterol. Indeed it does, but more people taking it died in a clinical trial, which was then stopped.

I am often asked, "Wouldn't it be great if we could do anything that we wanted and then to take a pill to cancel out the effects?"

The answer to that one is surely a big, "No!"

Fortunately such a solution - which would destroy personal responsibility - seems to be years in the future.

If ever.

We MUST take responsibility for the things that we do.

To do anything less is to accept the fantasy that we are no more than machines at the mercy of our brain cells.

We are all far more than that.

And deep down we all know it.

Probiotics: Caveat Emptor Part 2

After I posted about the new data on the apparent importance of intestinal microorganisms and weight management, I received some very helpful comments and emails.

If you look at the "comments" section of the post, you will see this:

"www.Probiotic-Lab.com is manufacturing and distributing Bacteroidetes as a natural bacteria supplement for weight loss."
Posted by an "R.Russell"

Now I have previously reported on a conference in London at which a number of experts expressed concern about some probiotics available in the United Kingdom. So on your behalf, I not only posted the following response, but also emailed the company. First, because there is nothing on their website about marketing probiotics for weight loss and second because it is important to have these questions answered whether they are marketing probiotics for weight loss or for skin care.

This is what I wrote on the blog and also in my email to the company:

On behalf of my many readers may I ask www.Probiotic-Lab.com two questions?
1. In my posting I referred to a short piece that I wrote about a conference in London, at which some of the speakers warned that some products on the market did not contain the active ingredients claimed on the label. How do you guarantee the activity of your preparations?

2. Though I am very familiar with the use of probiotics - I first used them in, I think, 1982 - I am intrigued that you are already distributing Bacteroidetes as a natural bacteria supplement for weight loss. What evidence do you have that they are effective? I could not find anything on your website or from a search of the literature. If you have some data to share I would love to analyze it, and if it's of good quality I will go ahead and write about it, both here and in my articles.

Kind regards,

RP

I wanted to give them time to respond because of the holidays.

But as of today - seventeen days later - there has still been no response to my communications.

I also checked the scientific references on the front page of Probiotic Lab's website. The first does not have anything to do with weight or skin infections, but actually refers to a study of ear infections. The second reference is problematic: it refers to the "American Medical Journal." But sadly I am not familiar with a journal of that name. I have looked at a range of American Medical Journals in case the journal name or date is wrong. But again I can find nothing.

I shall be delighted if someone can help.

I also looked to see if there is any published peer-reviewed literature on the use of probiotics and either weight management or skin disease, and again I have not been able to find anything.

So you can draw your own conclusions.

Should any data come to light I shall report it. Or if the company responds, I shall post what they say.

The Price of False Weight Loss Claims

It has just been reported that this afternoon the United States Federal Trade Commission has recovered more than $25 million ro settle allegations of deceptive marketing for four products:

1. Xenadrine EFX
2. CortiSlim
3. TrimSpa
4. One-A-Day WeightSmart

This is not a surprise. For anyone with any knowledge of human metabolism some of the claims made in television and print advertisements were really far-fetched.

The fines may sound large, but are probably just a drop in the bucket for the companies.

This legal action is all about false claims, but there is another worry, and that is that some of the alleged weight-loss products may also have side effects. Two months ago I mentioned that there are currently investigations underway of at least two people who appeared to have developed manic symptoms while on Cortislim. It remains to be seen if there is a causal relationship.

Pretty much ANYTHING will help you lose weight in the short term. But if these products really worked and were safe, then why on earth wouldn't doctors and nurses be using them themselves and prescribing them to their patients?

Sad to say weight loss does not come in a bottle: I only wish that it did!

Stick with the principles of gradually modifying your diet, exercise and be aware of the psychological traps that can sabotage healthy living. And please don't waste your money on quick fixes that cannot possibly work.

If it seems too good to be true, then it probably is.

Exercise Beats "Dieting" in Managing Obesity

An important report was presented at the Scientific Meeting of the United Kingdom Society for Behavioural Medicine in Cambridge earlier this month.

A team of researchers from Leeds Metropolitan University and the University of Hull studied 62 women aged 24 to 55. They all had a Body Mass Index (BMI) over 30, which is classed as clinically obese. (Regular readers will know that most experts have moved away from using BMI to evaluate metabolic and cardiovascular risks).

The program encouraged women not to diet but to take part in exercise classes. They were required to do four hours a week of exercise, such as t'ai chi, aqua aerobics or circuit classes.  So it was not necessary to become a hard core exercise freak!

The researchers found significant improvements in health and mental well-being.

The women in the study were also taught about good eating habits, including how to read food labels and cook food, and they received social support and behavioral therapy to help them respond to body cues such as hunger and feeling full.

After a year, the women had only lost a little weight but were significantly fitter and happier with themselves. Their blood pressure, heart rate and cholesterol fell and respiratory fitness increased. And the women also felt better in terms of general well-being, body image, self-perception and stress.

