Running head: REAL AGE HEALTH PROMOTION

Real Age Health Promotion, Risk Reduction and Disease Prevention Focused Assessment
Ronda A. Mott
Ferris State University

REAL AGE HEALTH PROMOTION

Real Age Health Promotion, Risk Reduction and Disease Prevention Focused Assessment
My individualized real age health status assessment identified several encouraging and
health affirming attributes and practices but also identified a few key health threatening risks. In
the following treatise, I summarize my personal real age test findings; analyze my foremost
health risk in light of evidence based literature; define wellness diagnostic strategies for reducing
the risk; characterize a specific risk reduction goal; and prescribe evidence backed interventions
toward achieving that goal, while evaluating my readiness and success potential in pursuing
those change interventions in light of the Transtheoretical Change Model.
The real age test determined that my real age is 5.5 years younger or 41.9, than my
chronological age of 47.4 years. My profile defined six health affirming practices and two health
threatening risks. The health affirming practices that imply that I am younger than my
chronological age include: 1) daily aspirin consumption, 2) joint, bone and spine protective
habits, 3) maintained healthy serum cholesterol, 4) lifetime nonsmoker status, 5) achievement of
adequate daily sleep and 6) control of ultraviolet light exposure. Health threatening
characteristics in my profile that signify that I would be older than chronological age included 1)
moderate hypertension (HTN) and 2) borderline body mass index (BMI). Both health
threatening aspects of my profile independently raise my risk for coronary heart disease (CHD)
(Sharecare, ).
When considering my current health practices, metrics, lifestyle and family history, I
surmise that my greatest health challenge and area of risk focus is the risk for developing
coronary heart disease (CHD). Atherosclerosis is responsible for most all coronary heart disease
(CHD). Traditional well established risk factors for CHD include age and gender, family history,
HTN, serum cholesterol levels, diabetes (DM) and lifestyle factors (specifically, cigarette

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smoking, diet, exercise, obesity and psychosocial or stress factors). These factors are further
categorized into modifiable risks (lifestyle factors, HTN, cholesterol, DM), and non-modifiable
factors (age, gender and family history) (Wilson, Cannon, & Downey, 2013).
Age contributes to the development of CHD. In individuals age 40 years or older the
prevalence of any vascular disease increases significantly with each decade of life. Gender
impacts the risk for CHD and associated morality. Male gender contributes to higher CHD and
mortality. Females had approximately 20 percent lower risk than males for all major
cardiovascular endpoints including cardiovascular death, myocardial infarction (MI), stroke and
heart failure (CHF) hospitalization and death. Family history is an independent risk factor for
CHD. Evidence asserts that a myocardial infarction (MI) or death from CHD in a first degree
relative (i.e., parent or sibling) prior to age 50 (males) or 60 (females) denotes a significant
family history. A wider definition of family history risk includes other manifestations of
atherosclerosis beyond MI or CHD death including stroke or transient ischemic attack and the
like. Familial risk definition may include presence of CHD disease in non-first degree relatives,
particularly biological grandparents (American Heart Association, 2013).
HTN is an established factor for CHD. Evidence asserts that patients with a systolic
blood pressure greater than 140 mmHg and a diastolic blood pressure greater than 90 mmHg are
considered hypertensive and at risk for CHD. Patients with prehypertension defined as a systolic
blood pressure between 120 and 139 mmHg or a diastolic blood pressure between 80 and 89
mmHg have an increased risk of CHD particularly at the higher end of the prehypertension range
(systolic 130 to 139 mmHg or diastolic 85 to 89 mmHg) (Wilson, Cannon, & Downey, 2013).
The prevalence of dyslipidemia is significantly increased in patients CHD and is thus
among the most important CHD risks. Disturbances in cholesterol are often familial. Evidence

