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FACTS ABOUT OBESITY

Experts subscribe to one or other of two theories of weight increase, which we can identify as either the PUSH or the PULL theories. The PULL theory suggests that weight is regulated by factors inside the body which pulls food in - like for example, there are lots of hungry fat cells waiting to be filled - OR the push theory suggests there is something external in the family or the culture which pushes food in.

 

There is a lot of evidence for the push theory. After all, we live in a culture which celebrates food. Holidays are centred around eating. If you want to celebrate something you don’t take your family to a salad bar. In our culture there are countless opportunities to eat together with countless messages telling you that you will be lacking something important - happiness even - if you do not eat. This “supermarket environment” fosters fat. In a recent experiment with rats in the US, Kelly Brownell found that rats exposed to what he described as a supermarket environment gained weight to the point that they were 300% fatter than their natural weight. In addition we are much more sedentary than we used to be and researchers in Britain measured the effect of our sedentary lifestyle compared to that of 30 years ago, estimating that our lifestyle alone - despite the fact that we eat marginally fewer calories than we used to - accounts for a gain of 5-10 lbs each year.

 

There is an evolutionary benefit conferred on people who are able to store fat. In olden times when food was scarce, it was fatter people - those who were able to store fat - who would survive illness and scarcity. Obesity would be rare in those times since periodic shortages made it impossible for weight to be gained progressively. However, although we live in the 20th century our bodies are still “in the caves” so to speak, because culture has galloped ahead of our biological response to culture. This means that our bodies have not adapted to an environment in which there is plenty of food. Weight gain MUST result.

 

On the family level, PUSH theory may operate. Some families foster overeating for emotional or cultural reasons, or simply from ignorance. Parents might teach bad habits, like forcing children to clear everything on their pates, eating quickly, or tie- in eating to relaxation such as watching television. Research indicates that eating in front of the TV may foster overweight because metabolism slows down when people are in a mild trance state and food energy is less likely to be converted to heat.

 

Stress is another factor in the external world which might lead to weight being gained. It is well known that obese binge eaters are more likely than thin people to eat in response to stress, loneliness or anger. This suggests a personality led vulnerability to responding to push factors in the environment, and indeed stress driven overeating is more common among deniers / avoiders. Overeating however is not a symptom of emotional distress - because if this were true the remedy would be to root it out. There are many people with emotional problems who are not overweight, similarly there are many overweight people who try psychotherapy, yet who remain overweight despite addressing their emotional issues. Obviously something else is going on.

 

 

Evidence For The Pull Theory

A) Fat cell biology

A lot of work is being done on the biology of fat cells. Researchers in Sweden recently discovered that people tend to drop out of weight loss programmes - not when they had attained their target weight but when their fat cells had reached normal size. For two people of the same height , this could occur at greatly different weights. This might be so because one person may have more fat cells than the other.

 

Overweight children and very obese adults are known to have more fat cells than usual. This is called hyperplastic obesity. Fat cells are usually formed at two critical periods of a persons life - in early childhood and at puberty. We now know that new fat cells can be formed at any time of life if weight is gained rapidly or if fat cells grow to over 50% of their normal size.

 

Similarly if people try to reduce their weight to the point where their fat cells shrink below their normal size they start to behave if they are starving ( even if they eat fairly well) and they display all the usual symptomology of people with eating disorders - craving, being obsessional and performing rituals etc. So there is obviously some kind of biological pressure to keep fat cells at approximately their normal size, even if technically this means that a person may be culturally “overweight. This provides evidence for the Set Point theory which is described below.

 

B) Set Point theory
Further support for the PULL effect comes from set weight theory. Question - do we all have a biological mechanism which determines what weight we are going to be stable at- and will pull food into our mouths until we have attained that weight? If you give healthy rats as much rat food as they can eat ( not the supermarket diet) - their weight remains remarkably stable. Also, look at people who lose weight - 97% regain all the weight they have lost, magically settling to more or less what they were before the diet. Good evidence for set weight. But this system breaks down at times - remember the rats in the supermarket environment - gaining weight to a level far in excess of their normal weight. So we can say that the environment will have an effect on our genetic levels of control.

