The epidemic of pre-diabetes: the medicine and the politics
BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g4485 (Published 15 July 2014) Cite this as: BMJ 2014;349:g4485
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Editor,
Yudkin and Montori make many valid points in their article on the epidemic of prediabetes (1) The topic of whether it is the medical profession's role to prevent disease is quite new, but important as we determine whether the disability and cost for diabetes complications can be prevented. From our perspective, the question is not whether we have a responsibility in prevention, but how we help individuals make good decisions for their own health, what the most evidence-based interventions are, and whether a person experiences better health outcomes as a result.
Health care in the U.S. is going through many changes with a distinct movement toward population health in addition to traditional health care. Looking upstream to prevent chronic disease in a systematic way, we believe, is an important aspect of new models of care. Working with our approximately 9.5 million members to restore them to health when they are ill, in addition to keeping them healthy as long as possible, is our core mission. We believe giving individuals information about their risk of developing diabetes is one area where we can leverage engagement of the individual, the health system, and the community to prevent chronic disease. In this way, we are choosing to lean into the complexity of the spectrum and develop approaches to support our members and our care teams to optimize health and prevent disease.
Since 2011, Kaiser Permanente has been developing a national approach to addressing prevention of Type 2 diabetes mellitus. This has entailed cohort development, testing interventions for prediabetes, and building capacity to offer members who want to address their risk and the options to do so. Today we have over 500,000 members with diabetes, and through our cohort development work we have identified just under 1 million with prediabetes out of the approximately 9.5 million members we serve.
While it is not our intent to engage in diagnosis creep given the broad HbA1c range defining prediabetes, we do feel we have an obligation to work with our members and let them know their risk for developing diabetes. Rather than wait for perfect evidence to guide us, we are working to determine rates of conversion to diabetes along the risk spectrum as we know those with higher BMI’s (>30) AND a higher A1c ( >6.2) are more apt to develop diabetes in a more accelerated timeline. There is an order of magnitude difference in diabetes risk across the spectrum of prediabetes.
We anticipate being able to further subdivide these risk strata to offer more intensive intervention bundles to those most likely to convert to diabetes, but offer anyone at risk an opportunity to address it in a variety of ways, whether in-person, online, telephonically, etc. We do feel an obligation to mention to our members that by criteria approved by the ADA that they may be at increased risk for diabetes, and that simple weight loss and exercise may prevent it.
We do recognize the Diabetes Prevention Program findings as being robust and the multiple subsequent translation trials demonstrate effectiveness of this program, even without the intensity of the original DPP. We feel that lifestyle is a reasonable first-line approach and that supporting our members with modest weight loss (goal of 5 percent) and improvement in activity levels (goal of 150 minutes/week) is possible in routine care delivery. We also recognize that not everyone who is at risk for developing diabetes will want or be able to take action. Part of our demonstration is also engaged in leveraging the latest science in behavior change and behavior design to determine the optimal engagement approaches for our members with prediabetes. We recognize the need to strike the right balance of on one side not over-medicalizing an issue and its solutions and on the other side the desire to partner with our members in maintaining optimal health. Given the changing role of health care in the U.S., we are mindful of playing the right role in this space.
1) The epidemic of pre-diabetes: the medicine and the politics John S Yudkin, Victor M Montori,: BMJ 2014;349:g4485
Competing interests: No competing interests
While I wholeheartedly agree with Yudkin and Montori in regard to their critique of the ‘pre-diabetes’ diagnosis, I am surprised that they did not also single out the closely related condition of ‘metabolic syndrome’ for criticism too. This is the name given to a group of cardiac/diabetic risk factors that include high cholesterol, insulin resistance, obesity, high blood pressure and high fat levels in the blood (Garber, 2004). The two conditions are often discussed together, with for example an International congress on ‘Prediabetes and the metabolic syndrome’ having been successfully held biannually since 2005 (Berlin 2005, Barcelona 2007).
