How to best define the metabolic syndrome

Abstract

The constellation of metabolic abnormalities including centrally distributed obesity, decreased high‐density lipoprotein cholesterol (HDL‐C), elevated triglycerides, elevated blood pressure (BP), and hyperglycaemia is known as the metabolic syndrome. Associated with increased risk of both type 2 diabetes and cardiovascular disease (CVD), the metabolic syndrome is thought to be a driver of the modern day epidemics of diabetes and CVD and has become a major public health challenge around the world . Since its initial description, several definitions of the syndrome have emerged. Each of these definitions used differing sets of criteria, the combination of which either reflected contrasting views on pathogenic mechanisms or clinical usefulness. The use of these definitions to conduct research into the metabolic syndrome in diverse populations resulted in wide ranging prevalence rates, inconsistencies and confusion, and spurred on the vigorous debate regarding how the metabolic syndrome should be defined. In response to this controversy, the International Diabetes Federation (IDF) has recently proposed a new definition, which is applicable to populations around the world . It is envisaged that the development of the new definition for the metabolic syndrome will help resolve the confusion caused by the number of earlier attempts to define this important entity.

• central obesity
• insulin resistance
• metabolic syndrome

Introduction

The concept of the metabolic syndrome can be dated back approximately 80 years to work by the Swedish physician, Kylin, who first noted a clustering of hypertension, hyperglycaemia and gout 2. Several decades later in 1947, Vague 3 observed that a particular obesity phenotype, upper body, android or male‐type obesity, was associated with the metabolic abnormalities often seen with type 2 diabetes and with cardiovascular disease (CVD). The clinical importance of the syndrome was crystallized only much later in 1988 by Reaven 4, who described the existence of a cluster of metabolic abnormalities with insulin resistance as the central pathophysiological feature, and labelled it Syndrome X. However, Reaven did not include obesity, a factor that has been linked with the metabolic syndrome in subsequent work.

The metabolic syndrome (also known by a variety of other names, including the insulin resistance syndrome and the ‘Deadly quartet’), is characterized by abdominal (visceral and retroperitoneal) obesity and clustering of other cardiovascular risk factors including impaired glucose regulation, raised triglycerides, decreased high‐density lipoprotein cholesterol (HDL‐C), elevated blood pressure (BP), and hyperinsulinaemia with underlying insulin resistance.

The pathogenesis of the metabolic syndrome is poorly understood, and likely to be complex and multifactorial. Insulin resistance and abdominal obesity have received the most attention as the putative underlying features which may explain the frequently observed clustering of the other components. The most favoured current hypothesis is that adipose tissue, in particular, visceral adipose tissue, expresses various factors which are involved in the regulation of insulin in skeletal muscle cells. One such factor, adiponectin, has been found tohave anti‐diabetic, anti‐atherosclerotic and anti‐inflammatory functions 5,6. Reduced production of adiponectin is associated with excessive intra‐abdominal adipose tissue and insulin resistance 7. However, further research is required to determine which factor(s) are central to the development of this syndrome. Whatever the pathophysiological mechanism, it seems highly likely that a sedentary lifestyle and dietary as well as genetic factors contribute to its development.

The objectives of this review are to examine the definitions of the metabolic syndrome, present the key limitations and advantages of the different approaches and to highlight the difficulties of defining the metabolic syndrome.

Key messages

• The metabolic syndrome is believed to affect at least one in five adults, and carries a high risk of cardiovascular disease and type 2 diabetes.

• The different definitions of the metabolic syndrome reflect diverse conceptual frameworks used to understand the aetiology of the metabolic syndrome.

• The new definition from the International Diabetes Federation, prioritizes central obesity, and accommodates the anthropometric differences between ethnic groups.

The need for consensus

An important feature of the metabolic syndrome is its association with type 2 diabetes and atherosclerotic CVD. Data from prospective studies have shown that those who meet the definition are twice as likely to die from, and three times as likely to have, a myocardial infarction than those who do not 8, and four to five times more likely to develop type 2 diabetes 9. The prevalence of the metabolic syndrome worldwide ranges from 10% to 50% and is highly age dependent 10. Perhaps of greatest significance is the fact that in concert with an ageing population and the rising prevalence of glucose intolerance and obesity 11, the burden imposed by the metabolic syndrome, already large, is set to increase. The scope for prevention of CVD and diabetes for those with the metabolic syndrome is indeed vast and poses a great challenge for the next decade.