 

As I have described elsewhere, although their is strong evidence for a set weight experts now feel that it is not an exact level of weight but rather a broad band and the position we take on that band will be affected by our lifestyle, food choices and exercise levels, and our age and gender.

 

C) Metabolism
Overweight people often claim that they have a slow metabolism, which we could ascribe to the pull theory. Food is pulled in but it cannot be burned. Metabolism is the rate at which we burn energy and is also affected by age and gender, body musculature and exercise levels. There is also a very important component of metabolism which is influenced by the food we eat and by our dieting history, It is true that metabolism varies among individuals - by up to 100 calories daily. Although their is evidence that overweight children can burn energy at a slower level than slim children ( perhaps because slim children feel more comfortable at running around - overweight adults do NOT have slower metabolisms - they have higher metabolic levels consistent with their additional body weight. Note that exercise has a profound effect on metabolism mostly due to changes in cell response to insulin ( ask if you do understand this) - and dieting has a strong effect on metabolic rate.


D) Genes
Another possible pull factor is in the genes. Is overweight hereditary? Well yes, it does run in families. Only 20% of children with no obese parents becomes overweight. 60% of children with one parent, and this rises to 80% of children who have two overweight parents. Could it just be bad eating habits being passed on? The answer may lie in adoption studies in Denmark where the weight of adoptees was compared to their natural and their adoptive parents. The weight of children as they grew corresponded most closely to their natural parents. Even more interesting were the studies done with identical twins raised apart. Thin separated twins grew up identical in size and weight. Overweight separated twins grew up overweight but there was much more variability in their body size, corresponding to other factors such as environment. From these studies we can estimate that genetics accounts for up to 70% of an influence on obesity.

 

E) Glands

Are they a pull factor? Glandular problems account for less than 5% of cases of obesity.

After looking at all these factors, while we cannot be specific about the causes of weight gain, we can at least dismiss some of the myths about fat people, namely “fat people are greedy”. There is no evidence that fat people are greedy. Fat people need to eat more than thin people to support higher energy needs due to their additional weight. What is true is that fat people are more likely to turn to food in times of stress than thin people and this may be due to personality factors but we can speculate that due to cultural and social pressures which lead fat people to feel bad about themselves they may be driven into ways of thinking which supports this kind of avoidance behaviour.

 

“I was born to be fat”. Twin studies might lead people to despair - “what’s the use, I can’t do anything about it. It is unfair, but it doesn’t mean that weight cannot be controlled.. All you inherit is a tendency to put on weight, careful eating and exercise habits lower the range at which you will settle.

 

“Fat people are lazy” Many fat people do not exercise due to embarrassment of because they find it uncomfortable, but many people do not exercise for different reasons.

 

“Fat people are responsible for their condition” This kind of thinking is unfair and misplaced.

 

So who does need to lose weight. Certainly not as many people as are concerned about it. Recent surveys show that almost 50% of people are concerned about their weight and half as many are trying to do something about it right now, even including large numbers of children, and people who acknowledge that they are not strictly overweight. There is a massive obesity phobia in the culture.


4 out of 10 women say that they are terrified about the prospect of gaining weight and children as young as 6 choose as a potential playmate a child who is disabled rather than one who is fat. The amount of distress in some women being half a stone over their ideal weight bears no relationship to the effect it has on their looks. Perhaps these biases arise from the importance we place in our culture on self denial and self control.

 

 

So Who Needs To Lose Weight?

Experts generally agree that health risks set in at about 30lbs excess weight and the risks of overweight are as follows

  • hypertension risk 6x normal
  • coronary artery disease - 3x normal
  • diabetes 4x normal
  • cancer - obese men are significantly at risk with higher rates of colon prostate and rectal cancer. Women have higher risk of bowel gallbladder and breast cancer at 30% overweight.

For people with upper body fat the health risks set in sooner.

 

 

Weight Control Devices

Reducing Calories
Experts favour a diet plan that will produce a weight loss of 1-2 lbs per week with modified calorie reduction, assuming a nutritional balance based on the food pyramid. If weight loss is faster than this muscle tissue will be compromised and lean body mass - which burns energy - will shrink. Dieting has an effect of metabolism and few people realise that at the end of a weight less program fewer calories are needed to maintain body weight. Long term dieting success rates are poor.

