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In the UK, more than 3.2 million live with diabetes, up from 2.1 million in 2005. The majority (90%) have type-2 diabetes, which is linked to poor diet and obesity.

Diabetes arises when the body loses its ability to use or make insulin, a hormone that helps regulate the amount of sugar in the blood, causing uncontrolled blood sugar levels. Patients with diabetes are at risk for macrovascular complications such as myocardial infarction and stroke, and microvascular complications such as nephropathy, retinopathy, and neuropathy. It can lead to devastating complications such as blindness, and was the cause of 22,000 early deaths last year.

Many diabetics experience peripheral neuropathy (nerve damage), which can result in a loss of sensation or persistent, nagging pain. The loss of sensation can lead to sores or infection in the feet, which, if left undetected necessitate lower limb amputation (135 per week across the UK); diabetic peripheral neuropathy can also cause gnawing, tingling, shock-like, or shooting pain in the extremities, which causes great distress and has no cure.

The spiralling numbers of diabetes patients, following the trend of obesity, shows that the public may still be unaware of the severity of these conditions.

Human cost aside, what about the NHS?

The dramatic growth in the numbers of people with diabetes underlines the urgent need for prevention, before the disease burden overwhelms the NHS.

  • The NHS spends 10% of its entire budget managing diabetes
  • Diabetes already costs the NHS nearly £10bn a year, and 80% of this is spent on managing avoidable complications
  • In 2014-15, there were 47.2 million items prescribed in England for diabetes
  • Diabetes prescription accounted for 4.5% of the total number of items prescribed and 10% of the total cost of all prescribing
  • Since 2005-6, prescribing of antidiabetic drugs has risen by 107%, with the net ingredient cost increasing by 138.6%

Despite this exorbitant spending, the charity Diabetes UK has warned that only 60% of patients receive all the care processes they require for effective monitoring and treatment. There is huge potential to save money and reduce pressure on NHS hospitals and services, but without successful diabetes prevention, this figure will unquestionably rise to unsustainable levels.

If nothing changes then what will happen?

The shocking recent headline that ‘Diabetes cases soar by 60% in past decade’ (1) is likely to have worried many, because – as with obesity – it is not an easily reversible trend. Many believe that obesity causes prediabetes (non-diabetic hyperglycaemia), a metabolic condition that almost always develops into type-2 diabetes

According to data from Public Health England, five million adults in England are pre-diabetic; using much broader criteria, Diabetes UK actually estimates a UK-wide figure of around 18 million people as being risk of developing diabetes; and the British Medical Journal suggests a staggering third of all adults in England are already pre-diabetic (2). However, some doctors have questioned the value of the pre-diabetic diagnosis (3), arguing that only a small number – perhaps one in 10 – will go on to develop diabetes.

Despite these widely variable outcome predictors for diabetes, the fact that diabetes prevalence has soared, and obesity – the greatest risk factor for developing DM – continues to “spread”, it is highly likely that diabetes prevalence will continue to grow.

Cause of diabetes: unhealthy lifestyle, genes or gut microbiota?

Diagnoses are not always clear-cut: obesity and diabetes result from complex interactions between environmental and genetic factors. However, with 80% of people with type-2 diabetes being overweight or obese at the time of diagnosis (according to the International Diabetes Federation), the explanation for the recent exponential increases in numbers of type 2 is being placed on the expanding waistlines of the nation. Excess abdominal fat is an especially high-risk form of obesity: abdominal fat causes pro-inflammatory mediators to be released from fat cells, which effectively reduce insulin responsivity, a major trigger for type-2 diabetes.

Recently gut microbiota has shown to be involved too. Using mice genetically predisposed to obesity and metabolic disorders Ussar and co-workers showed that this phenotype is the result of interactions between gut microbiota, host genetics, and diet (4). This is somewhat encouraging: individuals may be amenable “reprogramming” of microbiota for ameliorating the development of metabolic disorders and may offer hope for faecal transplants in the future.

So what’s new? Is it as simple as healthy eating and more exercise?

