I will start with this “We are what we eat”.
There is an adage that says “we are what we eat”.
The foods we eat every day contribute to our well-being.
Foods provide us with the nutrients required for healthy bodies and the calories we need for energy.
If we take in more calories than what the body burns, the extra food turns to fat and is stored in the body.
If we overeat regularly, we gain weight, and if we continue to gain weight, we may become obese.
Obesity is a disorder of body accumulation of relative or absolute excess of fat.
The excess body fat usually but not always results in higher body weight.
Obesity is an international epidemic. It is no longer a disorder of adults only; prevalence in children has accelerated rapidly.
ETIOLOGY AND PATHENOGENESIS
The cause of obesity is multifactorial. A large number of pathways such as biochemical, dietary and behavioral can contribute to the accrual of body fat.
Obesity represents interaction between environment and genetics. A permissive environment brings out the genetic predisposition to obesity.
i. Biochemical pathway refers to the hormones in the body.
ii.Dietary pathway refers to the quality and quantity of food we eat.
iii.While the behavioral means our lifestyles.
Three major factors modulate body weight: metabolic factors, diet, and physical activity, each being influenced by genetic traits.
Predisposition to common forms of obesity is probably influenced by numerous susceptibility genes, accounting for variations in energy requirements, fuel utilization, muscle metabolic characteristics, and taste preferences.
The WHO estimates that in 2005 approximately 1.6 billion people worldwide were overweight and that at least 400 million adults were obese. In 2015, approximately 2.3 billion adults were overweight and 700 million were obese.
In Nigeria, the prevalence of overweight individuals ranged from 20.3%–35.1%, while the prevalence of obesity ranged from 8.1%–22.2%.
With these statistics, it is obvious that obesity is increasing at alarming rate. This call for a serious concerns as professionals
Recent global figures from the World Health Organisation (WHO) indicate that the prevalence of obesity is not just a problem of the developed countries but is also on the increase in the developing world, with over 115 million people suffering from obesity-related problems.
CLASSIFICATIONS OF OBESITY
Obesity is commonly assessed in clinical practice by measurement of body mass Index (BMI) derived by dividing the body weight (in Kilograms) by the square of the height in meters OR by dividing the weight in pounds by the square of height in inches and multiply by 703.
BMI = Weight (kg) divided by Height (m2).
Classification of overweight or obesity based on BMI in adults and in children.
1. Normal weight for height 10th – 85th percentile
2. At risk for overweight 85th – 95th percentile
3. Overweight > 95th percentile.
With these, an individual can easily work out his or her BMI.
I can see some people trying to check their weight and height to know where they fall????????
CAUSES OF OBESITY
Essentially, obesity results from an imbalance between calorie intake and expenditure
1. Increased intake of calories
2. Energy expenditure: Some individuals undoubtedly metabolize at a more rapid rate than others. This may be due to increased expression of ‘uncoupling protein’ in mitochondria, and is certainly increased by thyroid hormone.
Such energy squanderers would be leaner than those with efficient energy metabolism (the ‘thrifty’ phenotype), despite ingesting the same quantity of food.
3. Low birth weight Metabolic imprinting of maternal nutritional status during fetal life influences tendency to develop obesity in later life. Adults who were low birth weight babies tend to develop a ‘thrifty’ phenotype’, depositing ingested calories as fat rather than burning them up in uncoupled mitochondria.
4: Emotional Eating releases mood-elevating neurotransmitters e.g serotonin, in the brain.
5: Genetic rarely causes obesity, but they teach us valuable lessons about normal control of fat mass.
The next cause will interest and this will catch our attentions;
This is central to development of obesity.
To regulate food intake, the brain must alter appetite. In the CNS, the hypothalamus is the key region involved in the regulation of appetite. The regulation of feeding, energy intake and expenditure, and body weight is a homeostatic process.
Apetite plays a central in development of Obesity. It is observed that obese people eat often than normal weight individuals.
The question will be be why is it so?
There are some hormones that are involved in this regulation:
They are Leptin, Ghrelin and Insulin and some others but these 3 hormones play the central role.
Leptin, the “satiety hormone”, or “thin hormone” is a hormone produced by adipose cells that helps to regulate energy balance by inhibiting hunger. Leptin is opposed by the action of the hormone ghrelin, the “hunger hormone”. Both hormones act on receptors in the arcuate nucleus of the hypothalamus to regulate appetite to achieve energy homeostasis.
In obesity, a decreased sensitivity to leptin occurs, resulting in an inability to detect satiety despite high energy stores. The amount of leptin circulating in the body is proportional to the amount of fat of an individual. Level of leptin is positively correlated with fat mass, being increased in obesity. Role of leptin is to maintain energy balance by regulating food intake and calorie burn rate. As fat stored in cells , leptin is secreted into the bloodstream and signals that make you eat more or less. Despite the high level of Leptin in obese individuals, the obese still consumed more food than what is required due to insensitive of the hormone.
Ghrelin is referred to as “hunger hormone”. Increase in ghrelin makes overweight individuals to eat more even when they did not need it. This create an imbalance between calorie intake and rate at which it is used up.