This small, simple study re-emphasizes what we have said to tens of thousands of people: fad diets will only help in the short term. For all practical purposes you can eat what you want, but in moderation. But try gradually to change the composition of your diet. I have written some advice on doing that. In Healing, Meaning and Purpose we also provide a number of tactics to help you tackle some of the psychological and social hurdles that may stand in the way of weight management. Which include something not often discussed: the twelve ego-fears that can be the hidden drivers to a lot of our behavior.

Understand them and you can gain a remarkable degree of control of your thinking and your emotions.

And it is exercise that should be the centerpiece of a weight management strategy.

This was re-inforced by a study published last week in the Archives of Internal Medicine: people who lost weight by restricting calories lost bone mineral density. Those with exercise-induced weight loss did not.

And as you doubtless know, loss of bone mineral density is one of the key risk factors for osteoporosis.

So please don't buy in to some new "miracle" diets: they simply don't exist.

Instead:

• Gradually increase your level of exercise
• Slowly change the composition of your diet
• Keep your internal organs - especially your intestine - in balance
• Develop your food awareness (I am going to do a whole post/article about that!)
• Learn how to deal with the psychological, social subtle and spiritual aspects of suboptimal eating (Check out the reources that I have already provided + a new eBook in the New Year)
  

And before you know it, you will be exactly where you want to be.

Promise!

 

Lack of activity destroys the good condition of every human being, while movement and methodical physical exercise save it and preserve it.”
--Plato (Athenian Philosopher, 428-348 B.C.E.)

“The way to cheerfulness is to keep our bodies in exercise and our minds at ease.”
--Sir Richard Steele (English Dramatist and Essayist, 1672-1729)

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)

Another Nail in the Coffin of BMI

In August I outlined some of our reasons for believing that the most common measure of overweight and obesity – the body mass index (BMI) – can be very misleading and should probably be abandoned, or at least consigned to the back burner.

A team at the Hammersmith Hospital in London led by Professor Jimmy Bell has been using a novel type of MRI scan to locate the distribution of fat in the body. The problem is that 40% of the population has "bad" fat around some of their internal organs including the heart, liver or pancreas, even though many appear thin. So even though they may look slim, they may still be at risk of conditions like insulin resistance, diabetes and hypertension because of this hidden fat.

As we have said before, from a health perspective, it is the distribution of fat that is all important, rather than just the amount of it. This study confirms what metabolic physicians have been saying for years: BMI gives you the wrong idea about how much fat you have.

Once you know about the distribution of your fat, we can design precise lifestyle changes to work on it. As an example, the strategies that we use for overall weight management are not the same as the strategies that we use for reducing intra-abdominal fat. There are very good physiological reasons why diet does little to reduce the fat around organs. It is there to provide fuel during exercise, so specific exercises are the way to rid yourself of this internal fat.

At the moment there are very few centers that can do this kind of scanning, but with the growing evidence of its importance, that is likely to change. In the meantime, be aware that aerobic exercise and strength training, particularly if it involves the large muscles of the back trunk and lower limbs is the quickest way to rid yourself of these dangerous fat deposits.

Fat in itself is essential for normal health, but fat in the wrong places can be a killer. And BMI tells you nothing about the fat lurking in the hidden parts of your anatomy.

Aerobic Exercise, Diet and Abdominal Fat

Most of us are probably aware of the difference between fat inside the abdomen – “intra-abdominal,” also called visceral fat – and fat on the hips or the outside of the abdomen. The fat inside the abdomen is associated with insulin resistance, diabetes and at least a dozen other medical problems. This fat is also covered in cortisol receptors and breaks down and reforms extremely rapidly. By contrast the fat on the outside of the body has relatively few metabolic consequences until the amount of it becomes extreme.

Excess fat in general is not a good idea, but it is the intra-abdominal fat that is the best target for treatment.

New research has shown that the addition of aerobic exercise to a standard dietary weight loss program can preferentially reduce abdominal fat in overweight people.

The investigators did a twenty week prospective study in which looked at 45 obese women with an average age of 58 years. During the study the participants bought their own breakfast in consultation with a dietitian, but had their lunch and dinner prepared by the kitchen staff of the hospital. They were either told to continue with their normal routine of daily activities, or to do low-intensity or high-intensity aerobic exercise. The investigators not only did all the standard measurement on their volunteers, they also did fat biopsies and measured the size of the fat cells.

They all lost weight, but in the people who did the high-intensity aerobic exercise, they also had a reduction in the size of the fat cells in subcutaneous tissue taken from the abdomen.

This is interesting, but it’s necessary to sound a note of caution about the experiment: the investigators were measuring subcutaneous fat cells rather than the all important intra-abdominal fat cells. The trouble with measuring those is simply getting at them. It is not easy trying to get fat out of the abdomen without some invasive procedures.

Hidden Harbingers of Weight: Salt Intake and Obesity

In Healing, Meaning and Purpose, I discuss some of the evidence for four previously little recognized causes of obesity:

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

Each of these has been widely discussed in the professional literature, but little has percolated out into the general population except in advertisements for agents like Cortislim. I remain skeptical about these products. Tinkering with just one of the 260 hormones and neurotransmitters implicated in the control of weight is unlikely to be crowned with success. And their ingredients may also have the potential for causing problems. Recent advertisements have also mentioned that one of these products may elevate mood. Sad to say, in the last year we have seen two people who developed manic symptoms after taking one of the supplements. We are urging colleagues to see if there are any other cases, or whether these two were just coincidental.

