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University of Colorado School of Medicine
 

Diabetes and Obesity Q&A

Dr Bessesen


      1. Why does someone ‘crave’ sugar?
        Research on addiction has identified a number of brain regions that are involved in the perception of pleasure and reward. Researchers who study this area use the terms “liking” and “wanting” to describe what they see as 2 different phenomena controlled by different brain regions. Liking refers to the pleasurable sensation that one gets when one say consumes sugar. It is a naturally rewarding substance. Wanting refers to a separate phenomenon that is what you might be calling craving. This is the urge to consume sugar or in people who are addicted, take cocaine, smoke, etc. People who are addicted to cocaine may not even really like the cocaine any more, yet they feel a strong compulsion to take it. The brain pathways responsible for this phenomenon likely relate to habit formation. There are differences in different people’s propensity to experience addiction and perhaps propensity for specific food cravings. The prevalent view currently is that people who are predisposed to addiction are hypersensitive to environmental stimuli relating to the substance that is the focus of the addiction but perhaps under-responsive to the actual rewarding stimulus.
      2. Can obesity be ‘learned’ from those you live around, such as your parents?
        Studies of families and other social networks suggest that food intake and physical activity habits which in turn determine weight do tend to cluster. Genetics play an important role, but only about 30% of weight seems to be determined by genetics. The rest is likely environmental and social interactions likely play an important role. In a famous study using the Framingham cohort, investigators tracked the weight of many people over time and found that groups of people tended to share a weight trajectory over time. Studies of families have demonstrated specific parenting styles that seem to be related to children’s weight over time, and most recently, studies of families of people who have had weight loss surgery demonstrate that those in the family who did not have the weight loss surgery also experience weight loss after one person in the family has surgery. It seems that social networks can potentially either promote or protect against weight gain.
      3. Do adipose cells for people with obesity predispose them to have a harder time keeping weight off if they had the same intake as a health individual?
        There are a number of adaptive responses that occur with weight loss. One is a reduction in energy expenditure/kg body weight which results in a tendency to gain weight despite eating the same number of calories as another person who weighs the same but has not lost weight. You are correct though that there are changes in fat cells following weight loss. This has been studied most closely in rats. We use to think that we had a fixed number of fat cells for our whole life. This turns out to be incorrect. Fat cells like most cells of the body are always turning over with some being newly minted every day and some dying. In people who have lost weight the average size of fat cells declines and new “baby fat cells” are recruited. This is associated with improvements in insulin sensitivity that occur with weight loss means that if a person who has lost weight overeats, they are predisposed to storing those calories in fat cells that are set up to store the excess nutrients.
      4. In your lecture your spoke about genetics and the environment as factors in metabolic disease. Does one or the other have a greater influence?
        A range of studies have looked at the role of genetics. Some of the most compelling look at the weight trajectory of identical twins raised in different households. Other studies have looked at the weight gain of identical twins who are overfed. Other studies have linked specific genes to the weight of large numbers of people. My view of this issue is that there are a small number of people who have a very strong genetic predisposition for obesity due to the presence of a gene that has a strong effect on weight. Other people have a strong genetic tendency to be thin. For these families/populations genetics plays a fairly important role. However, overall genetics probably only accounts for about 30% of the variation in weight between individuals. This means that the recent increase in the prevalence of obesity is largely due to changes in the environment.
      5. I have lost about 30 pounds in the past and have hit a sort of wall. How do I prevent weight regain or lose a little more weight?
        Congratulations! That is terrific. The body responds to weight loss with a number of adaptive adaptive responses toe weight loss including a fall in energy expenditure/kg body weight, increases in insulin sensitivity that promote a tendency to store fat, increased appetite mediated in part by changes in appetite hormones and others. The plateau you are experiencing is a reflection of your body reaching a new steady state between your current behaviors and your genetics. I find that one of the biggest barriers to long term success is peoples frustration with an inability to continue losing more weight. Often people say “well if I can’t lose more, then forget it, I will just go back to what I was doing before.” The best way to maintain your weight is to continue doing what you are doing now and making these habits the “new you”. There are people who maintain weight loss and they continue to monitor their weight and food intake. They typically maintain high levels of physical activity exercising 60-90 minutes per day, and they have specific dietary strategies that they use when the scale tells them that their weight is drifting up again. To lose more weight you would have to restrict your food intake more than you are doing now or increase your physical activity more. I am not sure how much you weigh, but a 30 lb weight loss is more than most people do. Perhaps the best approach for the short run is to see if you can maintain your weight for a while?