 

Liquid Diets

A recent development in weight control, this was associated in the early days with a few deaths attributed to poor quality protein. People are asked to take their meals in the form of specially prepared drinks which provide 300 to 500 calories daily in the form of protein with nutritional supplements. Weight loss is rapid but in the early days this consists of water and sodium because the body experiences shock. There are side effects, weakness and sickness. Outcomes are very poor, and these diets are associated with enormous post diet weight gain. Although they are on open sale experts agree that they are totally unsuitable for people who hare only moderate amounts of weight to lose. They nay have some value for severely obese persons under medical supervision.

 

Exercise

Always recommended for dieters, but we ,must not overestimate the value of exercise as a punitive measure. You have to run 11 miles to burn off the equivalent of one Mars Bar. To be of value in breaking down fat exercise has to be intense and prolonged, and different forms of exercise hare differing effects of calorie output, strength, fitness and stamina. Where exercise is of value is that it helps reduce appetite in the long run, it aids in relaxation and well-being and so has an effect on motivation and it has a profound effect on insulin receptivity in body cells - which burn glucose more readily.

 

Its importance in weight loss maintenance is undisputed. When we look at people who succeed in keeping their weight down over a 5 year period you will find over 70% exercising regularly as part of a lifestyle change, compared to only 20% of people who have regained their weight.

 

Drugs

There was a period in the 1970s where appetite suppressants especially amphetamine base drugs were very popular. They came to be associated with serious side effects, including emotional changes, tolerance and addiction and very poor outcome rates with weight being regained massively when drugs were ceased. They are currently out of favour among doctors.


Despite the introduction of new drugs to the armoury, such as amphetamine - like drugs and the serotonergic drugs like Prozac, we know very little about their long term effects. For example a drug marketed as Adifax was recently withdrawn because of damage that was discovered to the heart, and some serotonergic drugs damaged the receptors for serotonin in the brain rendering this valuable chemical ineffective.

 

It is sad that there is a proliferation of private clinics set up usually under franchises in which pills are dispensed to all comers irrespective of their body weight. They are being prescribed in many cases for cosmetic rather than medical reasons.

 

More recently there are Fat Binding agents such as Chitosan which has a mechanical action of dubious value, and Orlistat which blocks digestion of dietary fat. Trials using Orlistat show that the benefits of using this drug arise when people follow a reduced fat diet, rather than a normal diet. The long term side effects of this drug are as yet unknown and its effects are documented elsewhere in the Course.

 

At the time of writing as scientists become more familiar with the mechanisms affecting appetite, hunger, satiety and set weight mechanisms, there are many attempts to find the holy grail of weight control. But at present it does not exist.

 

Surgical Techniques

Jaw wiring and gastric bypass operations may have gone out of fashion but surgical interventions are regarded as suitable for people with serious life threatening conditions of obesity. The gastric balloon is being used in some severe cases, with moderate success. It can only be temporarily inserted. Also popular is gastric stapling which reduces the size of the stomach so that only minute amounts of food can be eaten There are mixed successes with this technique.

 

Popular as a cosmetic device is liposuction in which large amounts of fat are liquefied and sucked out through a pipette. But this method is only useful for selected areas of the body where fat has accumulated.

 

Behavioural Approaches

Most diets contain simple behavioural advice such as “keep naughty foods out of the house” or “pin a photo of yourself when fat to the fridge door”. A true behavioural modification programme employs a variety of techniques which are designed to

  • reward positive behaviour
  • help people become their own problem solvers through record keeping so that they can identify the attitudes, emotions, situations and habits which encourage overeating.
  • help people make permanent changes in stimulus control - the way they cook food, store it, buy it or expose themselves to it generally.
  • help them to control relapses
  • change the automatic thinking processes which influence behaviour, which is a deeper influence on simple behavioural changes.

True behaviour therapy aims for gradual but permanent changes in behaviour and can be successful when used in conjunction with a sensible eating plan.