Although diabetes medication is routine treatment, it basically helps to control the condition and is not preventative. These drugs fall into many categories, such as alpha glucosidase Inhibitors (slow carbohydrate digestion), incretin mimetics, and thiazolidinediones (reduce insulin resistance), to name but a few. With diabetes, the old adage – that prevention is better than cure – is a huge understatement.

Although to many, healthy lifestyle choices are common sense and almost intuitive, the NHS is preparing to roll out a diet, weight loss and exercise programme that has been shown to reduce the diabetes risk for a quarter of those who take it up. However implementing these recommendations into real world settings is a challenge for many.

Most people understand that in order to reduce risk of developing diabetes or reduce complications associated with diabetes they need to lose weight, exercise and eat healthily, but can find it difficult to maintain, so therefore patient support is critical. Mobile applications and web-based technology can be useful in self-management, and particularly for lifestyle changes in patients with diabetes.

A review of internet-based interventions highlighted that they were focused on management of glycaemic controls and drug titrations and rather than lifestyle changes, and that in this respect they lacked behaviour theory and educational components (5). This comes as a surprise as the lifestyle choices could be both cause and cure for the disorder. Promisingly, they found the tools available demonstrated improvements in behavioural, physiological outcomes as well as improved knowledge and self-efficacy. This suggests that utilisation of the almost ubiquitous smartphone as a motivational and educational tool may hold promise for managing type-2 diabetes for individual and peer-to-peer support using social media.

Another school of thought believes that a more drastic method is required: bariatric surgery. A recent study demonstrated that half of the type-2 diabetes patients who had weight loss surgery were cured for at least two years (6). Overall they were less likely to have heart problems (a common side-effect of uncontrolled diabetes), and reported improved quality of life and even those who weren’t cured were able to better manage their symptoms. In fact, so effective is this approach that NICE guidelines have reduced the threshold for consideration for surgery from a BMI of 35 with concurrent health to a BMI of 30-35 (7).

Clearly, in order to slow this wave of diabetes something must change, whether it is a more aggressive pre-symptomatic diagnostic phase with education and behavioural therapy, or decisive action regarding surgery at early stage or more effective symptomatic treatment. Technology must be embraced, so that patients can self-manage, self-motivate and prevent diabetes and its deleterious complications before NHS resources are overwhelmed with what is largely a preventable disease.

 

If you would like to comment on any of the issues raised by this article, particularly from your own experience or insight, Healthcare-Arena would welcome your views.

References

  1. http://www.bbc.co.uk/news/health-33932930.
  2. Wise J. A third of adults in England have “prediabetes,” study says. BMJ. 2014;348:g3791. Epub 2014/06/12.
  3. Yudkin JS, Montori VM. The epidemic of pre-diabetes: the medicine and the politics. BMJ. 2014;349:g4485. Epub 2014/07/17.
  4. Ussar S, Griffin NW, Bezy O, Fujisaka S, Vienberg S, Softic S, et al. Interactions between Gut Microbiota, Host Genetics and Diet Modulate the Predisposition to Obesity and Metabolic Syndrome. Cell metabolism. 2015;22(3):516-30. Epub 2015/08/25.
  5. Cotter AP, Durant N, Agne AA, Cherrington AL. Internet interventions to support lifestyle modification for diabetes management: a systematic review of the evidence. Journal of diabetes and its complications. 2014;28(2):243-51. Epub 2013/12/18.
  6. Arora T, Velagapudi V, Pournaras DJ, Welbourn R, le Roux CW, Oresic M, et al. Roux-en-Y Gastric Bypass Surgery Induces Early Plasma Metabolomic and Lipidomic Alterations in Humans Associated with Diabetes Remission. PloS one. 2015;10(5):e0126401. Epub 2015/05/07.
  7. http://pathways.nice.org.uk/pathways/obesity – path=view%3A/pathways/obesity/surgery-for-obese-adults.xml&content=view-node%3Anodes-people-with-recent-onset-type-2-diabetes.

 

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There’s nothing quite like diets to get people arguing. Calorie controlled, low-fat, Atkins, glycaemic index … they all bring out the worst in bigotry and charlatanism. There must be some truth somewhere, and you’d think science would find the answers, but recent experience is that a report of a study can generate apparently diametrically opposed press coverage: ‘Low-fat diets are better’ said the BBC while the Daily Mail headline said ‘Low-carb is best’ [1, 2].

