Could the Ebola epidemic end this year?

Although the Ebola epidemic is still raging in west Africa, US and European buzz about the disease spiked briefly and then all but disappeared, according to Google search data published in Vox’s in-depth report.

Liberia’s situation is the most promising, compared to the other two countries involved, writes Julia Belluz at Vox. Experts say that Guinea has “no discernible upward or downward trend” of cases, Sierra Leone is “the most challenging front,” and Liberia is the country closest to having the outbreak under control.

Ebola eradication is probably impossible, because the disease seems to simmer in wildlife populations, including bats, making occasional jumps into humans. Until recently, the outbreaks only killed dozens or hundreds of people before fizzling out, sometimes without another recorded case for years. The current outbreak, on the other hand, has been going on for over a year, with an official death toll of, at this writing, over 8,000.

Now, a new model of the epidemic suggests that it may be under control, at least in Liberia, by summer of this year.

I spoke with John Drake, whose team at the University of Georgia studies the dynamics of groups of living things, from wildlife populations to disease epidemics. They have a paper out in PLOS Biology today describing their prediction.

What’s the best case scenario and the worst case scenario here?

The worst case is that it could be quite terrible. If the current vigilance and investment and public buy-in isn’t maintained, it could take a turn for the worse.

I don’t think the worst case scenario is a very likely outcome, because I think that the public, the community, the politicians, the health community have all been galvanized by their battle with Ebola over the summer and fall of 2014. And they’ve made tremendous gains, and I think that they’re going to maintain that vigilance. And I’m optimistic that the great majority of transmission could be eliminated by the late spring, maybe even slightly earlier.

A lot of previous models focused on R0 [the number of new infections that each infected person can cause], but yours takes other factors into account.

A lot of models are based on an ‘if everything remains the same’ kind of assumption, and all that’s changing is the number of susceptible and infectious persons in the population.

But we said, well, no! The baseline is not staying the same, because they’re building Ebola treatment units. So hospital capacity is increasing. And what effect does that have on containing the outbreak? We included that trajectory, that sequence of Ebola treatment units being constructed in the development of our model.

Another important difference is that we focused on the different sites at which persons would acquire infection, whether that was in the hospital, at a funeral, or in the community, and how that would feed back into transmission. If a person acquires the infection in the hospital, then they’re very likely to be treated in the hospital, and the contact rate would be low.

On the other hand, a person who contracted the infection in the community might go to the hospital and effectively be isolated from the susceptible population. But they might be treated in the community, which means a larger number of persons might be exposed. And so this places an emphasis on the willingness of potentially infected persons to seek care and be treated, and allows us to explore better what’s the possible range of outcomes based on the frequency with which patients are isolated.

Another difference is in order to make our work tractable, we took a shortcut. We said, we don’t suspect that what epidemiologists call susceptible depletion, the extent to which previously infected individuals are removed from the population and therefore causing the epidemic to be self limiting—we don’t think we’re in that situation yet. And by making the approximation that susceptible depletion was negligible, that allowed us to make further progress on emphasizing the sorts of things we thought were important.

Your predictions are focused on Liberia, but the epidemic is also raging in Guinea and Sierra Leone. Do you think all three can contain it by this summer?

Our model is Liberia specific. There are differences among these countries; we don’t fully understand what those differences are.

My group decided to focus on Liberia because at the time we began this work, it’s where the epidemic was most out of control, it’s where we thought we could make the greatest contribution, and it’s where we had the best information. And we knew of other folks working particularly on Sierra Leone and Guinea.

Epidemiologically I think Sierra Leone is probably fairly similar. Transmission in Guinea seems to be a little bit different, and I think people are scratching their heads to understand first of all how is it different, and secondly what are the consequences of those differences.

I wouldn’t say the whole thing is coming to a close yet. I think that if Liberia is able to maintain their current level of response, and if they are able to prevent reinfection, reignition of the epidemic within Liberia, then I think we’re on a downward trend for Liberia. But it’s in a context in which there’s going to be interaction with neighboring countries, and there’s a possibility for subsequent flare-ups, so it requires vigilance and rapid response.

I think that the response in Sierra Leone and Guinea will ultimately contain those epidemics. I think that they are working very hard to accomplish that, and eventually that will happen in those places as well. But there needs to be continued investment in those places.

What do people need to know about Ebola now?

I do think the public’s been well informed about this particular epidemic, and I think that people understand that there’s not any reason for hysteria in western Europe or in the United States or places that are contributing health professionals to try and contain this epidemic.

I think that we are learning things about how collectively the world can respond to emerging infectious diseases like this that really pose a threat not just in one region or in a particular country or in the developing world, but that actually expose us all to some level of risk. And how to mobilize our scientists and medics and policy makers in a coordinated way.

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Black lives must matter more in health research

Anyone who thinks America is a ‘post-racial’ society is delusional. ‘Post-racial’ is political discourse that aims to deny any presence of racism or racial inequality in modern society. Racism is visible everyday. From visible neighbourhood segregation to everyday instances of white privilege to population-level statistics, it can be seen and felt (1-7). For example, in 2013, the average white family had a net worth 13 times greater than the average black family ($141,900 vs. $11,000), a gap twice the size it was prior to the Great Recession (1).

PewWealthGap

Why does racism matter for public health?

Racism is not only a social, cultural, political, and legal issue; it is also a health issue. Across history, racism has consistently been manifested in terms of the ultimate health outcome: death. When Europeans colonised the Americas hundreds of years ago, the aboriginal populations perished in scores. America’s legacy of slavery almost goes without mentioning. Still today, the life expectancy of American Indians and Alaska Natives is, on average, 4.2 years lower than all races and origins in the U.S. population combined (6).  Black men are more likely to die than non-black men, with a life expectancy 5 years lower than white men in America (see graph below) (7).

 lifeexpectancy

Recently, we’ve seen the ultimate outcome of racism dramatically played out in the streets of America. This form of overt violence, where unarmed yet ‘suspicious-looking’ black men are shot down by officers of the law is nothing new, yet requires contextualisation. Let’s not forget that while African Americans have been living in the United States for over 400 years, they have only had legal rights for about a tenth of that time. Let’s not forget how recent the civil rights movement was. It will take more than a couple of generations to repair the legacy of slavery, if it ever can be repaired.

The effects of racism on health, while undoubtedly negative, are not well understood. Racism is a personal experience, the manifestation of which is politically and socially situated in specific places and times. It is institutional, interpersonal, overt, covert, and violent.

The field of epidemiology and public health has only accumulated a small body of inquiry into racism and health, and most of it deals with the social experience of racial discrimination in people’s daily lives. As of 5 January 2015, a PubMed search of the term ‘racism’ returns 2,263 articles from all medical disciplines. By contrast, a search for the term ‘obesity’ returns 210,214 articles, about ten times more. This quick example is not meant to imply that obesity is not an important and urgent research topic (it is), or that these are even comparable topics, but rather to demonstrate the relative dearth of knowledge on racism in the quantitative health sciences.

