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30 Cards in this Set

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Canadian Statistics

2004 shows that 26%, Canadian children ages 2-17 years, are overweight or obese. Many obese children do not outgrow this condition.



Many more children who are not overweight or obese will gain excess weight in adulthood. Trends in weight gain forecast that approximately 1/3 of normal weight 20 year olds will become overweight within 8 years, and approximately 1/3 of overweight 20 year olds will become obese in 8 years.

Definitions

Overweight and obesity in adults is measured using body mass index, a person’s weight, in kg, divided by the square of their height, in m2. The adult ideal for BMI lies between 18.5 and 24.9 kg/m2; overweight is defined as 25 to 30 kg/m2; and over 30 kg/m2 is considered obese.



Ideal weight is based on growth chart due to different rates based on age and gender. The U.S uses the CDC growth charts, which will allow you to see what percentile the child's weight falls within.



Obesity is defined as BMI at or above the 95th percentile for age and gender.



There are sets of parameters for Birth to age 2, from ages 2-5 years and ages 5-19 years. In this latter category, overweight is assessed as BMI-for-age above the 85th percentile, specific for gender, while the criteria for obesity is BMI-for-age above the 97th percentile and severe obesity is above the 99.9th percentile.


Statistics Canada Data

Dieticians of Canada, in co-operation with the Canadian Pediatric Society, the College of Family Physicians of Canada and the Community of health Nurses of Canada recommended the adoption of the World Health Organization (WHO) growth charts as the gold standard for assessing growth in Canadian children.



In Canada, adolescents are the age group most affected by overweight and obesity. Rates doubles in those in the 6-11 year old age group, and again obesity appeared where it had not been seen before. Obesity in the 12-17 year old group tripled, while the proportion of overweight and obese just over doubles since the previous measurements.

Casual Web

Obesity is caused by an imbalance between energy in, in the from of intake of nutrient dense foods, and energy out in the form of activity level. Obesity is not a simple problem with a single cause and there are no simple solutions.



Conditions in the family and home as well as the availability of facilities for leisure-time activities can have an impact.


Public transportation, safety and quality of health care can also contribute. Education level may impact food and nutrition choices regionally or nationally. National perspective on education, healthcare and nutrition can also complicate the picture. Internationally, media and particularly food advertising are especially important for child nutrition

Ethnicity Involvement

Certain population are more susceptible to becoming obese, which is why the proportion of obese individuals amongst first nations people and those of Hispanic and African descents are so high.



Adolescent males of Hispanic decent and adolescent African-America females appear to be especially predisposed to the development of obesity.

Genetics

The biggest predictive factor in childhood obesity appears to be obesity in one or both parents. It is more strongly correlated with maternal obesity but genetics are not the whole story. Children obviously consume the same diet as their parents and have also been shown to mirror their activity level.

Parents may not recognize the problem!

Parents are responsible for food purchases and meal preparation, their lack of awareness may worsen the problem. Parents have the greatest opportunity to make the lifestyle changes necessary to ensure the health of their children but refusal to recognize the problem may lead to continued weight gain over the remaining childhood years and maintenance of overweight or obese status into adulthood.



Besides the risks to the child's health, their quality of life may suffer due to their extra pounds. Scores of the obese children were similar to those of cancer patients.

The Economist

In 2008, the last year reported, show 19 states with obesity levels between 25 and 30, and 6 states with an obese population of greater than 30%.



The magazine that the cover image was take from, talks about days gone by when the rich were fat and the poor were thin, as opposed to today’s situation where the rich are thin and the poor are fat and there is great concern over the epidemic of obesity that is sweeping the globe.



The problem of inactivity is compounded by the fact that playing video games or watching TV is often accompanied by snacking with high fat, calorie-dense foods.




The Trouble with FAT

Obesity can lead to poor self-esteem and in some cases depression. But an additional and perhaps more serious health issue is the dysregulation of body systems leading to chronic illnesses. Those who are obese are more likely to be diagnosed with cancer, liver disease, osteoarthritis, stroke, type 2 Diabetes and any of a number of cardio-vascular diseases.