 

 

Which Approach Is Best?

There are many weight loss techniques and lots of different approaches, ranging from Weight Watchers to Homeopathy and Hypnosis. No doubt there are some people who are permanently helped by any of these approaches. Comparing success rates scientifically you find that the behavioural approaches win hands down, although permanent success rates are still very low.

 

Behavioural approaches work best when “psychological readiness” is built into the programme. In other words, people need to be emotionally clear, not have other major issues to wrestle with, know how to elicit support from significant others be trained in the methods of maintaining commitment, and develop skills for dealing with lapses.

 

It is the greatest challenge of psychological medicine to fit the person to the right programme. People tend to blame themselves when they fail to lose weight and serious emotional damage can be done by exposing an overweight person to an unsuitable regime. Also there is evidence that repeated cycles of weight gain and weight loss can make it progressively harder for weight to be lost at all.

 

In general, moderate obesity responds best to a behavioural programme. Severe obesity responds better to the more aggressive approaches always under medical supervision.

 


Conclusion

Obesity is a complex issue. There are loss of different types of obesity with different causes.

It has different physiological and psychological manifestations and cannot be explained by a single label such as “gluttony”

 

There are no single guaranteed treatment programmes for obesity and individuals must be matched to treatments and any programme undertaken must be sensitive to personal motivation and the personal factors which affect long term commitment. The search is still on for a safe drug therapy which will reduce body fat, it being recognised that such a programme will have to be continued for the lifetime of an individual.

 


THE CAUSES OF OBESITY - IMPLICATIONS OF THE FAT CELL

What Is A Fat Cell?

Fat cells are the body’s storage depots for fat. Persons of average weight have 25 - 35 billion fat cells. Persons with severe obesity may have as many as 100 - 150 billion cells. Fat cells expand and contract as weight is gained and lost. There appear to be two critical periods for fat cell development ; the second year of life and, for females adolescence. Although these are the times when the number of fat cells increase most dramatically, new fat cells may be formed at any time a significant weight gain occurs.

 

 

Weight Gain And Fat Cells

The causes of overweight are multiple and varied. Independent of the cause, however, the effect is an excess of trigylceride or fat. This excess fat is stored in fat cells distributed throughout the body. The initial response to weight gain is to increase the size of fat cells. They do so in a manner similar to a balloon expanding to accommodate increase in air or water. As weight gain continues, fat cells reach their limit in capacity for storing fat. At this point, new fat cells are formed.

 

The degree of overweight at which new fat cells are formed is not exactly known, but it is estimated to be approximately 50 - 60% above ideal weight. Studies which have examined fat cell size across a wide range of body weights indicate that individuals with mild obesity have increased fat cell size called HYPERTROPHIC OBESITY. Moderate obesity is characterised by both increased size and an increase number of cells. Severe obesity results in no further increase in size, but a marked increase in number - known as HYPERPLASTIC OBESITY.

 

 

Weight Loss And Fat Cells

During weight loss, fat is mobilised from fat cells to provide energy. Since less fat is in the cell, the cell size is reduced. There are limits however on the degree to which the size of a fat cell can be reduced. Just as fat cells have an upper limit for storage before new cells are formed, they also have a lower limit. An average fat cell weighs 0.4 to 0.6 micrograms. Extreme cases, such as anorexia can result in fat cells being reduced lower than this, but in general fat cells are resistant to shrinking below their normal range.

 

One example of this biological defence is a s study by Per Bjorntorp and his colleagues in Sweden, They studied 26 patients who were losing weight and measured the fat cell size of the patients before weight loss and again when they stopped losing weight. Despite the fact that the patients varied greatly in their fat cell size before weight loss, 23 out of the 26 patients stopped losing weight when their fat cells reached between 0.4 and 0.6 micrograms. Some of these people were still overweight, however, because they had an excess number of fat cells. This study suggests that fat cell size may determine how much weight can be lost.


An equally interesting finding from this study was that when fat cells were reduced through dieting to below normal size, IRRESPECTIVE OF THE ACTUAL WEIGHT OF THE INDIVIDUAL, there was a significant increase in symptoms of eating disordered behaviour, cravings, depression, and ritualisation of eating behaviours.

