Lila Miller Goldberg is a 45-year-old diabetic. She had difficulty losing weight since her pregnancy years ago and has starte

SOC313 Introduction to the Miller Family

Sarah (40 yrs) and Joe Miller (43 yrs) are at the center of this family. [See the geneology maps (family

trees) for both Sarah and Joe below.] They are a middle aged couple, married 21 years with three

children. Their children are Lucy (20 yrs), Josh (17 yrs), and Abe (12 yrs). Lucy has had struggles with

substance abuse, along with having been diagnosed with bipolar disorder. Josh has been sneaking away

with friends and smoking pot. Abe is a good student but has started to act out recently.

Sarah’s parents are Donna and Manny Maldonado. Manny is third generation Hispanic American from

Mexico. Donna has long suffered from her “moods” which is mostly frustrating to Manny. He says it’s

“brujeria” (related to witches and magic). He worries that someone puts spells on her. They both are

fluent in Spanish, Donna having learned as a result of being with Manny and around his family. Sarah is

their oldest daughter followed by her brother, Mike (36) and then sister Becky (33). Becky, divorced,

has one child, Elías (10 yrs old) who was recently diagnosed with Leukemia. Mike is alone, having

recently suffered the loss of his companion of many years to AIDS. He is secretly also concerned that he

might be HIV+.

Joe’s parents are Ella and John Miller. Ella is at the center of our story as she has been trying to heal

herself from breast cancer through the use of a variety of natural means. She was raised on a farm and

is not very trusting of “modern medicine.” Her husband, (Joe’s father) John is of American Indian origin.

He uses a variety of traditional methods for health and well being and as a means of banishing bad

spirits from their home. Ella’s mother passed away over ten years ago but her father is still alive. He is

often referred to as the “shakey grandpa” by the grandchildren and great grandchildren due to the

manifestation of some symptoms of his Parkinson’s disease.

Joe has a sister, Lila (45 yrs), who has diabetes and who has always struggled with her weight. She and

her husband have one child, Alisha (20), who’s currently in college. Joe’s older brother Sam (50 yrs), was

married and then divorced years ago, has one son from whom he is estranged. He is an alcoholic who

hasn’t been able to keep a job for years.

The family and extended family get along well for the most part though the many cultural traditions and

backgrounds do clash from time to time. Manny, for example, has been known to say, “They’re crazy!”

when the family discusses some of the health issues that are going on and how they are being handled.

At one time, for example, Ella’s skin turned orange due to the amount of carrot and other juices she was

consuming in order to get rid of her cancer.

Sarah has been married to Joe long enough to know her well and when her sister Becky’s son Elias was

recently diagnosed with Leukemia, Ella was hopeful that Sarah would encourage Becky to use natural

means for treating him. Sarah isn’t really too sure about how she feels about it.

Sara Miller’s family tree

Joe Miller’s family tree

Learning Objectives

1. Describe why hypertension and diabetes are called silent diseases

2. Describe how hypertension and diabetes affect different individual, familial, and social domains

3. Explain how self-management and medication can be used to treat hypertension

4. Identify disparities in hypertension awareness, treatment, and control

5. Explain how both lifestyle changes and medication can be used to treat diabetes

6. Identify relationships between diabetes prevalence and larger social issues

Silent Disorders: Hypertension and Diabetes 5

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

5.1 Introduction to Hypertension and Diabetes

“Has Barbara been eating a lot of sweets lately?” the pediatrician asked Barbara’s mother, Margaret, on the phone. “No, she doesn’t have a sweet tooth and we don’t keep a lot of sweets in the house,” Margaret replied. Barbara was 11 and had come down with a particularly nasty stomach ailment. “Why do you ask?” “Well, most of the tests we did suggest that Barbara has a viral infection, but Barbara’s urine had a very high concentration of glucose. Let’s just monitor it for a while and see what happens.”

