TPE européen : Child obesity

Observation: child obesity in every day life

A. Definition of child obesity
Obesity is a medical condition characterized by abnormal or excessive fat accumulation in the fat tissues (which are also called adipose tissues). Children are considered obese by doctors and health professionals when their BMI (Body Mass Index) is superior to 20 if they are between 2 and 12 years old and 25 if they are 13 or more.
In obesity there are two degrees, degree1 which defines the overweight and degree 2 which defines pure obesity. The specialists use the BMI (BMI= weight / height²) in order to calculate if they are obese or not, and they confer with two different charts, graphs showing obesity in boys and obesity in girls. We have different type of obesity. Firstly on the graph we can see a zone showing a risk of being overweight, that zone is a slightly above the zone for normal people. Thus the people in this case are not so worrying. Then we have the overweight zone for obese people.

Let's take a look at these graphs: We can observe one graph for girls and another for boys.

We can see the graph which compares girls' BMI and boys' BMI: it depicts the difference between those two, so it explains why we have two different graphs !

B. Causes of obesity
The causes for obesity today have not been completely understood. However, it is a well-known fact that there are endless factors which cause this serious disease, some which appear to be very simple and others very complicated. Yet, in fact, being overweight and obese is the result of an energy balance over a long period of time, that is to say when consumed calories are greater than used calories. Energy balance for each individual depends of several factors, individual behaviour and environmental factors all contribute to the complexity of the obesity epidemic.
Furthermore, lipidic molecules are critical for good health, because they are foundations of cells membranes and source of energy when the body lacks the energy necessary to sustain life process. Indeed, if these lipids are not used, they are accumulated in the body. For every 7 500 calories, our body accumulates a weight gain of 1kg!

1. Lifestyle, main cause of obesity
The main cause of child obesity is lifestyle. Indeed, people of the 20th century have changed their tastes and it differs according to each person. So, various types of food are made in different restaurants (fast food, Chinese...) to satisfy people's demand. Furthermore, nowadays people eat more, during a meal because of larger portion sizes. People also eat at restaurants more frequently than in the 1970's ; and restaurants serve larger portions of caloric food than those made at home further more the indiscriminate increase of fast food restaurants increase the risk of obesity. All this may lead to the consumption of excessive calories, if people and children abuse this; that is to say, the consumed calories exceed the calories needed.

2. Advertisement, recent cause of obesity
Over consumption is also due to misleading advertisement which aims at attracting our curiosity. In this way, the influence of the media traps us into buying these new products which make us grow bigger and thus which increase the rate of obesity. Indeed, the media is an important aspect of life in our culture. About 95% of people own a TV set and watch it for an average of 3- 4 hours per day. By the end of the last century over 60% of men and 50% of women read a newspaper each day and nearly half of them are all girls, from the age of 7 read a girls magazine each week. A lot of advertising is devoted to the selling of foods that contribute to obesity. In particular, they are heavily advertised on television and specifically in connection to programmes that children watch. This is especially worrying partly because of the great increase in childhood obesity and partly because the food habits we acquire when we are young tend to persist throughout our lives.
Representatives of the food industry naturally disclaim any responsibility. They argue that it's the parents that decide what their children eat. Advertising, they claim, has no effect. It may sound odd that they are spending millions of pounds on something that they don't think helps them make money.
This is one aspect of their policy which has largely been ignored. This is the fault of the media which promotes unhealthy eating attitudes and which may be contributing to a national epidemic of obesity, which in itself will provoke damaging eating strategies as our ever expanding nation seeks to control its weight. An individual watching television for 2 hours per day will see over 20 000 food advertisements in one year, most of them promoting high in sugar and fat foods. The problem is ever worse for our children. During child-friendly broadcasting hours, they are exposed to a continual stream of advertisements for sweets, chocolate, and sugar laden cereals. This type of media supports the food industry and contributes to a significant effect on future problems with eating and with weight.

3. Physical inactivity contributes to obesity
However, changing lifestyles during the last century also reduced physical activity and this change is an important factor concerning the increase of children affected by obesity.
Children spend more time playing video games, surfing on the Internet, watching television instead of practising physical exercises, work enthusiastically during the sports lessons taught at school. In addition, many daily activities are facilitated by modern progress such as cars, buses, elevators, computers (to buy something without moving)... So, this lack of physical effort has reduced the overall amount of energy expended during the course of the day, contributing to the development of obesity. In addition to the lack of healthy foods, it increases obesity.

