TYPE 1 DIABETES 1

TYPE 1 DIABETES

by

Sonia Donaires

Applied Research Project Paper Submitted in Partial Fulfillment Of the Requirements

Forthe Degree of Master in Public Health MPH 500

Concordia University Nebraska

Dr. Rebeca Toland

August 14, 2014

Abstract

This is a studies of T1D from the point of view of the Domains of Public Health: epidemiology and biostatistics, biomedical basis, environmental factors, socialand behavioral factors, and policy. In terms of epidemiology, T1D is a disease that affects children, teenagers, andyoung adults. The prevalence is particularly in whites children more than others with an incidence of 26.6/100,000in US,and affecting million around the world. According to the biomedical basis,T1D is categorized as a chronic disease that destroys B-cells that impede the production of insulin in the pancreas; as a result of this the blood glucose levels increasewhich can cause serious harm to the body. In addition of the genetic, environmental factorsmay contribute to the disease, such as the prenatal influence, seasonal effects, viruses, possible reaction to cow’s milk, and vitamin Ddeficiencies in early childhood. Social and behavioral factors are based on research from two psychological models of health behaviors: The Health Believe Model and Ecological Model. These models determine if the person is likely to change behavior when faced with a health threat. The application of these models by patients with T1D involves a progressive step of acceptance of the disease:to follow a daily treatment and to provide psychological support to assume responsibility of the disease and to take control over patients’life.

Epidemiology of Type 1 Diabetes

Today, Type 1 Diabetes (T1D) is an autoimmune disorder affecting millions of children around the world, and is increasing at rates that cannot be explained. In this study I will discuss the risk factors and the distributions of T1D and I will review the epidemiologic studies and reports bypublic health agencies such as the WHO and itsMultinational Project for Childhood Diabetes, know as the DIAMOND Project, EURODIAB, and the SEARCH for Diabetes in Youth (SEARCH).

Studies conducted between 1990-1994 by the WHO revealed the incidence of T1Damong 75.1 million children in 50 countries was 19,164 cases. CDC reports a low of 0.1/100,000 per year in China and South America to a high of 36.5/100,000 in Finland and 36.8/100,000 per year in Sardinia, Finland, Sweden, Norway, Portugal, the UK, Canada, and New Zealand. Approximately half of the European population reported higher incidencerates 5-10/100,000 per year. (Karvonen, 2000)

An ethnicity study by SEARCH showed that T1D was most prevalent among Non-Hispanic whites at 2.0/1,000 with an incidence of 23.6/100,000 because of smoking, and a diet high in saturated fats.Among African American youth the prevalence of T1D was 0.57/1,000 for youth ages 0–9 years and 2.04/1,000 for youth 10–19 years. The incidence of T1D for 0–9 year olds and 10–19 year olds during 2002–05 was 15.7/100,000,of the African American youth that attended the research visit with T1D, 50% of those older than 15 were either overweight or obese.

The incidence of T1D in Hispanic youth in the SEARCH study was 15.0/100,000 and 16.2/100,000 for females and males 0–14 years of age. Poor glycemic control as well as high LDL-cholesterol and triglycerides were common and 44% of these youth with T1D were overweight or obese.The incidence of T1D among Asian and Pacific Islander youth was 7.4/100,000 for those 0–9 and 10–19 years olds, respectively. The Pacific Islanders were more likely to be obese as compared to the Asian or Asian-Pacific Islanders.

The majority of Navajo youth that were identified as having diabetes were diagnosed with T2D (66/83 in the SEARCH paper). The authors state that T1D is present in Navajos, but that it is infrequent; they estimate that the prevalence of T1D in Navajo youth is 0.5/1,000 and the incidence of 5/100,000 per year. The authors state that, regardless of age, Navajo youth likely to have poor glycemic control and a high prevalence of unhealthy behaviors and depressed mood.