Without empirical research we cannot record the effects of racism on population health and inequalities, we cannot transcribe the embodiment of discrimination in marginalised groups on a large scale.  By ‘embodiment’, I mean the literal embodying of social and ecological environments in terms of their biological effects in and on our bodies (8,9). A useful framework for quantitative health scientists wishing to investigate the effects of race and racism is ecosocial theory (8,9). The ecosocial theory of disease distribution concerns who and what drive social inequalities in health (8). I’ll leave the juicy bits to the paper and book referenced above, but will briefly describe what the theory posits with respect to racism:

Inequitable race relations simultaneously – and not sequentially

1)   Benefit the groups who claim racial superiority at the expense of those whom they deem intrinsically inferior,

2)   Racialize biology to produce and justify the very categories used to demarcate racial/ethnic groups, and

3)   Generate inequitable living and working conditions that, via embodiment, result in the biological expression of racism – and hence racial/ethnic health inequalities. (9)

These ideas are nothing new to those familiar with critical race theory, social constructionism, or intersectionality theory. However, they are often foreign to quantitative health scientists. We are taught how to count, classify, and categorise people in order to fit them into complex statistical models not designed to account for the social construction of biology. So, how do we move forward? We need to ground our work in theory (epidemiology, as a field, is notoriously atheoretical, although that’s a subject for another day), which means looking outside of our discipline to the social sciences. We need to collaborate with other fields and explore mixed methods. As epidemiology evolves, theories like the ecosocial theory may become entrenched in our discipline.

This is important because research is a key piece in the patchwork of knowledge, activism, policy, and public will that is required to make the world a more just place. The media attention and public demonstrations that have occurred in aftermath of Ferguson and other recent incidents of racialized violence perhaps signal a change in the public consciousness. Let’s keep moving in this direction.

 

 

Note: Although I refer to ‘black lives’ in this title, it not to privilege any minority group over any other. Linking to current public discourse and providing a focus for this article, the intent is purely demonstrative. The ecosocial framework can be applied to many inequitable social relations across place and time.

References

1)   Kochhar R, Fry R. Wealth inequality has widened along racial, ethnic lines since end of Great Recession. http://www.pewresearch.org/fact-tank/2014/12/12/racial-wealth-gaps-great-recession/ (accessed 1 January 2014).

2)   Nico Lang. It’s time to wake up from the myth of a ‘post-racial America’. Daily Dot. 25 November 2014. http://www.dailydot.com/opinion/ferguson-michael-brown-post-racial-myth/ (accessed 3 January 2015).

3)   McIntosh P. White privilege: unpacking the invisible backpack. Independent School, Winter, 1990, pp. 31-6.

4)   Vanhemert K. The best map ever made of America’s racial segregation. Wired. 26 August 2013. http://www.wired.com/2013/08/how-segregated-is-your-city-this-eye-opening-map-shows-you/ (accessed 3 January 2015).

5)   Baird-Remba R, Lubin G. 21 maps of highly segregated cities in America. Business Insider. http://www.businessinsider.com/most-segregated-cities-census-maps-2013-4?op=1&IR=T (accessed 3 January 2015).

6)   Indian Health Service: The Federal Health Program for American Indians and Alaska Natives. Disparities. http://www.ihs.gov/newsroom/factsheets/disparities/ (accessed 3 January 2015).

7)   Centers for Disease Control and Prevention. NCHS Data Brief: Death in the United States, 2010. http://www.cdc.gov/nchs/data/databriefs/db99.htm (accessed 3 January 2015).

8)   Krieger N. Methods for the scientific study of discrimination and health: an ecosocial approach. Am J Public Health 2012;102(5):936-45.

9)   Krieger N. Epidemiology and the people’s health: theory and context. New York: Oxford University Press; 2011.

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PLOS Public Health Perspectives Holiday Special 2014

Christmas_cookie_stack

Photo by Nathan2055 at Wikimedia Commons: CC-BY 2.5

The holiday season is here. We’ve compiled a short list of wintertime concerns that many people have:

1. Nutrition

If you’re lucky, the holiday season tends to be a time of over-nutrition. Knowing your body and what your energy requirements are is a first step to not overeating. Here is a simple calculator that will tell you how many calories per day you should eat (and how many if you want to lose or gain weight), based on your age, sex, BMI, and physical activity level: http://www.calculator.net/calorie-calculator.html. To make sure you eat what your body needs, there is one simple nutrition rule that everyone can follow:

“Eat food, not too much, mostly plants.”

These are the words of Michael Pollan in “Food Rules: An Eater’s Manual” (1). Avoid packaged, processed food products and eat a wide variety of real foods, and you will thank yourself for it.

And don’t forget our healthy holiday guide from last year[1] , with tips on navigating holiday buffets and squeezing in some exercise.

2. Exercise

Fur_trim_(4185547877)

This is one way of getting holiday fitness in – Photo by Magnus Manske at Wikimedia Commons: CC-BY 2.0

Exercise can be difficult over the holidays when schedules are disrupted and the weather can sometimes get in the way. Enjoy what you can, in balance with enjoying any downtime that you may have. At home exercise videos on YouTube are a great thing, as they are flexible time-wise and remove any financial and equipment barriers to working out. Whether it’s getting outside for a 30 minute walk each day, doing snow sports, or playing with kids or dogs around the house, exercise will help with not only balancing out any gastrointestinal over-indulgences but also with reducing stress and improving mental health.

3. Keep warm – but not too warm

Calvin and Hobbes by Bill Watterson. Available from Universal Uclick

Calvin and Hobbes by Bill Watterson. Available from Universal Uclick

Early winter snowstorms have been hitting parts of the USA and Canada. With feet of snow and temperatures well below freezing, it’s no surprise that cold weather contributes to ill-health and mortality in older and vulnerable people during the winter (2). Heating is expensive, and many people are fuel poor over the winter.

–          Wear layers of wool and thermal clothing, both at home and indoors. Long leggings and underwear, thick socks, and gloves are important. This sounds like a no-brainer, but it’s the first and obvious thing to do.

 

–          Take advantage of natural sunlight in your windows during the day, but draw your curtains at night to trap heat in. The thicker the curtains, the better.

 

–          Heat up a hot water bottle, or make your own rice bag – fill a sock (or other sack-shaped fabric) with rice, tie it up, and put it in the microwave for a couple of minutes (idea courtesy of Jack Monroe)

 

–          Drink hot drinks and eat warm food. Your body itself is a major source of heat, and you have to keep that engine running.

 

–          Get active – do some exercise at home to produce body heat.

 

–          Keep the central heating around 18 degrees Celsius – or slightly lower if you can stand it. Temperatures from around 15-17 degrees activate brown fat, which is metabolically active fat that burns calories to produce heat within our bodies (3). This process is called “non-shivering thermogenesis” – the production of heat without shivering. It’s a win-win for your health and your heating bill!

 

There are other recommendations from other sources as well – the BBC has compiled a list of tips to help keep your house warm, as well as Jack Monroe’s list from “a veteran of freezing houses, wooden floors, and big windows”.