4. Psychology and parents also play a role in childhood obesity
Obesity is also due to psychological changes according to recent researches as a cause and also as a consequence because psychological problems can influence the risk of people to become overweight.
In fact, parents have a great role to play in preventing childhood obesity. Parents have a strong influence on whether or not their children will become overweight or obese. When children grow up in households with bad eating habits and sedentary lifestyles, they are 33% more likely to become overweight or obese when they become young adults.
In addition, good self-esteem has a positive influence on body weight, and children whose parents received a higher level of education have a decreased risk of being overweight or obese.

The first graph shows that the relationship between parents and children influences their body weight control the most, but advertisement is the second major cause of the influence. To conclude, we can observe that the parents' responsibility and the advertisements have a great control on child obesity.

The second graph shows that 35% of the people in question cited lack of parental control over their children's diets, and 32% answered the growth in sedentary activities such as TV and computer and video games. 14% blamed too little physical education in schools, and 15% cited the heavy marketing of food and drink to kids.

Moreover, the consequences of obesity are many and varied, ranging from an increased risk of premature death to several non-fatal but debilitating and psychological complaints that can have an adverse effect on the quality of life.

C. Consequences of child obesity
1. Obesity causes social problems
Obese children are more likely to show evidence of psychological distress than non-obese children are and the effect is greater in girls and in boys. Obesity is associated with poor self-esteem, being perceived as unattractive, nervous breakdown, eating disorders, and body dissatisfaction.
Psychological distress and psychiatric disorders in children may be associated to parental psychological or psychiatric problems.
People have to contend with discrimination because in today's society, an obese person is not easily accepted and especially if it is in relation to a woman. For example, at school an obese person is not allowed to play with the rest of the children and is always the object of mocking and segregation, these people are mostly discriminated against. In this way, because of continuous rejection by today's society, obese children show all their feelings in eating constantly which leads to more and more serious problems.

2. Medical consequences

Then, obesity leads to many health problems such as heart and respiratory diseases, hypertension and some cancers, as well as early death.
The abdomen is more rigid and a bigger force is needed to displace the thoracic muscles for breathing so the person gets tired easily and has difficulty in breathing, even though in short movements, for what has to frequently interrupt walking as well as the rest.
When lungs are more rigid as previously mentioned, an increase of the lung's blood level takes place: small exchanges are formed in those zones where accumulations of blood can be formed and small thrombosis present, unleashing a pulmonary thrombosis.

Due to the excess of fat in the body caused by obesity, fat is deposited into the cerebral arteries and the flow of blood slow down each time, because diameter of blood vessels become narrow. So that, it easily clog, causing a vascular cerebral accident.
The same problem of overweight spoils joints: sedentary diminishes the transitory of the synovial liquid and their nourishment contribution, causing arthritis in the lowest members of the vertebral column, which can cause easily an inter-vertebral disc hernia.
What's more is that cohort and case control studies provide good evidence of a link between childhood obesity and cardiovascular and other risk factors. American post mortem studies for example have demonstrated consequences of childhood obesity such as atherosclerosis (which adverse lipid profiles) and coronary artery disease (sometimes due to a family history of coronary artery disease). Cardiovascular diseases account for a large proportion (up to one third) of deaths in men and women in most industrialised countries and their incidence in developing countries is increasing.
The accumulation of fat in obese people occurs in the subcutaneous tissue where it is deposited. The skin is composed of elastin, which provides a certain capacity for its elasticity and makes room for this excess fat. But it reaches a limit, which makes this tissue break and thereby forms stretch marks which, depending on the degree of obesity and genetics of each individual, the distribution and intensity differ. In the same way, when the skin breaks it starts to pigment these zones because the melanin uses it as a means to defend the breaking of the skin.
Obesity also provokes risk of developing asthma and the exacerbation of pre- existing asthma.
Although the link between obesity and cancer is less well defined, several studies have found an association between overweight and the incidence of certain cancers, particularly of hormone-dependent and gastrointestinal cancers. Greater risks of breast, endometrial, ovarian and cervical cancers have been showed in obese women, and there is some evidence of an increased risk of prostate and rectal cancer in men. The most obvious link is with cancer of the colon, for which obesity increases the risk by nearly three times in both men and women.
Indeed we can notice that from 30% to 20% obese children are likely to be affected by diabetes at the adulthood.

