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The metabolic syndrome: indispensable for some, meaningless for others... but what about the patients?
- Michele Coceani (22 March 2008)
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Not yet
- Thomas D R Hockaday (22 March 2008)
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Metabolic Syndrome – Dubious Value from a Public Health Perspective
- Franklin White MD, FRCPC, FFPH (23 March 2008)
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metabolic syndrome
- Richard J Jarrett, London SE26 4PA (26 March 2008)
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Metabolic Syndrome: Erasing the problem or constructing a better answer?
- Ali R. Khoshdel (29 March 2008)
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Are we using the wrong targets and the wrong terminologies in assessing the usefulness of the Metabolic syndrome?
- Sharmila P Seetulsingh-Goorah (29 March 2008)
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Michele Coceani, Cardiologist CNR Institute of Clinical Physiology, Via Moruzzi 1, 56124 Pisa, Italy
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A heated debate on the metabolic syndrome has been ongoing for several years now. However, amidst the various doubts surrounding the existence of the syndrome, a key figure, which theoretically should be at the center of this debate, has instead been consistently ignored: the patient. If the metabolic syndrome were to be accepted as a distinct clinical entity, it would be inappropriate, in my opinion, to hide such a diagnosis from our patients. But what would their reaction be upon learning of their apparently new disease? “Oh no! I have the metabolic syndrome!” or perhaps “I knew that I’m fat, have high blood pressure and diabetes, but no one ever talked to me about the metabolic syndrome!”. Personally, although I always keep the potential pathophysiological mechanisms underlying the metabolic syndrome in the back of my mind, I never explicitly use the term when discussing risk factor modification with my patients. I prefer to examine each risk factor separately and define therapeutic goals in a schematic manner that is easy to understand. Without a doubt, the concept of metabolic syndrome is intellectually appealing, but from a practical standpoint its routine clinical application may serve only to create unnecessary confusion and anxiety among patients. Competing interests: None declared |
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Thomas D R Hockaday, Retired Consultant Physician The Mulberries, Main St., East Hanney, OX12 0JF
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As with most good arguments, we don't know enough yet to settle the argument. Sadly neither Gale's typically lucid and logical text, nor Alberti and Zimmet's search to justify the widespread application of largely unhelpful measures confront the one issue that could validate the Metabolic Syndrome, however exactly defined. Does a single pathogenetic process promote the syndrome, with the phenotypic features varying with the background constitution, or do several different pathogenetic processes need to coincide? The authors agree that the syndrome's aetiology is unknown, and stating its 'underlying causes' to be obesity and sedentary lifestyle (Alberti and Zimmet) is superficial, when they both know that, placed in an arm-chair, they would rise up to act, and overfed they would be sated and reduce their intake. They will also have learnt that it's a minority of subjects who will follow long-term their wise recommendations to reduce adiposity by cutting energy intake and increasing its output. We don't yet know if there is something about the 'Metabolic Conformation' that leads to obesity and so decreased insulin sensitivity and liability to hypertension, or whether an associated obesity promotes insulin resistance and hypertension, hyperglycaemia and soon pancreatic islet-cell failure among the vulnerable. Just as the first chemical messengers were metabolites, so some metabolites would have been the first addictive substances, probably with the subject's phase of peak vulnerability pretty early in life. Therapy could be as arduous as detoxification from an addictive substance, but might benefit from being recognised as such. Prevention requires a better understanding of the entwined elements of Mother: Foetus and Child: and Familial nutrient movements. Competing interests: None declared |
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Franklin White MD, FRCPC, FFPH, President, Pacific Health & Development Sciences Inc. www.pacificsci.org 3164 Balfour Avenue, Victoria BC, CANADA V9A1S1
