Classification and evolution of increased cardiometabolic risk states

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It has been accurately observed that certain risk factors in humans appear to 'cluster' with clinical states such as obesity and type 2 diabetes. Specifically, this risk factor clustering, and the association with insulin resistance, led investigators to propose the existence of a unique pathophysiological condition1. Many names have been provided to describe this clinical state including 'metabolic syndrome', 'syndrome X', and 'insulin resistance syndrome'1. The particular names that refer to this risk factor clustering describe the human condition characterized by the presence of co-existing traditional risk factors for cardiovascular disease (CVD), such as hypertension, dyslipidemia, glucose intolerance, obesity, and insulin resistance, in addition to non-traditional CVD risk factors, such as inflammatory processes and abnormalities of the blood coagulation system2-6. Table 1.1 lists conditions and components associated with the clustering of risk factors. As seen, the components that are associated with risk factor clustering, e.g. 'metabolic syndrome', include not only many of the traditional risk factors, e.g. lipids, obesity, hypertension, but also components that represent aspects of vascular health, such as endothelial dysfunction, inflammation, and parameters assessing blood coagulability7. Recently, a joint statement released by the American Diabetes Association (ADA) suggested that, as a construct that denoted risk factor clustering, 'metabolic syndrome' has been a useful paradigm in that it draws attention to the fact that risk factors tend to cluster in patients1. However, the ADA felt that, while there is no doubt that certain CVD risk factors cluster, it was their impression that metabolic syndrome has

Table 1.1 Proposed components and associated findings felt to represent metabolic syndrome. The components listed represent not only many of the traditional risk factors, e.g. lipids, obesity, hypertension, but also components that represent aspects of vascular health such as endothelial dysfunction. In addition, parameters assessing inflammation, blood coagulability and insulin resistance are included. From reference 7, with permission

  1. Insulin resistance*
  2. Hyperinsulinemia*
  3. Obesity: visceral (central), but also generalized obesity*
  4. Dyslipidemia: high triglycerides, low HDL, small dense LDL*
  5. Adipocyte dysfunction
  6. Impaired glucose tolerance or type 2 diabetes mellitus*
  7. Fatty liver (non-alcoholic steatohepatosis, steatohepatitis)
  8. Essential hypertension: increased systolic and diastolic blood pressure
  9. Endothelial dysfunction
  10. Renal dysfunction: micro- or macroalbuminuria
  11. Polycystic ovary syndrome
  12. Inflammation: increased CRP and other inflammatory markers
  13. Hypercoagulability: increased fibrinogen and PAI-1
  14. Atherosclerosis leading to increased cardiovascular morbidity and mortality*

* Most widely incorporated into the definition of metabolic syndrome CRP, C-reactive protein; PAI-1, plasminogen activator inhibitor type 1

Natural history of type 2 diabetes

Natural history of type 2 diabetes

Time

Years to . decades

""Typical diagnosis of diabetes

Time

Years to . decades

""Typical diagnosis of diabetes

Figure 1.1 Schematic demonstrating where the presence of metabolic syndrome fits into the natural history of type 2 diabetes. Prior to the development of clinical overt hyperglycemia and the diagnosis of type 2 diabetes, it is observed that insulin resistance may develop in the majority of individuals, primarily associated with obesity. The development of insulin resistance in an individual will need to be compensated by hyperinsulinemia in order to maintain normal glucose tolerance. However, when the insulin secretory capacity of the p cell begins to diminish such that the pancreatic function now fails to compensate for the insulin resistance, a state of relative 'insulin deficiency' leading to hyperglycemia is observed. It is at this stage that impaired glucose tolerance and impaired fasting glucose may be present. With worsening pancreatic dysfunction and the inability to compensate fully for the degree of insulin resistance, hyperglycemia continues to increase and clinically overt type 2 diabetes develops. Adapted from reference 9, with permission been imprecisely defined1. For purpose of this Atlas, we will refer to the clustering of CVD risk factors as indicative of a state of increased cardiometabolic risk.

