Obesity Causes & Assessment Morbidity in Obesity



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Weight Management Course Dr A Blazos, 15/1/2001

Obesity

Causes & Assessment

Morbidity in Obesity

  • Cardiovascular e.g hypertension, heart disease, deep vein thrombosis

  • Respiratory e.g breathless, sleep apnoea, hypoventilation syndrome

  • Gastrointestinal e.g hiatus hernia, gallstones, fatty liver, colon cancer

  • Metabolic hyperlipidaemia, diabetes,polycystic ovaries,menstrual change

  • Neurology nerve entrapment

  • Renal proteinuria

  • Breast cancer, male gynaecomastia

  • Uterus endometrial cancer, cervical cancer

  • Urological prostate cancer, stress incontinence

  • Skin sweat rashes, fungal infections, lymphoedema, acanthosis nigracans

  • Orthopaedic osteoarthritis, gout

  • Endocrine growth hormone reduced, reduced prolactin response

  • Pregnancy obstetric complications, caesarian, neural tube defects

To read a short paper on the evidence linking obesity with diseases see: http://www.med.monash.edu.au/medicine/mmc/asso/complic.htm


The lowest mortality was observed among women who weighed at least 15% less than the US average for women of similar age and among those whose weight had been stable since early adulthood.

The relative risk of mortality increased by 60% at a BMI of 27.


In Asian populations
the equivalent risk occurs at a BMI between 23-25.

For more information see report: http://www.idi.org.au/download/obesity_report.pdf


Note that the mortality index rises only slightly as BMI values rise from 25 to 30, the overweight range. As BMI rises above 30 the risk can be seen to rise more steeply. BMI below 20 is also associated with increased mortality giving the characteristic ‘U’`shaped curve .

It is of particular interest to compare the mortality indices of smokers and non-smokers. Smokers of normal weight have an increased mortality index which represents the health risk of smoking. The health risk of smoking is significantly greater than the health risk of body weight in the overweight range. It is not until BMI is up to 35 or more that the health risk of obesity is approximately equivalent to being a smoker. This observation is important because a number of young women take up smoking or continue to smoke because they consider that it keeps their weight down. In fact, smoking probably does hold weight down to a small extent, however it does so at the cost of imposing a much greater risk to long-term health. When the obese person smokes the risk rises steeply, because the risks are additive.



 


Chemical pollutants tend to be fat-soluble and are stored in adipose tissue. It has been hypothesised that their presence in fat tissue may reduce the body’s ability to mobilise fats for energy generation. However, once these fats are mobilised through weight loss these pollutants may also be mobilised into the blood stream. Some of these are known carcinogens, but its not clear yet whether they have a cancer forming effect after release from fat cells. Psycho-social stress and inadequate sleep have been linked with abdominal obesity due to high levels of cortisol released in these states.


1. This is regarded as the main problem in modern societies because fat is energy dense, is addictive, is stored easily in the body and is easy to get. People with this as the main cause have a ‘fat
tooth’ and over-consume fatty foods. There is emerging evidence that saturated fat may be more 'fattening' than omega 3 fats and possibly monounsaturated fats - see Module C4 Dietary Advice on Fats.
2. If fat is controlled there can still be a problem with too many calories. Carbohydrate and protein are not turned to fat easily, but they can be if eaten in large quantities over an extended period.
People with this problem simply eat too big portion sizes.
3. Energy dense foods are too high in fat or sugar. Energy dense diets do not contain enough plant food, even if not high in total fat. These diets have been shown to increase the tendency to gain
weight. A low energy dense diet is very high in plant food and can also be high in fat - but this fat
is ‘diluted’ by the plant foods and has not been associated with weight gain
(see module B5 Weight Loss Diets )
4. Hunger can have a genetic component and hormones encouraging us to feel hungry are more
common in obese people.
5. Causes are often psychological and may need special treatment.
6.
Studies have shown we tend to eat more when other people are present at a meal. Social
|
eating can take some of the blame for the excessive food intake in some people.
7. This is ‘learned eating’; learned ways of acting e.g getting something to eat every time an ad appears on TV or learned ways of thinking e.g I feel depressed and worthless so I’ll have some chocolate
for comfort. Habitual eating needs to be unlearned to see weight loss results.
8. This is most common of men who are unaware of the energy density of different foods. Learning about high-energy dense foods can overcome the problem.
9. Adding fatty or high energy dense foods to a diet which also has alcohol can mean the alcohol is burned as energy and the other calories stored as fat.
10. The average person underestimates what they eat by 30%. It’s not lying. It’s the eye not seeing what’s going into the mouth.
11. Some people think they only over-eat on exceptional days. Don’t believe it.