Main question: Over all, we have already observed how lifestyle provokes obesity and its consequences more precisely. On top of that, we have noticed that children that have obese parents are more frequently obese. Indeed, 70% of obese couples have obese children, 40% of them have obese children if only one parent is obese and only 10% of non obese parents have obese children.
So does hereditary fragility play a role in child obesity?

Hypothesis: Obesity is due to genetic roots.

Experimental validation of what about genetic in Child Obesity

Lipid excess is associated with a variety of health problems. Studies show that individuals who are obese run a greater risk of developing diabetes, hypertension, heart disease and even some forms of cancer. The real cause for the accumulation of fat is lifestyle, that's why, some specialists; for example, dieticians and health professionals, are there to help obese people. But sometimes it is a genetic problem, that's why, there are researches on obesity. Here is an example:

A. Protocol

The maintenance of body weight stability requires that energy intake and energy expenditure must be regulated.
A experiment was done on 13 men who were between 18 to 27 years old. Thirteen young males were studied, six were lean (BMI < 24 kg/m2) and seven were overweight (BMI > 27 kg/m2). All participants were healthy, non-diabetic, non-smokers, taking no oral prescription medications and with a stable body weight during the previous three months. The characteristics of the 13 participants are shown in Table 1. The intervention was approved by the Clinical Investigation Ethical Committee of Navarra.

Table 1. Characteristics of
the 13 Study Participants in Basal Conditions

Leptin, the product of the ob gene, is presently assigned to have a critical function in the regulation of body weight, playing a key role in the regulation of body fat mass. This hormone, produced mainly by the adipose tissue, conveys information to the brain about the size of energy stores and activates hypothalamic centres that regulate the energy intake and energy expenditure. Serum leptin levels are elevated in obesity and usually correlate with body fat content and insulin both in lean and obese individuals.
The protocol consisted of a three-day baseline period followed by one experimental day. During the three-day baseline period participants consumed a eucaloric diet designed to maintain body weight, which provided 55% of energy as carbohydrates, 15% as protein and 30% as fat. On the experimental day, participants entered the metabolic unit between 07:30 and 07:45 a.m. (after a 10-hour overnight fast) and remained until 8.00 p.m. After the assessment of body weight and body composition, participants lay on a bed for 30 minutes until resting energy expenditure by indirect calorimetry was determined. A venous catheter was inserted into an antecubital vein for blood sampling. The fasting period was prolonged during 7.5 hours in order to obtain a depletion of glycogen stores and match all individuals for glycogen reserves
Some biochemical measurements were done by collecting blood samples before and after the high CHO load intake. They were frozen and centrifuged immediately and then stored at -40°C before essay. Enzymatic determinations were performed to measure serum glucose, free fatty acids and triacylglycerol concentrations. Insulin was analyzed by duplicate radioimmunoassay, Serum leptin levels were assessed with an enzyme-linked immunosorbent (ELISA) kit supplied by Diagnostic System Laboratories, USA.

B. Results
The pre-meal fasting values (measured after 17.5 hours of fasting) were significantly higher in overweight men for serum leptin, glucose and insulin as shown in Table 1. The Post absorptive leptin levels were found to be positively correlated with body fat in kg, serum insulin and triglycerides. After the high-CHO intake, both glucose and insulin increased in the two groups, (Table 2) between lean and overweight men in glucose, insulin, FFA or triglycerides concentrations. One hour after meal intake we saw a positive association between the leptin concentrations and the serum insulin as well as with body fat mass, triglyceride levels.

Table 2. Changes Measured over the Four hours after Meal Intake as Calculated by the Incremental Area under the Curve Taking into Account the Pre- and Post-Meal Values.

We also found that over the measured post-meal period, overweight men presented significantly higher energy expenditure as well as a significantly lower carbohydrate and lipid oxidation compared to lean men (Table 3).

Table 3. Cumulative Energy Expenditure (EE) and Nutrient Oxidation over the Four Hours after Meal Intake1

It has also been suggested that carbohydrate intake may have an important role in the regulation of leptin levels, possibly due to insulin mediated-changes in adipose tissue glucose disposal. Pre-meal and 60-minute post-meal insulin levels correlated positively with leptin concentrations, in agreement with data from others studies.