Fat cell size is reduced by weight loss, but what about fat cell number? Unfortunately a fat cell is a friend for life. Although some cases of reduced fat cell number have been reported with extreme weight loss, it is believed that fat cell number does not decrease with weight loss.

 

 

Implications For Weight Loss Goals

Since fat cell number can not be reduced with weight loss, the number of cells may identify how much weight a person can lose. If Mary has 40 billion fat cells and Joan has 60 billion , and both are enlarged to the same degree, if they diet they will both lose weight but Joan is destined to remain at above average weight. Her cells may be normal in size but excess in number and she will carry extra weight.

 

 

How Are Fat Cell Size And Number Determined?

Fat cell size and number are assessed by first determining the total amount of body fat. The most reliable method is underwater weighing. The difference between the weight in water and the weight outside can be used to calculate the density of the body, and from this measure of density the percentage of fat and muscle can be determined.

 

Once total body fat is determined, fat cells are removed from various parts of the body including buttocks and thighs. These cells are examined microscopically and measured for cell size. Total body fat is then divided by fat cell size to determine number.

 

In general, anyone who is overweight has increased fat cell size. Increased fat cell number is likely in people with childhood onset obesity or who have had significant weight gain in adulthood.

 


Distribution Of Fat

Fat cells are distributed throughout the body. Where the excess fat is stored has implications for health. Upper boy or android obesity is characterised by fat in the u[per body - abdomen chest and arms’ Lower body or gynoid obesity is where fat is distribute below the waist , hips thighs and legs. Upper body obesity is more prevalent in men and lower in women, although there are exceptions.

 

Waist to hip ratio gives an indication lower body obesity. Over 0.8 and 1.0 in men indicates upper body obesity, which is associated with increased risk of heart disease, stroke and diabetes.

 

 

Summary

Fat cell size and number have important implications for weight control. Significant increases in weight are associated with increase in fat cell number. Increased fat cell number can prevent the attainment of an ideal weight because fat cells will resist being reduced below normal levels.

 

Increased fat cell number is associated with childhood onset obesity, or severe weight gain in adult life.

People with increased fat cell numbers should set realistic weight loss goals and recognise the difficulty they may have in reaching an ideal weight.

 

Upper body obesity is more dangerous than lower body obesity.

 

 

THE CAUSES OF OBESITY - RESTING METABOLIC RATE

It is possible that one of the inherited pre-dispositions to obesity is reduced energy expenditure. Total energy expenditure is the sum of all the energy our body requires for rest, digestion and physical activity. Before reviewing what we know about energy expenditure and overweight lets review some basic of energy balance.

 

 

The Energy Balance Equation

Body weight is determined by the energy balance equation

  • If energy in = energy out, weight maintenance occurs.
  • If energy in exceeds energy out, weight gain occurs.
  • If energy in is less than energy out, weight loss occurs

Weight gain is the result of more energy coming into the body than the body is burning or expending. Energy comes into our body through the food we eat. Each food contains a certain amount of energy measured in calories.

 

Energy is used or expended by our bodies in three principal ways. The first is resting metabolic rate (RMR) which is the energy needed to keep our body functioning at rest, in breathing, heart pumping, digestion etc, and it accounts for 60-70% of all the energy we expend in one day. The energy required to digest and process the food we eat is approx. 10% of our total daily energy expenditure, and is called the thermic effect of food. The last and most variable component of energy expenditure is physical activity. Even persons who are not physically active spend 15 - 30% of their expenditure on every day activities.

 

Highly trained athletes may spend more energy on physical activity than their RMR.

Although all 3 components of energy expenditure may play important roles in the development of obesity, RMR is the primary focus of this discussion.

 

 

RMR In Lean And Overweight Individuals

Since most of the energy we expend is in RMR, a number of researchers have explained the relationship between RMR and overweight. One approach has been to examine differences in RMR between average weight and overweight individuals,. Studies have shown that overweight people as a group have a higher RMR than their lean counterparts of the same age, sex and height. Because these individuals weigh more, more energy is required to sustain the extra weight. The increased RMR is generally in proportion to the increased weight. The comparisons of RMR of lean and overweight individuals, however, are of limited use in understanding why obesity develops, because they describe the RMR of people after they are overweight.

