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
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.
Technorati tags: weight control obesity oxyntomodulin energy expenditure weight management