Barbara used urine glucose test strips for several months. At first, her urine glucose went back to normal, but a few months later it climbed back up and stayed there. She was diagnosed with type 1 diabetes, also known as diabetes mellitus. At the time Barbara was diagnosed, the family was undergoing quite a bit of stress, because Barbara’s teenaged step-siblings were moving into the family home.

5.2 Definition and Brief History of Hypertension and Diabetes

D iabetes and hypertension have been called “evil twins” and “bad companions,” because they are so often found together in the same person. Both are also “silent” disorders, in that they may cause no early symptoms but create extra work for the heart and blood vessels. Having hypertension makes it more likely that someone will develop diabetes, and hav- ing diabetes makes it more likely that the person will develop hypertension. Both hypertension and diabetes increase the risk for problems in the small blood vessels, known as microvascular disease, of the eyes, kidneys, and peripheral nerves, as well as problems in the large blood vessels, or macrovascular disease, of the heart, peripheral vascular system, and brain. The risk for both microvascular and macrovascular disease is even higher when a person has both hypertension and diabetes (see Table 5.1).

Table 5.1: Macrovascular and microvascular complications of hypertension and diabetes

Macrovascular complications

Atherosclerosis Disease of the arteries that can result in heart attack and stroke

Peripheral vascular disease Narrowing of arteries that can result in ischemia, or restricted blood supply to tissues, and ulcers

Microvascular complications

Retinopathy Damage to the retina that can result in loss of vision

Nephropathy and end-stage renal disease

Disease of the kidney that can result in kidney failure

Neuropathy Disease of the nerves that can result in pain, numbness, and weakness in the hands and feet

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

Table 5.2 gives a side-by-side comparison of the two disorders and their symptoms. In this sec- tion we compare and contrast the history of these two disorders, define them, and examine how the biology of each affects physical, mental, and social functioning. In the next section we apply Bronfenbrenner’s system of human ecology to each disorder. We then explore hypertension over the life span, approaches to its treatment, and its relationship to social issues. Finally, we discuss diabetes over the life span, its treatments, and related social issues.

Table 5.2: Characteristics of hypertension and diabetes

Aspect Hypertension Type 1 Diabetes Type 2 Diabetes

Age of onset Usually older adults Often in early childhood, but can be as late as adulthood

Usually in older adults, but recently seen in children and adolescents

Early symptoms None Excessive thirst and urination, weight loss

None

Later symptoms Severe headache, blurred vision, chest pain, difficulty breathing

Fatigue, blurred vision Excessive thirst and urination, weight loss, slowed healing, fatigue

Hypertension Hypertension is abnormally high blood pressure. Blood pressure is a measure of the force that the blood exerts against the walls of the arteries as the heart pumps blood through the body. It is

expressed as two numbers, written as if it were a fraction, for example, 120/70. The upper number is the force produced during the time the heart is con- tracting, called systolic blood pressure, and the lower number is the force produced when the heart is relaxing between beats, or diastolic blood pres- sure. The units for blood pressure measurement are millimeters of mercury, or mmHg. Watch a short video from Medline Plus for more detail about blood pressure:

http://www.nlm.nih.gov/medlineplus/ency/anato myvideos/000013.htm

Evidence shows that what was then called “hard pulse disease” was recognized as long ago as 2600 BCE. Of course, treatment at the time was rather crude by today’s standards and relied on reducing the blood volume either by bloodletting or apply- ing leeches (Esunge, 1991). The Reverend Stephen Hales is recognized as the first to measure intra- arterial pressure in a horse in 1733 (Kotchen, 2011). In the 1800s, Thomas Young and Richard Bright

Mary Evans Picture Library/Everett Collection

Hypertension, or what was then known as “hard pulse disease” was originally treated by bloodletting or applying leeches.

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

built on Hales’s work and gave us modern descriptions of hypertension (Esunge, 1991). In 1905, introduction of the blood pressure cuff with mercury columns, or the sphygmomanometer, together with arterial sounds associated with systolic and diastolic measurement heard via a stethoscope, allowed objective measurement of blood pressure for the first time (Kotchen, 2011).