1. If you are naturally inactive outside work hours, look no further than your job as a cause.
2.
In the past, the majority of the population walked or rode bikes to work/school. Increases
in urban sprawl and issues of safety mean this is no longer feasible.
3. This means taking time out for some activity such as walking.
4. Incidental movement is that which can be done for you by machines or other people. In an
age of remote controls, e-mails, paid help (cleaners, gardeners) we are not moving around as much.
5. Most people are not aware that all that is needed for weight loss is movement. It doesn’t
have to be vigorous and it doesn’t have to continuous. It just has to be.
6. Vigorous (anaerobic) exercise burns blood sugars, not fat. Slower (aerobic) exercise such as
walking burns fat (see module on Sport Nutrition). Weight supportive exercise like swimming and cycling does not require as much energy as movement where the body weight is not supported. Hence the wrong type of regular activity can lead to ineffectiveness in weight loss.
7. Fatigue is a 20th century phenomenon. The harder we strive the more tired we get. This
makes it difficult to do those physical things that would help us lose weight.
8. Injury often comes from being overweight and being overweight comes from being inactive.
9. Exercise can remind some people of tortuous sport or PE at school at which they always
failed. This can leave an unfortunate memory which doesn’t fit with the need for more movement than skill.
10. Stops us from objectively realising how active we are. The only way to really tell is by
measuring e.g pedometer

1. This is highly over-rated and occurs in a minority of people.
2. Over-rated excuse. However, metabolism may be negatively effected early in life by dieting
and inactivity and this can lead to later problems. Some families also have low metabolic rates and this can
only be confirmed by laboratory tests.
3. Bingeing and fasting throughout life (especially early adolescence) can cause long term changes in fat cells and metabolism that make lifetime weight loss a problem. Better to stop it in kids before it happens. Dieting improves the body's ability to store fat; doubles the lipogenic storage enzymes; can reduce lipolytic enzymes by 50%. Just one cycle of weight loss-regain can contribute to an increased risk of death from coronary heart disease independent of body fat levels. It is therefore important that weight loss be maintained if health benefits are to be gained.  
4. The causes of overweight and obesity are both genetic and environmental. 25-70% of individual differences of body mass may depend on genetic factors e.g weight problems do run in families. But if the family dog is also fat, this suggests the environment is more important.
5. Early experiences in life such as physical or sexual abuse can be linked to later weight problems.
6. Body fat is higher in women than men and increases gradually with age (this is not inevitable).
7. A number of studies have shown that it is lifestyle change rather than physiological change that is responsible for weight gain after pregnancy and menopause.
8. Can drive some people to become overly conscious of weight gain and sub-consciously react by eating more.
9. Success for some can be a problem with previous failures being the burden they have to carry, but which convince them they could never, truly be successful. Who needs enemies when you’ve got
yourself.

Around 50% of individual differences of body mass may depend on genetic factors. However, if you are able to adjust or control the lifestyle factors then the genetic predisposition may not be observed. For example, traditional hunter-gatherer societies mainly consumed foods of low energy density and physical activity was essential for survival; obesity was rare even though some individuals would have carried the 'obesity' gene.
Based on the association between DNA sequence variation at specific genes and obesity phenotype, a growing list of genes would seem to have the capacity to cause obesity or increase the likelihood of becoming obese when they are altered or dysfunctional in humans.


The Body Mass Index (BMI) provides a simple, yet accurate method of assessing whether a patient is at risk from either over-or-underweight. However, a proportionally greater lean body mass and/or skeletal frame size can contribute to apparent excess body weight. Many athletes, for example would be considered 'overweight', yet skin-fold tests show a sub-normal amount of adipose tissue.