Whereas the etiology of cardiometabolic risk is not specifically known, it is well established that obesity and insulin resistance are generally present2-4. Insulin resistance, defined as a clinical state in which a normal or elevated insulin level produces an impaired biological response, is considered to be a hallmark for the presence of metabolic syndrome. Insulin resistance can be secondary to rare conditions such as abnormal insulin molecules, circulating insulin antagonists (e.g. glucocorticoids, growth hormone, anti-insulin antibodies), or even secondary to genetic syndromes such as the muscular dystrophies8. However, the insulin resistance considered as part of the metabolic syndrome essentially represents a target-tissue (i.e. skeletal muscle) defect in insulin action and accounts for the overwhelming majority of cases of insulin resistance reported for the human condition8. The cellular mechanisms that contribute to insulin resistance are not fully understood, but will be discussed in more detail in Chapter 2.

The risk factor clustering that defines the state of increased cardiometabolic risk contributes greatly to increased morbidity and mortality in humans on several levels. First, these risk factors are present at the 'pre-diabetic' state. Specifically, and as demonstrated in Figure 1.1, it is now well accepted that the presence of insulin resistance in an individual will need to be compensated by hyperinsulinemia in order to maintain normal glucose tolerance10-14. It is also observed that in those individuals who develop diabetes, a progressive loss of the insulin secretory capacity of p-cells appears to begin years before the clinical diagnosis of diabetes. The pancreatic dysfunction fails to compensate for the insulin resistance and results in a state of relative 'insulin deficiency' leading to hyper-glycemia. It is at this stage that impaired glucose tolerance and impaired fasting glucose may be present. With worsening pancreatic dysfunction and the inability to compensate fully for the degree of insulin resistance, hyperglycemia continues to increase and

I 1 -

- 1 J

Glucose metabolism

Uric acid metabolism

Dyslipidemia

Hemodynamic

Novel risk factors

± Glucose intolerance t Uric acid I Urinary uric acid clearance

Small, dense LDL

  • SNS activity î Na retention Hypertension
  • CRP î PAI-1 î Fibrinogen
  • Glucose intolerance t Uric acid I Urinary uric acid clearance

Small, dense LDL

î SNS activity î Na retention Hypertension

Coronary heart disease

Figure 1.2 The current perspective on the relationship between metabolic syndrome and coronary heart disease. The presence of obesity in an individual is highly associated with the development of insulin resistance and hyperinsulinemia. Many traditional risk factors for CVD are related to the development of metabolic syndrome and these include glucose abnormalities, dyslipid-emia and hemodynamic factors. However, novel risk factors such as abnormalities in inflammatory markers, i.e. C-reactive protein (CRP) and coagulopathy (plasminogen activator inhibitor-1 (PAI-1)) also appear to play a role. BMI, body mass index; HDL-C, high-density lipoprotein cholesterol; LDL, low-density lipoprotein; PHLA, postheparin lipolytic activity; PP, postprandial; SNS, sympathetic nervous system; TG, triglycerides. These factors are highly related to the development of coronary heart disease. From reference 17, with permission clinically overt type 2 diabetes becomes present (Figure 1.1). Thus, the CVD risk factor clustering and the associated insulin resistance confers an increased cardiometabolic risk state and figures prominently in the natural history of type 2 diabetes (Figure 1.1).

A second major reason why a state of increased car-diometabolic risk contributes to increased morbidity and mortality in humans is the association with cardiovascular disease6,15,16. Coexisting cardiovascular risk factors, such as dyslipidemia, hypertension, inflammatory markers, and coagulopathy, are highly associated with the 'pre-diabetic' state as defined by obesity and insulin resistance, and have been defined in the past as components of the metabolic syndrome (Table 1.1). Therefore, as demonstrated, the presence of insulin resistance and obesity in 'pre-diabetes' will be associated with increasing prevalence of the CVD risk factors (Figure 1.2). Each risk factor, when considered alone, increases CVD risk but, more importantly, in combination they provide a 'synergis-tic' or 'additive' effect (Figure 1.3). For example, Lakka and his research team used definitions of metabolic syndrome by criteria as established by the National Cholesterol Education Program (NCEP) and the World Health Organization (WHO), and evaluated relative risk of death from coronary heart disease (CHD) during an 11-year follow-up in 1209 middle-aged men19. After correcting for multiple factors, the presence of the metabolic syndrome resulted in a 2.5-4-fold increase in relative risk for CVD death regardless of the criteria used (Figure 1.4). With the understanding that metabolic syndrome may precede the development of diabetes by many years (see Figure 1.1), the presence of this condition may partially explain the increase in CVD risk observed years before the diagnosis of diabetes, as outlined in Figures 1.5 and 1.6. Specifically, Hu et al. reported that the relative risk for CVD was significantly increased beginning as early