4. Getting sick

In the northern hemisphere, flu season typically peaks in February, which means the worst is still ahead of us (and holiday parties are a great opportunity for germ swapping). While the flu shot doesn’t protect against every cold, cough, and sniffle that’s going around, it does protect against more than half of the actual flu strains going around (yes, even when it’s a mismatch year.) A good read on the flu vaccine is Tara Haelle’s Debunking ALL the flu vaccine myths: Can the shot give you the flu? No. Is the flu actually dangerous? Yes.

To prevent colds and flu, wash your hands (although this is not a guarantee, because the flu is airborne, but hand washing still helps). Stay away from people who are sick, or if you’re the one who’s sick, keep yourself home for 24 hours after your fever breaks, as the CDC advises.

5. Travel

A lot of travel health concerns seem to focus on the air circulation: Is the air too dry? Does it pressurize us and squish our organs, like the Food Babe said? Read about how airplane pressurization really works on BrainStuff. The air outside the plane is cold, low-pressure, and dry, so it’s compressed (making it roughly equivalent to the air pressure in a mountainous place like Denver, so still less than most of us are used to), as well as heated by the engine, and mixed with air that’s been humidified by—ok this is just slightly gross—being in the air cabin already where people are breathing and releasing some moisture. That still leaves it fairly dry, but you can beat the dry nose feeling by drinking water and using saline nasal spray.

6. Stress

Stress can weaken your immune system, and can contribute to mental health issues like depression. This Mayo Clinic guide to managing holiday stress includes helpful tips like budgeting gifts rather than trying to solve problems by buying happiness, and planning some alone time every day to take a break from things that are pressuring you.

Enjoy the holidays, from all of us at PLOS Public Health Perspectives!

References

  1. Pollan M. Food Rules: An Eater’s Manual. New York: Penguin Group Inc; 2009.
  2. Berko J, Ingram DD, Saha S, Parker JD. Deaths Attributed to Heat, Cold, and Other Weather Events in the United States, 2006-2010. U.S. Department of Health and Human Services. 76, 2014.
  3. Wenner Moyer M. Supercharging Brown Fat to Battle Obesity. Scientific American 2014;311(2). http://www.scientificamerican.com/article/supercharging-brown-fat-to-battle-obesity/
  4. Haelle T. Setting the Record Straight: Debunking ALL the Flu Vaccine Myths. http://www.redwineandapplesauce.com/2013/10/28/setting-the-record-straight-dubunking-all-the-flu-vaccine-myths/
  5. Centers for Disease Control. Personal NPIs – Everyday Preventative Actions. http://www.cdc.gov/nonpharmaceutical-interventions/personal/index.html
  6. Brain, M. How Airplane Cabin Pressurization Works. http://www.brainstuffshow.com/blog/how-airplane-cabin-pressurization-works-keeping-you-comfortable-in-the-death-zone-at-33000-feet/
  7. American Academy of Otolaryngology. Your Nose, the Guardian of Your Lungs. http://www.entnet.org/content/your-nose-guardian-your-lungs
  8. Mayo Clinic staff. Stress, Depression, and the Holidays: Tips for Coping. http://www.mayoclinic.org/healthy-living/stress-management/in-depth/stress/art-20047544

 

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Chagas disease is turning up in (un)likely places. Who is ready for it?

Chagas

Photo by Clonny on Flickr. CC BY-NC-ND

Please welcome another guest post by Charles Ebikeme. –Beth

Chagas is a more dangerous and much more pervasive disease than we give it credit for. A tropical disease that is really no longer quarantined to the tropics, Chagas has been known to turn up in unlikely places — and those unlikely places are becoming more and more important.

Chagas is also known as American trypanosomiasis, and is found mainly in Latin America, where it is mostly transmitted to humans by the faeces of the triatomine “kissing bug”. About 7 to 8 million people are estimated to be infected with Chagas worldwide.

Recently, researchers at the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs can transmit Trypanosoma cruzi, the infectious parasitic agent that causes Chagas disease. They found that bed bugs, a not too unrelated cousin of the kissing bug, can transmit the parasite in the same way by which humans are usually infected. Both bed and kissing bugs only feed on blood, and both hide in household cracks and crevices waiting for nightfall and the opportunity to feed on sleeping hosts.

The discovery that bed bugs can transmit Chagas is not the first time the disease has turned up via an unlikely route.

Distribution of Chagas' disease.svg

Traditional distribution of Chagas’ disease by Tomato356 at Wikipedia. CC BY-SA 3.0.

In March of 2001, a 37 year old woman went into surgery in the US to have a kidney and pancreas transplant from a donor that had already passed away. She would die six months later, on the first week of October from Chagas. The parasite had been contracted from the organ transplant.

Outside of the bite and faeces of the kissing bug the parasite can be transmitted in more (extra)ordinary ways — from mother to child, and through contaminated blood or organ donations. In the US blood supplies have only routinely been screened for Chagas since 2007.

In southern states of the US, the kissing bug also roams, and recent research has shown that some cases of Chagas disease are originating domestically. There’s a need to look more carefully for local infections in Texas and elsewhere in the South. And given the pathology of the disease, many people who are infected may not know they carry the parasite.

In recent years, it has become more apparent that Chagas is now not just confined to the Americas. It hasn’t been for some time. Chagas has now spread to other continents, and Europe is its most recent port of call.

The first reported case of Chagas in Europe was in 1981. Ever since then, sporadic cases have been detected in different European countries. Since the turn of the millennium the numbers of reported cases have only increased, particularly in Spain, Italy, and Switzerland. In Europe, the currently estimated number of people with Chagas is somewhere between 68,000 and 122,000, yet by 2009 only 4,290 had been diagnosed.

Chagas is a real threat. The global cost of the disease worldwide is thought to be at around 7.2 billion US dollars per year — an amount that is comparable to cervical cancer.

How prepared is Europe for Chagas?

Researchers, publishing in PLOS, sent out questionnaires on health policy for T. cruzi infection to about a dozen European countries. They wanted to gauge policy on the possibility of infection via blood transfusion, transplantation, and congenital transmissions. Some European countries are slowly beginning to acknowledge this growing public health problem, and some changes in health policies have been implemented.

Some, but not all, European countries have implemented national or regional measures to control transmission, but many countries still have no legislation about Chagas disease within their borders.

For risk of infection via blood transfusions seven European countries have either already implemented, or are in the process of, changing recommendations to enhance detection of cases of infection (France, Italy, Portugal, Spain, Sweden, Switzerland, and the United Kingdom).

No country in Europe has a specific health policy against the risk of infection by organ transplantation. Only in Italy, Spain, and the United Kingdom are donors at risk of the infection being screened.

Of all the three possible routes of extraordinary infection, it is the congenital route that is the least well developed in terms of health policy. This in the face of the fact that control of congenital transmission has been demonstrated to be one of the most cost-effective measures to control the disease, since newborns with acute disease can be cured easily if treatment and diagnosis is early.