There are various risk factors for the development of T1D: age – the incidence rate increasesfrom birth and there is a high incidence in ages of 10-14, which declines after puberty and appears to stabilize between ages of 15-29. (Maahs, 2010); gender - females and males are equally affected with T1D in young populations; genotype - although the majority of T1D cases occur in individuals without a family history of the disease, T1D is strongly influenced by genetic factors. In the United States, individuals with a first-degree relative with T1D have a 1 in 20 lifetime risk of developing T1D, compared to a 1 in 300 lifetime risk for the general population(Redondo, 2001). Additional risk factors include those who are genetically susceptible or have reactions to cow’s milk, breastfeeding, wheat gluten, and vitamins D and E.

T1D is increasing especially in children under 5 years of age in Europe and in the U.S.Each year, more than 13,000 young people are diagnosed with T1D in U.S.,While in Europe the totals reach 28 million children who diagnosed with T1D.Today, the incidence rate of T1D is increasing 0-14.

Biostatistics for T1D

Diabetes has increased in the last decade among children and adults and today is the 7th leading cause of death in the U.S. My research includes biostatistics data for T1D collected between 2002- 2010.

The data collected in these research was derived from various data systems such as the CDC, the Indian Health Service’s (IHS), National Patient Information Reporting System (NPIRS), the U.S. Renal Data System of the National Institutes of Health (NIH), the U.S. Census Bureau, National Health Interview Survey (NHIS), 2009 IHS data, and 2010 U.S. resident population estimates.

The methods for estimating the percentage of people younger than 20 years with diagnosed Type 1 or Type 2 diabetes was obtained from the 2007–2009 NHIS data. Information on diagnosed diabetes was obtained from a knowledgeable family member under 18 years, and was self-reported for patients 18–19 years of age. Investigations reveals that among people under 20 in the U.S. in 2010, 215,000 have T1D or T2D, which represents. 26 percent of all people in this age group with 18.8 million people diagnosed yearly, and 7.8 million undiagnosed. (CDC)

SEARCH for Diabetes in Youth is another multicenter study funded by CDC and NIH to examine diabetes type 1 and type 2. SEARCH findings for youth under 20 include the following:

• During 2002–2005, 15,600 youth were newly diagnosed with T1D annually, and 3,600 youth were newly diagnosed with T1D.

• Among youth under 10 years, the rate of new cases was 19.7 per 100,000 each year for T1D and 0.4 per 100,000 for T2D. Among youth aged 10 years or older, the rate of new cases was 18.6 per 100,000 each year for type 1 diabetes and 8.5 per 100,000 for T2D

• Non-Hispanic white youth had the highest rate of new cases of T1D with 24.8 per 100,000 per year among those younger than 10 years and 22.6 per 100,000 per year among those aged 10–19 years.

• T1D was extremely rare among youth 10 and under. While still infrequent, rates were greater among youth aged 10–19 years than in younger children, with higher rates among U.S. minority populations than in non-Hispanic whites.

• Among non-Hispanic white 10–19 years, the rate of new cases was higher for T1D than for T2D. For Asian/Pacific Islander and American Indian youth aged 10–19 years, the opposite was true—the rate of new cases was greater for T2D than for T1D. Among non-Hispanic black and Hispanic youth aged 10–19 years, the rates of new cases of T1D and T1D were similar. (CDC)

Results from these studies indicate that the incidence of T1D is increasing in ages 0-10year and is decreasing in ages 11-20. Studies also show that T2D is increasing from 11-20 years. These data is used to analyze the incidence and prevalence of the disease, identify the risk factors for T1D, and to prevent, control, and implement programs of prevention. But, according to the research, there is no known way to prevent T1D. Several clinical trials for preventing T1D are currently in progress or are being planned. To survive, people with T1D must have insulin delivered by injection or a pump. Risk factors for T1D may be autoimmune, genetic, or environmental.

