Tag Archives: Diet

An Issue of BMJ with Multiple Studies on Diet

This News Blog often contains information about diet and health. For example, we have cited evidence that salt is enemy number one [1]; trans-fats are unremittingly bad news [2]; and large amounts of sugar are harmful.[3] After that the risks become really rather small – relative risks of about 20%. Fruit, and more especially vegetables, are good news. Milk is an unhealthy drink in adults (never intended for that purpose and galactose is harmful, unless removed during a fermentation process).[4] Three further studies of diet were included in a single recent issue of the BMJ.[5-7]

The first study by Etemadi, et al. looked at meat consumption in a large cohort of people (n= 536,969) who gave detailed dietary histories.[5] The evidence corroborates other studies in showing that red meat is harmful, increasing relative risk of death by about 20% in high meat eaters compared to moderate meat eaters. The difference is greater if the comparison is made with people who obtain almost all of their meat in the form of fish and chicken. The causes of death that showed greatest increases in risk with high red meat consumption were cancer, respiratory disease and liver disease. Surprisingly, perhaps, increased risk from stroke was nugatory. The increased risk in unprocessed meat is probably related to haem iron, and in processed meat to nitrates/nitrites – there are all pro-oxidant chemicals. Of course this is an association study, so some uncertainty remains. The main problem with meat, as the BMJ Editor points out,[8] is the harmful environmental effects; apparently animal husbandry contributes more to global warming than burning fossil fuels. I take the environmental effects seriously – perhaps we will one day vilify meat farmers more vociferously than we currently vilify tobacco farmers. After all, individuals don’t have to smoke, but cannot protect themselves from the harmful effects of pollution.

Meanwhile, for those who are interested, the other two relevant articles in this issue of the BMJ looked at avoiding gluten in people who do not have celiac disease (no benefit and evidence points towards harm),[6] and the beneficial effect of a low salt and fat diet on gout.[7]

— Richard Lilford, CLAHRC WM Director

References:

  1. Lilford RJ. Effects of Salt in Diet. NIHR CLAHRC West Midlands News Blog. 17 October 2014.
  2. Lilford RJ. On Diet Again. NIHR CLAHRC West Midlands News Blog. 23 October 2015.
  3. Lilford RJ. How Much Sugar is Too Much? NIHR CLAHRC West Midlands News Blog. 25 September 2015.
  4. Lilford RJ. Two Provocative Papers on Diet and Health. NIHR CLAHRC West Midlands News Blog. 12 December 2014.
  5. Etemadi A, Sinha R, Ward MH, Graubard BI, Inoue-Choi M, Dawsey SM, Abnet CC. Mortality from different causes associated with meat, heme iron, nitrates, and nitrites in the NIH-AARP Diet and Health Study: population based cohort study. BMJ. 2017; 357: j1957.
  6. Lebwohl B, Cao Y, Zong G, Hu FB, Green PHR, Neugut AI, Rimm EB, Sampson L, Dougherty LW, Giovannucci E, Willett WC, Sun Q, Chan AT. Long term gluten consumption in adults without celiac disease and risk of coronary heart disease: prospective cohort study. BMJ. 2017; 357: j1892.
  7. Rai SK, Fung TT. Lu N, Keller SF, Curhan GC, Choi HK. The Dietary Approaches to Stop Hypertension (DASH) diet, Western diet and risk of gout in men: prospective cohort study. BMJ. 2017; 357: j1794.
  8. Godlee F. Red meat: another inconvenient truth. BMJ. 2017; 357: j2278.

Exercise and Energy Expenditure: Not What You Think?