The rise in plasma leptin observed during weight gain and obesity may be a consequence of resistance to leptin action, which could consequently promote a greater fat accumulation and other metabolic changes. The data concerning macronutrient metabolism indicates that, after carbohydrate intake, insulin-inhibited lipid utilization was more pronounced in overweight individuals and was accompanied by higher circulating leptin levels. Furthermore, leptin has been implicated in controlling insulin release by inhibiting insulin expression and its anabolic effects on adipose tissue and also in promoting lipid oxidation in other tissues. Accordingly, resistance to leptin action or a reduced leptin sensitivity in these overweight subjects could subsequently be responsible for a lower lipid oxidation in the presence of carbohydrates.

C. Interpretation

Leptin is a protein considered as a peptide hormone that is produced by fat cells. It plays a role in body weight regulation by acting on the hypothalamus to suppress appetite and burn fat stored in adipose tissue. The hormone leptin, produced by adipocytes (fat cells), was discovered about three years ago in mice. Subsequently the human Ob gene was mapped to chromosome 7*. Leptin is thought to act as a lipostat: as the amount of fat stored in adipocytes rises, leptin is released into the blood and signals to the brain that the body has enough to eat. However, most overweight people have high levels of leptin in their bloodstream, indicating that other molecules also effect feelings of satiety and contribute to the regulation of body weight.

*: let's see the diagram of this chromosome 7, where we can see four genes with obesity severe due to leptin deficiency; obesity morbid with hypogonadism:

As the leptin is a protein let's see how it is formed in our cells: here is a diagram which depicts the protein's metabolism of construction:
Process whereby DNA encodes for the production of amino acids and proteins. This process can be divided into two parts:
1.Transcription : Before the synthesis of a protein begins, the corresponding RNA molecule is produced by RNA transcription. One strand of the DNA double helix is used as a template by the RNA polymerase to synthesize a messenger RNA (mRNA). This mRNA migrates from the nucleus to the cytoplasm. During this step, mRNA goes through different types of maturation including one called splicing when the non-coding sequences are eliminated. The coding mRNA sequence can be described as a unit of three nucleotides called a codon.
2.Translation : The ribosome binds to the mRNA at the start codon (AUG) that is recognized only by the initiator tRNA. The ribosome proceeds to the elongation phase of protein synthesis. During this stage, complexes, composed of an amino acid linked to tRNA, sequentially bind to the appropriate codon in mRNA by forming complementary base pairs with the tRNA anticodon. The ribosome moves from codon to codon along the mRNA. Amino acids are added one by one, translated into polypeptidic sequences dictated by DNA and represented by mRNA. At the end, a release factor binds to the stop codon, terminating translation and releasing the complete polypeptide from the ribosome. The protein, here leptin, goes to a blood vessel then to join brain in order to ensure its function. One specific amino acid can correspond to more than one codon. The genetic code is said to be degenerate.
Several studies have suggested that short-term energy balance has an impact on circulating leptin levels. No statistically significant changes in leptin levels during the four hours following CHO intake were observed, either in lean or overweight men; this is in agreement with a previous report in which leptin response to carbohydrate intake is delayed for four to five hours after meal intake. Thus, the apparent lack of response observed in our volunteers may be due to the short-time measurement period, since food ingestion may have a delayed effect on circulating leptin levels.
Carbohydrate intake may have an important role in the regulation of leptin levels, possibly due to insulin mediated-changes in adipose tissue glucose disposal. The rise in plasma leptin observed during weight gain and obesity may be a consequence of resistance to leptin action, which could consequently promote a greater fat accumulation and other metabolic changes. The data concerning macronutrient metabolism indicates that, after carbohydrate intake, insulin-inhibited lipid utilization was more pronounced in overweight individuals and was accompanied by higher circulating leptin levels. Furthermore, leptin has been implicated in controlling insulin release by inhibiting insulin expression and its anabolic effects on adipose tissue and also in promoting lipid oxidation in other tissues .Accordingly, resistance to leptin action or reduced leptin sensitivity in these overweight subjects could subsequently be responsible for a lower lipid oxidation in the presence of carbohydrates.
In our study, a negative association between protein and carbohydrate oxidation was found. Obesity is characterized by some muscle insulin resistance, which could be responsible for a lower insulin induced muscle glucose disposal and a subsequently higher protein utilization as fuel substrate showed by overweight men, although the later measurement was not statistically significant.
We observed no relationship between EE (absolute values or corrected for fat free mass) and leptin values both during fasting and after load intake. These results may be due to the small number of subjects or to the fact that lean and overweight men have a distinct sensitivity to leptin which could explain the lack of association between leptin and EE.
In a previous study, it was reported that postabsorptive serum leptin was inversely correlated with NPRQ ( non-protein respiratory quotient ) in obese individuals, with leptin concentrations higher in those subjects with low NPRQ. Interestingly, we found a positive trend (p = 0.09) between fasting leptin and NPRQ values and a strong positive relation (p < 0.01) between leptin concentrations and NPRQ values in all post-meal measurements. These findings indicate that higher leptin values were associated with higher proportion of oxidized carbohydrate in relation to fat, confirming the hypothesis that some degree of peripheral leptin resistance in overweight subjects may reduce lipid oxidation, at least after carbohydrate intake.
If one accepts that leptin values are an index of the degree of obesity and that a low rate of fat oxidation is considered a metabolic predictor of weight gain, it may be speculated with these data that circulating levels of leptin may also indicate fuel substrate utilization in obesity. Although further investigation in the impact of circulating leptin on fuel metabolism after food and macronutrient distribution intake is needed, these data suggest that the reduced fat oxidation commonly observed in the obese state may be, in part, due to some peripheral resistance to the lipolytic actions of leptin.