The medical community did not think that elevated blood pressure—hypertension—was a prob- lem until well after the insurance industry did. As early as 1918, the insurance industry began requiring blood pressure measurement for life insurance applicants and gathering actuarial data that related blood pressure to mortality (Kotchen, 2011). At the same time, the medical commu- nity suggested that rising blood pressure was a normal part of aging and that attempts to halt or reduce the rise were dangerous. Cardiologist J. H. Hay (1931) suggested, “There is some truth in the saying that the greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it” (p. 26).

We can only wonder what might have happened if President Franklin Roosevelt’s hypertension had been treated. His blood pressure was recorded as 162/98 mmHg in 1937 at age 54; 180/88 mmHg in 1940; 188/105 mmHg in 1941; between 180/110 and 230/140 mmHg in 1944, when he had a series of small strokes at the age of 62; and 260/150 mmHg in early 1945. He died of a stroke later that year at the age of 63. Just before his death, his blood pressure had been recorded as greater than 300/190 mm Hg (Moser, 2006).

One reason hypertension was not treated aggressively during the first half of the 20th century was the lack of treatments. Most of the medications of the time were either ineffective or had nasty side effects. The first clinical trial demonstrating efficacy and tolerability of a treatment for hypertension (the diuretic chlorothiazide) was published in 1959 (Moser & Macaulay, 1959). At first, diuretics were used as adjuncts for hypertension treatment, but later it was recognized that they could be used effectively alone to reduce the medical problems and death associated with hypertension (Moser & Hebert, 1996).

At the same time effective treatments were found, the underlying causes of hypertension were being uncovered, and hypertension was beginning to be understood as the result of multiple interacting systems, including the heart and the kidneys, and the vasculature, the endocrine, and the nervous systems. Later, the major proponent of this theory, I. H. Page (1982), added genetic and environmental aspects, bringing the theory current for the 21th century.

Two large studies published in the 1960s—the Veterans Administration Study (“Effects of Treat- ment on Morbidity in Hypertension,” 1967) and the Framingham Heart Study (Kannel, Schwartz, & McNamara, 1969)—finally convinced most medical practitioners that controlling hypertension reduces the rate of stroke, heart attacks, and kidney damage. At the same time, more medica- tions for treating hypertension were being introduced, including beta blockers and angiotensin- converting enzyme (ACE) inhibitors. Another class of medications, angiotensin receptor blockers (ARBs), was first introduced in 1995.

The U.S. National Hypertension Program was established in 1972, and the first report of the Joint National Committee (JNC) on detection, evaluation, and treatment of high blood pressure was published in 1977. Since then, the JNC has issued updates every few years through publication of

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

the JNC 7 in 2003 (Chobanian et al., 2003). The JNC 7 was the first to describe prehypertension as blood pressure that is higher than normal but not high enough to be considered hypertension. See Table 5.3 for blood pressure measurements.

Table 5.3: Blood pressure categories

Category Systolic Pressure mmHg

Diastolic Pressure mmHg

Normal Less than 120 and Less than 80

Prehypertension 120–139 or 80–89

Hypertension Stage 1 140–159 or 90–99

Hypertension Stage 2 160 or higher or 100 or higher

Source: Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., Izzo, J. L., . . . National High Blood Pressure Education Coordinating Committee. (2003). Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension, 42(6), 1206–1252.

Most hypertension does not have a clear cause—it is classified as essential hypertension. In con- trast, secondary hypertension results from an identifiable cause, such as kidney disease or as the side effect of a medication. We do know that certain traits and categories put people at higher risk for developing hypertension, such as:

• being Black, • having diabetes, • drinking too much alcohol (more than one drink a day for women, more than two

drinks a day for men), • being overweight or obese, • being older, • consuming too much salt, • smoking, and • experiencing frequent stress or anxiety.