Actually it was mainly the headlines that were confusing in this case as the actual results from the study were well reported in the articles but the issue with interpreting the results is how well they translate to the real-world setting.

The study involved a small number of obese subjects who followed a short (6-day) baseline diet of 2700 calories per day followed by the experimental 5-day diet where the calorific intake was reduced by a third either by reducing fat or by reducing carbohydrates. Subjects exercised daily. After a washout period of 2-4 weeks, the process was repeated with the other diet [3].

NHS Choices, which keeps a close eye on press coverage of medical research, explains that this was a well-designed study but because of the small number of subjects (19) and the short timeframe the results weren’t convincing enough to settle the debate [4].

In obese subjects fat loss is more important than weight loss and the prevailing view has been that fat loss is not possible without reducing the intake of carbohydrates [e.g. 5]. Hall’s study has shown that this is not the case and that fat loss is possible without reduction in carbohydrate intake.

Hall and his colleagues point out in the paper the difficulties of conducting randomised controlled trials of prescribed diets. For that reason Hall’s research involved subjects being admitted to the metabolic unit at the NIH Clinical Center in Bethesda, US where they stayed for the duration of the research with careful monitoring of all exercise and food intake – conditions that are neither practical nor cost-effective in outpatient studies.

The study showed that

  • Both diets led to weight loss
  • The low-carbohydrate diet affected the metabolism more than low-fat diet. Insulin levels dropped which increased fat burning and lowered carbohydrate burning
  • The low-fat diet led to more fat loss (measured as the difference between the fat taken in and the amount of fat burned) but no significant changes in fat oxidation or insulin secretion
  • Using the normal measure of % body fat, there was no change between the groups

As a result, the researchers were able to definitively reject the hypothesis [5] that carbohydrate restriction is required for body fat loss.

However, despite the clear results, Hall and colleagues stress that the opportunities to translate the results to real-world weight-loss diets for obesity are limited because the experimental model depended on strict control of food intake, which is unrealistic outside the clinic environment

It seems that the old truism remains: the best diet is the one that you can stick to!

Not all fat is equal

Our understanding of diet and how we store and process food is constantly changing. It was only in 2009 that studies showed the importance of brown adipose tissue (brown fat) in humans [6].

Brown fat is interesting because of its ability to burn food directly to produce heat; it can produce 300 times more heat per gram than any other tissue in the body but is also believed to release hormones that help to regulate the metabolism of glucose and fatty acids [see 7].

In general, slimmer people have more brown fat while obese people have less. The natural question to ask is whether the brown fat can be increased, enhanced or somehow made more active. The answer is that it can. Exposure to cold is known to activate the brown fat cells and recent studies suggest that capsaicin, the component of chilli peppers that provides the heat, stimulates brown fat in the same way [8]. Other pharmaceutical interventions to enhance the performance of brown fat could be in the pipeline, including mirabegron, which was developed originally for overactive bladder but has been found to stimulate receptors on the surface of brown fat cells [9].

Why do we need carbohydrates anyway?

From work recently published in the Quarterly Review of Biology it looks as though carbohydrates could have played a critical role in human evolution.

Our brains are bigger than those of our nearest relatives in the animal world, and they use about a quarter of the calories we consume. Karen Hardy and her colleagues outline the persuasive hypothesis that man’s brain did not develop as a result of moving from a plant-based to a meat-based diet. They propose instead that human brains were only able to evolve and grow as a result of including concentrated starch from plant food in the diet to meet the substantial increased metabolic demands of an enlarged brain – and the development of cooking would have to be a component of that development.

The evidence for the use of fire to cook food is – at present – primarily archaeological, but Karen Hardy and her colleagues have been examining the gene that produces the enzyme amylase that is essential to breaking down starch. Their hypothesis is that there must have been genetic selection for higher levels of amylase secretion at the same time as the processes of cooking were evolving. Better understanding of the amylase gene and ancient DNA data will therefore be important in the further refinement of the hypothesis [10].