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for the importance of serum cholesterol in CHD was determined in clinical trials which showed
that reductions in total and LDL-cholesterol levels reduce coronary events and mortality. DM is
associated with CHD. The 2002 National Cholesterol Education Program report designated
diabetes a CHD risk equivalent thereby elevating it to the highest risk category (Wilson, Cannon,
& Downey, 2013).
Lifestyle factors substantially impact the risk of CHD. Cigarette smoking is an important
and reversible risk factor for CHD. The incidence of a myocardial infarction (MI) is increased
six fold in women and three fold in men who smoke compared with subjects who never smoked.
Diets with a high glycemic index (GI) contribute to the risk of CHD. Evidence supports fruit
and vegetable consumption is inversely related to CHD risk, whereas intake of red meat is
directly related to CHD. Among 84,136 female nurses from the Nurses Health Study who were
followed for 26 years, those eating two or more servings of red meat daily had a 29 percent
higher risk for CHD compared with those who ate 0.5 servings daily. In two studies of health
professionals a low (GI) diet and 10 gram increase in total daily dietary fiber intake correlates
with reduced risk for MI. Exercise of even moderate degree has a protective effect against CHD
and all-cause mortality. Exercises beneficial effects include elevation in serum HDLcholesterol, reduction in blood pressure, less insulin resistance and weight loss. In addition to
the amount of exercise performed the degree of cardiovascular fitness (a measure of physical
activity), determined by duration of exercise and maximal oxygen uptake on a treadmill and is
also associated with reduced CHD risk and death (Wilson, Cannon, & Downey, 2013).
Obesity is associated with CHD and a number of associated CHD risk factors. In an
analysis of data from 4780 adults in the Framingham Offspring Study, obesity as measured by
body mass index (BMI) significantly and independently predicted the occurrence of CHD after

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adjusting for traditional risk factors. Psychosocial factors contribute to development of CHD
and precipitation of myocardial infarction (MI) and sudden cardiac death. The link between
psychological stress and CHD is both direct via damage of the vascular endothelium and indirect
via aggravation of traditional risk factors (Wilson, Cannon, & Downey, 2013).
In contemplating my desire to eradicate my CHD risk, wellness behaviors that I believe
would have great beneficial impact on risk reduction include: 1) control of HTN, and 2)
identification and management of psychosocial stressors. These wellness behaviors important as
truly modifiable risks within my personal CHD risk portfolio (Sparks & Taylor, 2010).
Health seeking behaviors related to HTN benefit individuals at risk for CHD. For
example, dietary changes and losing weight are effective treatments for reducing blood pressure.
Other lifestyle changes that reduce blood pressure include stopping smoking, reducing stress,
reducing alcohol consumption and exercising regularly. These changes are effective when used
alone but often have the greatest benefit in reducing CHD when used together (Kaplan, Bakris,
& Forman, 2013).
In addition, randomized controlled trials of antihypertensive drug therapy demonstrate
significant cardiovascular benefit in patients with systolic and diastolic hypertension designated
in both severe and moderate HTN categories with the magnitude of benefit high in both. In the
aggregate, the above findings support the recommended goal blood pressure of <140/<90 mmHg
in the general hypertensive population. Pertinent to my own status, evidence demands the blood
pressure goal to be even lower in persons with multiple risks for CHD (Mann, Hilgers, Bakris,
Kaplan, & Forman, 2013).
In assessing readiness to pursue HTN health seeking behaviors, several conclusions are
clear. My real age assessment identifies independent risk factors for CHD such as a positive