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As a public health physician, I recognize syndromic approaches as essential when we don't know what we are dealing with e.g., SARS. In other instances, when etiology is understood, some syndromes remain useful in prevention, diagnosis, treatment and health promotion e.g., AIDS. However, is it really likely that we could develop better public health strategies around “metabolic syndrome” than to address underlying determinants such as overweight, obesity and physical inactivity? Although useful papers have been published on its prevalence in various populations, for most actual public health applications, the answer to this question would be “no”. Just as Gale states for the clinical context, where “energetic screening and treatment for obesity, hypertension, and dyslipidaemia already form the basis of managing diabetes”, so too in public health, it is more practical to focus on the prevalence of its underlying determinants: overweight, obesity, physical inactivity, and poor nutrition practices, and then move further upstream to examine activity, nutrition and food marketing polices and practices. Measurement of these determinants and domains is more relevant in tracking the health of communities and in assessing the impact of health promotion initiatives. It is dubious to state that “the syndrome provides a simple public health strategy to define those at higher risk” (Alberti and Zimmet). We can already determine the prevalence of any such constellation of measurable risk factors without resorting to this syndrome as named. There is also a public health parallel to Coceani’s comments on the confusion this might give rise to in a startled patient: while keeping mechanisms in mind, most public health professionals would avoid using such a complex and medically loaded term when designing a health promotion strategy. Instead, it would be better practice to focus primarily on the determinants, and try to deal more directly with those realities through healthy public policy and community programming. Competing interests: None declared |
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Richard J Jarrett, emeritus professor 45 Bishopsthorpe Road, London SE26 4PA
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Soon after the concept of the metabolic syndrome various groups of "experts" have attempted to place a diagnostic straitjacket on the mixture of discrete and continously variable factors which have been found to associate statistically. Originally the value of the syndrome was in the prediction of diabetes and cardiovascular disease, so I agree with Edwin Gale that it is surprising the the International Diabetes Federation should now include the presence of diabetes as one of the optional components. Incidentally, as increased waist circumference is the basic requirement, if one had diabetes and a waist circumference below the cut- off level, one would escape the syndrome! The metabolic associations of the syndrome are undoubtably fascinating and deserve much more interdisciplinary research. But this will be hampered by arbitary - for that is what they are - definitions of the syndome based upon cut-off levels in continuous distributions in an attempt to provide clinical value, particularly as Alberti and Zimmet are only able to claim belief, ie no evidence, in favour. I would be happy to retain the term as a shorthand for the associations, but as a diagnostic label, then I am with Edwin Gale. Competing interests: None declared |
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Ali R. Khoshdel, MD, PhD, Clinical Epidemiologist (graduated from the University of Newcastle, AU), Assistant prof. Artesh University of Medical Sciences, Tehran, Iran, P.O. Box 16315-781
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The Metabolic Syndrome has been a useful construct in clinical practice as well as a valuable model to understand the interactions of diverse CV risk factors. However the increasing importance of the circulatory system in particular the role of the endothelium, in both connecting and controlling organ function, has underlined the limitations of the Metabolic Syndrome definition. Several epidemiologic evidence demonstrates that the cluster of the risk factors that has been involved in the metabolic syndrome is a part of a larger cluster of interacting risk factors. We have recently proposed “Circulatory Syndrome” as an attempt to refine the Metabolic Syndrome concept by the addition of recently documented markers of CV disease including renal impairment, microalbuminuria, arterial stiffness, ventricular dysfunction and anaemia to the previously known factors: hypertension, dyslipidemia and abnormal glucose metabolism; all of which are easily measured in clinical practice. These markers interact with each other as well as with other factors such as aging, obesity, physical inactivity, diet and smoking. The final common pathways of inflammation, oxidative stress and hypercoagulability thereby lead to endothelial damage and eventually CV disease. Circulatory syndrome is a cluster of risk markers with synergic effects. The proposed syndrome consists of eight major