Last week, the American Dietetic Association announced a new corporate sponsor: The Hershey Center for Health & Nutrition.  The press release is vague but states that they:

“…will collaborate with ADA on consumer and health professional initiatives including an innovative, national consumer-focused nutrition education campaign.”

Whatever that means.  But the goals of these partnerships are always primarily to improve brand image so more people will include their products in a “healthy” diet, or at least reduce negative perceptions of the brand.  Hey, if the ADA allows them to sponsor, their products must be ok to eat, right?  That is what I might think, or at least subconsciously perceive, if I didn’t study nutrition.

While clearly moderation does seem to be a good rule in most cases for food products, this is moving in the wrong direction.  The evidence clearly suggests that whole foods should be priority.  But people hardly understand the boundaries of a healthy diet, and partnerships with food companies that influence public perceptions may blur the lines even further.

This sponsorship adds to the growing list that also includes companies such as: Coca-Cola, PepsiCo, the National Dairy Council, General Mills, Kellogg’s, Mars, Soyjoy, and Unilever.

Now, I realize sponsorships help pay for conferences and other “ADA events and programs,” and I have no idea what is possible without their assistance.  But for an organization that proclaims its members are “experts in nutrition,” these corporate influences are very dangerous.  A large body of evidence suggests that processed foods often have negative effects on health, and there is still much to learn.  I wonder to what extent these companies change image perception among dietitians and the public?  We know that simple health halos on labels such as “organic” or “low fat” cause consumers to feel safer about the caloric content or health effects- what happens when they see these companies partnering with the major organization that tells us how to eat?

While I haven’t yet checked thoroughly to see if there is any relevant research on this, The Fodder File highlights a recent study (1) that should be considered here.  Social factors and preexisting perceptions (along with cognitive bias‘) seem to largely shape how people eat, and this helps to explain why counseling interventions generally aren’t that effective.  This study (more like an interview for trends, which is a limitation) suggests we need to have a deeper appreciation for how people are interpreting health messages.  People may be making changes (or not making them) based on how they interpret a healthy diet, but these interpretations may be incorrect.  The authors interviewed 46 mothers of a low socioeconomic status about issues relating to healthy eating messages and their interpretation and barriers to making change.  The first thing that made me cringe is that the subjects mentioned that television was their major source of diet information.  I don’t know about the UK (where this study was done), but I rarely see any good nutrition advice on TV in the U.S.  Additionally, all of the corporate sponsors of the ADA run television advertisements which influences purchases.

The authors note that: “Good food was discussed as flavorless, boring, and associated with self-denial.”  They seem to think that a healthy diet reduces immediate quality of life.  This reflects consumer surveys (FMI) show that Americans are increasingly less interested in nutrition and moreso taste.  Convenience was a main factor on food selection, as well as time, money, cooking skills, and food availability.  These are clear indications that food education is lacking, but companies that sponsor the ADA target all of these.  If the ADA is trying to reverse the trends of seeking only convenience, and promoting home cooking, they are at war with their sponsors.  Is the ADA instead accepting defeat in these areas?

Most of the mothers understood that an unhealthy diet was a main reason for poor health, but demonstrated a difficulty with interpreting what is healthy.  They note that for smoking, the message is clear, but for healthy eating it is more difficult to understand what constitutes a healthy diet, because there are so many different messages coming at them.  Interestingly, a number of the mothers misinterpreted the concept of a “balanced diet” as one that means balancing good food with bad food instead of balancing nutrient requirements.  It also seems that the people interviewed tended to justify their bad food choices (and guilt) with good ones (or good lifestyle activities).  People shouldn’t have to stress and rationalize about their choices in an ideal environment.  That isn’t healthy either.

Because behavioral change in general won’t occur unless the message is perceived as important, mixing corporate sponsorships with nutrition organizations may downplay the importance of reducing/eliminating processed foods.  To draw an analogy from smoking campaigns, they would certainly be less effective if smoking corporations sponsored major medical organizations and this was prominently displayed to the public.

Instead of relaying the responsibility to the individual dietitian as the ADA does, they should better understand how public health messages are perceived, and work to fund more research on how to build effective campaigns, because clearly what they are doing now isn’t working.  After that, this information should be taught to the dietitians to use in personalized settings to get to the root causes of poor eating habits and address the importance of change of these individual factors, because as the authors note “simply being exposed to public health messages is not enough to achieve lasting behavior change.”

