Overweight and Obesity Epidemic in America – Part V: Non-Modifiable Risk Factors

Suggested Citation: Garko, M.G. (2011, February). Overweight and obesity in America – Part V: Non-Modifiable Risk Factors. Health and Wellbeing Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.

Overweight and Obesity Epidemic in America – Part V: Non-Modifiable Risk Factors

Michael G. Garko, Ph.D.

Host – Let’s Talk Nutrition

Introduction

Americans are living in an obesogenic society. At nearly every bend and turn adults and children alike are tempted with and succumb to a veritable tsunami of fast foods. At home, school, work, entertainment venues, airports, train and bus stations, laundry mats, convenience stores, grocery stores, hospitals, churches and almost every other environment people frequent Americans are presented with an ever growing menu of processed foods low in nutritional value but high in calories, fat, sugar and sodium.

Contributing to the creation of our obesogenic society is the sedentary life style of Americans. More than 60% of American adults are not regularly active, with 25% of the adult population being totally sedentary during their leisure time. Only approximately 15% of U.S. adults are involved regularly (i.e., three times a week for at least 20 minutes) in vigorous physical activity during leisure time. About 22% of adults engage regularly (i.e., five times a week for at least 30 minutes) in sustained physical activity of any intensity during their leisure time (U.S. Department of Health & Human Services, 2000; U.S. Department of Health & Human Services, 1996).

The statistics for children and adolescents are not any better. Nearly 50% of American youths 12-21 years of age do not engage in regular, vigorous activity, with physical activity declining dramatically during adolescence. Twenty-five percent of young people report that they are not involved in any vigorous physical activity during their leisure time (see U.S. Department of Health & Human Services, 1996).

In addition to unhealthy eating habits and a sedentary lifestyle there are a number of other modifiable and non-modifiable risk factors and causes responsible for the obesity epidemic in America. This February, 2011, issue of Health and Wellbeing Monthly focuses on important non-modifiable risk factors contributing to a major health crisis in America in the 21st century.

Overweight and Obesity Defined

The term “overweight” refers to an excessive amount of body weight, which can be constituted of muscle tissue, bone, adipose or fat tissue and water, while the term “obesity” refers to an excessive amount of adipose or fat tissue (see National Institute of Diabetes and Digestive and Kidney Diseases, 2010).

Body Mass Index (BMI) is used to measure the amount of body fat/adipose tissue based on a person’s height and weight. Specifically, BMI is expressed as a person’s weight in kilograms divided by height in meters squared (kg/m2). Individuals with a BMI of 25.0-29.9 are classified as being overweight, while those with a BMI of 30 or more are classified as obese and those with a BMI more than or equal to 40.0 are classified as extremely obese (see Ogden and Carroll, 2010).

Risk Factors[1]

Risk factors are variables possessing the potential to increase the likelihood of developing a particular disease or health condition (e.g., overweight or obesity). They are linked to a disease or health condition by means of a statistical association or correlation. The stronger the statistical association is the stronger the inference that can be made about a particular factor putting a person at risk for becoming obese.

It is important to understand that while a particular risk factor or set of risk factors increases the likelihood of becoming overweight or obese, this does not mean that there is a certainty suffering from either condition (see Black, 1993).

In contrast to a risk factor, a cause is “that which produces or effects a result; that from which anything proceeds, and without which it would not exist” (Webster’s Online Dictionary, 2010). Thus, causes of obesity are definitive in producing it.

Modifiable and Non-modifiable

Risk factors and causes can be classified as being modifiable or non-modifiable. Non-modifiable risk factors are genetically determined traits (e.g., age, gender & race-ethnicity). Modifiable risk factors involve lifestyle variables (e.g., high stress levels, lack of exercise, poor nutrition, etc.) and acquired conditions (e.g., elevated blood pressure, insulin resistance, etc.). Lifestyle and acquired conditions are assumed in the literature to be changeable and ideally subject to improvement and prevention, while heredity based factors are viewed as fixed and unchangeable.

Multi-factorial and Interactional

Overweight and obesity are not associated with or caused by a single variable. Rather, they are multi-factorial in nature. The research on overweight and obesity provides convincing evidence that they result from a complex of interacting traits, acquired conditions and lifestyle variables that implicate various environmental, behavioral, psychological, physiological, social and genetic factors.