I recently mentioned some of the evidence for viruses as a cause of weight gain.

Now a new publication from the Universities of Helsinki and Kuopio is out in this month's journal Progress in Cardiovascular Diseases, that provides powerful support for the salt hypothesis.

The researchers report that an average 30-35 % reduction in salt intake during 30 years in Finland was associated with an extraordinary 75 % to 80 % decrease in both stroke and coronary heart disease mortality in the population under 65 years. During the same period the life expectancy of both male and female Finns increased by 6 to 7 years.

As expected, reducing salt intake has a beneficial effect on blood pressure.

But in my view the most interesting finding of the study is the close link between salt intake and obesity.

As bartenders, pub landlords and tavern owners have known since the beginning of time, increasing a person's intake of sodium produces a progressive increase in thirst. (You didn't think that those peanuts on the bar were put there out of the goodness of the establishment's heart did you??!)

The progressive increase in the average intake of salt explains the observed increase in the intake of sugar-containing beverages which, in turn, has caused a marked net increase in the intake of calories during the same period in the United States.

Here is an extraordinary statistic: Between 1977 and 2001, energy intake from sweetened beverages increased on the average by 135 % in the United States. During the same period, the energy intake from milk was reduced by 38 %. The net effect on energy intake was a 278 kcal increase per person a day. The American Heart Association has estimated that, to burn the average increase of 278 kcal a day and avoid the development or worsening of obesity, each American should now walk or vacuum 1 hour 10 minutes more every day than in 1977. As we all know, that has not happened.

In the decade from 1976-1980 to 1988-1994 the overall prevalence of obesity increased 61 % among men and 52 % among women. During 1999 to 2002, the prevalence of obesity was 120 % higher among men and 99 % higher among women as compared with the 1976 to 1980 figures. The increased intake of salt, through induction of thirst with increased intake of high-energy beverages has clearly made a significant contribution to the increase of obesity in the United States.

It is also of note that until 1983 the use of salt did not change or even showed a continuous decreasing trend in the United States. The prevalence of obesity was relatively low and remained essentially unchanged from early 1960s to early 1980s.

This new study suggests that a comprehensive reduction in salt intake, which would reduce the intake of high-energy beverages, would be a potentially powerful means in the so far failed attempts to combat obesity in industrialized societies.

There is now conclusive population-wide evidence that indicates that we could achieve powerful beneficial health effects simply by reducing our overall salt intake. These benefits include a decrease in obesity.

As an aside, the population-wide long-term experience from Finland indicated that a remarkable decrease in the salt intake has not caused any adverse effects.

A number of years ago we were engaged in some experiments in which we replaced regular table salt - sodium chloride - with potassium chloride. For the first three weeks food seemed rather tasteless. But then we all suddenly discovered a new universe of flavors that had previously been hidden under a thick coating of salt. So a dietary change does have a temporary effect on your taste buds.

Although the paper doesn't say so, there is also some data that salt may itself increase cortisol release.

The bottom line?

We now have clear, empirical data to support three out of the four points that I made in Healing, Meaning and Purpose, and there is some less robust data for the fourth.

I urge you to try gradually to reduce your personal intake or salt, and to encourage your family and friends to do the same. I mentioned that food may initially seem a little less flavorful, but then things change rapidly and for the better.

And your body will love you for the change!

Glycemic Index Revisited

If you are anything like me, you probably find loads of adverts in your mailbox for magical ways to lose weight, either by using some form of the Atkins diet, manipulating cortisol (it doesn’t work), or by paying attention to the glycemic index of the food that you eat.

Last January I summarized some of the recent research that showed that glycemic index and glycemic load were not related to measures of insulin sensitivity or secretion, or to the amount of fat in the body. However, the intake of fiber in the diet was found to have beneficial effects on insulin sensitivity, adiposity and the secretion of insulin by the pancreas. I went on to give some uncontroversial advice on how to eat.

Nobody thought that the glycemic index issue was dead: insulin and the other hormones involved in fat and carbohydrate metabolism are powerful and have multiple roles in the body.

A study published in the Archives of Internal Medicine in July, helps further refine our understanding about glycemic index. High carbohydrate foods with a low glycemic index are the best way to reduce your risk of cardiovascular disease. The problem is that you want to avoid sudden surges in glucose after you eat a meal. What normally happens is that those surges are accompanied by sudden rises in triglycerides and insulin. The three together can cause all kinds of mischief to the insides of your blood vessels. High protein and low glycemic index diets will help with weight, but it’s only the combinations of high carbohydrates with low glycemic index that reduces the risk of vascular disease.

My redoubtable Web Mistress, Carol Kirshner, has found a most useful resource at the University of Sydney, that you can use to help guide your food choices.

This is such a useful resource that we are going to attach it to our blogs and websites.

However, it’s essential that we don’t get seduced by the idea that high carbohydrate/low glycemic index eating is the solution to all of our ills.