However, although the metabolic syndrome term is widely used in the diabetes field and beyond, the concept has also been heavily criticised, with many medical professionals and health commentators raising the same concerns in regard to its clinical usefulness, as the authors highlighted in relation to ‘pre-diabetes’ (Kahn et al, 2005; Mitka, 2005). This has included criticism from Professor Gerald Reaven, the academic who first coined the term ‘syndrome X’ in 1988, who has questioned the validity of the metabolic syndrome diagnosis, as exemplified by the WHO (1999) and NCEP ATP-III (2001) definitions (Kim and Reaven, 2004). An issue also raised by James Meigs in a BMJ editorial on metabolic syndrome published in July 2003, where he asked whether the diagnosis was ‘a guidepost or detour to preventing type 2 diabetes and cardiovascular disease’.
It is interesting that it should be the American Diabetes Association (ADA) who has been instrumental in promoting the ‘pre-diabetes’ term, since they published a joint scientific statement (in conjunction with the European Association for the Study of Diabetes) in September 2005, which was highly critical of the ‘metabolic syndrome’ diagnosis, which again raised many of the same concerns now being levelled at their own ‘pre-diabetes’ term (Kahn et al 2005).
More recently, the BMJ published two further articles on metabolic syndrome in its ‘head to head’ section in March 2008, one by Edwin Gale (professor of diabetes at Bristol) in which he argued that the term was ‘a diagnostic artefact with little prognostic or therapeutic value’ (2008:640), while in an article defending the concept George Alberti and Paul Zimmet (key players behind the WHO (1999) and IDF (2005) definitions of the metabolic syndrome) argued that ‘the syndrome has an important role in public health and individual care’ (2008:641).
Earlier commentaries (also published in the BMJ) claim that conditions such as these are an example of the ‘medicalisation of risk factors’ by the medical profession, as well as ‘disease mongering’ by the pharmaceutical industry (Gotzsche, 2002; Moynihan et al, 2002). In the case of metabolic syndrome, it has been suggested that this is an example of the medicalisation of obesity, with professional organisations (such as the ADA) and the pharmaceutical industry both being implicated (Breitstein, 2004). My own research at Cardiff University (Chatterton 2014, PhD thesis – unpublished), however, showed that the medical profession, through disciplinary rivalries, has been the main driver behind the medicalisation of this concept, while the pharmaceutical industry has remained largely on the sidelines. Here medical organisations such as the American Heart Association (AHA) and International Diabetes Federation (IDF) were heavily involved in the process that led to the creation of the various definitions of the metabolic syndrome.
The negative side of labelling people as having ‘pre-diabetes’ and ‘metabolic syndrome’, or any other ‘lifestyle condition’ (such as obesity, diabetes or heart disease) is that this tends to individualise the problem, particularly in terms of responsibility and help seeking, with the result that other equally important issues such as the role played by social factors (including inequality and social stratification) become lost in the background. This tendency towards ‘blaming the victim’ has been highlighted by a number of workers, including the philosopher Daniel Wikler, who raised the issue back in 1987 in a publication entitled ‘Who should be blamed for being sick?’
The importance of social factors in the development of these so-called ‘conditions of western lifestyle’ (obesity, diabetes and heart disease) has been clearly illustrated in work conducted by epidemiologists led by Professor Michael Marmot at University College London. Their research, predominantly based on data collected from the Whitehall II Study of civil servants, has highlighted the key role played by factors such as stress, social stratification and economic inequalities (Brunner et al, 1997, 1998 and 2002; Chandola et al, 2006). Yet these are often overlooked, when a condition is largely seen in medical terms.
Of course, individuals should take some responsibility, but given that many people live under difficult economic and social circumstances, within an ever present ‘”obesogenic” enviroment’, they are often limited in what they can achieve on their own, and therefore we should stop blaming the victim and start tackling these wider issues (Pickett et al, 2005). But labelling individuals as having ‘metabolic syndrome’ (or ‘pre-diabetes’) does little to tackle these and may even prevent measures being taken, because too much emphasis is placed on the medical rather than social aspects of these conditions.