components, as follows [in the metabolic, arterial, renal, cardiac (“MARC”) order]:  Abnormal glucose metabolism  Dyslipidemia  Hypertension  Arterial stiffness  Microalbuminuria  Renal impairment  Anaemia  Left ventricular dysfunction All of these “markers” occur on a background of oxidative stress, inflammation, hypercoagulability and endotheliopathy (underlying factors) and can be accelerated by factors such as aging, obesity, smoking and physical inactivity (predisposing factors). Furthermore they can be simply and non-invasively assessed in outpatient clinical settings. While the mechanisms underlying the circulatory syndrome are poorly understood, it must be strongly stated that vascular-endothelial pathways link all and are of pathological significance. Activation of the renin-angiotensin system, insulin resistance and increased sympathetic activation are all by -products of the underlying pathogenic process. Since these markers represent the extent of the underlying disease process, they could also manifest as risk factors for other components and thereby enhance their development. Considering the interrelationships, the final outcome in this model can be considered to be CV events, stroke or renal failure; all of which are associated with general circulatory health. Consequently the condition of the circulatory system and these markers is directly related to the mortality rate. Consideration of this syndrome in clinical practice is expected to facilitate more effective prevention, early diagnosis and timely multidisciplinary treatment of diabetes consequences including renal and cardiovascular complications. Nevertheless, the Circulatory Syndrome, like its predecessor the metabolic syndrome, is only a small step toward a better understanding of these complex and as yet poorly understood markers of disease. Competing interests: None declared |
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Sharmila P Seetulsingh-Goorah, Associate Professor in Health Sciences Department of Health Sciences,Faculty of Science, University of Mauritius, Reduit, Mauritius.
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The 'popularity' which some may wish to equate with "clinical value" of the metabolic syndrome, is such that it has even been suggested that metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the US population (1). Whereas this may require much further investigation of the actual predictive value of the metabolic syndrome, it remains true that the clustering of risk factors grouped under the 'metabolic syndrome'mimics closely the clustered occurence of non-communicable diseases such as diabetes mellitus and cardiovascular disease (2), although I agree with M.Coceani that the metablic syndrome should not move from the status of 'predictor of relative risk' to the status of disease in its own right. Until an explanation is found regarding why all those with the 'metabolic syndrome' do not develop the diseases for which it is a proposed 'risk factor' or "risk predictor", the 'cigarette smoking' history will repeat itself. TDR Hockaday is right in questioning the reference to obesity and a sedentary lifestyle as 'underlying causes'of the metabolic syndrome. Obesity is itself the result of metabolic alterations which are brought about by aetiological factors, which remain largely unknown. Obesity therefore is itself part of a pathogenic mechanism triggered by 'underlying causes'. The question that may arise is therefore, is obesity a 'cause' or a 'risk factor' for diabetes mellitus and cardiovascular diseases, or is it part of a common pathogenic pathway for these conditions triggered by overlapping causes. In fact the other components of the metabolic syndrome are themselves better classified as pathogenic mechanisms/conditions rather than 'risk factors'. In any case, unless we can positively identify the pathogenic mechanism(s)that underlie the clustering of "risk factors" forming part of the metabolic syndrome, we remain unfortunately in a chicken and egg situation regarding whether, for instance,obesity or insulin resistance is the first to arise. I do not follow the logic that is used to conclude that focusing on the cluster of cardiovascular disease and diabetes "risk factors" emphasises the 'multifactorial nature of the risk for these diseases'. Terminologies must be put in their right perspectives: it is clear that the components of the metabolic syndrome are the result of some aetiological cause(s) and of some pathogenic process(es) and that they are not in themselves aetiological agents and cannot thus be classified as 'risk factors', epidemiologically speaking. I would say that clustering of the components of the metabolic syndrome points more towards a "commonality of cause(s) and pathogenicity" for these diseases. This issue has also been addressed elsewhere (3), but there is no proof as yet of the syndrome being the result of a common underlying pathological