I don’t doubt that the ADA has good intentions- they likely perceive sponsorships as potential to change corporate behaviors, working with them instead of against.  But it is a huge conflict of interest, and there is a high risk that the companies will use the partnership to improve their image- here is Hershey already using it (and RDs) to tell the public that their chocolate products are ok- never-mind doses or which types, or the other ingredients that may come with it.

It seems there is a growing resistance to what the ADA is doing.  Marion Nestle (twitter) (who is not an ADA member) has been outspoken about the ADA’s partnerships eloquently writes:

“Respected ADA colleagues: as long as your organization partners with makers of food and beverage products, its opinions about diet and health will never be believed independent (translation: based on science not politics) and neither will yours. Consider the ADA’s Nutrition Fact Sheets, for example, each with its very own corporate sponsor (scroll down to the lower right hand corner of the second page to see who paid for the Facts). Is the goal of ADA really the same as the goal of the sponsors–to sell the sponsor’s food products? Is this a good way to get important scientific messages to the public?  ADA members: how about doing something about this!”

Or from Michele Simon, who highlights a blogger who spoke up against Canada’s ADA equivalent:

“Professional associations such as the American Dietetic Association and Dietitians of Canada must renounce their corporate affiliations and stop taking money from the very companies that are undermining their own members’ ability to do help people eat right. Until they do so, these groups risk becoming little more than a tool of corporate interests, which is exactly what Big Food wants.”

One of my favorite bloggers, Yoni Freedhoff (twitter) frequently comments on industry’s influence on nutrition in Canada on his blog Weighty Matters.  Yoni covered a topic that I followed very closely this month: PepsiCo’s attempted “advertorial” sponsorship of ScienceBlogs.  ScienceBlogs is a prestigious blogging platform with many great bloggers who cover science topics much more accurately and in depth than you get from traditional media outlets.  So when the parent company, Seed, announced a new blog which from PepsiCo scientists would:

“Discuss the science behind the food industry’s role in addressing global public health challenges”

Many were angered with the decision that threatened to undermine the independence of science and advertising, something that is difficult to find anywhere.  In fact the debacle, dubbed “PepsiGate,” cause about a third of them to temporarily stop posting or move their blogs elsewhere.  It was quite a shift in a very fragile intelligent community from one offensive move.

The majority of the bloggers were not scientists covering nutrition (Obesity Panacea left as expected), either, simply concerned with upholding the integrity of science.  They were understandably furious, which makes me wonder… why isn’t the ADA, whose advice is purported to be evidence-based?  Why are these scientists so sensitive to these obvious commercial interests while most dietitians look the other way for the ADA?

Speak Up

I have no plans to become an ADA member, but will be sharing my opinions from the outside with my blog, and I suggest that others use social media outlets to do this as well.  If more people voice their opposition to these partnerships, the ADA will be forced to establish a dialog with nutrition professionals and corporate interests will become more transparent.  Please share your thoughts, especially if you are a RD, in the comments.

Reference

1. Wood F, Robling M, Prout H, Kinnersley P, Houston H, & Butler C (2010). A question of balance: a qualitative study of mothers’ interpretations of dietary recommendations. Annals of family medicine, 8 (1), 51-7 PMID: 20065279

Last year, I described a study that found an epigenetic mechanism of peripheral insulin resistance through methylation of the PGC-1alpha promoter.  Recently, Chang et al. explored an epigenetic mechanism in non-alcoholic fatty liver.

Fatty liver is closely linked with insulin resistance and diabetes as well as obesity.  As it is not yet fully understood, the only effective treatment is lifestyle intervention (exercise and weight loss).  However, one compound that has potential, Berberine, is a natural alkaloid that is sold as a dietary supplement in the U.S.  It has been studied in animal and human models in which it ameliorates metabolic problems like dyslipidemia and insulin insensitivity.  The authors also note that it has been found to reduce serum cholesterol and LDL-cholesterol by increasing hepatic LDL-receptor expression.  I have written previously a little about some of these biomarkers- I don’t think (in general) they are good representations for disease, at least yet.  Berberine does reduce fatty liver in some genetically altered mice, but these do not represent a normal milieu.  If berberine can improve the aforementioned dysfunctions and fatty liver in a normal mouse model, it has potential to go on to human trials and possibly be used therapeutically, or its structure used to develop more potent drugs for fatty liver.