 


RMR In The Development Of Overweight

A better way to determine the role of RMR in the development of obesity, is to follow people over time and determine whether a low energy expenditure is associated with weight gain. Two recent studies have done just that. One study by Dr Susan Roberts and the Massachusetts Institute of Technology, and her colleagues at the Dunn Nutrition unit in England, examined infants born to 6 lean and 12 overweight mothers. 50% of the infants born to the overweight mothers became overweight while none of the infants born to lean mothers became overweight.

 

The researchers found that the children who had become overweight at the end of one year had a 21% lower energy expenditure at 3 months than those children who had not become overweight.

 

Dr Eric Revussin and his colleagues at the National Institute of Health examined the contribution of increased energy expenditure to weight gain in a group of 286 SW American Indians. The researchers studied 3 groups; those with a low, medium or high RMR.


Of 89 subjects followed for 2 years, less than 5% of those with a high RMR gained 20 + lbs, while over 25% of those with a low RMR gained + 20 lbs. People with a low RMR gained an average of 6 lbs a year compared to a 0.2 lbw increase for those with a high RMR.

 

These studies suggest that a low total energy expenditure and / or a low RMR may contribute to weight gain and subsequent obesity. Both of the studies indicate that decreased RMR or total energy expenditure does not account for all of the weight gain - suggesting that environmental factors ( calorie intake) and / or biological factors ( fat cell size and number ) may also contribute to increased weight.

 

 

Relevance Of RMR To Weight Control

In addition to its role in weight gain, RMR certainly plays an important role in long term weight control, in fact, studies have shown that RMR is the single most important factor determining weight lost, where a specific number of calories are consumed. Is there any way to know what your RMR is? Conventional wisdom based on the pioneering studies of Harris and Benedict, 1990, suggest that age, weight height and sex were the key determinants of RMR, specifically male individuals who are younger heavier and taller would have a higher RMR than older lighter and shorter females, and therefore would be expected to lose more weight given the same calorie intake.

 

Recent studies have shown that these original assumptions about age weight height and sex may not be true, particularly for the overweight.


In a study done at the University of Pennsylvania in Columbia State university, Dr Waceen compared the predicted RMR based on age, weight height and sex, to actual RMRS in 80 overweight women. He found that the predictions were accurate for less than 60% of the women. A more striking finding was the marked variability of RMRs among the overweight.


He compared the measured RMR of 5 women who were the same age, weight and height. Theoretically these 5 women would have the same RMR - approx. 1740 calories per day. The RMR of these 5 women varied by almost 1000 calories per day. If they consumed a 1200 calorie a day diet for 3 months they would all lose different amounts of weight - between 11 and 40 lbs. Based on their predicted RMR, all 5 women would be expected to lose 27 lbs.


This study suggests that estimates of RMR are not useful in overweight people. This study also reveals that the RMR of individuals varies greatly, suggesting that weight losses among people will be very different even when they consume the same number of calories.

 

 

What determines this difference?

Several researchers have shown that RMR has a strong genetic component. Bogardus and his colleagues in Phoenix showed a high similarity in RMR within families, while Dr Bouchard and others at Laval University in Canada showed that genetic factors accounted for 40% of the differences in RMR when he examined parent- child groups, identical twins and fraternal twins. These studies do not suggest that genetics is the only determinant of RMR, but it does play SOME role in addition to age, height and sex.


Muscle also influences RMR - the more muscle you have the higher your RMR. This exercises that increase muscle mass ( e.g. weight training) may increase your RMR.

 

Effects of dieting on RMR

It is well documented that the body adapts to calorie restriction by decreasing RMR. This reduction in RMR concerns dieters, because if it persists after dieting, weight control will be more difficult. In any event RMR will decrease after dieting because a person weighs less - there is less body weight to sustain. For example it should take approx. 10% less calories to maintain weight after a 10% weight loss. The critical question is, whether the decrease in RMR is more than that expected from the decrease in weight.