So the proponents of the ‘Paleolithic diet’ are going to have to add back some starch!

 

If you would like to comment on any of the issues raised by this article, particularly from your own experience or insight, Healthcare-Arena would welcome your views.

References

  1. BBC News website. Low-fat diets ‘better than cutting carbs’ for weight loss [Internet]. BBC News. [cited 2015 Sep 4]. Available from: http://www.bbc.co.uk/news/health-33905745
  2. Daily Mail. Low-carb diets ‘are best for weight loss but forsaking fat is BETTER’ | Daily Mail Online [Internet]. [cited 2015 Sep 4]. Available from: http://www.dailymail.co.uk/health/article-3196738/STILL-great-diet-debate-rages-Low-carb-best-weight-loss-forsaking-fat-BETTER-health-latest-study-reveals.html
  3. Hall KD, Bemis T, Brychta R, Chen KY, Courville A, Crayner EJ, et al. Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity. Cell Metab. 2015 Sep 1;22(3):427–36.
  4. NHS Choices. Low-fat diet ‘better’ than low-carb diet for getting rid of body fat – Health News – NHS Choices [Internet]. 2015 [cited 2015 Sep 4]. Available from: http://www.nhs.uk/news/2015/08August/Pages/Low-fat-diet-better-than-low-carb-diet.aspx
  5. Taubes G. Why we get fat and what to do about it. New York: Alfred A. Knopf; 2011.
  6. van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JMAFL, Kemerink GJ, Bouvy ND, et al. Cold-activated brown adipose tissue in healthy men. N Engl J Med. 2009 Apr 9;360(15):1500–8.
  7. Lambert C. Grow fat, get thin? We put brown fat to the test | New Scientist [Internet]. [cited 2015 Sep 4]. Available from: https://www.newscientist.com/article/dn27265-grow-fat-get-thin-we-put-brown-fat-to-the-test/
  8. Yoneshiro T, Aita S, Matsushita M, Kayahara T, Kameya T, Kawai Y, et al. Recruited brown adipose tissue as an antiobesity agent in humans. Journal of Clinical Investigation. 2013 Aug 1;123(8):3404–8.
  9. Cypess AM, Weiner LS, Roberts-Toler C, Elía EF, Kessler SH, Kahn PA, et al. Activation of Human Brown Adipose Tissue by a β3-Adrenergic Receptor Agonist. Cell Metabolism. 2015 Jan 6;21(1):33–8.
  10. Hardy K, Brand-Miller J, Brown KD, Thomas MG, Copeland L. The Importance of Dietary Carbohydrate in Human Evolution. The Quarterly Review of Biology. 2015 Sep 1;90(3):251–68.

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Microbiome data now being gathered may form the basis for a ‘personalised’ approach to improving individual microbial populations

Image: ©Pixelbliss/Shutterstock #280702511

In May 2015, a molecular microbiology study was published in the Proceedings of the National Academy of Sciences (1). This study showed that gut bacteria could be DNA ‘fingerprinted,’ as their DNA sequences were shown to represent a unique form of identification in more than 80% of individuals examined (1). This study has little to do with ‘CSI’-style forensic identification but does have implications for our health, diet, development and genetics and our ability to defend ourselves from true microbial pathogens (1).

That the human body is believed to contain ten times more microbial cells than human cells (trillions of them) can be an uncomfortable thought. Even more remarkable is that, in terms of numbers, the population of these microbes accounts for up to 90% of the total number of cells associated with our bodies. Our human microbial population weighs between 1% and 3% of our total body mass (1.5 kg); this is equivalent to the weight of the largest human internal organ, the liver (2).

The terminology of the body’s flora and fauna can be confusing. This could be why someone, probably working in advertising, came up with the phrase ‘friendly bacteria.’ The term ‘microbiota’ is the collective noun that refers to the viruses, fungi and bacteria that inhabit our bodies, mainly in our gut and on the surface of our skin. The microbiota has a commensal and a symbiotic relationship with us. The term, ‘microbiome’ is used to refer to the collection of the genomes of these microbes. These two names, ‘microbiota’ and ‘microbiome,’ are often used interchangeably.