The recommendation from authors is an evolving health policy to control Chagas disease transmission in Europe. Across Europe, the map of policies is a mixed one — some laws and directives concerning blood banks and transplant programmes are urgently needed to avoid and reduce the risk of transmission. The differences in regulations emanating from the European Commission are not always in line with the Council of Europe, which should be addressed to give some coherence. Where laws and regulations do exists, more effort needs to be made to evaluate their implementation and impact.

About Charles

charles_ebikeme (1)

Charles Ebikeme is a science journalist with a PhD in parisitology who serves as a Science Officer with the International Social Science Council of UNESCO and writes frequently on global health, health policy, neglected tropical diseases and infectious diseases for The Huffington Post, The Guardian, Scientific American, and Think Africa Press. He is based in Paris. You can find him on Twitter @CEbikeme.

 

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The flu shot isn’t a good match this year. Is it ever?

The CDC announced recently that this year’s flu vaccine is missing a key strain, one that accounts for 48% of what’s circulating. That strain, a “drifted” version of H3N2, was discovered in March 2014, but the vaccine strains for the Northern hemisphere, including the US, had been decided a month earlier. (The Southern hemisphere vaccine will include the drifted strain.)

Cue the overreactions: Natural News framed the advisory as an announcement that the vaccine “doesn’t work” (um, no) and a Fox News affiliate called the shot “useless” (likewise nope). The vaccine’s match is still better than 50%; if you believed the hype and skipped the shot, you’d be protected against, oh right, 0%.

“Doesn’t this happen every year?” was my friend’s reaction to the announcement that the vaccine wasn’t a good match. So I pulled up the CDC’s past reports to see how well the shot has been matching the circulating flu strains over the past few years. Take a look:

flu_match

How well the flu vaccine matched circulating strains over the past 5 years, including partial data from 2014. Click to embiggen; feel free to share with attribution. CC-BY.

Well, hey. That’s actually pretty good.

Where these numbers come from:

There are two series of tests the CDC does. The first, which you’ll find under Virologic Surveillance in each report, gives the percentage of each type of flu relative to the others (A/H3N2, B, A/H1N1, etc) in samples that turned up positive at hospital labs. Not everybody gets tested, but we can assume the strains that show up here correspond roughly to what’s circulating.

To find out whether the vaccine is a match, animals’ antibodies are given a chance to attack samples of circulating flu strains. This is listed under Antigenic Testing. In a good year, the antibodies all do their job, or they do it maybe 99.5% of the time and the last 0.5% is beyond the resolution of my colored pencils. The caveat here: only a small number of samples are tested in this way, so there is a risk of sampling bias, but once again it’s our best source of these numbers.

Most of the mismatches over the last few years came from B strain viruses. Flu vaccines often have just three strains: two A and one B. That’s called a trivalent vaccine. But if you get a chance to get the quadrivalent vaccine (which includes the nasal spray this year, and some but not all of the needle shots), you’re getting a second B strain. Last year, there were two types of B viruses that showed up in the test, and both were present in that year’s quadrivalent shot.

There’s another year on this chart with a big mismatch, and you may remember it: 2009, the grand entrance of a very special version of H1N1. That’s another case of a strain that popped up after the vaccine components had been decided, and so you might say that giant orange bar should be striped as a mismatch. But the threat from H1N1 was great enough that authorities commissioned a special second vaccine just to provide H1N1 coverage; I’ve written before about how I made sure to get that shot. I, and others who got both shots, were protected against nearly 100% of the circulating flu.

An important caveat: we’re just talking here about which strains match; the question of the shot’s overall efficacy is an issue for another time. The shot doesn’t provide complete protection, although in most years, for most populations, it’s somewhere around 60-70% effective for all the circulating strains combined. A meta-meta-analysis from 2012 summed it up like this:

Most influenza vaccines have been shown to confer some protection against naturally acquired infection and no evidence for major harms has emerged. In adults and children, the efficacy/effectiveness of current seasonal vaccines was generally high for laboratory-confirmed cases (especially for [the nasal spray] in children aged 2–17 y), and modest for clinically-confirmed cases and for the elderly.

 

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Maintaining health literacy through being web-savvy and culturally engaged

Note: The research discussed on the blog today is work from my PhD dissertation, which was published last week and covered by several media outlets online. It was originally blogged about on the Health Behaviour Research Centre ‘Health Chatter’ blog.

BritishMuseum

The British Museum in London.

Ageing involves many challenges for health and well-being. One under-recognised problem is that of declining literacy skills. While we are familiar with general issues of ageing such as loss of eyesight or physical mobility, what happens to literacy skills during ageing is much less well understood. Literacy is important to health during ageing because literacy is fundamental to managing health. For example, proper taking of medications, understanding what the doctor says, and understanding of written medical information all rely on having adequate literacy. When literacy is used in health contexts such as these, we refer to it as ‘health literacy’. The American Institute of Medicine defines health literacy as “the degree to which individuals have the capacity to obtain, process, and understand basic health information and services needed to make appropriate health decisions” (1).

The consequences of low health literacy include poor self-care of chronic disease, unnecessary use of emergency services, low use of preventive health services such as cancer screening, and increased risk of mortality (2–4). Health literacy declines during ageing. This is thought to be caused by the normal ageing-related decline in cognitive abilities such as mental processing speed and memory (5,8).

In our study, we were curious to see whether cognitively stimulating activities would help older adults to maintain their health literacy skills, regardless of any cognitive decline they experienced.

In particular, we examined whether internet use and engagement in several different types of social activities might help older adults to maintain health literacy. We used data from almost 4500 men and women aged 52 years and over in the English Longitudinal Study of Ageing (ELSA). The ELSA is a population-representative longitudinal study of English adults aged 50 and over, which aims to capture the experience of ageing in England. Since 2002, the study participants have been interviewed every two years about their health, economic, and social conditions. Data on health literacy were measured in 2004 and again in 2010 using a basic reading comprehension test of a medicine label.

800px-Reading_glasses_

Health literacy was measured using a basic reading comprehension test of a medicine label

At the start of the study, we found that nearly one-third of adults had low health literacy, and that 18% of the study sample experienced a decline in their health literacy skills during the study follow-up period (9). People who were most at risk of declining health literacy were older, had no educational qualifications, had relatively low wealth, were ethnic minorities, and had difficulties with activities of daily living. On the positive side, consistent internet use over the six year study follow up period and engagement in cultural activities such as attending the opera, theatre, art galleries, museums, concerts, or the cinema appeared to protect against health literacy decline (9). The other types of social activities that we looked at were civic activities including being a member of a trade union, environmental group, neighbourhood group, and volunteering, and leisure activities including being a member of a sport or social club, or attending educational or musical classes. Alone, participating in civic or leisure activities had no effect on health literacy during ageing.

When we looked at the combined effects of engaging in none, one, two, three, or four of internet use and each of civic, leisure, and cultural activities, we saw an additive effect where the more activities adults engaged in, the more likely they were to maintain health literacy skills (9). People who engaged in all four of internet use, civic activities, leisure activities, and cultural activities over the study follow-up period had half the odds of losing health literacy skills as people engaged in none of these activities (Table). Importantly, all of these associations were independent of cognitive decline and other factors that might influence internet use and social activities such as wealth, social class, and health status.