The two main approaches to care for hypertension are lifestyle modification and medication. Although no one can control heritage or age, it is possible to modify many of these risk factors, as we see in the section on treatment of hypertension. Everyone can benefit from the suggested life- style modifications, but some people have to add medication (sometimes two or three) to reach recommended blood pressure goals.

The usual way to define overweight and obesity is by body mass index (BMI), which is calculated from weight and height. (The formula is weight in kilograms divided by surface area in square meters [kg/m2], but most people look it up in a table.) Table 5.4 shows the ranges of BMI that cat- egorize normal weight, overweight, and obesity. You can look up your own BMI by entering your weight and height on this NHLBI website:

http://www.nhlbi.nih.gov/guidelines/obesity/bmi_tbl.htm

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

Table 5.4: Body mass index (BMI) categories

Category BMI

Normal 18.5–24.9

Overweight 25.0–29.9

Obese 30.0–39.9

Extremely obese ≥ 40.0

Diabetes Diabetes is characterized by high levels of glucose in the blood. Glucose is a simple sugar that all cells use as an energy source. The two main types of diabetes are type 1 (T1D), which affects about 5% of people diagnosed with diabetes, and type 2 (T2D), which affects 90% to 95% of peo- ple diagnosed with the disorder. When one or another is specified, we use the terms T1D or T2D, but when we talk about the disorder in general, we use the term diabetes. A third type of diabe- tes, which may be becoming more common, is gestational diabetes. New diagnostic criteria for gestational diabetes have increased the number of women diagnosed to 18% of pregnant women (American Diabetes Association, 2013).

Type 1 diabetes (T1D) is a disorder in which the body’s own immune system attacks and kills beta cells in the pancreas that produce insulin, a hormone needed for cells to absorb glucose from the blood and transport it across the cell’s outer surface to the inside, where it can be used for energy. As a result, the body produces too little insulin. This kind of misdirected attack on the body is known as autoimmune disease. T1D was previously called insulin-dependent diabetes mellitus or juvenile diabetes. It is usually first diagnosed in children and young adults. In order to survive, people with T1D must have insulin delivered to their blood by injection or a pump.

In contrast to T1D, people with type 2 diabetes (T2D) produce enough insulin at first, but their cells do not respond to it properly, a condition known as insulin resistance, or insensitivity. As a result, more and more insulin is required, and the beta cells of the pancreas become exhausted and lose their ability to produce it. T2D was previously called non–insulin-dependent diabetes, or adult-onset diabetes. It is associated with older age, obesity, a family history of diabetes, physical inactivity, and certain racial or ethnic groups. As people have become more sedentary and obesity rates have risen, T2D is being diagnosed in a younger population.

Both T1D and T2D appear to need both an inherited susceptibility and some environmental trigger to set the disease process in motion. All the environmental triggers have not yet been identified, although in some cases, it appears that certain viral infections may trigger the body to produce antibodies to the virus that cross-react with and destroy pancreatic beta cells. This is probably what happened to 11-year-old Barbara in the case study at the beginning of the chapter.

Gestational diabetes is defined as excess blood glucose that shows up in the later stages of preg- nancy in women who did not have diabetes before they became pregnant. It appears to be a form of insulin resistance that develops perhaps in response to a hormone produced by the placenta. Gestational diabetes must be treated to avoid problems for both the mother and the child.

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

Egyptian texts as old as 1500 BCE have identified diabetes as a rare condition in which people have excessive volumes of urine and lose weight. Similarly, Indian texts from the fifth century BCE refer to people with excessive urine production that is sweet, accompanied by emaciation. The term diabetes mellitus, reflecting the sweet taste of urine from people with the disorder, was used by the Greek physician Aretaeus, who lived from about 80 to 138 CE and wrote one of the first accu- rate clinical descriptions of the disorder. Until well into the 18th century, when Matthew Dobson measured the concentration of sugar in the urine and blood, diabetes was thought to be a disease of the kidneys (Eknoyan & Nagy, 2005; Polonsky, 2012).