An issue also noted by Yudkin and Montori, who argued that by continuing to back the ‘pre-diabetes’ diagnosis, the ADA is at odds with other organisations such as the WHO, and indicative of ‘the dominance of the medical model over a public health approach’ (2014:4). They suggested that ‘we need a shift in perspective’ and that ‘rather than turning healthy people into patients with pre-diabetes, we should use available resources to change the food, education, health, and economic policies that have driven this epidemic (of obesity and diabetes)’ (2014:4). But whether liberal western societies, with their onus on individual freedom and choice, are serious about tackling these underlying causes, or the medical profession is ready to relinquish control of the issue, is another matter.
Competing interests: No competing interests
We believe that the use of classifications for elevated risk conditions for diabetes can act as an incentive for important behaviour change for some patients and is, therefore, a useful tool to use.
Insight research was undertaken in Merseyside in 2013 as part of the development of a local pathway for prediabetes. The research included 65 people aged 40 or over who were overweight or obese, some of who had been identified as having prediabetes.
The research explored reactions to prediabetes and found that people accepted lifestyle change as the main intervention for preventing Type 2 Diabetes if it was communicated in a way that made them take notice of the potential future consequences, whilst positioning lifestyle change as an opportunity to prevent these consequences from occurring.
The research explored reactions to the name prediabetes as well as ‘high risk of diabetes’, “borderline diabetes” and a range of clinical names for the condition. The name borderline diabetes was preferred by the majority of respondents as it has positive conations, suggesting that there is a chance of preventing the onset of diabetes. The term prediabetes suggested that diabetes was inevitable and this was just the precursor to be diagnosed with the condition.
A number of definitions of the condition were tested over two stages of research, and participants co-created a definition that they felt was provoking, yet motivational and which would engage them in making lifestyle changes.
The following definition has been adopted across Merseyside to introduce patients to the condition:
“Borderline diabetes is serious because it significantly increases your risk of getting Type 2 diabetes. It can also double your chances of suffering from heart disease or a stroke. The good news is that by achieving a healthy weight, eating healthier food and or being more physically active, you may be able to delay or prevent borderline diabetes from progressing any further.
This definition clearly positions lifestyle change as the key ‘treatment’ for preventing type 2 diabetes in the future.
The research found that again communication was key to engaging this group of people in lifestyle change. Applying a health motivation segmentation model to the research identified that patients would require different approaches to engage them with lifestyle change and to support them to actually make these changes. For example, some groups of patients would require significant emotional support whereas others had poor planning skills. Patient groups had different preferences as to whether individual or group support would motivate them. It is appreciating these differences and tailoring the support offered to patients that will lead to them engaging with lifestyle change.
Whilst participants in the research initially assumed that a ‘diagnosis’ would mean taking medication, clear communications about the role of lifestyle changes in ‘treating’ the condition were accepted, as long as tailored support was provided.
Similar research which has been undertaken in Liverpool exploring what could be done to improve self management of Type 2 Diabetes highlighted that diabetes patients typically perceive self management as taking their medicine and avoiding sugar. Other lifestyle changes are perceived to be part of being healthy in general, and are not associated with preventing diabetes complications. Developing a prediabetes pathway which clearly and effectively positions lifestyle change as the treatment for preventing diabetes and it’s complications provides an opportunity not only to prevent type 2 diabetes in those patients diagnosed with prediabetes, but could also improve self management of type 2 diabetes in patients who go on to be diagnosed with the condition – as they will already understand the important role of lifestyle change in self management.
Competing interests: No competing interests
We read with interest the point-of-view of Yudkin and Montori who, questioning the value of pre-diabetes as a clinical entity, suggest putting the term in “cold storage” [1].
We suggest that many of the concerns raised around disease-labelling are widely held and indeed this position reflects the WHO/IDF consensus guideline for the HbA1c range 6.0–6.4% termed “intermediate hyperglycaemia” [2].