Table. Additive effects of consistent engagement in any of internet use, civic activities, leisure activities, and cultural activities, the English Longitudinal Study of Ageing, 2004-11 (n=4368)

OR*

95% CI

Per additional activity

0.87

(0.81, 0.94)

Number of activities engaged in

 

 

     None

1.00

     One

0.93

(0.76, 1.14)

     Two

0.81

(0.63, 1.02)

     Three

0.70

(0.53, 0.94)

     Four

0.51

(0.33, 0.79)

*Adjusted for age, sex, ethnicity, educational attainment, net non-pension wealth, having a limiting long-standing illness, experiencing an IADL limitation, baseline executive function, baseline memory, executive function decline, and memory decline

Computer Keyboard

Internet use was associated with maintaining health literacy

What does this study mean? Well, first of all, that it is not inevitable that older people lose literacy skills as they age. It appears that internet use and social activities help with the maintenance of literacy skills. Even adults who experienced cognitive decline appeared to gain a benefit from using the internet and engaging in cultural activities. However, the main concerns are social inequalities in access to the internet and that cultural activities require time, money, and transportation. Older adults who are in poor health, have low wealth, and are from deprived backgrounds are the least likely to take advantage of the internet and to participate in cultural activities. They are also the most vulnerable to the loss of literacy skills as they age. Future research is needed to improve our understanding of how internet use and social engagement promote literacy skills, and to develop strategies to enable the most vulnerable individuals to benefit from technological advances and full participation in society.

This research was conducted at the Health Behaviour Research Centre at University College London, and funded by a Doctoral Foreign Study Award from the Canadian Institutes of Health Research, an Overseas Research Scholarship from UCL, and by programme grant funding from Cancer Research UK.

References

1.        Institute of Medicine. What is health literacy? In: Nielsen-Bohlman L, Panzer A, Hamlin B, Kindig D, editors. Health literacy: a prescription to end confusion. Washington D.C.: National Academies Press; 2004:31-58.

2.        Berkman ND, Sheridan SL, Donahue KE, Halpern DJ, Crotty K. Low health literacy and health outcomes: an updated systematic review. Ann Intern Med 2011;155:97–107.

3.        Kobayashi LC, Wardle J, von Wagner C. Limited health literacy is a barrier to colorectal cancer screening in England: Evidence from the English Longitudinal Study of Ageing. Prev Med 2014;61:100–5.

4.        Bostock S, Steptoe A. Association between low functional health literacy and mortality in older adults: longitudinal cohort study. BMJ 2012;344:e1602.

5.        Wolf MS, Curtis LM, Wilson EAH, Revelle W, Waite KR, Smith SG, et al. Literacy, cognitive function, and health: results of the LitCog study. J Gen Intern Med 2012;27(10):1300–7.

6.        Paasche-Orlow MK, Parker RM, Gazmararian JA, Nielsen-Bohlman LT, Rudd RR. The prevalence of limited health literacy. J Gen Intern Med 2005;20(2):175–84.

7.        Gazmararian JA, Baker DW, Williams M V, Parker RM, Scott TL, Green DC, et al. Health literacy among Medicare enrollees in a managed care organization. JAMA 1999;281(6):545–51.

8.        Federman AD, Sano M, Wolf MS, Siu AL, Halm EA. Health literacy and cognitive performance in older adults. J Am Geriatr Soc 2009;57(8):1475–80.

9.        Kobayashi LC, Wardle J, von Wagner C. Internet use, social engagement and health literacy decline during ageing in a longitudinal cohort of older English adults. J Epidemiol Community Health 2014;epub ahead of print. doi: 10.1136/jech-2014-204733

All images: Wikimedia Commons

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Interview with Joan Bloch: The connection between bus travel and preterm birth

bus_stop

Photo by Gray Monk, CC BY-ND 2.0

I spoke with Joan Bloch, PhD, CRNP, about her work on the causes of disparities in preterm birth. Although premature births are declining in America, African-American women are still far more likely than white women to have a baby born too early.

In a recent research project, presented at the American Public Health Association meeting, her team studied bus routes in the low-income areas of Philadelphia, PA where preterm birth is highest. They found that women likely spend upwards of 19 hours and $69 just for bus fare in the course of a healthy pregnancy—or, for a high risk pregnancy, 27 hours and $98.

On calculating bus travel for this project:

I have 30 years experience in caring for low income populations of women that take the bus to prenatal care, and I also work with people in my clinic and other clinics. So we had a panel of experts and a spatial analyst who rode around the city and we looked at different neighborhoods. We identified what would be a typical case, but maybe not such a dramatic case, right? Because we could go into a neighborhood where the houses are all boarded up and create a scenario where somebody has poor health behaviors and whatnot.

So we drove around and identified an apartment house, you know, young people often live in apartments. We identified an apartment house on a main street where there’s a bus stop right in front of it. And we said, [this hypothetical woman who lives here] gets pregnant, what would her travel through the bus system be like for prenatal care? And we just mapped it out.

On how to fix the situation:

I don’t know if we can make healthier places for everyone. That would be wonderful but that would take a long time. Maybe in 10 years we can make a bad neighborhood better, but in the meantime babies are being born every day, so what can we do to make it easier for those mothes to take care of their babies?

It would be great if we can have maternal/child centers, and mothers would come there, take care of their kids, and they can be cared for. [Agencies] could come together and make it one stop shopping. If the WIC program has their own building, maybe the prenatal care and infant care can be there too.

On why mothers travel just days after birth:

In efforts to decrease infant mortality, in this country we decreased the length of stay for mothers after childbirth in the hospital. Women who have a healthy normal delivery go home within 48 hours. But babies can go south quickly, so pediatricians, with good intentions, require that mothers bring their babies back to their pediatricians within two days after discharge.

So what that means is we’re sending mothers home right after this huge physological experience of childbirth and then they’re told they have to bring their baby back within 2 days. And the pediatricians in our city, at least at St. Christopher’s hospital, say that just about 100% of mothers do that.

I was talking to the medical students and they were saying “Ohh! Maybe that explains why we often see mothers with brand new babies on bus corners waiting for the bus. We thought they were totally negligent bringing out these newborn babies and taking them on the bus.”

And to think, what society has so little respect for the childbirth process we would expect a mother to leave her house just days after giving birth, and travel with her baby in tow? I think globally, from my experience and those of nurses around the world, we agree that mothers will do anything to make sure their babies are healthy. In most countries around the world they actually send nurses home to the mother’s house within that first week.

On changes in prenatal care over the years:

in the 1990s there were prenatal care adequacy indices that calculated the amount of prenatal care women got, to see if that was related to their outcomes, and that was actually based on 11 visits during the pregnancy. In our analysis, standards of practice have changed, increasing the number of visits. [Today, a woman] would have to make 25 different visits to get just regular prenatal care.