Each week I burn up to 1,500 kcals in my two hours of intense ‘spinning’. So you might have thought (like me) that I could indulge in 1,500 kcals worth of extra puddings. Well you (like me) would have thought wrong, at least according to careful animal and human studies described by Pontzer in this month’s Scientific American.[1] Apparently, short of being an absolute coach potato or an extreme sportsman like Mark Spitz, the rest of us burn the same number of Calories per day, adjusted for mass, irrespective of how much we exercise. Apparently the body compensates for activity by consuming less Calories at rest. Says Pontzer, “exercise to stay healthy, but restrict Calories to control weight

Richard Lilford, CLAHRC WM Director

Reference:

  1. Pontzer H. The Exercise Paradox. Scientific American. February 2017.

 

More on Fats and Their Effect on Cholesterol, Heart Disease, and Death

The accumulating evidence on the lack of association between eating saturated fat and heart disease has featured in previous posts.[1] [2] An intriguing re-analysis of an RCT carried out in nursing homes and hospitals for mental illness has recently been published in the BMJ.[3] In this trial saturated fats were replaced in the diet by polyunsaturated fats. The now familiar story was confirmed; yes, the polyunsaturated fat is associated with lower cholesterol levels, but no, there was no hint of a decrease in heart attack or all-cause mortality in the low fat group. The authors then carried out a systematic review, finding five RCTs examining the same hypothesis. They provided strikingly similar results; the meta-analysis corroborated the nursing home study. One intriguing point made in an accompanying editorial [4] is that the climate was so heavily slanted towards the fat and cholesterol hypothesis that the trial, which ended in 1973, was not published until 1989. But opinion has eventually caught up with the evidence and US dietary guidelines have finally removed dietary cholesterol and fat from the list of foods that should be avoided.[5] But note this point – the fact that saturated fats are no worse than polyunsaturated fats does not mean that there are not yet better sources of calories. And, yes, plants are better than meat, butter, etc. They are boring to eat, of course, but they are probably the best source for most of our calories.

— Richard Lilford, CLAHRC WM Director

References:

  1. Lilford R. More on Diet. NIHR CLAHRC WM News Blog. 14 August 2015.
  2. Lilford R. On Diet Again. NIHR CLAHRC WM News Blog. 23 October 2015.
  3. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 2016; 353: i246.
  4. Veerman JL. Dietary fats: a new look at old data challenges established wisdom. 2016; 352: i1512.
  5. US Department of Health and Humans Services and US Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th Washington, D.C.: USDA, 2015

 

 

Golden Rice Controversy

Genetically modified rice – called ‘golden rice’ – can increase yields and, since it produces beta-carotene, can prevent the sequelae of vitamin A deficiency that is common in those with a predominantly rice-based diet. For an interesting article on the controversy over use of this GM crop in Bangladesh, and its potential costs-benefit, please read Uttam Deb’s article from the Copenhagen Consensus Center.[1]

— Richard Lilford, CLAHRC WM Director

Reference:

  1. Deb U. Returns to Golden Rice Research in Bangladesh: An Ex-ante Analysis. Bangladesh Priorities, Copenhagen Consensus Center, 2016.

 

Caution should be Exercised when Synthesising Evidence for Policy

Policy should be formulated from all the available evidence. For this reason systematic reviews and meta-analyses are undertaken. However, they are often not conclusive. Indeed, there have been notable articles published in the BMJ over the last two years which are critical of the evidence or conclusions of reviews that have been conducted to inform important contemporary public health decisions.

A key theme that often emerges from articles critical of reviews is that only evidence from randomised controlled trials (RCTs) is strong enough to support policy decisions. For example, Teicholz [1] claimed that a number of important RCTs were ignored by a recent report explaining changes in dietary guidance in the US. This claim has since been refuted by a large number of prominent researchers.[2] Kmietowicz [3] argued that there were flaws in a meta-analysis of observational patient data that supported the stockpiling of anti-flu medication for pandemic influenza, casting doubt on the decision to stockpile. An upcoming analysis of clinical trial data was instead alluded to, despite these trials only examining seasonal flu. Recently, McKee and Capewell,[4] and later Gornall,[5] criticised the evidence underpinning a comprehensive review from Public Health England [6] on the relative harms of e-cigarettes. They noted that it “included only two randomised controlled trials” and that there were methodological weaknesses and potential conflicts of interest in the other available evidence. McKee and Capewell make the claim that “the burden of proof that it is not harmful falls on those taking an action.” However, this is illogical because any policy choice, even doing nothing, can be considered an action and can cause harm. This claim therefore merely translates to saying that the policy chosen should be that best supported by the evidence of its overall effects.