In 1788, Thomas Cawley became the first to suggest that the pancreas played a role in the devel- opment of diabetes. His observations were later confirmed in 1889, when Minkowski and Mering showed that removing the pancreas from dogs caused diabetes that could be reversed by implant- ing pancreatic fragments. Edward Sharpey-Schafer suggested that diabetes resulted from the lack of a single product of the pancreatic cells, which he named insulin (Eknoyan & Nagy, 2005; Polon- sky, 2012). In 1922, Banting and Best isolated insulin from cows and were the first to use it to treat patients with diabetes (Banting, Best, Collip, Campbell, & Fletcher, 1922).

The availability of purified insulin turned an inevitably fatal disorder into one that could be treated—one of the first instances in which scientific investigation was almost immediately trans- lated into clinical treatment. Insulin’s biology and chemistry became an intense area of research. Insulin is a peptide hormone made up of two linked chains of amino acids. Insulin was the first hormone whose amino acid sequence (the order that the amino acids appear in the peptide chain) was determined. It also became the first hormone to be produced by recombinant DNA techniques, so that fully human insulin could be produced in vast quantities rather than isolating insulin from pig or cow pancreas, which had been the method until then (Keen et al., 1980).

During the first half of the 20th century, it became evident that not all diabetes was caused by the lack of insulin. For a long time, people had noted that those who developed diabetes as children or young adults were usually underweight, while those who developed it when they were mature adults were usually overweight. Himsworth (1936) first proposed that some patients had diabetes because they were resistant or insensitive to insulin. Yalow and Berson (1959) devised the first immunoassay to measure circulating levels of insulin. Subsequently, they found that obese people with early diabetes actually released more insulin after an oral glucose tolerance test compared with normal controls—in other words, they didn’t have too little insulin, but they were insensitive to it, as Himsworth had proposed (Yalow & Berson, 1960).

Insulin resistance is difficult to measure in a clinical setting; therefore, having high blood glucose levels (higher than normal but not high enough to qualify as diabetes) is used in its place as a marker. This intermediate level of blood glucose is termed prediabetes, also known as impaired glucose tolerance or impaired fasting glucose (fasting plasma glucose [FPG] of 100–125 mg/dL).

There are three main ways of determining whether someone has prediabetes or diabetes:

• hemoglobin A1C (HbA1C) test, • FPG test, and • oral glucose tolerance test (OGTT).

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

The HbA1C test (or A1C test for short) reflects average blood glucose levels over the last 3 months. It is not as sensitive as the other tests, and certain conditions (e.g., abnormal hemoglobin, any- thing that changes red blood cell survival, possible racial differences) can alter the results. FPG measures blood glucose after fasting for at least eight hours. It is most reliable when done in the morning. OGTT measures blood glucose after fasting for at least eight hours, then drinking a liquid containing glucose, and measuring blood glucose two hours later. For all three tests, within the prediabetes range, the higher the test result, the greater the risk of diabetes (see Table 5.5).

Table 5.5: Blood test levels for diagnosing diabetes and prediabetes

Diagnosis A1C (%) Fasting plasma glucose (mg/dL)

Oral glucose tolerance test (mg/dL)

Normal About 5 99 or below 139 or below

Prediabetes 5.7–6.4 100–125 140–199

Diabetes 6.5 or above 126 or above 200 or above

Note. mg = milligram; dL = deciliter.

Even with the advent of insulin by injection in the 1950s, many people diagnosed with T1D went blind and developed kidney disease, and about one in five people died within 20 years of being diagnosed. At that time, people monitored their glucose levels with urine tests, which gave read- ings for what had been true in their blood several hours previously but could not recognize danger- ously low glucose levels (National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], 2010). In addition, because the kidneys do not excrete glucose into the urine until blood levels reach 160–180 mg/dL, the urine test is insensitive.