From 2000 to now, there’s been a plethora of health disparities research. But the reality is that even though we see so much in the literature, at the ground level, the teams I worked with 30, 20 years ago, we had much more resources.

We had a lot more time to spend with women. As a nurse practitioner, it’s not like I was scheduled like a mini doc every 15 minutes to see another patient. I could provide more well women’s health care.

In the past there was more ability to really work with a woman and her family and her support systems (or lack of support systems) and to run around in the neighborhood to get her what she needs. I think nowadays that has sort of been parceled out to funded safety net programs, so back then maybe we didn’t have them, but now there’s no real communication between all these different programs.

On how she got into her field:

I became a nurse in 1978, never knew a nurse in my life, but I was inspired, actually I was obsessed with racism as an adolescent. Like, why people could kill other people and harm other people just because they belong to a certain group. I had the opportunity to listen to Viktor Frankl and his words just resonated with me: Do something that’s going to be purposeful. Find meaning in your life, right? I looked through an occupational forecasting book and I saw nurses help people and I love math and science.

In nursing school when I saw birth it was like a miracle. Birth is a miracle. And I thought wow, I could help women and couples have healthiest birthing experience and babies.

When I went into the PhD program [after 20 years of nursing and teaching], I wanted to understand how the outcomes of health care services are evaluated, and particularly prenatal care. I grew up in nursing at a time there were a lot of changes. Childbirth classes, birthing rooms, I guess it was a product of the feminist women’s health movement. I wanted to know how this was evaluated on a public health level, and that led me into perinatal epidemiology.

On race and poverty:

I came into this work by just taking care of women & trying to promote each individual woman’s optimal health, and it wasn’t a race thing. In my dissertation work [on brain injury in newborns] I saw that if the mothers didn’t come to prenatal care, there was no relationship if the mother was white. But if the mother was black and she didn’t have prenatal care, those babies born to black mothers were two times more likely to have brain injury by 4 hours after birth.

But to tell you the truth once I did these maps, and saw the relationship with poverty and violence in the neighborhood & the racial segregation, it sort of shocked me, because it was so glaringly obvious, that it was more about living in bad neighborhoods. I think at the end of the day it really is about being poor. We need to take care of poor folks with a different approach than perhaps folks that have more resources. We need to take care of individual people and look at the context of their lives and help them be as healthy as they can be, and be sure they can take care of their children the best they can.

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Guest post: Economists should focus on the economy, not public health

Ed note: Please welcome Dr Travis Saunders back for another guest post. Travis Saunders has a PhD in Human Kinetics at the University of Ottawa. His research focuses on the health impact of physical activity and sedentary behaviour. He blogs regularly about both on his blog, Obesity Panacea.

We get it. Maclean’s Editor-at-Large Peter Shawn Taylor thinks that public health people (e.g. myself) should stay away from chronic disease (I guess it’s time to wrap up my research program and call it a career!). And he thinks that we should definitely stay away from any policies related to chronic disease that have anything to do with personal choice or the economy.

Earlier this month I sounded off on a recent Maclean’s editorial arguing that public health should prioritize infectious diseases like Ebola, rather than chronic diseases like cancer or obesity. This week, Mr Taylor repeated the same arguments in an opinion piece for the Globe and Mail concluding that:

It is not the job of public health to have an opinion on
taxes, economic policy, free trade or corporate control. Neither
should it be their business to interfere in the freely-made choices of adults.

Public health ought to stick to their needles, and leave the economy alone.

To recap: Mr Taylor (an economist and journalist) is well equipped to tell public health agencies how to run their business. Those of us trained in health research are not (one presumes it is because we are not economists). The level of condescension implicit in that line of reasoning is nothing short of astounding (if I ever meet Mr Taylor, I hope to ask him what he thinks of health economists… does their economic training qualify them to speak on important matters of public health, or are they disqualified by their training in public health?).

Unfortunately Mr Taylor does not present much in the way of arguments
to support his conclusions. He simply doesn’t believe that public health should include a focus on chronic diseases, because this might result in policies that impact the economy or personal choice. He does not claim that this would result in better policy, a healthier
society, or a stronger economy. The gist of his argument? We shouldn’t focus on chronic disease, because Mr Taylor doesn’t like it.

Here are some of Mr Taylor’s comments from the Globe and Mail, along with my responses (emphasis mine throughout):

The mission drift rampant in public health extends all the way up to the World Health Organization. At the peak of the
Ebola scare and with her organization under fire for mismanaging the on-the-ground response to the outbreak, last month executive director Margaret Chan was in Moscow attending a tobacco conference where she argued cigarettes are a bigger threat to global health than an African virus.
Last year she threw her lot in with the anti-corporate crowd, railing against “Big Food, Big Soda and Big Alcohol.”

As I noted last time around, this argument borders on willful ignorance for two reasons. First of all, Maclean’s (Mr Taylor’s magazine) has argued that the WHO failed to respond to Ebola not due to its focus on non-communicable diseases, but because it is chronically  nderfunded. Second, smoking is the # 1 preventable cause of death worldwide. At the risk of repeating myself, tobacco kills more people than Ebola every three days. So it absolutely makes sense to continue to focus on tobacco, even while we try to get a handle on the Ebola crisis.

The original − and very necessary − purpose of public
health was to combat infectious diseases and impose sanitary standards on water, food and waste. From this perspective, the field has enjoyed many successes, such as the eradication of polio and smallpox and the remarkable safety of Canada’s food system. Lately, however, public health departments seem to have lost sight of their primary mission. In a search for new things to control, or perhaps to pursue
personal ideological views, public health officials have pushed their way into areas they simply don’t belong.

As I noted in response to the Maclean’s editorial, this line of thinking is driven by ideology, rather than any clear logic. If you want to improve the health of a population, it makes no sense to draw an arbitrary line separating communicable and non-communicable diseases (keeping in mind that any line between the two is already blurring anyway).

By Mr Taylor’s logic, it would perfectly acceptable for public health campaigns to hand out condoms on university campuses, but not to warn people about the dangers of binge drinking, or drinking and driving (freely made choices of adults, etc). Take seat-belt laws – another unmitigated public health success story, despite infringing on our freedom to be thrown from a moving vehicle. A paper in the Review of Economics and Statistics concluded that “mandatory seat belt laws unambiguously reduce traffic fatalities”. And yet an exclusive focus on communicable diseases would have taken this option off the table
(unless, I assume, it was suggested by an economist).

Clearly Mr Taylor has an issue with public health agencies, in particular the public health unit in his hometown of Waterloo (although I know nothing of their policies, I can assure Mr Taylor that they did not invent the term “food swamp”). But I fail to see any convincing arguments (or any arguments at all really) in this new piece, or the earlier editorial from Maclean’s. There is no logical reason to allow public health to deal with infectious disease, but to bar it from dealing with other health-related issues. Arguing that you don’t like something isn’t really much of an argument.