Adipose tissue, the main storage depot for triglycerides, which are the most common form of lipid consumed in a meal, was considered somewhat passive. All that changed, a little over a decade ago, when it was discovered that adipose tissue synthesizes and secretes a number of substances including hormones and inflammatory molecules, now referred to as adipokines. These secreted substances allow different tissues in the body to interact to maintain lipid homeostasis.





Constant over-consumption of food, especially high fat diets, causes dysregulation of this homeostasis and leads to the pathologies.

Liver Disease


Over-nutrition leads to deposition of fat in liver cells. Insulin resistance, another consequence of constant overeating and inactivity, further enhances this fat deposition. There is increased risk of fatty liver disease amongst obese individuals and diabetes patients but it is present in nearly everyone who is morbidly obese and diabetic. Although those with fatty liver disease may start out asymptomatic. These fat deposits can lead to increases in inflammatory activity, fibrosis and eventually cirrhosis in some cases. Liver failure can result and the chances of hepatocellular carcinoma are increased as well.


Colon Cancer


Obesity increases the risk of colon cancer, especially central obesity. A high-BMI was associated with increased risk of colon cancer, especially in men, among the Framingham Study Cohort. Waist circumference was even more strongly correlated with the chance of colon cancer and risk was found to increase linearly with increasing waist size in both men and women. It seems that visceral adiposity, or fat deposits around the central organs, creates an even greater risk than elevated BMI alone.


Osteoarthritis

Increased weight adds extra stress to bones and joints. Osteoarthritis used to be associated with advanced age but is now being seen at earlier ages, as is diabetes, another former disease of old age, especially in those with elevated BMIs. In addition to the mechanical stress caused by excess weight, studies show that the adipokines secreted by adipose tissue, mentioned earlier, may have a role to play in causing and advancing osteoarthritis.



Inflammatory cytokines, such as tumor necrosis factor-alpha, or TNF-alpha, promote cartilage degradation and the advance of this disease.

Stroke

Obesity is a known risk factor for cardiovascular disease in general but manifestation as ischemic stroke is less clear.




Chance of stroke was examined in the Northern Manhattan Stroke study with respect to waist-to-hop ratio. There was an association shown between ischemic stroke and waist-to-hip ration, even after correcting for confounding factors. Greater wait-to-hip ratio increased the risk of ischemic stroke, in both men and women although the risk was greater in men. This effect seemed to be independent of atherosclerotic risk factors, so there may be some other mechanism involved in this association. Risk of stroke from greater waist-to-hip ratio was shown at all ages but there appeared to be greater risk among those younger than 65.


Type II Diabetes (FAT)


Obesity may lead to type II diabetes over time, first due to dysregulated lipid metabolism, which then causes insulin resistance. This insulin resistance may eventually lead to hyperglycemia when the pancreas fails to be able to produce sufficient insulin to affect glucose uptake in cells. Hyperglycemia, along with altered blood flow and vascular endothelial damage may lead to diabetic retinopathy and eventual blindness.


Vascular Disease


Obesity and inactivity are two of the biggest risk factors in the development of atherosclerosis, which can cause coronary artery disease as well as peripheral vascular disease. The altered lipid metabolism that results from a constant excess of nutrients as well as a diet high in fat leads to lower levels of high-density (HDL) or “good” cholesterol and higher levels of low-density (LDL) or “bad” cholesterol and triglycerides. The inflammatory process, that is also a result of lipid dysregulation, compounds the problem by increasing the influx of macrophages into vascular tissues where they remove LDL cholesterol from circulation, creating foam cells and advancing the atherosclerotic process.


Pathophysiology of Metabolic Syndrome


Predisposition to obesity may occur even before a child is born. If the mother is affected by gestational diabetes, this can have a profound effect on a child’s propensity for weight gain down the road. In addition, children, who have been born large for gestational age, (that is, big babies) are predisposed to both obesity and diabetes.



Babies born small for gestational age are also predisposed to diabetes and obesity, and they may manifest these characteristics, usually during adolescence, when triggered by the environmental conditions of inactivity and poor diet. It is thought that the fetal environment may permanently alter metabolic processes to a more “thrifty phenotype” so that glucose homeostasis malfunctions during conditions of overabundance of nutrients. The result may be insulin resistance, increased risk of cardiovascular disease and other evidence of the metabolic syndrome.