The benefits of deriving a clear, consistent definition for the metabolic syndrome are obvious. The establishment of a cohesive definition of the metabolic syndrome will allow the identification of individuals at high risk of these conditions for prevention and treatment purposes, and the ability to compare the prevalence of the metabolic syndrome among populations and over time. However, despite the urgent need for consensus, some controversy may still exist regarding the best approach to define or diagnose this condition.

Approaches to defining the metabolic syndrome

Efforts to understand and characterize the metabolic syndrome have led to several differing conceptual approaches when defining this syndrome, all of which begin from the simple observation of clustering of the key components. In one paradigm, an underlying feature (e.g. abdominal obesity or insulin resistance) is apparently clear, and any definition is derived from, and can be tested against, the association of potential components (and the proposed overall syndrome) with the identified underlying feature (Figure 1A). In a second paradigm, no assumptions are made about aetiology, but components are simply selected by the statistical strength of their association with other components, and investigation of these associations may then lead to insights into the underlying causes (Figure 1B). The tensions between these competing approaches are readily apparent, and are neatly illustrated by two recent papers 12,13. Both publications examined the associations between insulin resistance and the components of the metabolic syndrome, as defined by National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, Adult Treatment Panel III (ATPIII), and found that the associations were not universally strong 12,13. One group concluded that the ATPIII definition was, therefore, flawed, since it failed to adequately identify those with insulin resistance 13. In contrast, the other group suggested that since visceral fat was strongly related to all other components, it was the underlying cause 12.

Figure 1. The two most common conceptual frameworks used to describe the metabolic syndrome. InA, there is a presumed underlying feature which is related to and causes the other variables. In B, the metabolic syndrome is represented by a set of variables which cluster with each other and no variable is known to be at the aetiological core.

Superimposed on the two approaches noted above is the desire for clinical and public health relevance, which demands that any clinical decision (e.g. diagnosing the metabolic syndrome) is demonstrably valuable. This usually means that outcomes can be predicted, and preventative measures then taken. In the context of the metabolic syndrome, this means that it can be shown to be a good predictor of new cases of type 2 diabetes and CVD. However, since age, sex, smoking status and family history are not included in any definition of the metabolic syndrome (as they do not feature in the observed clusters); it is likely that the metabolic syndrome will never be the best predictor of either CVD or diabetes. Nevertheless, while risk prediction is a valuable asset, it may not be the single most important feature of any definition, even though it may dictate the extent to which the disorder is used in clinical practice. For example, in the general population, rheumatoid arthritis is unlikely to be useful as a predictor of joint replacements (most of which are due to osteoarthritis), but that does not mean that definitions of rheumatoid arthritis are without value.

Finally, there is a practical need to maintain simplicity. Thus, for example, it is desirable to have the cut‐points used to define hyperglycaemia and high blood pressure in the metabolic syndrome the same as those used elsewhere to define states of abnormal glucose metabolism and hypertension. This can limit the freedom of definition committees in their selection of cut‐points of the various components. The need for practicality also means that definitions that include insulin resistance, and perhaps even the oral glucose tolerance test, will be of limited value, as measurement of insulin resistance is difficult, and the oral glucose tolerance test is seen by some as inconvenient and impractical.

Potential causes of the metabolic syndrome

Insulin resistance is often thought to be the key factor in the development of the metabolic syndrome 1,4,14. This is supported by the fact that for the majority of components in the definition there are studies which implicate insulin resistance as contributing to their pathophysiology 4,14, in that insulin resistance induces the abnormality via more than one biological pathway. Supporters of the alternative concept state that while this is true for many components of the syndrome, there are exceptions and insulin resistance alone does not fully explain the metabolic syndrome. For example, in factor analysis, hypertension does not usually cluster with insulin resistance 15. Instead, the link between obesity, particularly, central adiposity, and the other components is very strong and the syndrome may well be best viewed as the metabolic consequences of central obesity.