High LDL-C Hypertension

: Metabolic syndrome

Coronary heart disease

Figure 1.3 The presence of individual cardiovascular disease risk factors (hypertension, dyslipidemia) is clearly related to the development of coronary heart disease. However, when many of these factors are present in the same individual (such as individuals with metabolic syndrome), an 'additive' or 'synergistic' effect may be observed. LDL-C, low-density lipoprotein cholesterol. Adapted from reference 18

WHO WHO NCEP NCEP

WHR a 0.90 Waist a 94 cm Waist a 104 cm Waist a 94 cm or BMI a 30

WHO WHO NCEP NCEP

WHR a 0.90 Waist a 94 cm Waist a 104 cm Waist a 94 cm or BMI a 30

  • Adjusted for age
  • Adjusted for age, exam year, LDL cholesterol, smoking, family history of CHD
  • Adjusted for age, exam year, LDL cholesterol, smoking, family history of CHD, fibrinogen, leukemia, alcohol and SES

Figure 1.4 Relative risk of death from coronary heart disease (CHD) for metabolic syndrome during an 11-year follow-up of 1209 middle-aged men. As observed, regardless of whether the criteria as established for metabolic syndrome for the World Health Organization (WHO) or National Cholesterol Education Program (NCEP) were used, individuals with central obesity had an increased relative risk for CHD. In addition, these observations persisted regardless of the various statistical adjustments for lipids, smoking, family history, and other socioeconomic factors. BMI, body mass index; LDL, low-density lipoprotein; SES, socioeconomic status; WHR, waist-to-hip ratio. Adapted from reference 19

as 15 years before the diagnosis of diabetes, and the CVD risk increased significantly in the years closer to the actual time the clinical diagnosis of diabetes was made (Figure 1.5)20. Thus, the current perspective of increase in cardiometabolic risk as it relates to development of coronary heart disease is outlined schematically in Figure 1.6. The relationship of risk factors to CVD will be covered in more detail in later chapters.

In the past, a number of criteria have been suggested to meet those for being classified as having 'metabolic syndrome' for any given individual. For example, Table 1.2 outlines the criteria as previously suggested by the National Cholesterol Education Program (NCEP-ATP III)18. Although ATP III did not make any single risk factor (e.g. abdominal obesity) a requirement for diagnosis, it nonetheless espoused the

Figure 1.5 Relative risk of myocardial infarction (MI) or stroke in pre-diabetes. Hu and his collaborators, from the Nurses' Health Study, reported that the relative risk for cardiovascular disease (CVD) was significantly increased beginning as early as 15 years before the diagnosis (dx) of diabetes, and the CVD risk increased significantly in the years closer to the actual time the clinical diagnosis of diabetes was made. Adapted from reference 20, reproduced with permission

Figure 1.5 Relative risk of myocardial infarction (MI) or stroke in pre-diabetes. Hu and his collaborators, from the Nurses' Health Study, reported that the relative risk for cardiovascular disease (CVD) was significantly increased beginning as early as 15 years before the diagnosis (dx) of diabetes, and the CVD risk increased significantly in the years closer to the actual time the clinical diagnosis of diabetes was made. Adapted from reference 20, reproduced with permission position that abdominal obesity is an important underlying risk factor for the syndrome. Abdominal obesity at these cut-off points (see Table 1.2) was not made a prerequisite for diagnosis because lesser degrees of abdominal girth often associate with other ATP III criteria. In fact, some individuals or ethnic groups (e.g. Asians, especially South Asians) appear to be susceptible to development of the metabolic syndrome at waist circumferences below ATP III cut-off points. Thus, ATP III specifically noted that some individuals having only two other metabolic syndrome criteria appear to be insulin resistant even when the waist circumference is only marginally elevated, e.g. 94-101 cm in men or 80-87 cm in women. The WHO had very similar criteria as outlined in Table 1.3. However, required criteria for WHO guidelines include the presence of impaired glucose tolerance (IGT), impaired fasting glucose (IFG), diabetes, or insulin resistance. The American Association of Clinical Endocrinologists (AACE) have also provided guidelines based on clinical signs, and these are compared with both the NCEP and WHO criteria (Table 1.4). In 2003, the AACE modified ATP III criteria to refocus