Some risk factors are described in the literature as being independent (e.g., overeating) because they have the potential to bring about overweight or obesity single-handedly. However, risk factors and causes can and most often interact and work together with one another to create a greater likelihood of becoming overweight or obese and have a greater deleterious impact on health. It stands to reason that the more risk factors and causes an individual possesses for obesity the greater the chances of that person developing and dying from it.

Non-Modifiable Risk Factors Related To Overweight and Obesity

As mentioned above, non-modifiable risk factors are genetically determined traits such as age, gender and race-ethnicity. Then, of course, there is the influence of genes themselves as a non-modifiable risk factor.

Age

The statistics on adult and childhood obesity indicate that obesity is a condition which can occur at any age (see Garko, 2010a; Garko, 2010b). However, as people age and move deeper into the life span, their hormone levels change. When these hormonal changes are coupled with a sedentary life style, body fat begins to accumulate and muscle begins to decrease. The decrease in muscle tissue is accompanied by a decrease in metabolism rate and efficiency, contributing further to the likelihood of becoming overweight or obese.

Gender

Gender makes a difference in whether a person will be either overweight or obese. Of the total percentage of adults 20 years of age and older who are either obese or overweight (i.e., 68%), 64.1% and 72.3% of women and men were overweight or obese, respectively (Flegal et al., 2010); Ogden & Carroll, 2010). Of the total percentage of adults 20 years of age and older who are obese (i.e., 33.8%), 35.5% and 32.2% of women and men are obese, respectively (Ogden & Carroll, 2010). Less than one-third (i.e., 31.6%) of adults 20 years of age and older is at a healthy weight. Of this total percentage of adults 20 years of age and older at a healthy weight, 36.5% and 26.6% are women and men, respectively.

In summary, there are more adult men 20 years of age and older who are overweight, while there are more adult women 20 years of age and older who are obese. At the same time, there are more adult women 20 years of age and older who are at a healthy weight.

Genetics[2]

The rather rapid rise of obesity in America cannot be attributable to genetics because changes in the genetic makeup of populations takes place at a rate that is far too slow to be responsible for the swift increase in obesity. That being said, genetics is implicated in the development of obesity. One way genes may contribute to obesity is their functional ability to regulate how humans capture, store, and release/burn energy from the food they eat.

Thrifty genotype hypothesis. Another explanation of how genes are implicated in obesity epidemic is the thrifty genotype hypothesis. According to this hypothesis, our ancestors millions of years ago evolved with a set of genes which allowed them to survive famines. Their genes were thrifty in holding on to the energy/calories they ate and were able to store that energy in the form of fat. Humans’ ability to store energy is still part of their genetic make-up. This becomes a problem because in today’s world most humans live in an environment not plagued continually by unpredictable food sources and famines. On the contrary, they live in environments in which there is a plentiful and even overabundant amount food year round. Thus, according to the thrifty genotype hypothesis, the very same energy-thrifty genes that contributed to the survival of humans in times of food scarcity are now responsible humans becoming obese. In other words, humans seem to genetically favor fat accumulation.

As part of the theory in which obesity is viewed as resulting from genetic variation interacting with shifting environmental conditions, it is contended that the thrifty genotype is just one way genes favor fat accumulation within the context of a given environment and contribute to humans becoming obese. These other ways “include the drive to overeat (poor regulation of appetite and satiety); the tendency to be sedentary (physically inactive); a diminished ability to use dietary fats as fuel; and an enlarged, easily stimulated capacity to store body fat” (The Centers for Disease Control and Prevention, 2011, p.1)

Support for the belief that genes play a role in the development of obesity is based on research showing that “not all people living in industrialized countries with abundant food and reduced physical activity are or will become obese; nor will all obese people have the same body fat distribution or suffer the same health issues” and that “this diversity occurs among groups of the same racial or ethnic background and even within families living in the same environment” (The Centers for Disease Control and Prevention, 2011, p.1).[3]

Race/Ethnicity

National Health And Nutrition Examination Survey (NHANES) data reveal significant racial and ethnic disparities in adult obesity. While NHANES data from 2007–2008 and 1988–1994 indicate no significant differences between racial and ethnic groups in the prevalence of obesity among men of different racial-ethnic groups, the prevalence of obesity among men increased between 1988–1994 and 2007–2008 in the following ways:

• From 20.3% to 31.9% among non-Hispanic white men.
• From 21.1% to 37.3% among non-Hispanic black men.
• From 23.9% to 35.9% among Mexican-American men (Ogden & Carroll, 2010, p.1)

With respect to women, NHANES data indicate significant differences between racial and ethnic groups in the prevalence of obesity among women. In 2007-2008, “non-Hispanic black women (49.6%) were significantly more likely to be obese than non-Hispanic white women (33.0%)” and in a similar fashion “Mexican-American women (45.1%) were more likely to be obese than non-Hispanic white women (33.0%)” (Ogden & Carroll, 2010, p.1).