 

Recent studies have provided good news in this regard. Although the short term drop in RMR in response to calories restriction is dramatic, the long term change is what would be expected from the decreased weight. This seems to be true whether the diet is moderate or more severe. Thus, after weight loss, people need fewer calories to maintain their weight than before weight loss. Lighter bodies need less energy. Exercise combined with dieting may be more helpful in preserving RMR, although this is still a matter of controversy.

 

 

Summary

Although overweight people have a higher RMR than their average weight counterparts, a low RMR seems to contribute to weight gain and subsequent obesity. RMR is extremely variable in the overweight , and this variability will result in different weight loss even when people consume the same diet. There is some evidence that dieting has no long term effects of RMR other than that predicted from weight loss. Although RMR may be under the influence of genetic factors and age, sex and height, choosing diets that minimise muscle loss and choosing activities that increase muscle mass, may increase RMR.

 


The Genetics Of Obesity

The question of genes vs environment has been highly debated in recent years and encompasses a wide variety of both physical and psychological characteristics. These characteristics include intelligence, athletic ability, heart disease and schizophrenia. Such traits are often examined within families for their genetic or environmental influences. For example, do you prefer certain foods because everyone in your family ate them as you were growing up ( (environment), or are the shared taste preferences in your family a result of heredity (genes).

 

As you might suspect, body weight is one trait that has attracted a considerable amount of attention. It is well known that obesity runs in families. For example, children with two obese parents have an 80% chance of being overweight, compared to 40% for children with one obese parent and 20% when neither parent is obese. One scientist even went to the extreme of documenting that obese pets are almost twice as prevalent in obese households as non obese households. These findings have been used to argue that environment is the key.

Because facilities share a common environment and common genes, it has been difficult to separate nature and nurture. However, studies in the last 5 years have greatly clarified the role of environmental and genetic factors. We will review what is known about genetics and what it means for weight control.

Adoption Studies

An intriguing method for assessing the genetic influence on body weight is to study adoptees. They are ideal for two interesting reasons. First, studying this group who are not biologically related to their adoptive parents allows scientists to attribute any similarities between adoptive parents and their children to environmental factors. On the other hand, similarities between adoptees and their biological parents can be attributed to genetic factors.

 

Dr Albert Stunkard at the University of Pennsylvania, and other colleagues, have recently conducted several studies on the role of heredity in determining body weight. In 1986, he and Dr Sorenson studied 504 adoptees and their biological and adoptive parent using the Adoption Register in Denmark. Denmark was chosen for this study because its adoption records are unusually comprehensive and include information about weight and height for adoptees as well as for both sets of parents. The adoptees were separated from their biological parents early in life, so they were not influenced by their biological parents eating or exercise habits.
The results were striking. The weights of the adoptees more closely resembled the weights of their biological mothers. The next strong resemblance was with the weight of the biological fathers. There was no relationship between the weights of adoptees and their adoptive parents. These findings were the first to document a strong genetic component in human obesity.

 

 

Twin Studies

Another method of separating genetic traits from environmental traits is the study of twins. In twin studies researchers study both identical and fraternal twins.


Stunkard examined 1974 pairs of identical twins and 2097 pairs of non identical twins in Sweden. Most of the variability in body weight was explained by genetic factors, which confirmed the heredity study of adoptees.


An even more interesting way of studying twins is to compare identical twins who have been raised apart. Twins raised together share the same genes and the same environment. Making the distinction between genes and environment is difficult. Twins raised apart have only their genes in common.

 

Stunkard and colleagues examined 673 pairs of twins, of whom 93 were raised apart. The body weights of the twins was the same irrespective of whether they had been raised together or apart, suggesting that environment plays almost no role in the development of body weight!

 

Dr Claude Bouchard in Canada has done much work on the power of genes on the ability of the body to gain weight. They took 12 pairs of identical twins and overfed them by 100 calories for 100 days. The results were remarkable. There was high variability of weight gain between different sets of twins but great similarity within each pair. One pair gained 9 lbs and one pair gained 29 lbs. Even though people vary in the way they gain weight ( even when given the same calorie intake ) these gains are largely under the influence of genes. The twins not only gained similar weight, they distributed the excess Wight in the same places i.e. some on the stomach and some on the thighs.