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Red meat and cancer: the biological evidence

 

original

Is it all about cooking at high temperatures? | Gizmodo

Two weeks ago, we discussed the link between red meat consumption and breast cancer risk. This relationship is particularly interesting, given that younger women and those taking birth control pills were at the highest risk for breast cancer, indicating some kind of interaction between sex hormones and eating red meat. What wasn’t so well covered is the actual biological explanation for how red meat may contribute to causing cancer.

Current evidence is from large-scale population studies, which actually cannot tell us much about biological mechanisms. The first way these studies are done is through recruiting people who already have cancer, and matching them to similar people without cancer for comparison. Both groups – the cancer ‘cases’ and the healthy ‘controls’ – are asked about their historical consumption of red meat along other dietary and lifestyle factors that may also affect cancer risk. This is called a ‘case-control’ study. The second strategy involves recruiting a large group of healthy people, assessing their red meat consumption and other risk factors in real time, and following them forward in time to see who gets cancer and who doesn’t. This is called a ‘prospective cohort’ study, and provides more scientific validity than a case-control study because it happens in real time.

Both of these epidemiological strategies tell us a lot about population trends. Several, high-quality case-control and prospective cohort studies have consistently found relationships between red and processed meat intake and risks of breast cancer, colorectal cancer, death from cancer and cardiovascular disease, and overall risk of death. These relationships were independent of major dietary and lifestyle risk factors, which were carefully measured and statistically adjusted for (1-5).

There are hypotheses put forward by epidemiologists and biomedical scientists to explain the link between red meat intake and cancer risk:

1. Carcinogenic by-products of cooking meat at high temperatures

pah

Structural formulas of some PAHs | ATSDR

When meat is barbequed, grilled, or otherwise cooked at a high temperature, chemical by-products, which have the potential to cause cancer are formed. They are called heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Both PAHs and HCAs have been found to be carcinogenic in rodents, but the biological evidence for humans is not yet well established (6).

HCA

The formation of HCAs during cooking |
Precision Nutrition

HCAs are formed when nutrients in meat – amino acids, sugars, and creatine – react together at high temperatures (6). PAHs are formed when fat and juices from meat drip onto an open flame, causing PAHs from the flame to stick to the surface of the meat (6). PAHs are also found in cigarette smoke and emissions from diesel fuelled-engines, so they are often studied in relation to air pollution (7). They have been linked to breast cancer in epidemiological studies, and this evidence is supported by biomedical research showing that PAHs are stored in the fat tissue of the breast, that they weakly mimic estrogen, and that they bind to DNA, forming damaging PAH-DNA adducts (7-9).

2. Nitrites and nitrates in processed meats

Nitrites and nitrates are found in processed meats, such as bacon, sausages, and hot dogs. In the large intestine, these compounds react with naturally occurring amines in meat to form carcinogenic N-nitroso compounds (NOCs). NOCs have been found to cause cancer in over 40 different animal species (10). Prospective studies have found a link between NOCs and gastrointestinal cancers, including oesophageal, stomach, and colorectal and rectal cancers (11-13). There is some evidence that the antioxidant vitamins C and E could help counteract the effects of NOCs (12,13), but further research is needed.

3. Hormone residues in meat

This explanation is one of the most worrying, as it would be due to growth hormones fed to cattle during farming. There is the least amount of evidence for this hypothesis, and surely there is strong political resistance from the meat industry against this possibility. In many places, use of growth hormones such recombinant bovine growth hormone (rBGH), which is actually more of a concern for dairy products, is banned or has been reduced in its usage. The Huffington Post has an interesting article on this issue.

4. Heme in red meat

The final hypothesis I will cover here is that of heme. Heme is the iron-containing chemical compound in red meat, also providing its pigment or colour. While dietary iron is crucial to good health, heme is also toxic in the digestive system. It has its own toxicity, but also acts to promote the formation of NOCs (14). Population-based cohort studies have found mixed evidence on the relationship between dietary consumption of heme from red meat and cancer incidence (15).

gut

The curiosity of the human gut microbiome | CR Way

Another current question is the role of genetics in how red meats are metabolised, and whether genetic differences may make some people more susceptible than others to any potential effects of eating red meat (16,17). An even newer and dynamic avenue of research is how the gut microbiome interacts with foods to produce health conditions (18). It also may be as simple as people who eat excessive amounts of red meat are probably not eating enough of other healthy foods that might help prevent cancer.

A lesson learned here is that science moves forward incrementally. Although the epidemiological evidence shows strong trends, not all of it is in perfect agreement. There is always some degree of human error present in the practice of research (19), which might obscure the truth. And, as we learn more, we also learn how much we don’t know. There are probably variations in metabolic genes and the gut microbiome within human populations that we don’t even know about yet, not to mention the biological and chemical factors in meat itself. Years from now, we may look back on today’s research as clunky and unrefined, unable to pick up more subtle aspects of the diet-cancer relationship.

In any case, the editors of the journal JAMA Internal Medicine have advocated that “Reducing meat consumption has multiple benefits for the world’s health” (20), a bold statement that future research will tell us more about.

 

References

1)Farvid MS, Cho E, Chen WY, Eliassen AH, Willett WC. Dietary protein sources in early adulthood and breast cancer incidence: prospective cohort study. BMJ 2014;348:g3437

2)Farvid MS, Cho E, Chen WY, Eliassen AH, Willett WC. Adolescent meat intake and breast cancer risk. Int J Cancer 2014; Published Online First 15 September 2014: doi: 10.1002/ijc.29218

3)Norat T, Bingham S, Ferrari P, Slimani N, Jenab M, Mazuir M, et al. Meat, fish, and colorectal cancer risk: the European Prospective Investigation into Cancer and Nutrition. J Natl Cancer Inst 2005;97(12):906-16.

4)Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Stampfer MJ, et al. Red meat consumption and mortality: results from 2 prospective cohort studies. JAMA Intern Med 2012;172(7):555-63.

5)Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people. JAMA Intern Med 2009;169(6):562-71.

6)National Cancer Institute. Chemicals in meat cooked and high temperatures and cancer risk. http://www.cancer.gov/cancertopics/factsheet/Risk/cooked-meats (accessed 16 November 2014).

7)Breast Cancer Fund. Polycyclic aromatic hydrocarbons (PAHs).  http://www.breastcancerfund.org/clear-science/radiation-chemicals-and-breast-cancer/polycyclic-aromatic-hydrocarbons.html (accessed 17 November 2014).

8)Rundle A, Tang D, Hibshoosh H, Estabrook A, Schnabel F, Cao W, et al. The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer. Carcinogenesis 2000;21(7):1281-9.

9)Gammon MD, Santella RM, Neuget AI, Eng SM, Teitelbaum SL, Paykin A, et al. Environmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts. Cancer Epidemiol Biomarkers Prev  2002;11:677-85.

10)Bogovski P, Bogovski S. Animal species in which N-nitroso compounds induce cancer. Int J Cancer 1981;27:471-4.

11)Jakszyn P, Gonzalez CA, Nitrosamine and related food intake and gastric and oesophageal cancer risk: a systematic review of the epidemiological evidence. World J Gastroenterol 2006;12(27):4296-303.