Going back to the period 1988-1994, a similar pattern of racial-ethnic disparity among women existed in that “22.9% of non-Hispanic white women, 38.3% of non-Hispanic black women, and 35.3% of Mexican-American women were obese” (Ogden & Carroll, 2010, p.1).

Trends in the prevalence of obesity among women of different racial-ethnic groups increased between 1988–1994 and 2007–2008, with greater increases among non-Hispanic black women and  Mexican-American women in the following ways:

• From 22.9% to 33.0% among non-Hispanic white women.
• From 38.2% to 49.6% among non-Hispanic black women.
• From 35.3% to 45.1% among Mexican-American women (Ogden & Carroll, 2010, p.2).

Conclusion

It is clear that the non-modifiable risk factors of age, gender, genetics and race/ethnicity have an impact on people becoming overweight or obese. Experts use such terms as “unchangeable,” “predetermined” and “uncontrollable” to describe non-modifiable risk factors. Using such terms to describe non-modifiable risk factors reinforces a fatalistic approach to health, whereby, any health related condition (e.g., being overweight or obese) and event (e.g., contracting cancer or having a heart attack) in a person’s life is inevitable or otherwise predetermined. We all end up with a death certificate. However, our departure from this earth does not need to be premature. Nor does it need to be characterized by protracted, debilitating diseases and disorders stemming from being overweight or obese, which are for the most part brought on by a failure to practice prevention and take personal responsibility for one’s health (a hallmark of the fatalistic approach).

Healthy Choices

While some people may be put at a potential health disadvantage by their increasing age, genetics, gender or race-ethnicity, they do not have to live their lives with a feeling of impending doom created by the belief that they will die from some obesity related condition or disease because they suffer from non-modifiable risk factors. Contrary to a fatalistic approach to health, we are not necessarily ill-fated to die from non-modifiable risk factors associated with overweight or obesity. Even with non-modifiable risk factors, we are not rendered helpless and without choices to prevent from becoming overweight or obese.

One choice people can make is to become familiar with the non-modifiable factors associated with overweight and obesity. Having even a rudimentary understanding of non-modifiable risk factors can help people (1) determine if they may be at risk, (2) assess their level of risk, (3) teach them about and alert them to the early warning signs for becoming overweight or obese and (4) make them more vigilant and health conscious, all of which reduces the danger of suffering or dying from being obese.

Another choice people can make is to adopt a healthy diet and lifestyle designed to modulate the effects of non-modifiable risk factors and prevent being overweight or obese. Generally speaking, a healthy diet and lifestyle would include day-to-day habits that prevent the consumption of excess calories derived from processed foods low in nutritional value and high in saturated and trans fats, sugar and sodium, while engaging in regular physical activity.

A third option for people whose age, gender, genetics, or race-ethnicity may put them at risk for becoming overweight or obese is to keep the number of modifiable risk factors to a minimum (e.g., excessive calories, sedentary lifestyle, foods high in fat, sugar and sodium, insomnia, stress, etc.). In addition to the scientific findings on the health consequences of having more rather than less risk factors for overweight or obesity, common sense dictates that the more non-modifiable and modifiable risk factors a person has the greater the likelihood for becoming overweight or obese and either becoming debilitated by or dying from obesity.

Non-modifiable Risk Factors As Modifiable

On the one hand, aging and genetics are non-modifiable in the sense that they possess programmed qualities. On the other hand, they are not immutable to the extent that people are left without any choices to moderate their impact on the development of overweight or obesity. Moreover, thinking about non-modifiable risk factors for overweight and obesity in less conventional terms opens the up the opportunity to make heart-healthy choices.

Aging. For example, rather than construing aging as a chronological phenomenon it is more useful to think about aging in functional/biological terms. That is, aging is not just about the passage of time. Rather, it is also about the bio-physical health status of a person at any given point in time. It is theoretically possible for an individual to be chronologically 50 but biologically 35 or chronologically 50 and biologically 65.

The point is that while chronological age (i.e., the passage of time) is non-modifiable, functional/biological age is modifiable. Diet/nutrition and lifestyle or otherwise what is put into the body and what is done to and with the body greatly influences the functional age of the body.