One other predisposition to insulin resistance that has not yet been discussed is the onset of puberty. Puberty results in reduced insulin sensitivity and a compensatory increase in insulin secretion. This was first discovered because of the increase, by about 30%, for insulin by Type I diabetics entering puberty. Non-diabetic children and adolescents were then tested for insulin sensitivity and it was found to be true for all children entering puberty.


Type II Diabetes (Metabolic)


This results from the metabolic disturbances that occur when the body is constantly overwhelmed by trying to deal with an overabundance of food, especially when this is compounded by lack of activity, or sedentary lifestyle. This dyslipidemia, or disturbed lipid metabolism, also greatly increases the risk for cardiovascular disease. The levels of good cholesterol drop, the levels of triglycerides are elevated and this is true of low-density lipoprotein or LDL, the “bad cholesterol” as well.


Atherosclerotic process


Immune cells that deposit in the arteries, beginning the atherosclerotic process, take up the oxidation of this excess LDL in the blood stream. This process can begin very early in those eating a diet high in fat, especially saturated and trans fat. Fatty streaks, which are the first signs of the atherosclerotic process, have even been found in coronary arteries in children nine years of age.


Hypertension

Blood pressure is maintained in the body through the Renin-Angiotensin-Aldosterone System, as shown in the diagram. Adipocytes have also been shown to release angiotensinogen along with the other adipokines, and the amount is related to adiposity. Body mass index is positively correlated with plasma concentrations of angiotensinogen, as well as renin and angiotensinogen, as well as renin and angiotensin-converting enzyme activity.


Acanthosis Nigricans


Condition common in obesity, usually caused by insulin resistance. It is an area of hyperpigmentation, usually found in body folds, such as at the back of the neck, under the arms and in the groin area. It can appear brown to black and is an area of thicker, velvety skin. Once the underlying cause is treated, usually through diet change and increase in activity, the skin problem is resolved.


PCOS and NAFLD

Polycystic ovary syndrome is associated with obesity and hyperandrogenism, and again with hyperinsulinemia related to insulin resistance. Hyperandrogenism results in excess body hair, acne, and often-elevated levels of testosterone. Failure of ovulation appears to be the cause of cysts that develop on the ovaries and the condition is usually accompanied by menstrual irregularities.



Non-alcoholic fatty liver disease is related to obesity as well and may be caused by dysregulation of lipid metabolism. This condition can be asymptomatic but may eventually progress to cirrhosis and could ultimately lead to liver failure. Both of these conditions improve with weight loss and exercise.

Dyslipidemia

Constant excess caloric intake leads to an increase in the size of adipocytes, the cells in adipose or fat tissue. This tissue secretes “adipokines”, a combination of hormones and cytokines, which are small immune system molecules, such as TNF-alpha. Enlarged adipocytes, filled with fat, produce and secrete excess adipokines and this causes problems in normal lipid metabolism. The enlarged adipocytes also have little capacity to take in more lipids so the fat may begin to be deposited into the muscle cells.



The excess TNF-alpha causes an increase in free fatty acids in the bloodstream by causing some of the fat in the adipose tissue to break down. This cytokine also inhibits the clearance of very low-density lipoprotein (VLDL, which is the main transporter of triglycerides (and some cholesterol) in the bloodstream. The lipoproteins, which you will hear more about in pharmacology related to cholesterol transport, atherosclerosis and heart disease, are the body’s mechanism for transporting lipids (or fats) through the bloodstream, which is a water-based system.



TNF-alpha is also involved in increased production of more VLDL by the liver and lowering of levels of HDL in the circulation in response to increased adiposity, or weight gain. All of these extra circulating triglycerides and free fatty acids interfere with insulin signaling in muscle and liver tissue. Insulin, released by the pancreas after a meal, binds to receptors on cells in muscle and liver and signals the cells to take up the glucose that is flooding into the bloodstream from the digestive system. Binding of insulin leads to signaling in the cells that allows the cells to take up glucose. High concentrations of free-fatty acids in the blood interfere with this signaling, preventing the cells from taking up the glucose in response to insulin.