      6. Can you discuss the benefits of an active sex life versus an active gym life?
        Now there is a study I would like to be involved in! I am wondering how many hours per week of each activity would be needed for health benefits and if the injury rates associated with the 2 strategies would be different? I also wonder if there would be divergent effects on food intake? It is clear that as people gain weight and become obese the rate of low testosterone in men and menstrual/reproductive problems in women increase. Obesity is also associated with sleep apnea which can have an independent effect on the reproductive system. Weight loss and treatment of sleep apnea can improve reproductive function. Women with severe obesity who have weight loss surgery often regain lost fertility and men experience improved sexual function.
      7. With the epidemic of childhood obesity and its link to diabetes, why isn’t the public stepping up to the plate and demanding changes in our schools (dietary and exercise)?
        This is a logical question and I agree with you that the levels of obesity in children are alarming and warrant some action. However, one would like to know that an investment in a particular intervention would lead to a measurable effect. Unfortunately, studies of school based interventions have not shown dramatic beneficial effects. It has been very difficult to show that changes in lunch options and physical activity options at schools results in any clinically significant changes in the weight of students or the prevalence of obesity in the school. It may be that the effects of the environment outside school have a greater effect. Things like TV time, computer time, food options in the neighborhoods around schools, safety and recreation options in neighborhoods may have more potent effects on weight. There is evidence that exposure of fetuses in the womb to high levels of glucose, fat and insulin can predispose to obesity in childhood. What then is the best way to address the childhood obesity epidemic? Better pre-natal care for mothers? Changes in infant nutrition? Pre-school interventions? High school health classes? Re-designing neighborhoods? Unfortunately as you can see this is a very complex issue without simple clear answers.
      8. Why do rats and humans have the trajectory of weight gain over a lifetime? Is there an evolutionary purpose?
        This is a fascinating question and one that I could only speculate about. The human lifespan was probably much shorter 10,000 years ago and starvation leading to illness or predation likely was common. I can only guess that having a drive to eat that was strong and metabolism that was designed to store weight gave a selective advantage over time. It seems likely that the “weight trajectory” I showed is a reflection of how the biology works in an environment where food is always available and physical activity levels are restricted and is not a reflection of how the system worked in the harsh environment that existed thousands of years ago.
      9. Why do women gain weight during peri-menopause and menopause?
        I am sorry, but for most women weight gain is a natural part of menopause. With the fall in estrogen levels most women not only gain weight but redistribute fat mass away from hips and thighs towards the abdomen. It is not entirely clear why this happens although there is evidence for a fall in energy expenditure and changes in insulin sensitivity with the onset of menopause.
      10. Can you talk about the correlation between environmental exposures and obesity? (i.e., obesogens and genetic changes in the body’s ability to metabolize fat)
        Most investigations have been directed at associating specific environmental factors with obesity. These studies have found statistical associations with changes in the composition of the diet, portion sizes, time spent watching tv or using computers, reductions in sleep time, increases in average home temperature, increases in the age of first pregnancy, increases in the concentrations of specific environmental toxins, differences in the availability of sidewalks and many others. These studies are based on the notion that genetics have not changed in the last 100 years and so the predominant cause of obesity is changes in the environment. However, recently it has become increasingly clear that external factors can actually modify genes in a process that is called epigenetic influences. The field of epigenetics has largely focused to date on the effects of maternal factors on the fetus. Studies in animal models including non-human primates has demonstrated that maternal obesity actually results in changes in fetal DNA that can lead to obesity in the offspring. Studies in rats shows that not only diet, but maternal stress can affect fetal DNA in a manner that changes the weight of offspring.
