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!
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:
- Stress
- Salt
- Viruses
- Pesticides
- 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
- Receive regular colorectal cancer screenings beginning at age 50 if you are at normal risk
- 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
- Eat between 25 and 30 grams of fiber each day from fruits, vegetables, whole grain breads and cereals, nuts, and beans
- Eat a low-fat diet: colorectal cancer has been associated with diets high in saturated fat, particularly fat from red meat
- Eat foods with folate, such as leafy green vegetables
- Try to drink at least 80 fluid ounces of pure water a day unless you have a medical reason for not doing so
- Drink alcohol in moderation: 2 units of alcohol or less each day
- If you smoke, here is another good reason for quitting. Alcohol and tobacco in combination are linked to colorectal cancer and other gastrointestinal cancers
- 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
- 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
- Maintain a healthy weight. Obesity may increase the risk of colorectal cancer
- 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.
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.)