Public health decisions should be made on the basis of all the currently available evidence. What then are reasons one might write off a piece of evidence entirely? One might object to the conclusions reached from the evidence on an ideological basis, or one might view the evidence as useless. In the latter case, this opinion could be reached by taking a rigid interpretation of the ‘hierarchy of evidence’. RCTs may be the only way of knowing for sure what the effects are, but this is not tantamount to concluding that other evidence should be rejected. RCTs are often, correctly in our view, regarded as an antidote to ideology. However, it is important not to let matters get out of hand so that RCTs themselves become the ideology.

In a recent paper, Walach and Loef,[7] argue that the hierarchy of evidence model, which places RCTs at the top of a hierarchy of study designs, is based on false assumptions. They argue that this model only represents degrees of internal validity. They go on to argue that as internal validity increases, external validity decreases. We don’t strictly agree: there is no necessary decoupling between internal and external validity. However we do agree that in many cases, by virtue of the study designs, RCTs may provide greater internal validity and other designs greater external validity. Then how could we know, in the case of a discrepancy between RCTs and observational studies, which results to rely on? The answer is that one would have to look outside the studies and piece together a story, i.e. a theory, and not ignore the observational evidence as recognised by Bradford-Hill’s famous criteria.

The case of chorion villous sampling, a test to detect foetal genetic abnormalities, serves as a good example of how different forms of evidence can provide different insights and be synthesised. Observational studies found evidence that chorion villous sampling increased the risk of transverse limb deformities, which was not detected in any of the RCTs at the time. To make sense of the evidence and to understand whether the findings from the observational evidence were a result of random variation in the population or perhaps poor study design, knowledge of developmental biology, teratology, and epidemiology were required. It turned out that the level of the transverse abnormality – fingers, hands, forearm, or upper arm – corresponded to the embryonic age at which the sampling was conducted and also to the development of the limb at that point. This finding enabled a cause and effect conclusion to be drawn that explained all the evidence and resulted in recommendations for safer practice.[8] [9]

Knowledge gained from the scientific process can inform us of the possible consequences of different policy choices. The desirability of these actions or their consequences can be then assessed in a normative or political framework. The challenge for the scientist is the understanding and synthesising of the available evidence independently of their ideological stance. There often remains great uncertainty about the consequences of different policies. In some cases, such as with electronic cigarettes, there may be reason to maintain the current policy if, by doing so, the likelihood of collecting further and better evidence is enhanced. However, in other cases, like stockpiling for pandemic influenza, such evidence depends on there being a pandemic and by then it is too late. Accepting only RCT evidence or adopting an ideological stance in reporting may distort what is reported to both key policy decision makers and individuals wishing to make an informed choice. It may even be potentially harmful.

— Richard Lilford, CLAHRC WM Director
— Sam Watson, Research Fellow

References:

  1. Teicholz N. The scientific report guiding the US dietary guidelines: is it scientific? BMJ. 2015; 351: h4962.
  2. Centre for Science in the Public Interest. Letter Requesting BMJ to Retract “Investigation”. Nov 5 2015.
  3. Kmietowicz Z. Study claiming Tamiflu saved lives was based on “flawed” analysis. BMJ. 2014; 348: g2228.
  4. McKee M, Capewell S. Evidence about electronic cigarettes: a foundation built on rock or sand? BMJ. 2015; 351: h4863.
  5. Gornall J. Public Health England’s troubled trail. BMJ 2015;315:h5826
  6. McNeill A, Brose LS, Valder R, et al. E-cigarettes: an evidence update: a report commissioned by Public Health England. London: Public Health England, 2015.
  7. Walach H & Loef M. Using a matrix-analytical approach to synthesizing evidence solved incompatability problem in the hierarchy of evidence. J Clin Epidemiol.  2015; 68(11): 1251-1260
  8. Olney RS. Congenital limb reduction defects: clues from developmental biology, teratology and epidemiology. Paediatr Perinat Epidemiol. 1998; 12: 358–9.
  9. Mowatt G, Bower DJ, Brebner JA, et al. When and how to assess fast-changing technologies: a comparative study of medical applications of four generic technologies. Health Technol Assess. 1996; 1: 1–149.