The pancreas produces greater and greater quantities of insulin in response to this insulin resistance. The pancreas is able to overproduce insulin to compensate for insulin resistance, for a while, which is why the first signs of impending Type II diabetes are elevated triglycerides and impaired glucose tolerance. Eventually the beta cells become exhausted from producing all this extra insulin and failure of the beta cells is the point at which glucose levels in the blood begin to rise and hyperglycemia results.


Aiden's Case

He’s an 11 year-old boy who has left friends behind because of the recent split of his parents, which has resulted in a move to a new school. He has therefore been less active and has begun to take comfort in food.



Father tends to indulge him and adds to his weight by taking him out to eat. Father denies that his son has a weight problem, but his mother is concerned for his health.

Changes in lifestyle


Modification of eating behaviors is a goal of the Children’s Exercise and Nutrition Centre program. This must be accomplished gradually and result in a permanent change in dietary choices in order to be effective. Choosing to be physically active after school and breaking the habit of sitting in front of the TV with an unhealthy snack is one way to modify a behavior that leads to excess weight gain.


Failure in Diets

The reason that diets fail and the reason that they are not recommended as part of the program in the Children’s Exercise and Nutrition Centre or CENC because basal metabolic rate drops in response to a decrease in availability of food through dieting, this causes weight to be quickly regained when previous foods levels are reinstated. The only way to permanently reduce weight is to change the eating behaviors for good as well as increasing levels of physical activity.

Normal Values

The values for triglycerides and LDL cholesterol would likely be higher in obese children and teens. The glucose levels could be normal or high, depending on the degree of metabolic derangements. The value of HDL cholesterol would likely be lower. High levels of LDL cholesterol and low levels of HDL cholesterol could lead to deposition of oxidized LDL cholesterol in the artery walls, the beginnings of atherosclerosis, which would put these individuals at higher risk for heart disease in the coming years. High triglyceride levels would compound the problem of glucose and insulin dysregulation, and could eventually lead to type II diabetes, if left unchecked.



*Check Chart*

Measurement of Body Composition

The gold standard is underwater weighing, although it requires specialized equipment and is difficult to do with children. Triceps skinfold thickness tests are not nearly as reliable and can vary greatly depending on who is doing the measuring. Bioelectrical impedance can be done easily, using either a stand-on device or a hand held one. This gives an accurate measure of body fat that correlates well with values derived by underwater weighing.


Reversal of Metabolic Disorders through Exercise


As the child grew taller, they managed to pretty much maintain their weight lost.





Exercise increases insulin sensitivity, even in those with type II diabetes, as well as reducing glucose production by the liver. Studies also showed that a bout of exercise, an hour before consumption of a high fat meal, reduced blood triglyceride levels versus the high fat meal with no exercise. Glucose transporters migrate to the surface of muscle cells in response to signals transmitted by insulin binding to its receptor. Translocation of these glucose transporters to the cell surface has also been shown to occur with exercise alone, independent of insulin binding. This allows more glucose to be taken up by muscle cells to fuel further activity. Finally, in studies of those with dyslipidemia, exercise combined with a low-fat diet was shown to improve blood lipid profile.

Glucose Uptake by Glucose Transporter System


Glucose transporters migrate to the surface of muscles cells in response to signals transmitted by insulin binding to its receptor. Translocation of these glucose transporters to the cell surface has also been shown with exercise alone, independent of insulin binding. This allows more glucose to be taken up by muscle cells to fuel further activity.


Sweet Drinks

Foregoing sweet drinks is on of the pieces of nutritional advice offered in the CENC program. As mentioned, even 100% fruit juices contain a considerable amount of sugar. In a 12-ounce can of pop there are about 40g of sugar, the equivalent amount of orange juice contains about 33g of sugar, apple juice has about 39g and grape juice has a whopping 58.5g of sugar.



The label lists the serving size as 8 ounces but the servings per container as 2. It is unlikely that someone would deink only half of this bottle, so 50g of sugar are actually being consumed for a total of 200 calories, with in this case, very little nutritional value.