Genetics. Nutrition and lifestyle also influence the course of heredity. In this regard, a variation of an often cited principle is that genetics loads the gun, while diet and lifestyle pull the trigger. Even those who are gifted with a “healthy” set of genes can accelerate the process of aging and disease through poor diet and an unhealthy lifestyle. On the flipside of the genetic coin, individuals who may possess a set of genes making them more vulnerable to aging and disease can live a long and vibrant life through practicing nutritional and lifestyle principles that promote good health.

Preventing the potentially deleterious effects of non-modifiable risk factors for overweight and obesity is an achievable health goal. It all comes down to the nutritional and lifestyle choices that are made.

References

Black, W.K. (1992). Cardiovascular risk factors. In B. L. Zaret, M. M. Moser & L. S. Cohen (Eds.),Yale university school of medicine heart book (pp. 23-35). New York: Hearst Press.

Centers for Disease Control and Prevention (2011). Obesity and genomics. Centers for Disease Control and Prevention, Office of Surveillance, Epidemiology, and Laboratory Services, Public Health Genomics. Retrieved January 21, 2011 from http://www.cdc.gov/genomics/resources/diseases/obesity/obesedit.htm

Flegal, KM, Carroll, MD, Ogden, CL, & (2010). Curtin, LR. Prevalence and Trends in obesity among US adults, 1999–2008. Journal of the American Medical Association. 235–241.

Garko, M.G. (2010a). Overweight and obesity epidemic in America – Part I:  Prevalence and trends among adults. Health and Wellbeing Monthly. October, 1-12. www.letstalknutrition.com

Garko, M.G. (2010b). Overweight and obesity epidemic in America – Part II:  Prevalence and trends among children an adolescents. Health and Wellbeing Monthly. November, 1-9. www.letstalknutrition.com

Garko, M.G. (2010c). Overweight and obesity epidemic in America – Part III: The immediate cause. Health and Wellbeing Monthly. December, 1-7. www.letstalknutrition.com

Garko, M.G. (2011). Overweight and obesity epidemic in America – Part IV:  What risk factors and causes are and why it is important to know about them. Health and Wellbeing Monthly. January, 1-5. www.letstalknutrition.com

Hernandez, L.M. & Blazer, D.G. (Eds.). (2006). Genes, behavior, and the social environment: Moving beyond the nature/nurture debate. Institute of Medicine (US) Committee on Assessing Interactions Among Social, Behavioral, and Genetic Factors in Health. Washington (DC): National Academies Press (US).

National Center for Health Statistics (2009). Chartbook on trends in the health of Americans. Health, United States, 2008. Hyattsville, MD: Public Health Service.

National Institute of Diabetes and Digestive and Kidney Diseases (2010). Overweight and obesity statistics. Retrieved September 25, 2010, from http://www.win.niddk.nih.gov/publications/PDFs/stat904z.pdf

Webster’s Online Dictionary (2009). Cause. Retrieved December 1, 2010, from http://www.webster-dictionary.org/definition/cause

Ogden, C.L. & Carroll, M.D. (2010).  Prevalence of overweight, obesity, and extreme obesity among adults: United States, trends 1976–1980 through 2007–2008. NCHS Health E-Stat. Hyattsville, MD: National Center for Health Statistics. Retrieved September 25, 2010, from http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm.

U.S. Department of Health and Human Services (2000). Healthy people 2010: Understanding and improving health and objectives for improving health ( 2nd ed.). (Vol. 2, pp. 22/1 – 22/39).  Washington, DC: U.S. Government Printing Office.

U.S. Department of Health and Human Services (1996). Physical activity and health: A report of the surgeon general. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion. Atlanta, GA.

Suggested Citation: Garko, M.G. (2011, February). Overweight and obesity in America – Part V: Non-modifiable risk factors. Health and Wellbeing Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.


[1] See Garko (2011) for a definition and complete discussion on risk factors.

[2] The discussion on genetics is borrowed heavily from Centers for Disease Control and Prevention (2011).

[3] The influence of genetics on the development of obesity is more complicated than can be addressed here. It is recommended that readers refer to Hernandez, L.M. & Blazer, D.G. (Eds.). (2006). Genes, behavior, and the social environment: Moving beyond the nature/nurture debate. Institute of Medicine (US) Committee on Assessing Interactions Among Social, Behavioral, and Genetic Factors in Health. Washington (DC): National Academies Press (US). This is an excellent book on the topic.