So the authors tested this, and elucidated an epigenetic mechanism in which it develops.  A short summary is available at the end. The study was done in Sprague-Dawley rats.  Split into 3 groups, one group consumed a high fat diet to induce fatty liver and received 200 mg berberine per kg/day (BSA HED ~32 mg/kg per day if I calculated correctly), one group consumed a high fat diet and received a placebo, and a “normal” diet group received the placebo.

Genes involved in lipid metabolism were chosen after real-time PCR analysis of liver mRNA expression- genes differentially expressed between the high fat group taking berberine and the high fat group taking placebo were chosen for DNA methylation analysis.

The researchers measured body weight, visceral fat, and lipids for 16 weeks in the groups.  On a high fat diet, rats tended toward obesity as expected, but in the high fat diet with berberine treatment, bodyweight was reduced to levels similar of non high fat diet rats.  It should be noted that this does NOT mean berberine will do this in humans as some supplement companies will claim- many compounds reduce bodyweight in rodents but fail in human trials.  Visceral fat, serum total cholesterol, and LDL-cholesterol, but not serum triglycerides were also lowered in the berberine group, though these were not affected until toward the end of the treatment.

Liver analysis showed that berberine prevents derangement of liver cells, excessive lipid droplets in the cells, and decreased the total liver weight of the liver compared to the placebo group.  Hepatic triglycerides, and serum ALT and AST were also reduced.  These suggest that liver steatosis is improved with berberine.

Fasting glucose and insulin were reduced in the berberine group, as well as AUCs after a glucose challenge.  These suggest that insulin resistance is ameliorated with berberine treatment.

Next came genetic analysis.  mRNA and protein of the following genes were found to be down-regulated in the livers of rats consuming a high fat diet (without berberine) compared to a non high fat diet: CPT-1alpha, MTTP, LDLR.  Berberine prevented the down-regulation of CPT-1alpha and MTTP induced the the high fat diet.  SCD-1 mRNA was lower in the berberine treatment.  PPARgamma and GPAT were not affected by berberine, nor ACC, DGAT1, DGAT2, PPARalpha, and UCP-2, all of which are involved in fat storage and oxidation.  So berberine seems pretty selective in its targets.

So next they chose to examine if these gene expressions are altered by DNA methylation.  They looked at the promoters of MTTP, CPT-1alpha, and LDLR.  They found that the MTTP promoter was methylated differently in each of the test groups, while CPT-1alpha and LDLR was not.

So they focused on the MTTP promoter, finding that on average it was methylated more in the high fat diet rats compared to the non high fat diet rats (38% vs 12%), as well as more at each CpG site that was individually analyzed.  Berberine lowered the methylation level of the promoter with a high fat diet down to about 17% on average, as well as at individual CpG sites. An inverse correlation between MTTP mRNA expression and methylation of 2 of the 3 CpG sites was found.  Together, this suggests that berberine influences gene expressions that influence lipid metabolism (MTTP for sure) by altering the methylation of its (MTTP) promoter, which prevents fatty liver.

To further verify this, they performed subsequent in vitro experiments with berberine against a demethylating agent, which corroborated the theory.  If you read my previous post about the epigenetic modifications of the PGC-1alpha promoter, you may recall that certain metabolic factors influenced the activity of a DNA methyltransferase isoform which mediated the effect of these variables on the methylation of the promoter.  In this study, that DNA methyltransferases weren’t affected, but serum homocysteine was higher in the high fat diet group compared to the non-high fat diet group, and berberine restored this to normal levels, but other molecules in this pathway (SAM, SAH, SAM/SAH ratio) were not different.  This suggests that berberine prevents methylation by altering the methyl donor pool, or by altering DNA demethylases, or other mechanisms that need to be further explored.

Lastly, since MTTP is needed for VLDL secretion and triglyceride accumulation in VLDL fractions, they found that berberine indeed increased the triglyceride content (as well as higher apoB-100 and -48), compared to a high fat diet which reduced it.

It should be noted that in the previous study on PGC-1alpha that I described, many of the epigenetic changes were on non-CpG sites (which was a novel finding), while this appeared to only examine CpG methylation.  I don’t know why this is.