Our view of our personal microbial health has changed during the past 20 years. Until the 1990’s there was the ‘germicidal view’ that all bacteria were harmful and that we should be doing all we could to sterilise our home environment, ourselves and our food. There are now increasing numbers of scientific and healthcare news stories, as well as television commercials, which advise us to encourage and nurture our own, resident, and very personal ‘friendly bacteria.’

As with the dietary anti-oxidant ‘industry’ that arose from cardiovascular research in the 1980’s, the food industry has been swift to promote the sales of dietary probiotic supplements. Global sales of probiotics have been reported as £13.6 billion ($21.6 billion USD) in 2010 and are expected to exceed £19.6 billion ($31.1 billion USD) during 2015 (3).

In February 2015, an editorial collaboration between the journals, Nature and Scientific American, resulted in the publication of a series of special reports entitled, Innovations in the Microbiome(4) These and other recent publications have helped to place the importance of the normal human microbial population further into the medical spotlight.

For almost a century, epidemiological studies have shown that diet has a profound effect on human health. Recently, the link has been made between diet and the gut microbiota, with emphasis on the effects that a ‘western’ diet of refined foods and high protein have on these organisms. In 2011, a study linked long-term dietary patterns to changing gut bacterial enterotypes in humans (5). In 2014, a study in wild mice clearly demonstrated that dietary change can induce gut bacterial ‘enterotype switches’ within hosts (6). ‘Biome reconstitution’ has been proposed as a treatment approach to immune disorders, including allergy and autoimmune disease and to preventing colonic cancer, obesity, diabetes, and metabolic disease (7, 8).

In the past ten years, sequencing technologies have allowed the development of a detailed reference database of the diverse microbes that inhabit our bodies. In 2007, in the US, the National Institutes of Health (NIH) Human Microbiome Project (HMP) Consortium was launched, consisting of more than 200 members, from nearly 80 universities and scientific institutions (9). In its 2012 report, the HMP listed the major ways in which knowledge of the human microbiome may change the future of science and medicine (10). The HMP has considered the potential privacy issues surrounding knowledge of the individual microbiome, the flow between human microbes and those found in nature (in water and soil) (10).

The microbiome data now being gathered may form the basis for a ‘personalised’ approach to improving individual microbial populations. Most importantly, solutions to microbial antibiotic resistance may be found through increasing knowledge of microbial interactions. At this same time comes the realisation that overuse of antibiotics, as part of our ‘war on germs’ mentality, has allowed true microbial pathogens to develop antibiotic resistance. The lack of a functioning and complete personal microbial population leaves us vulnerable to bacterial pathogens that we may be increasingly less able to fight.

In 2013, the Chief Medical Officer for England highlighted the increasing problem of antibiotic resistance. These concerns led to the Department of Health launching a five-year Antimicrobial Resistance (AMR) Strategy, which is supported by NHS England’s Antibiotic Awareness Campaign (11,12). In October 2014, Public Health England produced the first report on the English Surveillance Programme for Antimicrobial Utilisation and Resistance (ESPAUR) (13). These latest initiatives by the medical profession and healthcare regulators to reduce antibiotic prescribing is just one approach that has to be made.

The European Molecular Biology Laboratory (EMBL) annual conference, held in Heidelberg in June 2015, was devoted to the topic of the Human Microbiome (14). This meeting included discussions on the design of possible therapeutic or dietary interventions to prevent and treat disease. An announcement was made at the meeting of the first results from the Personalised Nutrition Project, run by research groups in Israel (15). The u-Biome Project is a crowdfunded ‘citizen science’ initiative that is set to analyse the microbiome in the context of individual health and is currently recruiting participants (16).

The rationale for learning more about the ‘normal’ or ‘optimal’ microbiome, and how to reconstitute or nurture it, is an important component of individual healthcare (17, 18). For the future development of interventions for resistant microbial pathogens, the human microbiota may play more than just a ‘friendly’ role, it may be life-saving.

If you would like to comment on any of the issues raised by this article, particularly from your own experience or insight, Healthcare-Arena would welcome your views.