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family history of CHD in maternal grandparents, age greater than 40 and borderline BMI at 26,
in addition to confirmed HTN. When viewed individually, HTN clearly increases CHD risk but
that CHD risk is compounded in the face multiple risks (Wilson, Cannon, & Downey, 2013).
Further, my baseline blood pressure trends are in the moderate HTN category, in which
blood pressure control confers maximal benefit and risk reduction (Mann, Hilgers, Bakris,
Kaplan, & Forman, 2013).
My personal motivations for CHD risk reduction are galvanized by my desire for
maximal longevity toward raising a 6 year old daughter and pursing physically challenging
family leisure activities and lifestyle. Lastly, I recognize that early, successful HTN control at
age 47 imparts considerable lifetime health benefit, less end-organ complications and reduces allcause mortality, as opposed pursing this change later in life (Mann, Hilgers, Bakris, Kaplan, &
Forman, 2013).
Health seeking behavior that reduces psychosocial stress bestows benefit to those at risk
for CHD. Acute and chronic stress are risk factors for myocardial infarction (MI) and sudden
cardiac death and now evidence supports a link between CHD, MI and the role of psychosocial
factors in acute disease precipitation and prognosis. Emotional upset is a factor in a significant
proportion of CHD patients. A worldwide study of cardiac risk factors demonstrated that social
factors and stressful life events occurred frequently within the previous year CHD patients with
acute events. Stressful life events include marital separation or divorce, retirement and job loss,
crop or business failure, violence, major intra-family conflict, major personal injury or illness,
death or major illness of a close family member, death of a spouse or other major stress. In
addition to acute events, chronic levels of stress are associated with acute coronary syndromes.
High levels of psychological distress are detected in 75 percent of cardiac patients. Sources of

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chronic stress found in CHD patients consist of work, home and financial stress. Patients with a
first MI report considerable stress in these categories compared to controls. Evidence supports
that hostility, cynicism and anger form a critical "toxic" component of type-A behavior that is
associated with CHD risk. Finally, multiple social factors correlate positively with CHD and MI
risk, including recreational drug and marijuana consumption, exposure to air pollution, seasonal
variation (winter as greatest cardiovascular risk season), vehicular traffic congestion and a
predictable circadian impact that increases CHD and MI presentation (Mondays mornings,
Christmas and New Years Day holidays) (Tofler, Silver, & Soloman, 2013).
In assessing my inclination to pursue stress reduction behaviors to reduce CHD risk, I
recognize the considerable presence and variety of chronic stressors in my personal and
professional life. Though fortunate to have survived but a few typical, time limited, event driven
acute stressors, such as the miscarriage of my first pregnancy at 5 months; the death of my
maternal grandmother with whom I shared an almost maternal bond; several years of intrafamily discord surrounding the dissolution of her estate and the loss a beloved pet cocker spaniel,
Nickie after 11 years, I still nonetheless, encounter a variety of insidious, chronic stressors that
imperil my health. For example, living in the four season climate of Michigan with extended
winter is a perpetual chronic stress that is currently unavoidable without relocation. Life in the
second largest urban center in the state of Michigan magnifies exposure to the chronic stressors
of air pollution, vehicular traffic, crime and violence, all of which are a stark contrast to my rural,
low risk origins. Modern day work and life balance produces a unique set of tensions in the form
of family interactions, child rearing, finances and activities of daily living. Finally, imposed
professional stresses, such as those I experience in a demanding, fast-paced radiation oncology

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clinic include the hostilities, indignations and disappointments born out of staff interactions and
organization dysfunction.
My SMART goal to reduce CHD risk is HTN control. Control of HTN, based on the
aforesaid evidences, confers not only the greatest health benefit to my risk portfolio but is the
most urgent to address, given my age of 47 and other comorbidities. The goal of HTN control
qualifies as a SMART goal for me in that; 1) the benchmark is numeric, (<110/60mmHg) which
is specific, 2) blood pressure measurement in human beings is a time tested, achievable metric in
individuals for which current technologies allow for precise determination, reproducibility and
calibration of results across reporters to avoid bias, 3) is attainable in that my strategies for
reduction have been validated, and have resulted in goal achievement for clients of similar age,
gender and risk as myself, with all of the tools necessary for success within my locus of control
and 4) is realistically time bound, with current treatment guidelines for moderate HTN, under the
direction of a physician, requiring benchmark achievement within 3 months (Kaplan, Domino,
Bakris, & Forman, 2013) (Pender, Murdaugh, & Parsons, 2011).
The planned interventions for HTN control are 1) employing regular exercise as a nonpharmacologic tactic and 2) use of prescribed drug therapy under the direction of a physician.
Exercise confers benefit on the reduction of blood pressure (BP) in persons with HTN. Both
aerobic exercise and resistance training lower resting blood pressure. Most studies have shown a
sustained reduction in BP determined more by the intensity of exercise than on its frequency.
Studies of untreated hypertensive patients who exercised for eight weeks at an intensity of 50
percent of estimated maximal oxygen consumption only two times a week for a total of 60
minutes had almost as much of a drop in BP (about 12/6 mmHg) as those who exercised more
than five times a week for a total of more than 120 minutes. In addition, to its antihypertensive