Whilst advocating that the definition “pre-diabetes” should be restricted and used appropriately, to abolish it would firstly neglect the accepted wealth of data around IFG and IGT elegantly described in the article, and secondly would eliminate a readily comprehensible public health message and marker of a condition carrying a recognised increased risk of cardiovascular disease.
Moreover, as reported in the article, available observational evidence would indicate a graded continuum of the risk of vascular events for FPG values ≥5.6 mmol/L (≥100 mg/dl) in subjects not on anti-hyperglycaemic treatment [3, 4]; therefore, using such rationale not only the definition of “pre-diabetes”, but also of “diabetes”, should be questioned.
Lastly, the existing evidence over the psychological harm of being defined as “pre-diabetic” is very limited [5, 6].
In conclusion, we believe that the term “pre-diabetes” should not be abandoned, but used objectively within existing terms of reference for plasma glucose.
References
1. Yudkin JS, Montori VM. The epidemic of pre-diabetes: the medicine and the politics. BMJ 2014;349:g4485.
2. http://www.idf.org/webdata/docs/WHO_IDF_definition_diagnosis_of_diabetes... accessed 24/07/2014
3. Emerging Risk Factors Collaboration. Diabetes mellitus, fasting glucose, and risk of cause-specific death. N Engl J Med 2011;364:829-41.
4. Emerging Risk Factors Collaboration. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies. Lancet 2010;375:2215-22.
5. Andersson S, Ekman I, Lindblad U, Friberg F. It's up to me! Experiences of living with pre-diabetes and the increased risk of developing type 2 diabetes mellitus. Prim Care Diabetes 2008;2:187-93.
6. Troughton J, Jarvis J, Skinner C, Robertson N, Khunti K, Davies M. Waiting for diabetes: perceptions of people with pre-diabetes: a qualitative study. Patient Educ Couns 2008;72:88-93.
Competing interests: No competing interests
Yudkin and Montori [1] suggest that maybe there is too much diagnosis of prediabetes and conclude by suggesting that major organizations should seek to define the characteristics of the various measures of prediabetes as a predictor of future risk of both diabetes and arterial disease in different populations. The insulin disposition index (DI), which is essentially b-cell function relative to insulin resistance, is a well defined predictor of progression to diabetes [2-4]. We recently created a gold standard based on this index and demonstrate unequivocally that contrary to the discussion by Yudkin and Montori [1], the oral glucose tolerance cutoff for normality of less than 7.8mmol/L is not too generous at all but probably too high and could be lowered to less than 6.7 mmol/L [5]. Given the seriousness of the implication of this finding, we have also put the entire dataset online as a Stata file in the supplementary material for interested readers and would welcome any thoughts.
References
1. Yudkin JS, Montori VM. The epidemic of pre-diabetes: the medicine and the politics. BMJ. 2014 Jul 15;349:g4485. doi: 10.1136/bmj.g4485. PubMed PMID:25028385.
2. Cnop M, Vidal J, Hull RL, et al. Progressive loss of beta-cell function leads to worsening glucose tolerance in first degree relatives of subjects with type 2 diabetes. Diabetes Care 2007;30:677–682
3. Utzschneider KM, Prigeon RL, Faulenbach MV, et al. Oral disposition index predicts the development of future diabetes above and beyond fasting and 2-h glucose levels. Diabetes Care 2009;32: 335–341
4. Abdul-Ghani MA, Williams K, DeFronzo RA, Stern M. What is the best predictor of future type 2 diabetes? Diabetes Care 2007;30:1544–1548
5. Doi SA, Ward GM. Examination of the fasting and 2-h plasma glucose in the light of impairment in beta-cell function: what does the epidemiological data tell us? Endocrine. 2014 Jun 1. [Epub ahead of print] PubMed PMID: 24880620.
Competing interests: No competing interests
Professors John Yudkin and Victor Montori, have explored the evidence and value of pre-diabetes as a category or diagnosis and argue that current definitions risk unnecessary medicalisation and create unsustainable burdens for healthcare systems.(1) This represents, amongst other issues, cause for concern.