  • Metabolic syndrome'
  • Metabolic syndrome'
Age (years)

Figure 1.6 Schematic demonstrating the development of metabolic syndrome in the natural history of type 2 diabetes. As shown, with the development of metabolic syndrome, there is an increasing prevalence of the associated risk factors that are observed many years before the diagnosis of type 2 diabetes is made. In addition, the CVD risk is greatly accelerated during this time. Therefore, CVD risk is elevated many years prior to the diagnosis of diabetes in large part owing to the presence of metabolic syndrome. When the pancreas fails to compenstate for the insulin resistance, hyperglycemia ensues, which also contributes greatly to CVD risk. From reference 14, with permission on insulin resistance as the primary cause of metabolic risk factors23. Major criteria included were glucose levels indicative of impaired glucose tolerance, elevated triglycerides, reduced HDL cholesterol, elevated blood pressure, and obesity. No specified number of factors qualified for diagnosis, which was left to clinical judgment.

In April of 2005, the International Diabetes Federation (IDF) presented a new consensus definition that is an important modification of the previously used ATP III definition24. The IDF definition clearly outlined the complexity of the syndrome and also suggested that central obesity should be a prerequisite for the syndrome. More importantly, the IDF

Table 1.2 Diagnosis of metabolic syndrome

as suggested by the

National Cholesterol Education Program. As

outlined, diagnosis is established when a 3 of these

risk factors are present. From reference 18, with

permission

Risk factor

Defining level

Abdominal obesity* (waist circumferencet)

Men

>102 cm (>40 in)

Women

> 88 cm (> 35 in)

TG

a 150 mg/dL

HDL-C

Men

<40 mg/dL

Women

< 50 mg/dL

Blood pressure

a 130/a 85 mmHg

Fasting glucose

a 110 mg/dL

HDL-C, high-density lipoprotein cholesterol; TG, triglycerides

  • Abdominal obesity is more highly correlated with metabolic risk factors than is increased body mass index
  • Some men develop metabolic risk factors when the circumference is only marginally increased

HDL-C, high-density lipoprotein cholesterol; TG, triglycerides

  • Abdominal obesity is more highly correlated with metabolic risk factors than is increased body mass index
  • Some men develop metabolic risk factors when the circumference is only marginally increased

Table 1.3 The World Health Organization (WHO) definition of metabolic syndrome*. As outlined, the parameters appear similar to the National Cholesterol Education Program ATP III criteria. However, WHO criteria would include measures of insulin resistance, if these are available in a particular subject

Impaired glucose tolerance, impaired fasting glucose,

diabetes and/or insulin resistance

And a 2 of the following:

Abdominal obesity

BMI

> 30 kg/m2 or

Waist-to-hip ratio

> 0.85 women

> 0.90 men

Dyslipidemia

Triglycerides

a 150 mg/dL or

HDL

< 35 mg/dL in men

< 39 mg/dL women

Blood pressure

a 140/90 mmHg

Microalbuminuria

Urinary excretion rate

a 20 ^g/min or

Albumin-creatinine ratio

a 20 mg/g

*WHO Definition, Diagnosis and Classification of Diabetes and its Complications. Report of WHO Consultation. Geneva: WHO, 1999

BMI, body mass index; HDL, high-density lipoprotein

*WHO Definition, Diagnosis and Classification of Diabetes and its Complications. Report of WHO Consultation. Geneva: WHO, 1999