Home blood glucose monitor- ing first became possible in the 1970s. At first, test strips sim- ilar to urine test strips were used and compared with a color chart. This proved impractical, and meters were developed to automatically read the strips. Today’s home glucose meters require a single drop of blood on a test strip that is fed into a small meter for reading.

People with diabetes must learn to keep their blood glucose within a normal range—neither too high (hyperglycemia) nor too low (hypoglycemia). Blood glucose levels depend on a variety of fac- tors: when and what meal was last eaten, exercise, and other medications. Self-monitoring blood

Joerg Sarbach/Associated Press

A blood glucose meter is used to self-monitor blood glucose.

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CHAPTER 5Section 5.2 Definition and Brief History of Hypertension and Diabetes

glucose can help keep glucose in the normal range. Results can also be reviewed periodically with the clinician to determine how well diabetes is being controlled. Self-monitoring is particularly useful for people who tend to have episodes of hypoglycemia, for instance, after participating in an active exercise session or sports game. Hypoglycemia can be extremely dangerous, as it can cause accidents, injuries, coma, or death. More information about hypoglycemia can be found on the American Diabetes Association website (http://www.diabetes.org/living-with-diabetes/treat ment-and-care/blood-glucose-control/hypoglycemia-low-blood.html).

Modern technology has changed the experience of people with diabetes. Today, systems allow for continuous glucose monitoring (CGM) through a small needle inserted beneath the skin. However, blood glucose still needs to be measured periodically with a conventional meter, as CGM readings lag about 15 to 20 minutes behind blood levels.

In addition to changes in detecting glucose, technology has affected how insulin is delivered and the types of insulin available. When insulin was first administered in the 1920s, it was delivered via glass syringes with rather large needles that were painful to use. Syringes and needles were reused after sterilization. Disposable syringes with smaller disposable needles that were less pain- ful to use came next. Insulin pens that allow discreetly injected insulin were developed in the 1990s. Pens combine the insulin vial with a syringe, can store a 3- to 5-day supply of insulin, and are less painful to use.

Insulin pumps were first explored in the late 1970s. The first ones were large, heavy, and not really suited for home use. Pumps have the advantage of more closely approximating how the pancreas works, with a steady infusion of insulin that can be tailored to the individual. At first they were used only for patients who had high insulin requirements. With the development of smaller and lighter insulin pumps, however, they have been more commonly used by people with T1D. Pumps are cost- lier than syringes and insulin vials but result in tighter glucose control, as measured by decreased A1C, and fewer hypoglycemic episodes. Perhaps more important, they allow “more freedom, flex- ibility, and spontaneity in the person’s daily life” (Yaturu, 2013, p. 2). More detail about delivering insulin and monitoring glucose can be found online (http://effectivehealthcare.ahrq.gov/index .cfm/search-for-guides-reviews-and-reports/?pageaction=displayproduct&productid=1240#toc).

Most people are reluctant to begin injecting themselves. Many people would rather not let oth- ers know that they need to inject—they find it embarrassing or shameful. For those people with T1D, there is little choice, and people adjust over time. What may be more surprising is that, for reasons that are unclear, clinicians tend to avoid prescribing injected insulin for their patients who have T2D, even if it is the best available option for treatment.

Science and technology continue to advance the treatment of diabetes. Better understanding of immunology may make it possible to intervene in early T1D and prevent continued autoimmune attack on pancreatic beta cells. Closed-loop insulin delivery, which has also been called the artifi- cial pancreas, is in the testing stage. Combining glucose detection, wireless communication with an insulin pump, and software that continuously determines how much insulin needs to be deliv- ered, this technology delivers insulin without the need for intervention (Yaturu, 2013). People with T1D who were born in the 1970s have gone from having to inject themselves multiple times daily to using insulin pumps. And they may see the use of an artificial pancreas become common in the near future.

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CHAPTER 5Section 5.3 Using

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