How have we reached a point where pre-diabetes is being considered? The role of the diabetic diet is a key issue: Historically dietary recommendations for diabetes were based on low carbohydrate and normal fat consumption, for example: A 1970s UK study of two hundred newly diagnosed, overweight diabetics concluded that control of diabetes in obese patients who respond to diet alone is due to carbohydrate restriction rather than to weight loss, this result was achieved in 80% of the participants. A highly significant statement regarding this research was - They did not start drug treatment until it was clear that diet alone had failed, which was usually after at least four months.(2) This study was led by some of the world’s most eminent diabetologists.
A further 1979 study concluded that in Type 2 diabetes a high carbohydrate diet composed of readily available cereal foods and tuberous vegetables (wholefoods) resulted in lower fasting and preprandial blood glucose concentrations than a standard low carbohydrate diet. (3)
However, by the 1980s national diabetes associations were recommending diets with a substantial amount of carbohydrate and fibre and little fat to improve glycaemic control and reduce the risk factors for ischemic heart disease.(4)(5) No doubt driven by the controversial 'diet heart' hypothesis.
Have the low fat and high carbohydrate diets wreaked havoc within the diabetes epidemic? Fats are a vital component of the human diet and within normal homeostatic function. It should also be borne in mind that without appropriate fats we cannot absorb nutrients such as vitamin D. Unsurprisingly vitamin D is often found to be deficient within the diabetes population. Crucially vitamin D plays an important role in insulin secretion and insulin sensitivity for glucose homeostasis. (6) The balancing role of fat also plays a vital role in the prevention of diabetes complications such as retinopathy and in renal health. Fat consumption also provides satiety within the diet and so may prevent overeating. Carbohydrates are converted to glucose (sugar) by the action of insulin. In a population of people with marked insulin resistance, the high carbohydrate diet approach makes little sense.
The diabetes epidemic has been spread around the world by the adoption of the western type diet and lifestyle as dominant factors. The introduction of highly processed foods and fats contribute to a diet which is destructive to health and promotes pro-inflammatory conditions, such as type 2 diabetes. It has also promoted obesity and, as a consequence, a very lucrative slimming industry. This trend has been compounded by the greed and stealth of the vested interests in the food and drug industries which have substantially benefitted from the diabetes/obesity epidemic.
Recently there has been much controversy over cholesterol (statins) management of people not considered at high risk of cardiovascular disease (Pre-cardiovascular disease?). (7) http://www.bmj.com/content/348/bmj.g3306 The article Adverse effects of statins by BMJ editor Fiona Godlee attracted 86 responses, However it appears that concerns raised have been brushed aside. Why the reluctance to honestly review the evidence concerning the role of fat (lipids) within the diet and also the medicalisation of a healthy population? A negative correlation between statin use and diabetes has also been highlighted. (8) Isn’t the treatment of pre-diabetes a similar issue? Where are the meaningful preventative measures? Where is the realistic educational support to help people live a healthy life with fully diagnosed T2DM? World health systems are being crushed under the burden of T2DM. Those diagnosed? with ‘pre-diabetes’ will potentially be medicalised at an earlier date. Including being placed on dubious diets and barely tested drugs. It appears there is nothing in place to ensure that medicalisation will not take place, or indeed the potential prevention of diabetes which represents a golden opportunity.
(1) The epidemic of pre-diabetes: the medicine and the politics John S Yudkin, Victor M Montori,: BMJ 2014;349:g4485
(2) Effect of Carbohydrate Restriction in Obese Diabetics:Relationship of Control to Weight Loss J. R. Wall, D. A. Pyke, W. G. Oakley British Medical Journal, 1973, 1, 577-578
(3) Simpson, R W, et al, British Medical Journal, 1979, 1, 1753.
(4) American Diabetes Association. Nutritional recommendations and principles for individuals with diabetes mellitus. Diabetes Care 1987;10: 126-32.
(5) Diabetes and Nutrition Study Group of the European Association for the Study of Diabetes.Nutritional recommendations for individuals with diabetes mellitus. Diabetes, Nutrition and Metabolism 1988;1:145-9.