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effect regular aerobic exercise also provides other anti-CHD benefits. These include reductions
in total cholesterol, improvement in HDL-cholesterol, weight loss and diminished cardiovascular
mortality. Strength and weight training exercise also reduces resting blood pressure significantly
by 4/4 mmHg with moderate-intensity resistance training (Kaplan, Bakris, & Forman, 2013).
Pharmacotherapy with prescription antihypertensive medication is the cornerstone
strategy for HTN control. Multiple guidelines and meta-analyses conclude that the amount of
blood pressure reduction is the major determinant in mitigating cardiovascular risk in patients
with hypertension, and that drug therapy is by far the most effective option for achieving and
maintaining target goals in treatment. Single drug, multiple drug and nocturnal drug regimens as
well as specific conditions outside of HTN determine drug selection. In summary, the specific
drug used is far less important than the amount of blood pressure reduction achieved (Kaplan,
Domino, Bakris, & Forman, 2013).
Refer to Appendix A for HTN interventions, blood pressure trends and exercise log.
After reflection on readiness to employ the above interventions, I have reached the Action
Stage described in the Stages of Change of the Transtheoretical Model. Having past the
Contemplation and Preparation phases through a health risk versus benefit analysis regarding
action versus inaction once diagnosed with HTN (further fortified by real-age test results); a
thorough review of my personal motivations for change and the establishment of cooperative
partnerships with my spouse, physician and friends who value my health in preparation for
action, I began the Action Stage with the interventions toward reducing CHD risk through HTN
control. The selected interventions of exercise and drug therapy attain the criterion consistent
with the Transtheoretical Model, that scientists, professionals and the evidence based literature
agree is sufficient to actually reduce disease risk. My experience during these interventions

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includes validation of the transtheoretical independent variable of Decisional Balance and its
relationship to my Action Stage of change. For the healthy intervention of regular exercise,
maintenance has indeed been achieved, because the tangible pros for my exercise remain high
(weight loss, feeling of wellness, sense of accomplishment) and due the fact that I must
purposefully decide to actually exercise on the appointed days. On the other hand, with the
intervention of drug therapy, the Decisional Balance concept is manifest in having to regularly
weigh the pros and cons of this change in terms such as future health benefits of HTN control
versus the immediate risk of side drug effects; the self-approval and sense of integrity fostered by
drug compliance versus; the risks of disapproval from my physician and spouse for drug
noncompliance. These experiences in the Action stage thus far, bear witness to the fact that my
vigilance against relapse at this stage truly is critical for intervention success (Velicer, Prochaska,
Fava, Norman, & Redding, 1998). (Appendix A).
An evaluation of progress toward the SMART goal of HTN control with exercise and
drug therapy reveals that after 6 months, though progress has been made through the combined
interventions, the overall goal of HTN control target level of <110/60mmHg within 3 months has
not yet been achieved. Regular exercise intervention has been achieved and maintained. I
currently exercise using a combination of aerobic and resistance training schedules (3 times per
week) for one hour periods. This intervention is verifiable through my own exercise log, the
attendance records maintained by the professional trainer who supervises my training and the
monetary receipts for the funds invested for each exercise session (Appendix A).
Regarding the drug therapy intervention for HTN control, regular, daily compliance with
prescription consumption has been achieved and maintained. This intervention is verifiable
through my own self reporting, validation of prescription use by my spouse, who is a health care