Factor analysis has been used to show that there are several dominant, independent factors/components which underpin the metabolic syndrome. This work by Hanson 9 suggests that insulin resistance, body mass index (BMI) or waist circumference and BP, and lipid factors (triglycerides/HDL‐C) are important factors of the metabolic syndrome. Similar analyses by Wang et al. 16 suggest that insulin resistance, and BMI and waist‐hip ratio are very closely related. Others believe that excess abdominal adiposity is a factor that decreases insulin‐medicated glucose disposal, which then in turn can result in obesity implying that obesity is a modifier rather than a central component or a direct cause of the syndrome. This latter notion has met with some disagreement, as not all insulin resistant individuals are obese and vice versa15.

Such controversy over which components are the most important is not limited to insulin resistance and abdominal obesity. Some argue that a definition should not have diabetes as a component if it is an outcome of the syndrome 15. However, since the links between hyperglycaemia and each of the other components are very clear, it is hard to justify the exclusion of diabetes simply because many researchers choose to attempt to predict one component of the syndrome using the other components.

How best to define the metabolic syndrome

Several factors need to be considered when developing a definition for the metabolic syndrome. These include deciding which variables best capture the condition, the relative weighting of each component, how each component is assessed, what the thresholds are for identifying abnormalities in each component, how these thresholds might need to change for different ethnic groups, and the usefulness in clinical practice. The complex nature of this task is further limited by lack of consistency in the data and thus has led to the emergence of several definitions with differing components, various ways to measure components and separate thresholds.

Current working definitions

In recent years, several working definitions and/or statements have been developed for the metabolic syndrome, the most widely recognized of which are from the World Health Organization (WHO) 17, Adult Treatment Panel III (ATPIII) 18, the European Group for the Study of Insulin Resistance (EGIR), the American college of Endocrinology Task Force on the Insulin Resistance Syndrome 14, and more recently the International Diabetes Federation 19 (Table I and II).

Table I. Current definitions of the metabolic syndrome.

WHO 1999	EGIR 1999	ATPIII 2001	IDF 2005
Diabetes or impaired glucose tolerance or insulin resistance*	Insulin resistance^† or hyperinsulinaemia (only non‐diabetic subjects)		Central obesity
			Waist circumference (ethnicity specific)^‡
Plus two or more of the following:	Plus two or more of the following:	Three or more of the following:	Plus any two of the following:
1. Obesity: BMI>30 kg/m^2 or waist‐hip ratio>0.9 (M)>0.85 (F)	1. Central obesity: waist circumference⩾94 cm (M), ⩾80 cm (F)	1. Central obesity: waist circumference>102 cm (M), >88 cm (F)	1. Raised triglycerides⩾150 mg/dL (1.7 mmol/L) or specific treatment for this abnormality.
2. Dyslipidaemia: triglycerides⩾150 mg/dL (1.7 mmol/L) or HDL‐C<35 mg/dL (0.9 mmol/L) (M)<39 mg/dL (1.0 mmol/L) (F)	2. Dyslipidaemia: triglycerides>177 mg/dL (2.0 mmol/L) or HDL‐C<40 mg/dL (1.0 mmol/L)	2. Hypertriglyceridaemia: triglycerides⩾150 mg/dL (1.7 mmol/L)	2. Reduced HDL‐C<40 mg/dL (1.03 mmol/L) (M)<50 mg/dL (1.29 mmol/L) (F) or specific treatment for this abnormality
3. Hypertension: blood pressure⩾140/90 mmHg or medication	3. Hypertension: blood pressure⩾140/90 mmHg or medication	3. Low HDL‐C:<40 mg/dL (1.03 mmol/L) (M), <50 mg/dL (1.29 mmol/L) (F)	3. Hypertension: blood pressure⩾ 130/85 mmHg or medication.
4. Microalbuminuria: albumin excretion⩾20 μg/min or albumin:creatinine ratio⩾30 mg/g	4. Fasting plasma glucose⩾110 mg/dL (6.1 mmol/L)	4. Hypertension: blood pressure⩾130/85 mmHg or medication	4. Fasting plasma glucose⩾100 mg/dL (5.6 mmol/L) or previously diagnosed type 2 diabetes^§
		5. Fasting plasma glucose⩾110 mg/dL (6.1 mmol/L)

*Defined under hyperinsulinaemic euglycaemic conditions, glucose uptake below lowest quartile for background population. ^†Defined as the top quartile of fasting insulin in the non‐diabetic population. ^‡For guidelines on how to accurately measure waist circumference see table II. If BMI is>30 kg/m² then central obesity can be assumed, and waist circumference does not need to be measured. ^§In clinical practice, IGT is also acceptable, but all reports of the prevalence of the metabolic syndrome should use only the fasting plasma glucose and presence of previously diagnosed diabetes to assess this criteria. If fasting plasma glucose is above 5.6 mmol/L, OGTT is strongly recommended but is not necessary to define the presence of the syndrome.