 

Reversible Environmental Factors and the Global Burden of Disease

The Global Burden of Disease study is an extraordinary collaborative effort to document the health of the human race. It produces a series of weighty publications every four years, packed with interesting detail. The most recent set of papers have been published and the first deals with life years lost.[1] The study documents the recent epidemiological transition in which non-infectious diseases have taken over from infectious diseases as the main cause of life-years lost across the world. Childhood malnutrition is no longer enemy number one, relegated to fourth place globally, but it retains the number one slot in sub-Saharan Africa. High blood pressure, smoking and obesity now occupy the first three slots globally. CLAHRC Africa includes a programme of research on salt. Salt is now enemy number two, after smoking, in unhealthy behaviours. Research into methods to reduce salt intake is a priority, even as the debate continues into whether sodium levels can fall too low – some data suggest a J-shaped distribution of risk with rising salt intake. Unsafe sex is the major risk factor in East, and Southern Africa, while South Africa is the country with the world’s highest burden of disease associated with reversible environmental factors. Areca nut (another interest of CLAHRC Africa) does not make it onto the list. Along with smokeless tobacco, the CLAHRC WM Director thinks this risk should be considered for inclusion in further versions. Another criticism is double counting – high sodium intake and high systolic blood pressure both appear on the list, yet the former is a prominent cause of the latter. To be fair, the authors do recognise this issue. In a future blog we will report on a further analysis of the remarkable GBD dataset to consider not just the deaths, but the total burden of disease (for instance in Disability Adjusted Life Years [DALYs]).

— Richard Lilford, CLAHRC WM Director

References:

  1. GBD 2013 Risk Factor Collaborators. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015; 386: 2287-323.

The Obesity Challenge is Very Real, but What About Extreme Low Weight?

A body mass index under 16 in women is associated with anorexia in rich countries, but with malnutrition in low- and middle-income countries. It is associated with reduced life span, but the effects of energy supplementation in people who were seriously malnourished as children are uncertain. A recent cross-sectional study of over 40 countries using Demographic and Health Surveys shows a pooled incidence of extreme underweight of 1.8% (standardised for age). The prevalence is highest in India at over 6% and Bangladesh at over 3%.[1] Rates are declining quite rapidly in these countries, but overall at a very low rate and in some countries they are actually increasing.

— Richard Lilford, CLAHRC WM Director

Reference:

  1. Razak F, Corsi DJ, Slutsky AS, et al. Prevalence of Body Mass Index Lower Than 16 Among Women in Low- and Middle-Income Countries. JAMA. 2015; 314(20): 2164-71.

Diabetes – a Lens for our Health Woes

Let us start with the premise that a fat, inactive group of people has poorer wellbeing than a thin, active one and it is desirable to try and move people from the former to the latter. Prevention of chronic disease and improving resilience of the population should reduce pressure on overstretched health service worldwide. Diabetes is a classic example, with NICE continuing to recommend a diet consisting of 50% carbohydrates for a disease caused by insulin resistance! It seems illogical not to have carbohydrate restriction as first line management for diabetes.[1]

We also need to clear the confusion around inactivity and obesity. Firstly, becoming active will not make you become thin. More activity makes you hungrier and if you diet you become more sedentary.[2] To state that obesity is merely a function of calories in and calories out is unhelpful when trying to bring about behaviour change in a species that has evolved to deal with under supply of calories.[3] The problem is not obesity per se, but fat storage. The human race has genetically evolved to store fat. If you were someone who could store fat efficiently, then you would survive wars, famines, droughts, and plagues, and pass those genes on to the next generation. In the last 60 years or so the food industry has worked out how to produce loads of carbohydrate rich foods at immense profit. We still store fat very efficiently so this has created the obesity epidemic. One of the reasons that NICE still recommends a high carbohydrate diet is that fats in particular are energy dense foodstuffs, but this also presumes rather illogically that humans will consume the same weight of food irrespective of calories!