BMI, body mass index; HDL, high-density lipoprotein

Table 1.4 A comparison of the specific criteria necessary for the definition of metabolic syndrome from the American Diabetes Association

(ADA), National Cholesterol Education Program (NCEP), World Health Organization (WHO), and the American Association of

Clinical Endocrinologists (AACE). From reference 7, with permission

ADA

NCEP*

WHO*

AACE*

Glucose intolerance

Fasting plasma glucose

Type 2 diabetes, impaired glucose

Fasting plasma glucose

110-125 mg/dL

tolerance, or insulin resistance by

110-125 mg/dL or 2-h post-75 g

HOMA-IR

glucose challenge > 140 mg/dL

Central obesity

Waist circumference

BMI > 30 or waist-to-hip ratio > 0.90

BMI a 25 or waist circumference

> 40 in (men) or > 35 in (women)

(men) or > 0.85 (women)

> 40 in (men) or > 35 in (women)

Dyslipidemia: high TG,

TG a 150 mg/dL, HDL < 40 (men),

TG a 150 mg/dL,

TG a 150 mg/dL, HDL < 40 (men),

low HDL, small dense LDL

HDL < 50 (women)

HDL < 35 (men), HDL < 39 (women)

HDL < 50 (women)

Hypertension

Blood pressure a 130/85 mmHg

On medication or

High blood pressure

untreated blood pressure

a 130/85 mmHg

a 140/90 mmHg

Microalbuminuria > 20 ^g/min

  • NCEP: must meet 3 of 5 criteria (low HDL and high triglycerides are 2 criteria) +WHO: must meet glucose/insulin criterion and 2 more
  • AACE: these key clinical signs are considered risk factors. Other risk factors include: polycystic ovary syndrome; sedentary lifestyle; age; ethnicity (certain groups); and family history of type 2 diabetes, hypertension, or cardiovascular disease

BMI, body mass index; HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment; LDL, low-density lipoprotein; TG, triglycerides

  • NCEP: must meet 3 of 5 criteria (low HDL and high triglycerides are 2 criteria) +WHO: must meet glucose/insulin criterion and 2 more
  • AACE: these key clinical signs are considered risk factors. Other risk factors include: polycystic ovary syndrome; sedentary lifestyle; age; ethnicity (certain groups); and family history of type 2 diabetes, hypertension, or cardiovascular disease

BMI, body mass index; HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment; LDL, low-density lipoprotein; TG, triglycerides definition attempted to provide a more appropriate definition for abdominal obesity. When such is present, two additional factors originally listed in the ATP III definition are sufficient for diagnosis. The IDF recognized and emphasized ethnic differences in the correlation between abdominal obesity and other metabolic syndrome risk factors. For this reason, criteria of abdominal obesity were specified by nationality or ethnicity based on best available population estimates. The most recent American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) statement, in contrast to IDF, maintains the ATP III criteria except for minor modifications (Table 1.5)25. They suggested lowering of the threshold previously set for impaired fasting glucose to 100 mg/dL and they did not adjust the existing US waist circumference cri-

Table 1.5 Criteria for clinical diagnosis of metabolic syndrome. From reference 25, with permission

Measure (any 3 of 5 constitute diagnosis of metabolic syndrome)