process. It is however clear that the choice of the unifying pathogenic factor is important and that components such as insulin resistance and hyperinsulinaemia, not universally associated with other components of the metabolic syndrome, may themselves be the results of common upstream pathogenic mechanism(s). I can appreciate that the concept of the metabolic syndrome has shed light on the commonality of pathogenic pathways leading to these two Type 2 diabetes and CVD , but how has the metabolic syndrome rendered the "management" of type 2 diabetes better? Type 2 diabetes, on its own, has clinical complications worthy of ensuring a proper clinical management of the disease with or without the looming risk or presence of cardiovascular disease. I also do not agree that "the syndrome provides a simple public health strategy to define those at higher risk". In fact, I think that the authors are not doing justice to the 'metabolic syndrome' by attributing to it multiple and sometimes unjustified merits and refusing to admit its limitations. Addressing these limitations may serve it better in the long run. The assessment of the risk predictive value of the metabolic syndrome should continue to be the a focus for research and, public health policies and community health promotion programmes should not just cast it aside prematurely. Research has so far focused on the risk predictive value of the syndrome in adults from different age, gender and ethnic groups. However, research focus should also depart from these classical target groups because if we truly want to define "those at higher risk", with a view, I assume of halting, as early as possible, the appearance of overt disease, then, targeting adults is already too late in the pathogenic process comprising disease development. We should thus target children and adolescents. Using current definitions, metabolic syndrome has been found to have a high prevalence amongst children in the US (4,5).More studies should focus on children and adolescents for whom however, the current definitions used to assess presence and prevalence of metabolic syndrome may not be appropriate, requiring thus more studies on paediatric definitions of the syndrome. This is especially so when treatment options for conditions like obesity in youth, includes pharmacotherapy and surgery (6). The impact and usefulness of different definitions of the metabolic syndrome and of the thresholds of the components of the metabolic syndrome in primary healthcare and different target groups, known to vary (7), should be further researched to avoid unecessary alarm and to increase cost-effectiveness. Metabolic syndrome has been described as the result of the maladaptation to overnutrition of genes selected to survive undernutrition because of the limited nutrition on which mankind is assumed to have evolved(8). This situation of overnutrition affects the whole of society and not just those classified as "overeaters". On the evolutionary scale, the emergence of obesity within a couple of generations is classified as too rapid to be accounted for by a genetic change and is believed to be the result of a change in environment instead (8). So again the issue of appropriate targets for studies arises. Studies on any link between the metabolic syndrome and oestrogen levels/metabolism must not be forgotten, in view of the association of gender, polycystic ovary syndrome and fat distribution (central obesity) with the metabolic syndrome. References: 1)Gogia A, Agarwal PK. Metabolic syndrome. Indian J Med Sci 2006;60:72-81. 2)Grundy SM. Metabolic syndrome : Connecting and reconciling cardiovascular and diabetes worlds. J.Am. Coll. Cardiol. 2006; 47: 1093- 1100. 3) Kahn R, Buse J, Ferrannini E, Stern M. The metabolic syndrome : Time for a critical appraisal. Diabetes care. 2005.28(9):2289-2304. 4) Kranz S, Mahood LJ and Wagstaff DA. Diagnostic criteria patterns of US children with metabolic syndrome: NHANES 1999-2002. Nutrition Journal. 2007; 6:38. doi:10.1186/1475-2891-6-38 5)Dhuper S et al. Utility of the modified ATP III defined metabolic syndrome and severe obesity as predictors of insulin resistance in overweight children and adolescents : a cross-sectional study. Cardiovascular Diabetology.2007;6:4. doi:10.1186/1475-2840-6-4 6) Jolliffe CJ, Janssen I. Vascular risks and management of obesity in children and adolescents. vascular Health and Risk management. 2006; 2(2) :171-187. 7) Moebus S et al; Impact of 4 different definitions used for the assessment of teh prevalence of the metabolic syndrome in primary healthcare : the German Metabolic and cardiovascular Risk project (GEMCAS). Cardiovascular Diabetology. 2007; 6:22 doi: 10.1186/1475-2840-6- 22 8)Wilkin TJ, Voss LD. Metabolic Syndrome ; maladaptation to a modern world. J R Soc Med 2004;97 : 511-520. my e-mail address : seetulg@uom.ac.mu Competing interests: None declared |
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