WHO = World Health Organization; EGIR = the European Group for the Study of Insulin Resistance; the American college of Endocrinology Task Force on the Insulin Resistance Syndrome; ATPIII = National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III); IDF = International Diabetes Association; F = female; M = male.

Table II. ‘Identifying abnormalities’ according to the American College of Endocrinology position statement on the Insulin Resistance Syndrome.

Identifying abnormality	Cut point
1. Triglycerides:	>150 mg/dL (1.7 mmol/L)
2. HDL Cholesterol:
Men	<40 mg/dL (1.03 mmol/L)
Women	<50 mg/dL (1.29 mmol/L)
3. Blood Pressure:	>130/85 mmHg
4. Glucose:
Fasting	110–125 mg/dL (6.1 mmol/L)
2 hour post glucose challenge	140–200 mg/dL ( 7.8–11.1 mmol/L )

Before such definitions were available, those characterizing this condition applied their own constructs which varied considerably in regards to number and weighting of the components, and the thresholds used for the various abnormalities. This approach has led to a range of prevalences of the metabolic syndrome reported in the literature based on differing components and cut points.

The first official definition of the metabolic syndrome to be developed was by a WHO consultative group 17. This had glucose as a central theme, such that those with insulin resistance (measured using an euglycaemic clamp), impaired glucose tolerance (IGT) or diabetes, together with at least two of raised BP, hypertriglyceridaemia and/or low HDL‐cholesterol, obesity, as measured by waist‐hip ratio or BMI, and microalbuminuria are classified as having the syndrome. This definition also highlighted several other factors that have been associated with the metabolic syndrome but are not necessary for recognition of the syndrome. These include inflammatory or haemostatic variables such as hyperuricaemia, coagulation disorders and raised plasminogen activating inhibitor. The crux of the WHO definition was the biological and physiological description of insulin resistance. Its main focus was to detect cases with insulin resistance and then its associated co‐morbidities. However, it must be borne in mind that this definition was initially promoted as a working model, with the authors acknowledging that it should be improved on as new data came to light 20.

Critics of the WHO definition identified several limitations, of which the most important related to the use of the euglycaemic clamp to measure insulin sensitivity, making the definition almost impossible to use in either clinical practice or epidemiological studies. They also contended that microalbuminuria was not a key metabolic component, though it may be an important consequence of the syndrome, and that the use of waist‐hip ratio as a measure of central obesity is not appropriate as it is an index of the relative accumulation of abdominal over peripheral fat rather than an absolute measure of visceral adiposity.

Recognizing that this WHO definition may be too complex to apply in many settings, and relied heavily on insulin resistance, the EGIR released a modification of the WHO definition which would be easier to use as it relied on fasting insulin levels, instead of the euglycaemic clamp, to measure insulin resistance 14. This definition still retained insulin resistance as an essential component, arguing that this was a rational decision since much of the evidence to date suggested that insulin resistance was the underlying theme to the metabolic syndrome. This is turn meant that their modified definition had to be restricted to those in whom insulin resistance could be easily and reliably measured, and so the definition was restricted to those without diabetes (as the addition of significant beta‐cell dysfunction, which occurs in diabetes, to insulin resistance makes estimates of insulin sensitivity unreliable). This definition also introduced waist circumference as the measure of adiposity, and contained modified cut points for the other components.

Several years later, the ATPIII definition of the metabolic syndrome was developed 18. The authors of this definition wanted to develop a definition which would be simple, and hoped that its widespread use would ultimately lead to prevention of CVD and type 2 diabetes. Designed to have clinical utility, this definition did not include a specific measure of insulin sensitivity, but rather adopted a less glucose‐centric approach by treating all components with equal importance. Notably, it retained waist circumference as the measure of obesity (though with higher cut‐points than EGIR). This definition has been noted for its simplicity in that its components are easily and routinely measured in most settings, but studies have shown that it fails to identify all those with insulin resistance 21, which has incurred some criticism. Unlike the WHO definition, the ATPIII definition does not incorporate inflammatory and haemostatic variables as part of an extended definition.