      11. How effective is behavioral therapy in combating obesity?
        Broadly there are 3 treatment strategies for obesity: lifestyle change/behavioral therapy, medications and surgery. In general behavioral therapy produces about a 5-7% weight loss. Some people can lose as much as 15-20% of their baseline body weight with behavior change alone, but this is uncommon. Men tend to lose more than women but participate in behavioral therapy less often. The amount of weight lost is a function of the intensity of the intervention and the person’s adherence to the treatment. Lifestyle change treatment has been shown to prevent the onset of obesity with even a 5% weight loss. There are a range of behavioral theories that have been used as foundations for behavioral treatment. Currently a skills based approach that uses cognitive behavioral therapy as the core theoretical approach is the gold standard.
      12. With respect to hypothyroidism and obesity, have the number of people with hypothyroidism increased along with the obesity numbers?
        The number of people diagnosed with hypothyroidism has increased at the same time that the prevalence of obesity has increased. Most investigators however do not think that the 2 things are causally related. It may be that with the broad availability of assays for TSH more people are screened for hypothyroidism now than were in the 60s, and the diagnostic criteria commonly used to make a diagnosis of hypothyroidism (increased TSH levels) are more liberal now than they were even 15 years ago when we often wanted to see a low level of T4 before making a diagnosis of hypothyroidism.
      13. Can you address eating according to your blood type?
        This idea was offered in a popular diet book. The idea was that your blood type reflected your genetic background and as a result gave a clue as to what kind of a diet would be the best for you. I was asked to comment on this book by the Denver Post a number of years ago. I had not read the book but that did not stop me from saying it was ridiculous. I was ashamed and could not sleep for a week. I then read the book and looked into the claims. There is a very important idea in this book. The idea is that as individuals we are not genetically identical and so it is possible that different diets (high fat versus high carb for example) will work better or worse for different people. This is an important idea and is likely true. There is recent research trying to link insulin sensitivity to what diet might be best for weight loss and other more sophisticated measures of specific genes and their ability to predict responsiveness to specific diets. However, there is no evidence that blood type is related to responsiveness to particular diet and the mechanisms proposed for these hypothesized relationships in the book are not supported by and convincing scientific studies.
      14. Are sugar consumption and hyperactivity related?
        While most parents have behavior that they see as supporting this relationship it has been very difficult to demonstrate experimentally. Importantly attention deficit hyperactivity disorder is a growing and disruptive condition that some have argued has a dietary basis. ADHD appears to involve some of the same brain regions that are engaged following sugar consumption (and other substances such as drugs of addiction). It may be that genetic variability between children in the brain areas and neurotransmitter systems that might be involved in this hypothesized relationship make it difficult to conclusively show that sugar consumption per se has an effect on behavior. Bottom line: there is no conclusive scientific evidence that these 2 are consistently related.
      15. Can you talk about the relationship between food choices and building muscle (i.e., eat more protein at regular intervals & especially shortly after exercising). – This is about building muscle for overall health not ‘bulking-up.’
        Most of us who eat a relatively normal diet consume enough protein to build new muscle tissue if we are exercising regularly. That is to say, protein intake is not limiting for muscle building. In addition, unlike the situation where eating more fat results in more fat tissue, eating more protein does not result in more muscle. This is because the function of fat tissue is to store fat, the function of muscle is not to store protein. In fact the body is not able to store excess protein and when protein is consumed in excess the body burns it and excretes the nitrogen in the urine. If a person is on a reduced calorie diet to lose weight and exercising, protein may become more of a limiting factor. It is very difficult to gain muscle mass while simultaneously losing weight. The best one can usually do is to not lose muscle mass. Most weight loss interventions including those using both exercise and calorie restriction result in a loss in muscle mass (the loss is less in those who are exercising as compared to those on diet alone). There is some evidence that protein is more satiating and so having a good level of protein intake while consuming an energy restricted diet may be helpful although careful studies comparing the weight loss associated with diets that are low or high in protein do not show substantial differences.
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