(6) Role of vitamin d in insulin secretion and insulin sensitivity for glucose homeostasis. Alvarez JA, Ashraf A. Int J Endocrinol. 2010;2010:351385.
(7) Adverse effects of statins. Fiona Godlee. BMJ 2014;348:g3306
(8) Do statins cause diabetes? Goldstein MR1, Mascitelli L. Curr Diab Rep. 2013 Jun;13(3):381-90. doi: 10.1007/s11892-013-0368-x.http://www.ncbi.nlm.nih.gov/pubmed/23456437
Competing interests: No competing interests
An awareness regarding obesity and obesity related complications is the need of the hour. In obese individuals as well as in family members with a susceptibility to diabetes a screening for pre-diabetes may prove useful. There is already the practice of screening and diagnosing metabolic syndrome in vogue. Therefore it becomes prudent to look for proper diagnostic or say screening methods for obesity and obesity related disorders including pre-diabetes in a population.
Competing interests: No competing interests
I agree with much of what John Yudkin says here, but when he mentions 'harms of overdiagnosis -a label of pre-diabetes brings problems of self image'. I must point out that this very much depends on how the clinician uses this information.
In my practice I have found the diagnosis of pre-diabetes to be an ideal opportunity to have a 'lifestyle review' with my patients. In this the HbA1c result needs weighing up along with other factors such as weight, waist measurement, liver function tests, BP and so on.
At the point of having a raised HbA1c result I find the patient particularly interested in exploring improvements in lifestyle- particularly diet. We discuss the choices open to them, especially the idea of reducing sources of sugar.
Surprisingly out of 26 newly diagnosed pre-diabetics and type 2 diabetics I have interviewed over the past year- 24 have cheerfully joined our practice weight loss group (with me!) and far from this resulting in 'problems of self-image' they are proud of taking control of their lives, seven patients came off medication.
Results: Paired t test
Weight (Kg) pre diet 100.9 (93.4, 108.3), post diet 91.3 (83.6, 99.0) p<0.001
HbA1(mmol/mol) pre diet 50.2 (45.5, 55.0), post diet41.2 (38.2, 44.1) p<0.001
I feel we have all eaten our way into this diabesity epidemic and we must all take every opportunity to help patients eat their way out of it again.
John Yudkin asks for a shift in perspective - I suspect it would help if doctors prioritized working on lifestyle changes with our patients well before initiating drug therapy. The diagnosis of pre-diabetes far from being a threat can be a turning point and a golden opportunity.
Ref; Unwin DJ, Low carbohydrate diet to achieve weight loss and
improve HbA1c in type 2 diabetes and pre-diabetes:
experience from one general practice. Practical Diabetes 2014; 31(2): 76–79
Competing interests: No competing interests
Yudkin and Montori outline clearly (July 16th) the morass of arbitrary cut-points on the glycaemia distribution that are said to define type 2 diabetes. Yet the authors may have missed wood for those trees.
All the randomised trials directed at lowering blood glucose have failed to reduce outcomes that matter to patients, namely vascular end-points and mortality, which has been increased. The intensive treatment trials also all suffer from visit or treatment bias - as in ‘Advance’ where the intervention group averaged 33 visits over 5 years and the control group just 12. Systolic blood pressure variability and maximum values were the most powerful predictors of small and large vessel damage in Advance (1).
T2 diabetes is a vascular disease, most probably linked to inflammation in abdominal fat prior to onset of hyperglycaemia, as excess events in pre-diabetes show. Blood vessels develop problems early (2-4). Blood glucose now seems a late, secondary factor in diabetes development - multiple metabolic, mainly lipid, markers are disturbed before blood glucose, as shown by metabolomic techniques (5). It is important to note that statins reduce vascular events by some 30% in people with type 2 diabetes (6).
.