A modification of the ATPIII definition was also developed by the American Association of Clinical Endocrinology 14, and was based on the belief that insulin resistance was the core feature, and aimed to identify individuals with insulin resistance. The statement, deliberately labelled as such to allow the diagnosis to rely strongly on clinical judgement rather than satisfying specific criteria, lists four factors as ‘identifying abnormalities’ of the metabolic syndrome. These were elevated triglycerides, reduced HDL‐C, elevated BP, and elevated fasting and post‐load glucose. Factors such as obesity, diagnosis of hypertension, gestational diabetes or CVD or family history of diabetes, hypertension, non‐European ancestry or age greater than 40 years and a sedentary lifestyle, are classified as factors which increase the likelihood of the syndrome rather than as key identifying abnormalities. While similar to the ATPIII definition, in that it excludes hyperinsulinaemia, it also differs as it excludes obesity as a component, since abdominal obesity is viewed as a contributory factor in the development of insulin resistance rather than as a consequence of insulin resistance. The authors rationalize this approach on the basis that insulin assays are not standardized and the evidence implicating elevated plasma insulin as an independent risk factor for CVD is limited 10. Furthermore, omission of abdominal obesity as an identifying component in this statement has evoked much criticism, especially in light of the growing evidence that central obesity is a major risk factor for type 2 diabetes and CVD 22,23.

Clearly, the development of these definitions over the years has led to considerable confusion, an inability to accurately compare prevalences of the metabolic syndrome between populations, and has hampered the progress of research into the area. To a large extent, the approach with each definition reflects different conceptual frameworks underlying each construct. For those who see the metabolic syndrome as a collection of components which reflect the clinical manifestations of insulin resistance, the WHO and EGIR definitions are the most appropriate. Others who believe the metabolic syndrome to be the consequence of abdominal obesity, a constellation of risk factors which predict CVD risk or merely a statistical phenomena, the ATPIII definition may be more relevant. Not surprisingly, the choice of definition does matter, as each definition categorizes a distinct group of people 10. The choice of the most suitable definition for the metabolic syndrome therefore depends on first deciding on what we are trying to achieve by having a definition for the metabolic syndrome. Amongst the many competing criteria a definition should meet, the highest priority may be the identification of those at risk of diabetes and CVD.

To this end, most of the current evidence suggests that the WHO definition is better able to predict those at risk of CVD than the ATPIII 24, a feature which has been attributed by some to the central position of insulin resistance in the WHO construct. In these studies, when insulin resistance was added to the ATPIII, it performed similarly 24. For this reason, many favour the inclusion of insulin resistance in the definition, but because the measurement of insulin resistance is problematical, the inclusion of insulin resistance as a component in any definition can also represent a weakness. A more extensive comparison of the predictive ability of various metabolic syndrome definitions to conventional risk prediction tools such as the Framingham Risk Score and the Diabetes Predicting Model produced disparate results. Using data from the San Antonio Heart Study, Stern et al. 25 showed the ATPIII definition to be superior to the WHO definition in the prediction of CVD, while the glucose‐centric WHO definition was superior for predicting incident diabetes. However, both metabolic syndrome definitions were inferior to the Diabetes Predicting Model and the Framingham Risk Score for predicting type 2 diabetes and CVD, respectively. More recently, a meta‐analysis of prospective studies of metabolic syndrome and CVD and diabetes, showed those with the metabolic syndrome had a pooled relative risk for CVD (1.93 and 1.65) and diabetes (6.08 and 2.99), using exact WHO and ATPIII definitions, respectively 26. Consideration of these findings must be tempered by the fact that there are very few studies using both definitions and measuring both outcomes.