Biomedical Basis of Type 1 Diabetes

T1D is a metabolic disease that commonlyaffects children. The two most common forms of diabetes are Type 1 and Type 2; and have very different etiologies and different clinical presentation. In this study, I will show how the body reacts in the absence of pancreatic B-cell, compare T1D with T2D, and describe the biological and molecular characteristics of T1D.

After a personeats food that contains carbohydrates, a healthy body breaks down the chemicals in the small intestine tosingle sugar molecules. The cells that are resting in the intestine absorb the glucose which passes into the bloodstream; when it reaches the pancreas, the pancreatic B-cells inside detect the rising glucose level and release insulin into to the bloodstream and keep glucose levels in a healthy range. Most cells in the body have receptors on the surface that attract to the circulating insulin. Insulin acts like a key that open up the doors of the cells so that the circulating glucose can get inside the cell. The cells can use the glucose to produce energy that the body needs to function properly.

T1D is a polygenic T-cell dependent autoimmune disease characterized by the selective destruction of the B-cells of the islets of Langerhans; it is susceptible to individuals that have inherent defects that increase the risk of a pathogenic response rather than protective immune response. When the body is affected for Type 1 diabetes, the pancreas does not produce insulin; a hormone the body needs to maintain proper blood sugar levels. In Type 1 diabetes the pancreatic B-cells lose the ability to produce insulin, resulting in high blood glucose levels and other complications in the body. The immune system, specifically the white blood cells, mistake the pancreatic B-cells for foreign invaders and as an autoimmune response, they secrete antibodies (T-cells) that destroy their own B-cells. As a result, the pancreas produces little or no insulin. Without insulin, glucose cannot enter the cells, so the cells are starved for calories that they should be receivingand as a consequence of this failure glucose level builds up in your bloodstream resulting in a condition called hyperglycemia. T1D is an autoimmune response of the body that destroys the pancreatic B-cells that are very important to producing insulin in the body.

In comparison with T2D, the loss of pancreatic B-cells also occurs in T2D, but with a different mechanism, and more often, in adults.T2D is typically linked to metabolic syndrome and the presence of insulinresistance. However, a large subset of T1D patients routinely exhibits insulin resistancecontributing to the metabolic distress in islets (regions of the pancreas).In T2D, as weight increases theinsulin resistance appears, the pancreatic B-cells become overworked and die from high glucose levels. As the fat content in the body increases, the B-cells die. T1D and T2D have similar consequences in terms of glycemic control and the emergence of long-term complications. With the rising incidence of T1D and T2D, it is now being argued that both T1D and T2D are essentially disorders of altered insulin resistance set against the backdrop of genetic susceptibilityand the inflammatory process. (Sarkar, 2012). In type 1 diabetes (autoimmune diabetes) the loss of B-cells is often close to absolute with less than 1% of beta cells remaining in patients with long-term diabetesthat have prolonged C peptide production.(Buttler, 2007)

In most patients with almost no remaining B- cells, essentially all of the islets are devoid of B- cells while isletscontain cells expressing glucagon and somatostatin. Nevertheless, some beta cells often remain as scattered single cells in the parenchyma and ducts.In a small subset of patients, even with long-term type 1 diabetes, significant C-peptide is present and lobules of pancreas remain where all the islets contain beta cells and appear essentially normal in terms of expression of insulin while the rest of the pancreas is devoid of beta cells in islets.Shrinkage in overall pancreatic mass in patients with T1D has long been noted. (Henderson) Analysis of decreased pancreatic volume was recently combined with imaging of iron particle pancreatic accumulation to help distinguish patients with T1D from normal controls. (Gaglia, 2011)

According toWitebsky, the definition and classification of autoimmune disease has been difficult to establish. Definition of a disease as an autoimmune state depends on detectable circulating or cell-bound antibodies reactive with an auto-antigen, identification of the auto-antigen, presence of mononuclear cell inflammation in the target tissue, and ability to transfer disease with lymphoid cells or with serum. In Type 1 diabetes, there is still uncertainty regarding the nature of the auto-antigens. Taken together, these observations indicate that B-cell destruction in T1D cannot yet be definitively classified as an autoimmune disease, but certainly as an immune-medicated disease. (Eisebarth, 2004)

The increasing deficit of pancreatic B-cells is correlated with increasing the incidence of T1D. All genetic studies point to two cells types: the T cell in the immune reaction and the pancreatic B-cells.