We still need to follow the basic principles of a balanced diet:

1. It is important for you to maintain your energy balance, between input and output
2. Calories do count
3. What you include in your diet is as important as what you exclude: we are designed to consume not just rice and lettuce, but an array of other nutrients
4. Make only moderate dietary changes at any time: making big dietary changes can be a violent attack on your body and your mind
5. Avoid the “trans-fatty acids”
6. Try to consume some Mercury-free omega-3 fatty acids every single day
7. Eat fewer simple carbohydrates
8. Use weight management and exercise strategies that enhance your overall health and well-being
9. Take more exercise: even small amounts can have a big effect.
10. Make it a goal to gradually reduction your overall intake of cereals

Food, Reward and Weight Gain

There's a short review with a link to an online research paper that you might find interesting.

Although the paper has to do with the mechanisms of weight gain in people with schizophrenia, many of the same principles apply to many people with weight problems. The systems of the brain involved in salience - deciding what is important in the environment - appear to be disrupted.

Gene-Jack Wang at the Brookhaven National Laboratory has discovered that the brains of morbidly obese people seem constantly to be turned toward finding food: The regions of the brain connected to the mouth lips and tongue are overly active, and, like the addicts who get the biggest rush from drugs, they seem to have fewer dopamine receptors in the reward systems. Perhaps like the addict, the morbidly obese eat to compensate for an underactive dopamine system.

In Healing, Meaning and Purpose, we coined the term, “Salience Disruption Syndrome,” to describe a group of problems that are normally thought of as separate entities, but which are inextricably linked. They include not just over-eating, but:

• Impulse control disorders
• Substance abuse disorders
• Pathological gambling
• Pathological shopping
• Attention deficit with ot without hyperactivity
• Bipolar disorder

The list is a long one and the reason for highlighting it is that we have been able to devise new treatments based on this new principle of a disruption in salience. If there is interest, I shall post some more about the methods that we have devised.

Thrifty Genes, Thrifty Bodies and the Barker Hypothesis

“They have sown the wind, and they shall reap the whirlwind.”
--The Bible (Hosea, 8:7)

In 1962, a geneticist named James Neel first proposed a “thrifty gene” theory to explain why 60% of adult Pima Indians living in the United States have diabetes, and 95% are overweight. Neel’s theory was that populations like the Pimas, that have for millennia relied on farming, hunting and fishing for food, would experience alternating periods of feast and famine. Neel hypothesized that in order to adapt to these extreme changes in caloric needs, people developed a “thrifty gene” that allowed them to store fat during times of plenty so that they would not starve during times of famine.

A similar theory was advanced to explain the high rates of diabetes in people from the Indian subcontinent, once they are exposed to plentiful supplies of food. These was traced by the great Diaspora from central Asia at the end of the last age, when the ancestors of modern Indians and Pakistanis made the great trek through modern Afghanistan into the Indus valley. A journey that had been impossible at the height of the Ice Age and which was still difficult. The idea was that people who could quickly lay down a lot of intra-abdominal fat would have a huge survival advantage.

This is an attractive hypothesis, but here have always been some problems with it:

1. The gene or genes would have to be able to work with the environment: the Pimas of Mexico and people living in rural India do not have the high rates of diabetes and obesity
2. Despite looking for over 40 years, no such gene has yet been found
3. If the thrifty gene is so advantageous, why doesn’t everyone have it?
4. Until recently, famines were rare and usually occurred every 100-150 years. As John Speakman has pointed out that would mean that most human populations have experienced at most 100 famine events in the course of their evolutionary history
5. Famines do increase mortality but only in about 10% of the population
6. In famines most people die of disease rather than starvation, and the worst affected are the young. Having a “thrifty gene” would not help them survive starvation OR disease
7. Simple genetic models would suggest that famines would not provide enough selective advantage and there has not been enough time for a “thrifty gene” to have penetrated the population

There could yet be some complex genetic model involving “reserve” genes that appear when needed, or some epigenetic inheritance, but we have no evidence for that either.

A second concept is gaining a lot of traction. It is what is known as the “Thrifty phenotype,” and is part of a larger theory called the “Barker Hypothesis.” I’m going to stick my neck out, and predict that David Barker may receive the Nobel Prize in medicine for his discoveries. They are that important.

Essentially the Barker Hypothesis suggests that in addition to genetic, epigenetic and environmental factors in disease, there is another, and that is the intrauterine environment. The idea is that if a mother is malnourished, she can modify the development of her unborn child. From an evolutionary perspective, her body is preparing the unborn child to survive in an environment where food is in chronic short supply, resulting in the “Thrifty phenotype:” smaller body size, lower metabolic rate and a propensity to be less active.

The problem is this. If you are born with the thrifty phenotype and actually grow up in an affluent environment, you are more likely to develop obesity, diabetes and vascular disease later in life. If true – and virtually all the evidence suggest that it is – then it has serious implications for countries that are transitioning from sparse to better nutrition, and may have contributed to some of our current health problems. Many of us were born to mothers who had poor nutrition, either because of the Great Depression, the Second World War, poverty, or just plain poor information about good nutrition during pregnancy. And now we are reaping the whirlwind.