 

 

What Does It All Mean?

You may be thinking what’s the use, its all in the genes! Genes DO influence body weight as well as the ability to gain weight and store fat. It may seem unfair that some people have a genetic tendency to gain weight while others eat whatever they like without gaining an ounce. These facts however do not mean that you cannot control your weight.

 

Obesity is not a trait like eye colour, which is determined at the moment of conception and does not change. A tendency for obesity is inherited This tendency needs to have an environment that will nurture its development before it becomes a reality. All of the studies above were conducted in western industrialised societies that consume a large percentage of their calories as fat.

 

These societies are also characterised by an increasing dependence on labour saving and calorie saving devices such as remote controls, garage door openers, electric can openers, computers, cordless telephones and so forth. The message should now be coming into focus. Changing eating and exercise habits can make a difference, even if an individual has been born with the genetic tendency to store energy.

 

Modifying the environment to decrease high fat food and to increase physical activity will lower the chance that a genetic tendency will become a reality. Many medical disorders such as diabetes and high blood pressure are influenced by genetic factors but can be controlled by diet and exercise.

 

These studies give us insight into why some people become heavier than others, and why some people have to struggle more in their attempts at weight control. We hope these findings also provide some relief. There is now scientific evidence for what you may have suspected for years. Overweight people are not weak willed or lazy. Losing weight and keeping it off may not be as easy for some as it is for others, if a tendency to be overweight is inherited. Weight control may not be easy, particularly if you have inherited the tendency to be overweight but it can be done. Providing an environment of low fat foods and increase physical activity can stifle even the most stubborn genes.

 

 

THE CAUSES OF OBESITY - GENETICS Ctd

The Ob - Gene

Farmers have known for centuries that they could selectively breed animals for fatness or leanness. Scientists also know that selective breeding indicates a genetic influence in laboratory rats and mice.


Recently, research has shown that certain strains of lab animals become massively obese because of the effects of a single gene, i.e. there is one gene among the many in animals that seems to account for its obesity. Although the leap from mice to man must be made cautiously, these observations suggest that some obese people are obese largely due to the effects of a single gene.

 

For the sake of science, a genetically obese persons is defined as one who would be obese even in an environment in which less that 10 per cent of the population would be obese. With this definition in mind, scientists estimate that only approx. 21% of people who are obese are genetically obese.

 

 

Leptin

An obesity gene has been identified in mice, but so far no single human has been identified with this mutation. However, there is a protein, LEPTIN, produced by the OB Gene that circulates in the blood of humans. It is believed that Leptin acts on the brain to signal satiety and thereby reduce food intake. Injections of Leptin reduced feeling and weight in mice. Thus far however, no human has successfully been treated with injections of Leptin, which is at present expensive to produce ( $millions for a vial).

 

 

The DB Gene

The diabetes gene is of greater significance to weight control in humans. It is believed that DB codes for the receptor of the OB protein., enabling humans to experience the effects of Leptin.

 

 

Does Genetics Affect Metabolism?

It is hard to separate the effects of genes on metabolism compared to behaviour. However Dr John Castro carefully monitored fraternal vs identical twins eating habits, and found that identical twins were significantly more similar in what they chose and how they ate. This leads us to assume that eating habits and exercise patterns ARE influenced by genetic makeup.

 

 

Genetics Versus Environment

Genetic studies have taught us two very important things about the effect of environment on obesity.
First, most environmental influences on weight gain are “unique” rather than “common” environmental influences. ‘Unique’ means circumstances each individual experiences in his own life. Common refers to factors shared by members of a group - like all living in the same house.


Secondly, environmental influences are transient in nature. This means that growing up in a healthy eating household does not guarantee that these eating habit will be maintained as an adult.

 

 

Summary- “Fat Is A Cultural Issue”

As a society the only way we can reduce obesity is through environmental changes, not just target specific families or persons. These changes must be pervasive and enduring. This is thus far the only way to reduce ever increasing obesity in our society.

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