HEALTH CONSEQUENCES OF OBESITY
1. Type 2 Diabetes Mellitus
The risk of type 2 DM increases linearly with increasing BMI. BMI greater than 40 (obesity class 3) in a person under 55 years of age increases with the risk of T2DM by 18.1 folds in men and 12.9 folds in women.
Overweight (BMI 25-30) increases the prevalence of T2DM three to fold in both men and women under 55 years of age.
The worrisome and remarkable features of obesity is the increased type 2 diabetes in the children and teenagers. This may eventually lead to premature heart disease, renal failure, blindness and erectile dysfunction among the teenagers.
High blood pressure is the most common health condition associated with overweight or obesity. The relationship between hypertension prevalence and obesity for both men and women increases as risk of obesity increases. The prevalence is much higher with aging.
3. Hyperlipideamia and Dyslipidemia
The presence of overweight or obesity is associated with moderate high blood cholesterol but the relationship with other blood lipid parameters such as hypertriglyceridemia, low HDL cholesterol is much stronger.
The differences in serum TG concentration between individuals with BMI less than 21 and those with BMI greater than 30 is about 65mg/dl (in women) and 62-118 mg/dl (in men) depending on age.
Also each 1-unit of BMI change is associated with an HDL-cholesterol decrease of 1.1mg/dl in men and 0.7 mg/dl in women.
Let me quickly add this, we all believe cholesterol is more dangerous(permit me to use the word) among lipid but Triglyceride is even more. At times we focus much more on Cholesterol forgetting that TG can cause more havoc.
4.vAtherosclerotic heart disease and Stroke.
Prevalence of coronary artery disease shows a significant linear relationship with BMI for both genders and all ages.
Increased incidence of cerebrovascular accidents is also associated with obesity.
5: Early onset of puberty
6. Metabolic syndrome
Metabolic syndrome is a cluster of conditions such as increased blood pressure, high blood sugar, excess body fat around the waist(central Obesity).
It is also more prevalent in association with higher body weights and the symptoms often improve with weight loss.
such as Endometrial, breast, prostate and colon cancer are associated with obesity as a result of hormonal imbalance.
9: Sleep apnea
This is also highly associated with BMI greater than 30.
It is serious sleep disorder that occurs when a person’s breathing is interrupted during sleep. It is associated with overweight.
10: Menstrual irregularity, infertility and polycystic ovarian syndrome are more prevalent in women with higher BMIs.
I think I have done a little justice to this topic, thanks for the audience.
QUESTIONS AND ANSWERS:
Q1: Pls sir Kola, the knowledge about obesity keeps coming clearer each day!
Pls can you make a little elaboration between obesity and its effect on fertility both in males and females?
A: Thank you. Infact I missed it out in the course of presentation. Obesity plays a major role in infertility both in males and females.
(a) Testosterone potentiates the action of growth hormone to enhance muscle mass and decrease fat deposition. This accounts for the higher muscle/fat ratio of young men compared to women, and slow decline of growth hormone from young adulthood explains the gradual replacement of muscle with fat as individuals age – to so-called Somatopause’. For those that can afford it, GH replacement will slow this process.
Obesity can affect fertility in women by causing hormonal imbalances and problems with ovulation, particularly for obese women having their first baby. Obesity is associated with poly-cystic ovary syndrome (PCOS), a common cause of infertility.
Q2: Sir, I will like to know how inadequate sleep causes obesity?
A: sleep apnea is cuased by excess weight and obesity. This is associated with soften of tissue of the mouth and throat. During sleep, when throat and tongue muscles are more relaxed, this soft tissue can cause the airway to become blocked.
This is why the obese people snore.
Statement by Sct. Ogunwale:
To surprise us more, obesity cause insulin resistance and glucose intolerance
Response by Sct. Collins
And sir this is probably why it is attributed to Type 2 DM?
A: In obesity, abundance of circulating fatty acids and liver-derived triglyceride (VLDL) provide an excellent fuel for muscle, decreasing their requirement for glucose (the ‘Randle’ cycle).
Exercise stimulates glucose transport into skeletal muscle (via induction of the glucose transporter GLUT-4). Obese subjects tend to be sedentary, and thus muscle consumes less glucose.
Increased delivery of fatty acids to liver (as in visceral obesity) enhances gluconeogenesis i.e. hepatic glucose output. In lean individuals, this only happens in during starvation, where it is appropriate.
Increased FFAs cause insulin resistance directly by activating enzymes that decrease the response to insulin, thereby aggravating the pre-existing insulin resistance.
There is recent evidence showing that rather than simply a passive fuel store, adipose tissue is an active endocrine organ, secreting peptide hormones than can either impair (TNF-α) or enhance (adiponectin) insulin sensitivity in liver and muscle. An imbalance in secretion of such hormones in obesity may explain the insulin resistance. In this context, lipodystrophic individuals, who have no adipose tissue at all, are profoundly insulin resistant and develop hypertriglyceridaemia. Interestingly, this condition is remarkably responsive to leptin therary and probably forms the major clinical use for leptin at present.