Which Theory Asserts That Each Individual Has An Ideal Body Weight That Is Resistant To Change

Learning Objectives

Describe how hunger and eating are regulated in the homo body

Understanding Hunger

There are a number of physiological mechanisms that serve equally the basis for hunger. When our stomachs are empty, they contract, causing both hunger pangs and the secretion of chemical messages that travel to the encephalon to serve as a signal to initiate feeding behavior. When our blood glucose levels drib, the pancreas and liver generate a number of chemical signals that induce hunger (Konturek et al., 2003; Novin, Robinson, Culbreth, & Tordoff, 1985) and thus initiate feeding behavior.

For most people, once they accept eaten, they feel satiation, or fullness and satisfaction, and their eating behavior stops. Like the initiation of eating, satiation is also regulated by several physiological mechanisms. As blood glucose levels increase, the pancreas and liver ship signals to shut off hunger and eating (Drazen & Woods, 2003; Druce, Small, & Bloom, 2004; Greary, 1990). The nutrient's passage through the gastrointestinal tract likewise provides important satiety signals to the brain (Woods, 2004), and fat cells release leptin, a satiety hormone.

The various hunger and satiety signals that are involved in the regulation of eating are integrated in the brain. Research suggests that several areas of the hypothalamus and hindbrain are particularly important sites where this integration occurs (Ahima & Antwi, 2008; Woods & D'Alessio, 2008). Ultimately, activity in the brain determines whether or not we engage in feeding behavior (Effigy 1).

An outline of the top half of a human body contains illustrations of the brain and the stomach in their relative locations. A line extends from the location of the hypothalamus in the brain illustration, out to the left, past the outline, where it meets a box labeled

Metabolism and Torso Weight

Our body weight is affected by a number of factors, including gene-surround interactions, and the number of calories we consume versus the number of calories we burn down in daily activity. If our caloric intake exceeds our caloric utilize, our bodies store excess free energy in the course of fat. If we consume fewer calories than we burn down off, then stored fat will be converted to free energy. Our energy expenditure is plainly affected by our levels of activity, but our body's metabolic charge per unit likewise comes into play. A person'southward metabolic charge per unit is the corporeality of free energy that is expended in a given period of time, and in that location is tremendous individual variability in our metabolic rates. People with high rates of metabolism are able to burn off calories more easily than those with lower rates of metabolism.

Nosotros all feel fluctuations in our weight from time to fourth dimension, but by and large, most people'due south weights fluctuate within a narrow margin, in the absence of farthermost changes in diet and/or physical activeness. This ascertainment led some to propose a set-signal theory of body weight regulation. The ready-point theory asserts that each individual has an platonic torso weight, or set point, which is resistant to modify. This gear up-bespeak is genetically predetermined; efforts to move our weight significantly from the set-point are resisted by compensatory changes in free energy intake and/or expenditure (Speakman et al., 2011).

Obesity

I common mensurate of wellness and torso weight, and to differentiate the status of someone'southward weight from underweight, normal, overweight, and obese is the Body Mass Index (BMI).

When someone weighs more than what is by and large accepted equally healthy for a given height, they are considered overweight or obese. According to the Centers for Disease Control and Prevention (CDC), an adult with a body mass index (BMI) between 25 and 29.9 is considered overweight (Figure 2). An adult with a Torso Mass Index (BMI) of thirty or higher is considered obese (Centers for Affliction Command and Prevention [CDC], 2012). People who are so overweight that they are at risk for death are classified as morbidly obese. Morbid obesity is defined as having a BMI over 40.

However, it should be noted that recently the utility of the BMI has been questioned.^[one] Specifically, the BMI has been used as a healthy weight indicator by the Earth Health Arrangement (WHO), the CDC, and other groups, its value as an assessment tool has been questioned. The BMI is most useful for studying populations, which is the piece of work of these organizations. Information technology is less useful in assessing an individual since tiptop and weight measurements neglect to account for important factors like fitness level. An athlete, for instance, may take a high BMI because the tool doesn't distinguish between the body's percentage of fat and muscle in a person'southward weight.

A nautical chart has an x-axis labeled 30" area covers approximately 140–350 pounds at height 4'11" and extends to approximately 265–350 pounds at height 6'6."" width="614" height="502">

Figure 2. This chart shows how adult BMI is calculated. Individuals find their height on the y-axis and their weight on the x-axis to decide their BMI.

Beingness extremely overweight or obese is a risk cistron for several negative health consequences. Negative health consequences include, but are not express to, an increased risk for cardiovascular disease, stroke, Type 2 diabetes, liver disease, sleep apnea, colon cancer, breast cancer, infertility, and arthritis. Given that it is estimated that effectually 1-3rd of the adult U.South. population is obese and that near ii-thirds of adults and ane in 6 children qualify every bit overweight (CDC, 2012), at that place is substantial interest in trying to understand how to combat this important public health business.

Watch Information technology

Watch this video to learn nigh aberrant eating behaviors, including the nigh common eating disorders (which we'll examine in particular soon), and a summary of basic treatment strategies.

You can view the transcript for "Eating Disorder: Presentation & Treatment" here (opens in new window).

Dig Deeper: Prader-Willi Syndrome

A painting shows Eugenia Martínez Vallejo.

Figure three. Eugenia Martínez Vallejo, depicted in this 1680 painting, may have had Prader-Willi syndrome. At only eight years former, she weighed approximately 120 pounds, and she was nicknamed "La Monstrua" (the monster).

Prader-Willi Syndrome (PWS) is a genetic disorder that results in persistent feelings of intense hunger and reduced rates of metabolism. Typically, affected children have to be supervised effectually the clock to ensure that they practise not engage in excessive eating. Currently, PWS is the leading genetic cause of morbid obesity in children, and it is associated with a number of cognitive deficits and emotional problems.

While genetic testing can exist used to make a diagnosis, there is a number of behavioral diagnostic criteria associated with PWS. From nativity to two years of age, lack of muscle tone and poor sucking beliefs may serve every bit early signs of PWS. Developmental delays are seen between the ages of 6 and 12, and excessive eating and cognitive deficits associated with PWS normally onset a footling later.

While the exact mechanisms of PWS are non fully understood, there is evidence that affected individuals take hypothalamic abnormalities. This is not surprising, given the hypothalamus's role in regulating hunger and eating. All the same, as you will learn in the next department of this module, the hypothalamus is also involved in the regulation of sexual behavior. Consequently, many individuals suffering from PWS fail to reach sexual maturity during adolescence.

There is no current handling or cure for PWS. Withal, if weight can be controlled in these individuals, so their life expectancies are significantly increased (historically, sufferers of PWS often died in adolescence or early on adulthood). Advances in the apply of diverse psychoactive medications and growth hormones go along to raise the quality of life for individuals with PWS (Cassidy & Driscoll, 2009; Prader-Willi Syndrome Association, 2012).