Environmental Factors of Type 1 Diabetes

Studies show that T1D is a genetic disease that typically appears within the first few months or years of a child’s life. Scientists have proposed a multiple hypothesis to explain the increase of T1D. In addition to genetic factors, environmental causes include prenatal influence, seasonal effects, viruses, genetic susceptibility to cow’s milk and other early nutritional factors, and vitamin D.

Prenatal risk occur if parents of siblings have T1D the child has from to 2%-6% risk of developing the disease, when he has a higher birth weigh, or when he is born from a mother who is old his chances increases. (Baker, 2013)

Seasonal pattern of T1D increases during late autumn, winter, and early spring.

Reports on the seasonality of T1D in adults have been mixed, but a recent report from Sweden on more than 5800 patients ages 15–34 found higher incidence during January–March and the lowest during May–July with no difference by gender

Viral infections can provoke autoimmune responses or interfere with beta cell function; this may cause acute cell rupture with exposure of intracellular antigens to the immune system causing the destruction of beta cells.

Research indicates that breastfeeding for at least three month decreases the risk of T1D. Other studies conclude that exposure to cow’s milk-based formula before one year of age may increase diabetes risk. (Baker, 2013)

Vitamin D is presented in skin in response to sunlight. Studies show that young people with T1D have lower circulating levels of VD, which is correlated, with an increase of T1D. But there are not enough studies to prove that the increase of VD can decrease T1D. (Gale, 2013)

Social and Behavioral Factors

In this study, I will review the social and behavioral factors related to T1D, the psychological models of health behavior, the health belief model, and the ecological model of health behavior.

T1D is a chronic disease and a potentially life-threatening condition, which has a life-long impact on those diagnosed with it and their families. T1D is an autoimmune disease that is not extensively researched and therefore not preventable. The major concern is preventing the disability that is inevitable when the disease is not well controlled (Schneider, p.184). The multiple complications of T1D, if blood glucose is not controlled well, are atherosclerosis, blindness, nerve damage, and kidney disease.

The social and behavioral factors such as family behavior and support, peer support, and stress and emotional status of the patient heavily impact the presence of T1D. T1D has major psychological impact on adolescents.

Family behavior and support

T1D is a chronic illness, affecting children 0 – 10 whose parents are then responsible for controlling the blood glucose levels and following treatment advice. According to research, adolescence is the most difficult stage to be diagnosed with T1D because the relationship between parents and teens is often weak. A study of 58 adolescents with T1D concluded that youths with well-controlled diabetes reported less conflict among family members and parents. Studies have shown that a child who lives with parents and relatives who poorly control his diabetes will exhibit negative side effects noticeable in his personality, physical well being, schooling, and participation in activities away from home. (Carline, 2013)

Other studies concluded that proper treatment includes targeting family communication and implementing conflict resolution to improve adaptation to Insulin Dependent Diabetes Mellitus (IDDM), treatment, adherence, and diabetic control. Different types of therapies have been developed to support patients as well their families to deal with the impact of the disease such as the efficacy of Behavioral Family Systems Therapy (BFST-D) that according the studies has improved glycemic control.

Mental Health Problems

Adolescents with T1DM face a number of stressors and daily challenges as a result of their chronic illness. Treatment regimes includes daily insulin injections, self-monitoring of blood glucose, a prescribed meal plan, regular exercise, problem solving tactics to regulate blood glucose in the school (social interaction with friends and teachers) and at home (family members).