So the major research challenge now is to find out how most visceral fat develops into 'bad' fat. The hypothesis becomes 'T2 diabetes is not diabetes as understood but a vascular disease before 'hyperglycaemia'. The important practical question becomes 'Can we treat and improve such blood vessel dysfunction early, while reducing food intake?'.
1. Hata J, Arima H, Rothwell PM, Woodward M, Zoungas S, Anderson C, Patel A, Neal B, Glasziou P, Hamet P, Mancia G, Poulter N, Williams B, Macmahon S, Chalmers J; ADVANCE Collaborative Group. Effects of visit-to-visit variability in systolic blood pressure on macrovascular and microvascular complications in patients with type 2 diabetes mellitus: the ADVANCE trial. Circulation. 2013 Sep 17;128(12):1325-34.
2. Banerjee M, Anderson SG, Malik RA, Austin CE, Cruickshank JK. Small artery function 2 years postpartum in women with altered glycaemic distributions in their preceding pregnancy. Clin Sci (Lond). 2012;122:53-61.
3. Schofield I, Malik R, Izzard A, Austin C, Heagerty A Vascular structural and functional changes in type 2 diabetes mellitus: evidence for the roles of abnormal myogenic responsiveness and dyslipidemia. Circulation. 2002 Dec 10;106(24):3037-43.
4. Cruickshank JK, Riste L, Anderson SG, Wright JS, Dunn G, Gosling RG. Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation. 2002 Oct 15;106(16):2085-90.
5. Anderson SG, Dunn WB, Banerjee M, Brown M, Broadhurst D, Goodacre R, Cooper GJS, Kell DB, Cruickshank JK. Evidence that multiple defects in lipid regulation occur before hyperglycemia during the prodrome of type-2 diabetes. Plos-ONE 2014 accepted.
6. Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ, Thomason MJ, Mackness MI, Charlton-Menys V, Fuller JH; CARDS investigators. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 2004 Aug 21-27;364(9435):685-96.
Competing interests: JKC's centre was the largest global recruiting site in the Advance trial.
Re: The epidemic of pre-diabetes: the medicine and the politics. IT IS JUST ONE MANIFESTATION OF THOUGHTLESS PREVENTIVE MEDICINE
We have a prevailing mind-set in medicine which passionately believes in identifying biochemical markers which herald DEATH.
We have forgotten that at least SOME of us do not want to live for ever. Give me a short life but a happy one. I speak for myself.
And please, do not threaten me - if you say that “ untreated”, I will develop diabetes and develop heart disease and die in five years, I do not mind - if I am in my eighties. But once you have made such prediction, I develop a neurotic obsession with “healthy eating”. And you, dear Preventive Medicine Practitioner! You start on your next preventive obsession.
You tell me, a man, that I should have my PSA determined, Regardless of my age. Regardless of whether I have any urinary symptoms, or any reason to suspect prostatic metastases. I know and have known for sixty years - from pathology textbooks - that most people above the age of 80, do have malignant cells in their prostate, that these malignant cells do not always make an appearance, that such people die of other disease, blissfully unaware that they had been peacefully co-existing with CANCER.
Please see health.harvard.edu which tells us that the American Urological Association does not recommend PSA screening for men 70 or older or with a life expectancy of less than 10 to 15 years.
Then there is your obsession with searching for breast cancer with mammograms. Please read Bewley, Blennerhassett, Payne, BMJ 2019;365:1293, on AgeX programme. Why should I, a woman, listen to you, obey you?
To end, may I please remind you, dear reader, of the paper by Sackett, DL, “The arrogance of preventive medicine". Canadian Association Journal, Aug 20, 2002, 167, (4) 363-364.
Preventive medicine displays all 3 elements of arrogance - aggressive assertion......., presumptuous....that it will do more good than harm......overbearing, attacking those who question .......”
Thank you for reading.
Dr JK Anand
FFPHM DPH
Retired public health physician
Peterborough, England
Acknowledgement
The idea in the rapid response is of a joint effort of Dr Friedrich Flachsbart of Göttingen. I am responsible for the phraseology.
Competing interests: No competing interests