The hypothesis has become sophisticated. If you are born small or premature, then your liver and kidneys may not have completed their final growth spurt, which might predispose you to metabolic problems and hypertension.

The story of how this all came to light would be worthy of Sherlock Holmes himself. English counties used to have people who were responsible for providing midwifery services. In the county of Buckinghamshire a single midwife collected data for almost thirty years. Information about the mother, the length and weight of the baby and the weight of the placenta. Information that would be impossible to collect these days. Some civil libertarian somewhere would probably dream up some way of hiding this enormously important information.

David Barker discovered these extraordinarily good records, and then set about finding the adults that these babies had become. And what he found has changed medicine: babies who had small placentas – a good measure of being small or premature – were more likely to develop obesity, diabetes or hypertension as adults. Then he and others turned their attention to other early physical characteristics and found correlations with health later in life. The highest risk of coronary heart disease was seen amongst people who were born small and became heavier during childhood.

The practical implications?

Find out your own birth weight and anything else that you can about your early development.

If you were a very large baby (bigger than nine and a half pounds), it implies that your mother may perhaps have had a metabolic problem. If you were small (less than five and a half pounds), then you should get the regular health checks that we recommend for anyone in a “high risk” group.

BMI R.I.P.

For experts in metabolism, we have long worried about the over-emphasis on the use of body mass index (BMI) as the arbiter of a "healthy" weight. It is one of those measurements that is in some senses too easy, and the results are deceiving. I regularly see people claim that a certain BMI will "predict" the risk that someone will develop cardiovascular disease or diabetes. The truth is very diferent.

There are two ways to calculate your BMI:
1. Metric system - Kilograms and Metres
[Your weight] divided by [Your height squared]

2. Imperial System - Pounds and Inches
[You weight] divided by [Your height squared] times 703.5

A person is said to be healthy if his or her BMI is between 18.5 and 24.9.

The trouble with this is that the calculation lumps together fat and muscle: a muscular six foot tall football player weighing 300 pounds and with 3% body fat, would have an "unhealthy" BMI of 26.3. That is clearly absurd, and one of the reasons that most experts use BMI only as one part of an evaluation of health.

Our scepticism has been confirmed by an important study from the Mayo Clinic in Rochester, Minnesota, and published in this week's issue of the medical journal The Lancet.

The researchers looked at 40 studies involving 250,152 patients. Their analysis revealed that people with a BMI of 30-35 were at lower risk of cardiovascular disease than those whose BMI was below 20.

BMI does not correlate well with fat. A better way to distinguish between fat and muscle is to take a cross-sectional view of the abdomen, and to focus on the waist-hip ratio.

A separate study by researchers at the London School of Hygiene and Tropical Medicine of 14,833 people over the age of 75 was published in the American Journal of Clinical Nutrition. They also came to the conclusion that BMI is a poor indicator of health in both men and women in this age group. These researchers also agreed that waste-hip ratio was a better indicator of mortality risk.

This is all music to my ears. For almost three decades we have been teaching about the importance of  different stores of fat and the limitations of the BMI calculation. It has been known since the 1940s that gaining weight on the hips, or developing "lover's handles" are only very weak predictors of diabetes and vascular disease: it is the intra-abdominal fat that is the problem.

There are particular problems with using BMI in the elderly and in some ethnic groups, especially people from the Indian sub-continent and Japan.

The bottom line?

BMI is misleading, and in some age groups and races, grossly misleading.

Much better to use weight and waist-hip ratio.

And BMI only if there is a space on the medical forms where they still need to have it filled in.

 

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
Acne
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.

Gall Bladder Disease and Insulin Resistance

When I was a young student, everyone learned that gallstones were more common in people who were “Fat, female, fair and forty.” As you can see we lived in different times and nobody would say anything quite like that today. Not least because it’s now only partially correct. Gallstones are occurring at ever-earlier ages, because they are a recognized complication of obesity. And we all know that we are in the midst of a pandemic of overweight and obesity.

We have also been remarking on the number of people with bipolar disorder who have a history of gallstones.

For many years now, the explanation for the link has been to do with an increasing levels of cholesterol, which are a major precipitant of gallstones. There’s also evidence that high carbohydrate diets increase the risk of gallstones. Weight loss reduced the risk of developing them, though suddenly losing a lot of weight with an unbalanced diet may increase the risk of gallstones.

Now a paper from colleagues at three medical schools has just been published this month, and it helps clarify the connection. The conclusion of the scientists is important: insulin resistance itself seems to cause problems with the normal emptying of the gallbladder, and that would predispose people to the development of gallstones.

Insulin resistance is a feature of increasing weight. Several studies that have found increased rates of insulin resistance in people with bipolar disorder implying an increased risk of gallstones. Though gallbladder disease didn’t show up in a recent study from some friends in Toronto, I could not find any systematic studies of gallstones and bipolar disorder. And it is a study that needs to be done.

So there’s a tip for a researcher who can’t think of a project!

There's More to Weight Than Meets the Eye

There's an interesting article about the associations between obesity and mental illness.

We've all become so used to people telling us about the physical consequences of carrying extra weight, so it is interesting to learn that obesity may also be associated with higher rates of mental illness. We have here a typical chicken and egg problem.