Categorical cut-off points

Elevated waist circumference*+

a 102 cm (a 40 inches) in men a 88 cm (a 35 inches) in women

Elevated triglycerides

On drug treatment for elevated triglycerides*

Reduced HDL-C

On drug treatment for reduced HDL-C*

Elevated blood pressure

a 130 mmHg systolic blood pressure or a 85 mmHg diastolic blood pressure or

On antihypertensive drug treatment in a patient with a history of hypertension

Elevated fasting glucose

a 100 mg/dL or

On drug treatment for elevated glucose

  • To measure waist circumference, locate top of right iliac crest. Place a measuring tape in a horizontal plane around abdomen at level of iliac crest. Before reading tape measure, ensure that tape is snug but does not compress the skin and is parallel to floor. Measurement is made at the end of a normal expiration
  • Some US adults of non-Asian origin (e.g. white, black, Hispanic) with marginally increased waist circumference (e.g. 94-101 cm (37-39 inches) in men and 80-87 cm (31-34 inches) in women) may have strong genetic contribution to insulin resistance and should benefit from changes in lifestyle habits, similar to men with categorical increases in waist circumference. Lower waist circumference cutpoint (e.g. > 90 cm (35 inches) in men and > 80 cm (31 inches) in women) appears to be appropriate for Asian Americans Vibrates and nicotinic acid are the most commonly used drugs for elevated triglyceride (TG) and reduced high-density lipoprotein cholesterol(HDL-C). Patients taking one of these drugs are presumed to have high TG and low HDL
  • To measure waist circumference, locate top of right iliac crest. Place a measuring tape in a horizontal plane around abdomen at level of iliac crest. Before reading tape measure, ensure that tape is snug but does not compress the skin and is parallel to floor. Measurement is made at the end of a normal expiration
  • Some US adults of non-Asian origin (e.g. white, black, Hispanic) with marginally increased waist circumference (e.g. 94-101 cm (37-39 inches) in men and 80-87 cm (31-34 inches) in women) may have strong genetic contribution to insulin resistance and should benefit from changes in lifestyle habits, similar to men with categorical increases in waist circumference. Lower waist circumference cutpoint (e.g. > 90 cm (35 inches) in men and > 80 cm (31 inches) in women) appears to be appropriate for Asian Americans Vibrates and nicotinic acid are the most commonly used drugs for elevated triglyceride (TG) and reduced high-density lipoprotein cholesterol(HDL-C). Patients taking one of these drugs are presumed to have high TG and low HDL

teria. Depending on the definition, it has been estimated that one in four adults may have either diabetes or the metabolic syndrome (Figure 1.7)26.

Given the CVD significance of the clustering of risk factors, the fact that a state of increased car-diometabolic risk may be three to four times as common as diabetes, and the observation that obesity and other risk factors (i.e. dyslipidemia and diabetes) have become global health epidemics, a state of increased cardiometabolic risk represents a serious public health concern. Currently, it is estimated that approximately 7-8% of the population in the USA suffer from the complications of adult-onset diabetes27. However, the prevalence of diabetes in the USA has increased dramatically over the recent past. Figure 1.8 demonstrates the estimated prevalence of diabetes as established for the USA in the year 1990, where an estimated prevalence was 4.9%, compared with the data as obtained in the year 2001 with an estimated prevalence of 7.9%28.

In large part, the increase in diabetes appears to be secondary to the increase in obesity. Clearly, there is no question that the US population has had a significant increase in obesity over the past 40 years. Figure 1.9 demonstrates the percentage of the population since 1960 that are now classified as either obese or overweight. As shown, there has been a steady increase in individuals classified as obese29. Since 1990, however, the prevalence of obesity has increased by 61%30-32.As seen in Figure 1.10, the increasing prevalence of

Table 1.6

Diabetes has become a worldwide health

concern.

As observed, there appears to be no area

. of the world

that has not observed a tremendous rise

in new cases

of diabetes. On current estimates, approximately

360 million people worldwide will have diabetes by

the year 2030. From reference 21, with permission

2000

2030

People with

People with

diabetes

diabetes

Ranking

Country

(millions)

Country

(millions)

1

India

31.7

India

79.4

2

China

20.8

China

42.3

3

USA

17.7

USA

30.3

4

Indonesia

8.4

Indonesia

21.3

5

Japan

6.8

Pakistan

13.9

6

Pakistan

5.2

Brazil

1 1.3

7

Russian

4.6

Bangladesh

1 1.1

Federation

8

Brazil

4.6

Japan

8.9

9

Italy

4.3

Philippines

7.8

10

Bangladesh

3.2

Egypt

6.7

Figure 1.7 Schematic representing prevalence of metabolic syndrome. Estimates have suggested that over 18 million individuals residing in the USA have diabetes, with significant numbers undiagnosed. Depending on the criteria used, it is estimated that one in four adults may have diabetes or the metabolic syndrome. From references 26 and 28, with permission

Figure 1.7 Schematic representing prevalence of metabolic syndrome. Estimates have suggested that over 18 million individuals residing in the USA have diabetes, with significant numbers undiagnosed. Depending on the criteria used, it is estimated that one in four adults may have diabetes or the metabolic syndrome. From references 26 and 28, with permission