Since the initial release of the WHO and ATPIII definitions, there has also been much controversy about how best to measure obesity. It is generally accepted that BMI, though widely used, is not sufficiently sensitive to detect abdominal obesity in different ethnic groups. For example, South Asians have higher upper body and visceral fat for a given BMI when compared to Europids (people of white European origin). Furthermore, the risk of type 2 diabetes 27 and CVD 28 for those with the metabolic syndrome in this ethnic group is apparent at much lower levels of adiposity than in Europids. The likely inappropriateness of the ATPIII waist circumference cut‐points for non‐Europid populations is exemplified by data showing the application of the ATPIII definition to an Asian population. This resulted in a very low prevalence of the metabolic syndrome, which seems out of keeping with the high prevalence of diabetes in such populations 27,29. This issue has been partly addressed by the recommendation by the WHO and others 30 that a lower BMI (BMI>23 kg/m²) should be used to classify South Asians as obese 26. Unfortunately, it has been argued that this modification only serves to add more confusion to already murky waters.

In light of the controversy over the various limitations in the current definitions, the IDF decided that a more practical definition, which would be applicable globally for the identification of people at high risk of CVD, and diabetes, was urgently required 1,19. A consensus group was formed comprising members of IDF from all regions and representatives from organizations including those who had contributed to the previous definitions. The primary aim of this group was to develop a new definition which would be clinically useful, facilitate the comparison of data on the metabolic syndrome across countries and populations, and highlight areas where more research was needed. Recognizing that abdominal obesity is an important determinant in the causative pathway of the metabolic syndrome and that there is a strong association between waist circumference, CVD and other components of the metabolic syndrome, central obesity was placed in a central position of the construct. This has the further public health advantage of highlighting the importance of obesity, as the definition can be viewed as encompassing the key metabolic consequences of central obesity.

The consensus group also placed particular emphasis on developing criteria for obesity which were appropriate for a wider variety of populations. Using all the ethnic‐specific, body composition data available, they derived cut points for abdominal obesity based on waist circumference, which were applicable to individual ethnic groups (Table III). It was also decided that the definition should be less glucose‐centric and relegated diabetes status to a non‐central position. Moreover it was recognized that since there are practical difficulties in accurately measuring insulin resistance, it was omitted as a component. This was thought to be reasonable given that other included components such as waist circumference and triglycerides were so highly correlated with insulin resistance 23, that few of those with insulin resistance would be missed. The position and thresholds of other components were similar to those used in the ATPIII except for glucose, where the cut off of 100 mg/dL (5.6 mmol/L) recently recommended by the American Diabetes Association 31 was adopted for impaired fasting glucose.

Table III. Country‐/ethnic‐specific values for waist circumference.

Country/ethnic group*		Waist circumference^† (as measure of central obesity)
Europids^‡	Male	⩾94 cm
	Female	⩾80 cm
South Asians^§	Male	⩾90 cm
	Female	⩾80 cm
Chinese	Male	⩾90 cm
	Female	⩾80 cm
Japanese	Male	⩾85 cm
	Female	⩾90 cm
Ethnic South and Central Americans	Use South Asian recommendations until more specific data are available
Sub Saharan Africans and Eastern Mediterranean and Middle East (Arab) populations	Use European data until more specific data are available

*Ethnicity should be the basis for classification, not the country of residence. ^†In the USA the ATP III values (102 cm male; 88 cm female) are likely to continue to be used for clinical purposes. ^‡In future epidemiological studies of populations of Europid origin, prevalence should be given using both European and North American cut points to allow better comparisons. ^§Based on a Chinese, Malay and Asian‐Indian population.

In line with the WHO definition, the IDF definition also describes several other components which are sometimes associated with the syndrome but whose evidence is not sufficient as yet for inclusion in the definition. These include markers of body composition, inflammatory markers, thrombotic markers, additional lipid‐based factors, insulin resistance and others. It was recommended that these additional variables should be included in future research studies of the metabolic syndrome so that when sufficient data concerning these additional markers does accumulate, the presence or absence of these factors may allow refinement of the definition of the metabolic syndrome especially in different ethnic groups.

Is this the last word?

At the end of a long and arduous task such as defining the metabolic syndrome, one must ask whether this latest definition is the end of the story. Although the definition developed by the IDF consensus group does in part find some compromises between the WHO and the ATPIII definitions, and also begins to address ethnic differences between populations, it may not completely resolve all of the confusion and inconsistencies in defining the metabolic syndrome. Care must be taken when viewing it as the solution, and instead, it should be seen as an important advance along a potentially long road!