Do people become depressed because they are overweight, or does depression and its treatments cause obesity? The answer is probably "Yes." It is both.

Depression may cause insulin resistance and hypercortisolemia, which may result in weight gain. But insulin resistance alters the kinetics of some of the amino acids that are the building blocks of key neurotransmitters in the brain.

And this study re-emphasizes the importance of treating the physical, psychological, social, subtle and spiritual aspects of a problem simultaneously. If we address only one of these dimensions, people will continue to suffer needlessly.

When our clinicians see overweight people with depression or bipolar disorder, they start by treating the mood disorder, but then immediately get to work on the weight problem. And all of it is part of the five vector, or five dimensional approach to treatment: physical, psychological, social, subtle and spiritual.

If we fail to respect and work with every aspect of a person, each problem will return to make us respond appropriately.

After all, illnesses are like any other problem: sent to educate us. Not just you, but also the person to whom you went for help.

Insulin Resistance, Diabetes and the Timing of Meals

At a meeting of the American Diabetes Association in June 2006, Professor Markus Stoffel from the Eidgenossische Technishe Hochschule in Zurich and Rockefeller University in New York, received the Outstanding Scientific Achievement Award for his extremely interesting and important research on the molecular mechanisms involved in the developmental insulin resistance.

This may sound as interesting as watching paint dry, but in actual fact the research is supremely practical, and may lead to a complete re-working of some commonly used dietary strategies.

Many physicians have not yet been taught that the liver is the key organ involved in the genesis of insulin resistance and of type 2 diabetes mellitus. Up to 90% of the glucose circulating in your blood has come from your liver. As the liver becomes less sensitive to the actions of insulin, it starts producing more glucose, particularly after meals. This in turn causes blood glucose to rise and with it insulin levels. One of the other consequences of insulin resistance is that the liver stops storing triglycerides, which then start circulating, while at the same time storing other types of fat, leading to what we call, not surprisingly, fatty liver. Or in the dog Latin that doctors use to confuse the general public, hepatic steatosis.

When we are fasting, the liver switches on banks of genes that produce the enzymes responsible for oxidizing fatty acids to produce fuel.

The main objective of a balanced diet is to maintain balance: we want to avoid sudden swings in glucose, fatty acids or insulin: it is these sudden changes that can cause inflammatory changes in blood vessels and in the liver and may lead to some of the circulatory problems that are such distressing complications of diabetes. We want to try and keep our insulin levels smooth and low. The best way not to do that is to have frequent high calorie snacks and to eat late at night. The best way is to follow the plans that I’ve talked about before. Eat little and often, keep the balance of nutrients just right, and be aware of the exact times at which you eat. Nothing except a little protein in the 2-3 hours before you retire for the night, and go very easy on alcohol, which can wreck your metabolism.

“The secret of life is balance, and the absence of balance is life's destruction.”
--Hazrat Inayat Khan (Founder of the Sufi Order of the West, 1882-1927)

Technorati tags: Insulin resistance Diabetes mellitus Fasting Weight management

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.

Technorati tags: Insulin resistance Insulin resistance syndrome Metabolic syndrome Cardiovascular disease Hypertension Inflammation Hyperlipidemia Weight gain Integrated medicine

Acupuncture for Obesity

I was recently astonished to realize that it is now 25 years since I began my training in acupuncture.

It is an extraordinary system of prevention and treatment, yet one of my biggest disappointments has been the lack of effect in smoking and obesity. I have plenty of friends and collegues who have had great results, but I just have not. In fact I find that the "tapping therapies" seem to be a lot more helpful.

So I was interested to see a note about a report from Germany, that claimed modest success in treating the weight gain that can accompany treatment with some prescription medications. It will be interesting to see if anyone else is able to replicate the study. If they do, I shall report it immediately.

In the meantime, we have enjoyed considerable success with an integrated weight management strategy that addresses the physical, psychological, social, subtle and spiritual aspects of the issue. If you try only to diet and/or exercise, the long term results are usually disappointing.

Address everything at once in a very carefully coordinated manner, and the results can be spectacular. Remember the adage: Combinations are Key.

I outline our strategy in the last chapter and CD of Healing, Meaning and Purpose. Later this year we shall be publishing the entire program, and inviting researchers to examine our approach objectively.

Technorati tags: Obesity Weight management Acupuncture Integrated medicine The Atlanta Approach

Another Controller of Appetite and Weight

We recently discussed the role of cytokines in modulating appetite and energy balance. Now a study in mice has shown that animals deficient in interleukin-18 (IL-18) develop a voracious appetite, very marked obesity and insulin resistance. The insulin resistance is secondary to the obesity that was induced by increased food intake and occurred in the liver as well as muscle and fat.

When the little creatures were given recombinant IL-18 their food intake returned toward normal.

Only recently discovered, IL-18 is an important regulator of innate and acquired immune responses. The fact that a modulator or immunity and inflammation has a key role in feeding and in energy metabolism shows us once again just how closely all these systems are tied together. You lose weight when you are sick or depressed because the body is battling the illness. As you recover, the body needs to replace everything that was lost and re-establish your resilience. These systems don’t just exist in humans, they are found in all mammals and even some birds and fish. So they have evolved over millions of years and we need to be very careful about tinkering with these complex systems. Or of allowing stress or environmental toxins to compromise these protective mechanisms.