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professional and local pharmacy records that authenticate prescription receipt and refill. Despite
the personal successful compliance both interventions, according to my physician, failure to
reach target goal of <110/60 mmHg by 3 months has been plagued by medication side effects
that risked harm (hypokalemia and electrolyte shifts), physical side effects (persistent cough),
which have forced physician directed readjustments in drug selection and dose. Necessary drug
changes have undermined establishing a consistently effective and tolerable regimen within the
first 4 and months of drug therapy. Future intervention changes in drug therapy regimen will
require timely physician initiated and approved drug selections to achieve target results with
minimal side effect (Appendix A).

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Appendix A

Interventions: monitoring blood pressure trends, exercise log and observe food intake.
Decrease salty, fatty, fried foods, red meats and increase vegetable and fruit intake. No
medications at this time frame.
March 19, 2013 right arm

142/82 HR 68

Boot camp with weight lifting class

March 20, 2013 right arm

156/85 HR 70

Weight lifting

March 21, 2013 left arm

154/95 HR 68

Boot camp with weight lifting class

March 24, 2013 right arm

148/86 HR 67

March 25, 2013 right arm

153/82 HR 76

March 26, 2013

Boot camp with weight lifting class

March 27, 2013 right arm

150/90 HR 74

Weight lifting

March 28, 2013 left arm

151/89 HR 67

Boot camp with weight lifting class

April 1, 2013 left arm

157/95 HR 67

April 2, 2013

Boot camp with weight lifting class

April 3, 2013 right arm

149/88 HR 76

Weight lifting

April 4, 2013 left arm

152/90 HR 68

Boot camp with weight lifting class

April 5, 2013 right arm

150/82 HR 64

April 8, 2013 right arm

155/88 HR 72

Positive HTN trend and Lisinopril started. Continue to monitor and document as above.
April 9, 2013 left arm

110/62 HR 68

Boot camp with weight lifting class

April 10, 2013 right arm

108/66 HR 64

Weight lifting

April 11, 2013 right arm

106/68 HR 66

Boot camp with weight lifting class

April 12, 2013 left arm

108/70 HR 70

April 15, 2013 right arm

112/62 HR 69

April 16, 2013 left arm

114/59 HR 61

Boot camp with weight lifting class

Great response to prescribed oral medication however a chronic harsh non-productive

cough has started. Will monitor cough for a few more weeks and will return for another follow
up visit in the office.
April 17 June 28, 2013 -

blood pressures averaging 106/68 for the past 6 weeks. Continue

with the above exercise program of 3 times per week. Harsh chronic nagging cough continues.

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Follow up visit with physician and Lisinopril stopped due to side effects and Diovan with HTCZ
started.
July 3 8, 2013

Prescribed medication started however unable to monitor blood pressures

while on vacation.
July 9, 2013 left arm

121/89 HR 109

Boot camp with weight lifting class

July 11, 2013 right arm

122/68 HR 103

Boot camp with weight lifting class

July 12, 2013 left arm

114/74 HR 69

Weight lifting

July 16, 2013 right arm

119/73 HR 78

Boot camp with weight lifting class

July 17, 2013 left arm

118/75 HR 83

Weight lifting

July 18, 2013 right arm

113/71 HR 80

Boot camp with weight lifting class

July 22, 2013 left arm

111/69 HR 76

July 25, 2015 right arm

106/67 HR 99

Boot camp with weight lifting class

Blood pressures not as controlled with this medication and frequent leg cramps and
headaches. Physician again changed the medication to Diovan only. Continue with above
monitoring and report to physician blood pressure results.
August 5, 2013 left arm