For children and adolescents, special growth charts need to be used in relation to BMI because BMI alters considerably throughout childhood - it rises steeply in infancy, then falls up to about the age of 5 before rising again in adulthood.

Individuals with the same BMI may have quite different degrees of body fatness because BMI does not differentiate between muscle mass and fat mass. For e.g a body builder may have a high BMI despite relatively low level of body fatness, where as a sedentary person with the same BMI will have a much higher level of body fatness assuming other factors like age, gender and ethnicity are equal.

Polynesians appear to have less body fat compared with Caucasian Australians at any given BMI suggesting there may be some ethnic differences.

Click here to calculate your BMI on-line: http://health.med.monash.edu.au/healthyeating/BMI/

For more information about calculating your body mass index and other anthropometric measurements such as skinfold measurements, abdominal circumferences click here



The cutoffs for BMI classifications are recommended by the World Health Organisation. These cutoffs are recommended for Caucasian populations.
A recent report (: http://www.idi.org.au/download/obesity_report.pdf) recommends that for Asian populations: overweight: BMI 23-25 obesity: BMI >25. The reason for these lower cutoffs is that significant increased risk of morbidity from diabetes and cardiovascular disease begins at a BMI as low as 23 in Asian populations where as in taller Caucasian (and possibly Eurasian) populations this risk occurs around a BMI of 27. Recommended cut-off are not currently available for Eurasian populations.


The distribution of body fatness abdominally is known to be the major contributor to the adverse effects of body fat on health and has a strong genetic component (up to 70% can be explained by the genes).

Although obesity is generally considered a health hazard, results from several prospective and metabolic studies have shown that it is not the absolute excess of adipose tissue that is associated with an increased prevalence of diabetes, hypertension, hyperlipidaemia and cardiovascular disease, but rather the regional distribution of body fat. Abdominal fatness caused by excess fat around the intestines (known as visceral fat) rather than caused by fat located under the abdominal skin (known as subcutaneous fat) is particularly harmful.

Abdominal fat, irrespective of body size, will predispose to such conditions.

Compared with subcutaneous fat, visceral fat has more cells per unit, higher blood flow, more glucocorticoid (cortisol) receptors, possibly more androgen receptors and greater catecholamine-induced lipolysis. The average woman has a size 10 top and 14 bottom = pear shape. The more pear shaped, the greater the sensitivity to effects of estrogen; weight tends to be gained first on the hips and lost last from the hips and thighs. Fat cells in lower body are larger and have more lipogenic storage enzymes.

The WHR is not closely related to total body fat (r=0.39) but it has fairly close relationships with the amount of visceral adipose tissue in men (r=0.5 to 0.8).

The simplest measure that reflects body type is waist to hip ratio (WHR), which is calculated by dividing the waist/abdominal circumference by the hip circumference (greatest gluteal protuberance). WHR has been measured differently by various researchers, but they have all been found to have similar predictive strength in relation to lipid and carbohydrate metabolism:

1. minimal waist & maximal hip ; 2. maximal umbilical & greater trochanter ; 3. abdominal (midway between iliac crest/hip bone and lowest rib margin) maximal hip circumference (greatest gluteal protuberance)

The maximal umbilical and greater trochanter have been used successfully in many populations (including Chinese, Greek, Indian, Anglo-Celtic elderly) by researchers in the International Health & Development Unit at Monash University to describe abdominal obesity.

The last measure (also known as the abdominal hip ratio) has been recommended recently by the World Health Organisation in order to standardise all future measurements. WHR greater than 0.9 for men and 0.8 for women indicates central or android fat distribution. If the WHR is accompanied by a high body mass index (>25) this will compound the risk for morbidity and mortality.



Recent research has shown that abdominal circumference is a better predictor of health risks than BMI and waist hip ratio. Waist circumference is measured at the narrowest circumference between the lower border of the ribs and the upper border of the iliac crest. Increased waist circumference is associated with an increased risk of type2 diabetes, dyslipidaemia, hypertension and cerebrovascular disease in patients with BMIs over 25.

In ethnic groups where the build is slight, such as in many Asian countries, a lesser degree of abdominal fatness may still put the person at risk of developing chronic diseases, especially if BMI is over 23.



To read a short on-line article go to: http://www.idietclub.com.au/library/weight/bodyfat.php


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