This finding may well pave the way not just for new pharmacological approaches to weight management, but also to some non-pharmacological approaches.

Technorati tags: Cytokines Weight management Insulin resistance Interleukin-18 Inflammation

Cytokines and Weight

Anyone who has ever had a sick child knows that one of the surest signs that he or she is recovering is a return of appetite. From a biological perspective, this is an attempt by the body to make up for any losses that took place during the illness. The major mediator of this effect is one set of a group of chemicals known as cytokines.

Cytokines are glycoproteins that behave like hormones and neurotransmitters, serving as chemical messengers between cells. There are many families of cytokines, including leptin, that we have met before. In recent years most of the attention of researchers has been directed not at the cytokines themselves, but at their receptors, whose activity is far more subtle.

Cytokine receptors are involved in the regulation of cell growth and repair and have important roles in immune responses. Apart from their role in feeding behavior, cytokines have roles in fatigue, fever, sleep, pain and stress. Some key cytokines: interleukin (IL)-1,  IL-6 and IL-8 are dysregulated in fibromyalgia.

At a meeting of the 6th International Congress of Neuroendocrinology in Pittsburgh last month, researchers from the Centre National de la Recherche Scientifique (CNRS) at the Pasteur Institute and the University of Lille, France, presented evidence that The cytokine interleukin-7 (IL-7) is not only involved in immune function, but also prevents obesity-prone mice from getting fat. This is the converse of those cytokines that cause weight gain. IL-7 interacts with the regions of the hypothalamus involved in appetite control. This is yet another piece of evidence indicating that the immune and neuroendocrine systems are closely inter-linked.

This is not really a surprise. One of the big problems I people with many chronic illness, particularly cancer, is that they tend to lose appetite and weight. Sometimes they lose a great deal of weight even while maintaining a decent diet. The anorexia of cancer is caused by many factors working on the signaling pathways in the hypothalamus that modulate energy homeostasis. Research has shown that cytokines are major mediators of weight and appetite loss in cancer patients, by working on two systems known as melanocortin and neuropeptide-Y. It also seems likely that the weight loss that happens with stress, depression and chronic inflammation are all mediated by specific cytokines. These same cytokines increase the risk of developing heart disease. A recent study from Ireland has shown that treatment with an SSRI antidepressant reduces measures of systemic inflammation.

It may be that this new insight into the relationship between inflammation and weight will offer up some more solutions for the problems of obesity, but we are going to need to be alert to the possibility that anything that modulates cytokines may increase the risk of vascular disease.

The more that we learn, the more that we understand about the miraculous checks and balances that keep us healthy.

Technorati tags: Cytokines Leptin Cancer cachexia Weight control Inflammation

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.

Technorati tags: Rimonabant Acomplia Cannabinoid receptor Weight management The Atlanta Approach

Sleep, Weight, Insulin Resistance and Diabetes

I am often asked why there seem to be such close links between food and mood. Not just comfort eating, or the sudden shock of lots of carbs when we need an energy jolt, but why drugs that alter mood so often alter appetite?

You will probably not know this, gentle reader, but I only learned of it from reading scholarly papers. Apparently many people report that using marijuana makes them very hungry. On the other hand, cocaine and amphetamine affect not just the metabolism, but also appetite. The link has to do with the evolutionary development of feeding behaviors with the motivation to find food and to be satisfied by it.

Another link that has interested me for many years is the connection between metabolism and sleep. We have always presumed that this link has to do with hibernation: even humans have maintained some hibernation responses.

There is extremely good evidence that there is an inverse relationship between the number of hours that you sleep and an increase in your weight. There have been a great many studies on this, but one of the best was published by a group of researchers from the Mood and Anxiety Disorders Program, at the National Institute of Mental Health, the Psychiatric University Hospital, Zurich, Switzerland; University of Pittsburgh School of Medicine and the Department of Psychosocial Medicine, Zürich University Hospital, Switzerland in the Journal Sleep in 2004.

A report from the BBC concerning a study presented to the American Thoracic Society International Conference in San Diego provides yet more evidence of this link between sleep and weight. Researchers from Case Western Reserve University in Ohio, followed nearly 70,000 women for 16 years. They found that women who slept five or fewer hours a night were a third more likely to put on at least 33lbs (15kg) than sound sleepers during that time. It also found that compared with women who slept for seven hours a night. lighter sleepers were 15% more likely to become obese (have a Body Mass Index (BMI) of 30 or more. {BMI is calculated by dividing your weight in kilograms by the square of your height in meters}).

Previous studies, some of which I have reported before, have shown that after just a few days of sleep restriction, the hormones that control appetite cause people to become hungrier. However the women in the study appeared to eat less. I say “appeared to,” since the use of personal evaluations of food intake are notoriously inaccurate.