122/67 HR 90

August 6, 2013 right arm

130/89 HR 92

Boot camp with weight lifting class

August 8, 2013 left arm

142/90 HR 91

Boot camp with weight lifting class

August 9, 2013 right arm

143/89 HR 95

Weight lifting

August 12, 2013 left arm

136/86 HR 88

August 13, 2013 right arm

140/82 HR 76

Boot camp with weight lifting class

August 14, 2013 left arm

141/76 HR 81

Weight lifting

August 15, 2013 right arm

140/80 HR 72

Boot camp with weight lifting class

Physician notified and blood pressure trends reviewed. Diovan discontinued immediately
due to poor response in controlling blood pressures. Norvasc started. Continue with monitoring
blood pressures and report results to physician.
August 19, 2013 left arm

126/82 HR 74

August 20, 2013 right arm

119/78 HR 76

Boot camp with weight lifting class

August 21, 2013 left arm

121/83 HR 69

Weight lifting

August 22, 2013 right arm

132/74 HR 71

Boot camp with weight lifting class

August 26, 2013 left arm

123/77 HR 79

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August 27, 2013 left arm

139/80 HR 83

Boot camp with weight lifting class

August 28, 2013 right arm

129/74 HR 73

Weight lifting

August 29, 2012 left arm

122/72 HR 72

Boot camp with weight lifting class

September 5, 2013 right arm 118/76 HR 73

Boot camp with weight lifting class

September 6, 2013 left arm

138/84 HR 78

September 9, 2013 right arm 119/77 HR 84

Physician notified and blood pressure trends reviewed. Physician agreed that blood
pressure goal has not yet been meant and added Indapamide to current prescribed medication.
Continue with monitoring and return a call to the office with results. Schedule a follow up
appointment for December 10, 2013 to re-evaluate health status.
September 11, 2013 left arm 124/81 HR 88

Weight lifting

September 12, 2013 right arm 119/79 HR 78

Boot camp with weight lifting class

September 13, 2013 left arm 129/82 HR 82

September 17, 2013 right arm 134/76 HR 91

Boot camp with weight lifting class

September 18 November 1, 2013 average blood pressure trend is 120/79 HR 83

Physician notified and blood pressure trends reviewed. Physician agreed that blood
pressure goal still has not yet been achieved. No change in medications at this time. Continue to
monitor blood pressure trends. We will discuss further HTN management interventions on the
December appointment.

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References

American Heart Association (2013). Family history and heart disease, stroke. Retrieved from
http://www.heart.org/heartorg/conditions/more/myheartandstrokenews
Kaplan, N., Bakris, G., & Forman, J. (2013). Exercise in the treatment and prevention of
hypertension. Retrieved from http://www.uptodate.com
Kaplan, N., Bakris, G., & Forman, J. (2013). Patient information: High blood pressure, diet and
weight (beyond the basics). Retrieved from http://www.uptodate.com
Kaplan, N., Domino, F., Bakris, G., & Forman, J. (2013). Overview of hypertension in adults.
Retrieved from http://www.uptodate.com
Mann, J., Hilgers, K., Bakris, G., Kaplan, N., & Forman, J. (2013). What is goal blood pressure
in the treatment of hypertension? Retrieved from http://www.uptodate.com
Pender, N., Murdaugh, C., & Parsons, M. (2011). Health promotion in nursing practice (6 ed.).
Upper Saddle River, NJ: Pearson Education, Inc.
Sharecare (n.d.). Realage Profile. Retrieved from http://www.sharecare.com/user/ronda-mott
Sparks, S., & Taylor, C. (2010). Nursing diagnosis reference manual. New York, NY: Lippencott
& Williams.
Tofler, G., Silver, J., & Soloman, D. (2013). Psychosocial and other soical factors in acute
myocardial infarction. Retrieved from http://www.uptodate.com
Velicer, W. F., Prochaska, J. O., Fava, J. L., Norman, G. J., & Redding, C. A. (1998). Detailed
overview of the transtheoretical model. Retrieved from
http://www.uri.edu/research/cprc/TTM/detailedoverview.htm
Wilson, P., Cannon, C., & Downey, B. (2013). Overview of the risk equivalents and established
risk factors for cardiovascular diseases. Retrieved from http://www.uptodate.com

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