12)Zhu Y, Wang PP, Zhao J, Green R, Sun Z, Roebothan B, et al. Dietary N-nitroso compounds and risk of colorectal cancer: a case-control study in Newfoundland and Laborador and Ontario, Canada. Br J Nutr 2014;111(6):1109-17.

13)Loh YH, Jakszyn P, Luben RN, Mulligan AA, Mitrou PN, Khaw KT. N-nitroso compounds and cancer incidence: the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study. Am J Clin Nutr 2011;93(5):1053-61.

14)Bastide NM, Pierre FH, Corpet DE. Heme iron from red meat and risk of colorectal cancer: a meta-analysis and a review of the mechanisms involved. Cancer Prev Res 2011;4(2):177-84.

15)Kim E, Coelho D, Blachier F. Review of the association between meat consumption and risk of colorectal cancer. Nutr Res 2013;33:983-94.

16)Ananthakrishnan AN, Du M, Berndt SI, Brenner H, Caan BJ, Casey G, et al. Red meat intake, NAT2, and risk of colorectal cancer: a pooled analysis of 11 studies. Cancer Epidemiol Biomarkers Prev 2014 (in press).

17)Ho V, Peacock S, Massey TE, Ashbury JE, Vanner SJ, King WD. Meat-derived carcinogens, genetic susceptibility, and colorectal adenoma risk. Genes Nutr 2014;9(6):430.

18)Feltman R. The gut’s microbiome changes rapidly with diet. Scientific American. 14 December 213. http://www.scientificamerican.com/article/the-guts-microbiome-changes-diet/ (accessed 17 November 2014).

19)Ioannidis JPA. Why most published research findings are false. PLOS Med 2005;2(8):e124.

20)Popkin BM. Reducing meat consumption has multiple benefits for the world’s health. JAMA Intern Med 2009;169(6):543-5.

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Does it even matter if gluten sensitivity is bogus?

Gluten Free "Wheat" Thins

Photo by Elana Amsterdam, who made these gluten free crackers. (CC BY-NC-ND 2.0)

This one goes out to all the Americans who are wondering if they really need to make gluten-free stuffing for Thanksgiving.

Gluten-free eating is popular; according to one industry trend study, a third of American adults are trying to avoid gluten, and most of those believe it’s healthy for people in general (rather than avoiding it for medical reasons). Lindsay Kobayashi wrote a great post here about why gluten-free is not the same as healthy, although the processed food industry doesn’t mind if you think it is.

With any trend, of course, comes a backlash. Last year, Australian researchers ran an experiment in which they gave gluten-free or glutenful muffins to people who said they feel like they are gluten intolerant. They had no terrible reaction to the gluten.

Cue the gleeful headlines about gluten sensitivity being “fake” or “bullshit.” (One reporter was researching an unrelated story about gluten free beer and was told by a somewhat confused press officer that, as a result of that study, “gluten free” no longer exists as a concept.)

I get it. You’re sick of hearing about gluten. Maybe you have a friend who shops the gluten-free aisles and you suspect she’s just making it up. Whoopie for you.

But does this line of research help your friend?

Who needs to know?

The situation reminds me of the Saturday Night Live skit about a “Home Headache Test.” In it, a woman complains of agonizing pain in her head, but is told “Honey, you don’t have a headache!”

Likewise, many people who are on a gluten-free diet have chosen it to try to deal with symptoms they are having. Whatever the cause, those symptoms are real. (Those who are trying gluten-free diets as a fad or a temporary challenge will eventually move on to the next fad. I wouldn’t worry about them.)

Scientifically there are two groups of people who believe they benefit from gluten free diets: those with celiac disease, in which an immune system reaction to gluten results in damage to the digestive tract, and those who have similar symptoms but test negative for celiac. In other words, they have “non celiac gluten sensitivity.”

One reason I can’t jump on the backlash bandwagon is because most people with celiac disease don’t know they have it. A study in 2012 that tried to determine the prevalence of celiac disease found it in 35 of the 7.798 people they tested. The kicker? 29 of them didn’t know until the study that they had it. If a fad encourages them to shun gluten, and it helps, that sounds like a win. The University of Chicago Celiac Disease Center estimates that 97% of people with celiac disease don’t know it.

With the average case of celiac taking 6 to 10 years to diagnose, it’s not surprising that people who discover a medical reason, and a simple diet-based solution, for their problems are ecstatic to celebrate that victory and share the news with others. Here is how the blogger and author known as Gluten Free Girl felt, after years of agonizing symptoms and inconclusive medical tests:

When I received the official diagnosis – you have celiac – I clapped my hands and said yes! The naturopath was a little surprised to see my celebration.

The gastroenterologist was even more surprised, the next week, when I showed up for my follow-up appointment in great health, blood test results in hand. He confirmed it – I have celiac. And he left the room, embarrassed.

I’ve written here before about how people embrace changes in diet because they are something you can take action about. Dropping gluten and curing your celiac disease definitely fits in that category. Few other conditions are that easy and dramatic; the only ones I can think of are food allergies and vitamin deficiencies, like when James Lind, in 1753, tested oranges as a scurvy cure.

A celiac diagosis is a get-out-of-jail-free card when it comes to the gluten backlash, but I want to go further.

Remember the Australian study that supposedly proved non-celiac gluten sensitivity to be fake? As some of the better reports explained, the study really did come with a helpful breakthrough for those patients: the symptoms they were chalking up to gluten may come from FODMAPs, a little-known group of carbohydrates that are found in many of the same foods as gluten. Before the study began, researchers put the 37 subjects on a low FODMAP diet, and found that patients’ symptoms improved right away, and weren’t affected by the introduction of low-FODMAP but gluten-laden muffins.

Peter Gibson, the senior author of that study, explained in an interview that a low-FODMAP diet is easier to follow and in his experience is a better initial recommendation: “Our approach is to use a low FODMAP diet as our first dietary approach, and we would only restrict gluten in a very small proportion of patients where we’re not winning and we have a very strong belief that wheat is a cause of their symptoms.”

That’s a recommendation that can actually help patients, and is also something worth getting out the word about. FODMAPs are harder to keep track of than simply avoiding wheat or looking for a gluten-free label, but this may be a worthwhile diet. Here is a cheat sheet for foods to avoid and foods that are safe on a low FODMAP diet.

But 37 patients don’t completely answer the question; it’s a small study, and FODMAPs may not be the issue for everyone who seems to have trouble with wheat. For example, other wheat proteins (besides gluten) may also trigger symptoms. The scientific understanding of wheat/gluten intolerance is just beginning, not ending, and solutions will likely to turn out to be more complex than slapping gluten-free labels on products and selling them at a higher profit.

Bottom line: the science of nutrition exists to serve public health, which in turn exists to serve individuals’ health. If cutting out gluten seems to help, you don’t need a scientist’s permission to eat what you want while you wait for more research to roll in. And if that gluten-eschewing person is your friend? Just pass the wheat-free stuffing already.

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