The food industry is cunning, however, and is now trying to blame simple sugars solely for this problem so diet drinks are now literally becoming the flavour of the month. The problem is that all carbohydrates are problematic, even the so called ‘healthy stuff’, such as potatoes, rice, bread, pasta, etc. Carbohydrates are the only component of food to stimulate an insulin response leading to conversion to free fatty acids and then triglycerides – within 2-3 hours the individual is hungry again. Having one of the most sedentary populations in the world and our grazing culture creates the perfect storm.

I should say at this point that we are a divided country and if you are active in the first place then it probably doesn’t matter very much what you eat as you merely use it as fuel.

There is also the commonly held belief that fat consumption clogs up your arteries, but several studies, including meta-analyses, have consistently failed to show reduction in levels of heart disease with low fat diets.[4]

Finally just to really push the boat out one should question the mantra of five (fruit and vegetables) a day. Although studies have shown some reduction in cardiovascular disease, there is little evidence for the reduction of rates of cancer.[5] My suspicion for the mixed message is that fruit and vegetables are not the same. Five 100g portions of random fruits will give you around 380 calories. Five 100g portions of vegetables will give you around 80 calories. So not only an insulin response and fat storage with fruit, but also an extra 300 calories.

Many people engage with activity to lose weight and disengage because their primary motive is not achieved. Inactivity has been shown to be the single worst thing you can do to yourself. A massive study of 364,000 patients over 12 years published earlier this year showed it is twice as likely to kill you as obesity.[6]

So the bottom line is get active but be aware that is so much easier to do that if you are thin. To do that, get rid of the carbs!

— Dr Ewan Hamnett, Birmingham’s Champion for Physical Activity, Board Member UK Active

References:

  1. Feinman RD, Pogozelski WK, Astrup A, et al. Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition. 2015; 31(1): 1-13.
  2. Malhotra A, Noakes T, Phinney S. Its time to bust the myth that you can outrun a bad diet. Br J Sports Med. 2015. [ePub].
  3. Ludwig DS. Increasing adiposity. Consequence or cause of overeating. JAMA. 2014; 311(21): 2167-8.
  4. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010; 91: 535-46.
  5. Boffetta P, Couto E, Wichmann J, et al. Fruit and vegetable intake and overall cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). J Natl Cancer Inst. 2010; 102(8): 529-37.
  6. Ekelund U, Ward HA, Norat T, et al. Physical activity and all-cause mortality across levels of overall and abdominal adiposity in European men and women: the European Prospective Investigation into Cancer and Nutrition Study (EPIC). Am J Clin Nutr. 2015. [ePub].

Another Day, Another (Badly-Reported) Health Story in the Media…

Recent health issues reported in the British media have included the link between consumption of red and processed meat with an increased risk of cancer and the need for a ‘sugar tax’ to curb the ever-increasing rates of obesity and its associated health problems. These are big, newsworthy issues relating to the effect of diet and lifestyle on health: the World Cancer Research Fund estimate that around 6,000 cases of bowel cancer in the UK could be prevented by reducing consumption of red and processed meat,[1] while a 20p/litre tax on sugar-sweetened beverages could reduce the number of obese adults in the UK by 180,000 according to the Faculty of Public Health.[2]

So one has to feel a little pity for a journalist tasked with writing a piece about a study investigating whether the composition of a mother’s breast milk was associated with infant weight and body composition.[3] The journalist from The Times seemed to approach this task by jumping on the obesity bandwagon; two key quotes from the story are: “A mother’s milk can increase the chance of a child growing up obese” and “A study … identified sugars in breastmilk that heightened a baby’s risk of being overweight by the age of 6 months”. This seemed to fly in the face of almost everything I had ever read about breastfeeding, so I decided to look at the evidence in a bit more detail.

The paper was based on a sample of 25 breastfeeding mothers and their babies. No babies were formula-fed. Outcomes were infant growth (weight and length) and body composition (percentage fat, total fat and lean mass). Whether or not the baby was ‘overweight’ or ‘obese’ was not an outcome. An association between the level of different human milk oligosaccharides (HMOs) in breast milk and infant weight and body composition was identified by the study authors, adding to the evidence base regarding the factors influencing a baby’s growth and development. The authors themselves made no direct claim that breastfeeding causes childhood obesity (three separate meta-analyses have, in fact, shown the opposite [4-6]), with the smallest of these studies including data for almost 30,000 babies.