References

(1) Franzosa EA, Huang K, Meadow JF, Gevers D, Lemon KP, Bohannan BJ, Huttenhower C. Identifying personal microbiomes using metagenomic codes. Proc Natl Acad Sci U S A. 2015;pii 201423854. http://www.pnas.org/content/early/2015/05/08/1423854112 Accessed June 10, 2015

(2) The Human Microbiome Project. Structure, function and diversity of the healthy human microbiome. Nature 2011;486:207-14. http://www.nature.com/nature/journal/v486/n7402/full/nature11234.html Accessed June 10, 2015

(3) Business Communications Company (BCC) market research data for sales of probiotic foods and supplements, 2010 and 2015. http://www.bccresearch.com/pressroom/fod/global-market-for-probiotics-reach-$36.7-billion-2018 Accessed June 10, 2015

(4) Special Report. Innovations in the Microbioma. Scientific American Vol 312, Feb 2015. http://www.scientificamerican.com/editorial/innovations-in-the-microbiome/ Accessed June 10, 2015

(5) Wu GD, Chen J, Hoffmann C, et al. Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes. Science 2011;334(6052):105-108. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368382/ Accessed June 10, 2015

(6) Wang J, Linnenbrink M, Kunzel S, et al. Dietary history contributes to enterotype-like clustering and functional metagenomic content in the intestinal microbiome of wild mice. Proc Natl Acad Sci USA 2014; 111:E2703-E2710. http://www.pnas.org/content/111/26/E2703.full Accessed June 10, 2015

(7) Parker W, Ollerton J. Evolutionary biology and anthropology suggest biome reconstitution as a necessary approach toward dealing with immune disorders. Evolution, Medicine, and Public Health 2013;2013(1):89-103. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868394/ Accessed June 10, 2015

(8) Grice EA, Segre JA. The Human Microbiome: Our Second Genome. Annual Review of Genomics and Human Genetics 2012;13:151-170. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518434/ Accessed June 10, 2015

(9) The National Instututes of Health (NIH) Human Microbiome Project website http://commonfund.nih.gov/hmp/index Accessed June 10, 2015

(10) National Institutes for Health (NIH). Human Microbiome Project defines normal bacterial makeup of the body. Genome sequencing creates first reference data for microbes living with healthy adults. June 13th 2012. http://www.nih.gov/news/health/jun2012/nhgri-13.htm Accessed June 10, 2015

(11) The Department of Health Antimicrobial Resistance (AMR) Strategy 2013 to 2018. First published September 10, 2013. https://www.gov.uk/government/publications/uk-5-year-antimicrobial-resistance-strategy-2013-to-2018 Accessed June 10, 2015

(12) NHS Antibiotic Awareness Campaign. Last revised 24th Sept 2014. http://www.nhs.uk/NHSEngland/ARC/Pages/AboutARC.aspx Accessed June 10, 2015

(13) Public Health England. English Surveillance Programme Antimicrobial Utilisation and Resistance (ESPAUR) Report. Published Oct 10, 2014. https://www.gov.uk/government/publications/english-surveillance-programme-antimicrobial-utilisation-and-resistance-espaur-report Accessed June 10, 2015

(14) European Molecular Biology Laboratory (EMBL) website. http://www.embl.de/aboutus/general_information/index.html Accessed June 10, 2015

(15) The Personalised Nutrition Project website. http://newsite.personalnutrition.org/WebSite/Home.aspx Accessed June 10, 2015

(16) u-Biome – Sequencing Your Microbiome website. https://www.indiegogo.com/projects/ubiome-sequencing-your-microbiome#/story Accessed June 10, 2015

(17) Grogan D. Microbes in the Gut Are Essential to Our Well-Being. Scientific American. Feb 17, 2015. http://www.scientificamerican.com/article/microbes-in-the-gut-are-essential-to-our-well-being/ Accessed June 10, 2015

(18) Parums D. ‘Indigenous’ Human Microbes – the Microbiota and the Microbiome. Thomson Reuters Life Sciences Connect. May 26, 2015. http://lsconnect.thomsonreuters.com/indigenous-human-microbes-the-microbiota-and-the-microbiome/ Accessed July 6, 2015

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