Conclusion: genetic factors of Child Obesity
Our experiments proved that the ob gene is responsible for obesity because it can prevent our body to react to leptin messages.
It has been shown that children with obese parents are more likely to become obese. One estimate says that heredity is a major factor for obesity. The remaining risk is attributed to environmental and behavioural factors. Others believe that genetics may play a bigger role. Regardless, the interrelationship between genetics and the environment is clear: parents provide genes, a model role, and food. If one or both parents are overweight, then children have a poor example being set to them. Children tend to imitate their parents. While they do not copy all of their parents' behaviours, they almost always emulate those behaviours we would most want them to avoid. However environment and genetics play a role in obesity.
Moreover we know that a child having two obese parents, has 70% of chance to be obese, and a child having one obese parent has 40% of chance to be obese. On top of that, it is known that more than 15 million French (children + adult) are affected by obesity of degree1, so we can deduce that this disease becomes more and more alarming.
We can conclude, thanks to all those elements, that Genetics have an important role. Indeed, Genetics explain why some people are affected by obesity and some other not. Learning how variations in genetics affect susceptibility to become or remain obese leaded us to a greater understanding of how obesity occurs and, hopefully, how to prevent it and treat this condition with successful outcomes.

A risk of obesity: diabetes type 2
Type 2 diabetes (the standard of diabetes which normally develops during adulthood and it is associated with overweight people) is called non-insulin-dependent diabetes mellitus (NIDDM) and has the strongest association with obesity and overweight people. Indeed, the risk of developing Type 2 diabetes is more important if someone is obese (so if the BMI reaches the number 30). On the one hand, women who are obese are more than twelve times more likely to develop type 2 diabetes than women of a healthy weight. On the other hand, the risk of Type 2 diabetes increases with BMI, especially in those who have a family history of diabetes, and decreases with weight loss.
Type 2 diabetes are characterized by a hyperglycaemia (when the glycaemia is around 1.26 g.L-1) associated to a normal or a strong insulinemy. This form of diabetes is due to an insensitivity of the muscle of the liver cellular receiver to insulin's action: one talk about the insulino-resistance. So it triggers the increase of insulino-resistance but the decrease of insulino-secretion (the caloric reduction also decreases the insulino-secretion).
Diabetes of type 2, also called "fat diabetes" represents more than 80% of cases of obese people. It affects from 2% to 5% of the European population. What's more, one third of obese people are diabetic but above all, 80% of diabetic people are obese.
It is shown that if one of the parents is diabetic the risk for the child to become diabetic is about 40%. We know that if a dizygotic twin, so who has two different alleles (an allele is a gene version) is affected by diabetes, the risk for the second one is 20%. And if a monozygotic twin, someone who has two of the same alleles; is touched by diabetes of type 2, the risk for the other person to be affected by diabetes is from 50% to 90%.

We can observe a diagram related to diabetes which summarizes what happens:
To put it in a nut shell, we have observed especially the ob gene, the leptin and the diabetes and they depict us that the obesity can also be due to genetics roots. However environmental and familial influence must also be considered as one of the main cause of child obesity.

A great thanks to the Doctor FHLEGEL Céline, a dietician and Mrs. Bucquet, the school doctor, for having answered our questions.

Bibliography
http://www.iaso.org
http://hcd2.bupa.co.uk/fact_sheets/html/child_obesity.html
http://www.medicms.be
http://www.hhdev.psu.edu/