Figure 1.8 Estimated prevalence of diabetes in the USA in 1991 and 2001 based on a telephone survey of 195 005 adults aged 18 or over. As shown, several states had higher prevalence of diabetes in 1990, many > 7%. As also shown, by the year 2001, most of the other states had observed an increase in prevalence of > 7%, with the increase being much higher in many states. From reference 28, with permission

Figure 1.8 Estimated prevalence of diabetes in the USA in 1991 and 2001 based on a telephone survey of 195 005 adults aged 18 or over. As shown, several states had higher prevalence of diabetes in 1990, many > 7%. As also shown, by the year 2001, most of the other states had observed an increase in prevalence of > 7%, with the increase being much higher in many states. From reference 28, with permission

NHES I (l960—62) NHANES I (l97l-74) I NHANES II (l976—80) I NHANES III (I988-94) I NHANES 1999

NHES I (l960—62) NHANES I (l97l-74) I NHANES II (l976—80) I NHANES III (I988-94) I NHANES 1999

Overweight or obese

Overweight

Obese

Overweight or obese

Overweight

Obese

Figure 1.9 The increase in numbers of individuals classified as being overweight or obese since 1960. As clearly shown, the percentage of the US population classified as obese has increased dramatically. NHES, National Health Examination Survey; NHANES, National Health and Nutrition Examination Survey. From reference 29, with permission

Diabetes

Mean body weight

Diabetes

Mean body weight

1990

1992

l994

l996

2000

1990

1992

l994

l996

2000

  • Prevalence of obesity increased 61% between 1991 and 2000
  • More than 60% of US adults are overweight
  • Only 43% of obese persons advised to lose weight during check-ups
  • BMI and weight gain major risk factors for diabetes

Year

Figure 1.10 Prevalence of diabetes and obesity in the USA since 1990. As shown, the increase in diabetes prevalence appears to mirror the increase in rates of obesity. It is observed that the prevalence of obesity increased by 61% from 1991 to 2000. These observations support the well-observed concept that weight gain is a major risk factor for diabetes. BMI, body mass index. Compiled from references 30, 31 and 32, with permission

Figure 1.11 Estimated number of individuals with type 2 diabetes who are expected to have diabetes by the year 2010. This would represent a 45% increase since the year 2000. Adapted from reference 33

diabetes appears to mirror closely the increasing prevalence of obesity. However, despite the findings of obesity and diabetes in the USA, this is truly a global problem. Based on the estimated number of people with diabetes, it is projected that by the year 2010, there will be 221 million people worldwide with diabetes (Figure 1.11) and 360 million by the year 2030 (Table 1.6). As is outlined in Figure 1.12, it is clear that very few areas of the world are immune to developing diabetes. The major concern with the epidemic of diabetes will be the development of the devastating complications of diabetes as outlined in Figure 1.13. With specific reference to metabolic syndrome, it is clear that the obesity epidemic contributes greatly to the presence of metabolic syndrome and that the prevalence of the metabolic syndrome increases with age. It is estimated that, by the time individuals reach the age of 60 years, approximately 40% may have the metabolic syndrome (Figure 1.14)26. Minority ethnic groups are at even greater risk. Therefore, it is not surprising that the WHO considers it to be one of the top ten most dangerous diseases in the world today35,36.

Figure 1.12 Global projections for the diabetes epidemic. As shown, an increase in new cases of diabetes will be observed in all parts of the world. From reference 34, with permission

Complications of diabetes

Figure 1.13 Schematic demonstrating micro- and macrovascular complications of diabetes
Figure 1.14 Metabolic syndrome prevalence among US adults. Clearly there is increasing prevalence in older individuals such that, by age 60, over 40% of the population may have criteria for metabolic syndrome. From reference 26, with permission

Successful strategies to intervene in the development of the 'metabolic syndrome' are urgently needed. Such interventions will be discussed in later chapters.

In summary, the development of metabolic syndrome is a threat to public health worldwide and is increasing at epidemic proportions.

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