In dozens of countries arond the world, I am regarded as an authority in the fields of endocrinology, metabolism and nutrition. But when a group of us tried to estimate our daily intake and compare it with meticulous diaries, we discovered that we – a group of internationally renowned experts – were off by around 500 calories per day.

All kinds of explanations have been advanced, from people who didn’t sleep getting up and binge eating; to the effects of sleep-deprived people craving high carbohydrate, high fat food; to insomnia being a result of anxiety or depression that releases hormones that cause us to lay down fat in our tummies.

For all kinds of complex biochemical reasons, I have always felt that a lack of sleep would lead to an increase in insulin resistance, that may cause an increase in the deposition of fat in key regions of the body.

Some new research suggests that I may have been right on this one. A group based at Yale University School of Medicine, in New Haven, Connecticut has just published a report that should be of interest to all of us, and in particular you multi-tasking insomniacs out there.

The investigators studied a cohort of men from the Massachusetts Male Aging Study who did not have diabetes at baseline (1987–1989) and who were followed until 2004 to look for the development of diabetes mellitus. They came to the conclusion that BOTH very short and extra long sleep durations increase the risk of developing diabetes, independent of confounding factors.

The take home message?

If you do not get 7-8 hours sleep each night, you are vulnerable to a great many problems, and perhaps the biggest of all is the risk of weight gain, insulin resistance and diabetes mellitus.

I do not recommend using sleeping tablets unless absolutely necessary, and then for just a few days at a time. Instead follow all the sleep strategies that I have talked about in earlier blog entries.

During a recent visit to Danville, Virginia, I was delighted to learn that one of the non-pharmacological approaches that I have found helpful – putting a cold compress on the abdomen – was used by General Stonewall Jackson who used this very technique that I had to learn by going all the way to China.

The bottom line? Before your sleep gets disrupted by being  overweight and you develop sleep apnea, try some simple sleep hygiene, and a few of these novel techniques.

Technorati tags: Insulin Insulin resistance Insulin resistance syndrome insomnia alternative medicine resilience 

More on the Neurology of Obesity

The last year has seen a mass of new obesity research linking intestinal hormones and the brain.

Over the last 25 years, there has been increasing evidence that many people with significant weight problems have problems in a region of the brain called the hypothalamus that is involved in the control of appetite, feeding, temperature and a range of other bodily functions. On April 18th, I mentioned the intriguing possibility that viruses could be one previously unrecognized explanation for the obesity pandemic. It is hypothesized that these viruses might alter the normal functioning of the hypothalamus, causing an increase in feeding, and perhaps also of appetite and inactivity.

A study from Albert Einstein Medical College in New York, published in this month’s Journal of Clinical Investigation provides further evidence that there may be something wrong with the normal functioning of the hypothalamus.

We normally have a sensitive mechanism in the hypothalamus for sensing fats, which provide a strong signal to stop eating and also to start normalizing blood glucose. There are strains of obese rats, and in these little creatures the fat sensing mechanisms do not work properly. Not only do they keep eating, but also they cannot control their blood glucose properly. Those two things together conspire to produce yet more obesity. What was so interesting in this study, was that the researchers found that if they inhibited a single enzyme involved in fat metabolism, the levels of fatty acids rose in the hypothalamus, the animals were once again able to sense fat levels, and both their feeding and glucose levels normalized.

This is one of the first times that it has been possible to find a single enzyme that would normalize metabolism. The next question is to see whether this might constitute a viable treatment for obesity, or if the body would quickly work around the treatment and return to its old ways.

Technorati tags: weight control hypothalamus obesity

More Advances in Understanding Weight Control

I have on many occasions discussed the problem of over-simplifying the mechanisms controlling our weight and appetite. They are complex and have multiple fail-safes and multiple levels of redundancy, which is why most weight loss programs only last for short periods of time. The body gets used to the diet, believes that it is starving, and immediately gets to work to conserve energy: our metabolism slows and our physical activity levels begin to fall.

We can tinker with leptin, cortisol or insulin to our hearts’ content, and each will probably help for a while. But if we ignore the body’s starvation-protection mechanisms, to say nothing of the psychological, social and subtle aspects of weight, our efforts will usually be fairly short-lived. Most of us now understand that food intake is only part of the equation; we also need to maximize our metabolic rate and increase our level of physical activity. One of the problems has been how to help someone exercise whose body wants to go into starvation mode.

Steve Bloom’s group at Imperial College and the Hammersmith Hospital in London has published another valuable report helping to elucidate some of the complex mechanisms involved in appetite, weight and metabolism. Steve has been working in this area since the early 1970s, and is one of the most highly cited scientists in the world. In a field that constantly sees new discoveries replacing the old, he is unusual in that that virtually all of his work has stood the test of time.

This report concerns the intestinal hormone oxyntomodulin, which has a dual action, increasing energy expenditure as well as reducing food intake. It appears that oxyntomodulin may let the brain know it has an adequate energy supply and that it can afford to do productive things rather than just concentrating on food seeking behaviors or energy conservation. The hormone signals the brain that it can increase exercise by letting it know that the energy is available to do so.

At the moment oxyntomodulin has to be given by injection, and, given the complexity of the weight maintenance systems it is unlikely to be the whole answer.

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