The journalist’s train of thought may have gone thus:

44 GB Health Story in Media Fig 1

The first step in this chain was identified by the study authors. But was the journalist justified in making the second?

The increase in risk of adulthood obesity given a high weight-for-age percentile in infancy has been known for some time,[7] so the second link is plausible. But can it automatically be inferred from this study? To do so relies on the increases in body fat/fat mass being of such magnitude to class some of the infants in this study as overweight or obese at six months and we simply don’t know if this was the case. Instead, it could be possible that babies receiving alternative combinations of HMOs to those shown in the diagram were actually underweight and that those at the upper end of the weight range were still of ‘normal’ weight. We also don’t know how the weights and body compositions of the babies in the study would compare to those who have been formula-fed: even if breast milk containing high levels of certain HMOs did increase the risk of obesity, the risk with such HMOs could still be lower than that from infant formula.

That some HMOs were shown to have a negative relationship with body weight and/or composition seemed to make the journalist even more confused, since the story ended by stating “However, scientists also found that breast milk could protect against obesity.” The meta-analyses quoted above have demonstrated this, but once again, such a conclusion cannot be drawn from this particular study.
Reporting of current research in the media is invaluable to help increase uptake of its findings, yet the dangerous misinterpretation of the findings of the study by Alderete et al. mean that I hope the story in The Times (not the research study) was ignored by all who read it.

— Celia Taylor

References:

  1. World Cancer Research Fund. Bowel cancer. 2015. [Online]
  2. Faculty of Public Health. A duty on sugar sweetened beverages. A position statement. 2013. [Online]
  3. Alderete TL, Autran C, Brekke BE, et al. Associations between human milk oligosaccharides and infant body composition in the first 6 mo of life. Am J Clin Nutr. 2015. [ePub].
  4. Arenz S, Rückerl R, Boletzko B, von Kries R. Breast-feeding and childhood obesity – a systematic review. Int J Obesity. 2004; 28: 1247-56.
  5. Owen C, Martin R, Whincup P et al. The effect of breastfeeding on mean body mass index throughout life: a quantitative review of published and unpublished observational evidence. Am J Clin Nutr. 2005; 82: 1298-1307.
  6. Harder T, Bergman R, Kallischnigg G et al. Duration of breastfeeding and risk of overweight: a meta-analysis. Am J Epidemiol. 2005; 162:397-403.
  7. Charney E, Goodman HC, McBride M, et al. Childhood Antecedents of Adult Obesity – Do Chubby Infants Become Obese Adults? N Engl J Med. 1976; 295: 6-9.

Cost-Effectiveness of Exercise and Diet for Diabetes Prevention

I promised that I would report on the cost-effectiveness studies in the systematic review of exercise and diet therapy for the prevention of diabetes discussed in a previous post.[1]

Most studies end three years after the start of the intervention, while the most substantial potential benefits accrue later. Some studies did not model these longer-term benefits, but most extrapolated over ten years or more. Most used previously published model structures such as the Archimedes model. Incremental Cost-Effectiveness Ratios (ICERs) were calculated in 22 studies, all but two of which showed that the intervention (whether group- or individual-based) was cost-effective at a $50,000 Willingness-to-Pay (WTP) threshold. Two studies (both concerning a group intervention) actually suggested the intervention was cost releasing. Averaged across all studies the ICER was about $13,000 per QALY (quality-adjusted life year). CLAHRC WM is collaborating with CLAHRC East Midlands on a study to prevent later onset diabetes in women who have had gestational diabetes. These models will be useful for the calculation of the incremental cost-utility of our intervention.

— Richard Lilford, CLAHRC WM Director

Reference:

  1. Li R, Qu S, Zhang P, et al. Economic Evaluation of Combined Diet and Physical Activity Promotion Programs to Prevent Type 2 Diabetes Among Persons at Increased Risk: A Systematic Review for the Community Preventative Services Task Force. Ann Intern Med. 2015; 163(6):452-60.