Their interpretations

The authors describe the functions of MTTP (microsomal triglyceride transfer protein), which include assembling and secreting VLDL and LDL which export lipids from the liver; down-regulation of its expression in other research increases liver dysfunction.  The results of this study match what would be expected if MTTP had a major role in liver lipid homeostasis.  However, other genes come into play that were not affected by methylation- LDLR, which regulates LDL-cholesterol levels, was affected by berberine in a non-methylation fashion.  CPT-1alpha expression, key in mitochondrial beta-oxidation, and SCD-1, which converts saturated fats to monounsaturated fats were also altered through non-methylation mechanisms by berberine.  These alterations could be from other epigenetic mechanisms, e.g. histone modifications or by miRNA.

Quick Summary

Berberine prevents fatty liver in rodents on a high fat diet in one way by reducing the methylation of the MTTP promoter, which restores triglyceride accumulation in VLDL and export from liver cells.  It also affects several other gene expressions through unknown mechanisms, possibly epigenetic, that have not been explored yet.

No practical relevance yet, but interesting to those who like this area.  Elucidating these specific pathways will allow us to find precisely how diet, exercise, and environmental factors interact to influence metabolic functions, and model them for manipulation and medical purposes.

Reference

Chang X, Yan H, Fei J, Jiang M, Zhu H, Lu D, & Gao X (2010). Berberine reduces the methylation of the MTTP promoter and alleviates fatty liver induced by a high-fat diet in rats. Journal of lipid research PMID: 20567026

I have often wondered why, when buying coffee from the same establishment on different days, or the same size from different establishments- they do not have an equal effect on my subjective alertness.  It probably has a lot to do with internal milieu- hormones, neurotransmitters and the like, but I came across another reason: the amount of caffeine in coffee can vary quite a bit, even when bought at the same place on different days.  If fact it was pretty shocking to me, so I thought I would report it here for those who may not know.  There are also health concerns- if you are expecting a certain dose and it is actually well above it, it may cause anxiety in those prone to it, interact with medications, or negatively effect the cardiovascular system.

Prior to the study by McCusker et al. (1), it was established that preparation of coffee and the source of the coffee bean influences caffeine content dramatically.  The average value in a 150mL/5oz cup is approximately 85 mg.  But McCuster and colleagues tested specialty coffees to see how much they differed.

They tested by gas chromatography with nitrogen-phosphorous detection 20 caffeinated and 7 decaffeinated samples from coffee shops in Maryland, as well as samples of Starbucks Breakfast Blend bought over 6 consecutive days from the same shop in Florida.

Here are the results of the 20 caffeinated coffees:

As you can see, the expresso coffees varied a bit, but the brewed coffees were more dramatic- from 143 mg to 259 mg for an equal amount.  The average amount was 188 mg per 16 oz, or 59 mg per 5 oz, which is lower than the previously reported 85 mg average.

The authors note that the 7 decaf coffees had concentrations less than 17.7 mg.  They further explored decaf coffees in a subsequent study, finding up to 13.9 mg per 16 oz in specialty coffees and up to 15.8 mg/shot of decaf espresso from Starbucks, so if you are particularly sensitive to caffeine or are supposed to completely restrict it for medical reasons, this information may be relevant.

Here are the results of the Starbucks product purchased on 6 consecutive days from the same shop:

This was the most surprising to me- the same product from Starbucks varied from 259 mg to 564 mg on different days.

The authors note several variables that may influence caffeine content: variety of bean, roasting method, particle size, proportion of coffee to water, and length of brewing time. But even with standardized conditions in the Starbucks coffee, which is a “blend of Latin American coffees,” caffeine content varied by over 2-fold.

Another study by Hackett et al. (2) used a different analysis method: LC-diode array detection to test 32 coffee powder samples for caffeine content after using a microwave to extract the caffeine.

The results show again a dramatic difference in the amount of caffeine- from 5.2 to 12.2 mg/g of powder.

The simplest solution to get the most consistent amount to me would be to brew your own at home, which would give you more control over the variables that influence caffeine content.  If you are extra sensitive to caffeine, be careful when trying a new brand/product and start at a lower amount of coffee in case there is a significantly greater amount of caffeine in it.

Getting your “fix”

With such inconsistencies in dosing, I now have a reasonable explanation for why it sometimes feels like I don’t get much of a boost in alertness.  Though as a recent study suggests (3), alertness is only really returning to baseline in regular coffee drinkers.  The “fix” is only really eliminating withdrawal symptoms from acclimation to coffee’s effects.  The study, on 379 subjects, found that in habitual coffee drinkers, after doses totaling 250 mg of caffeine (not from coffee and standardized), had alertness levels only reached those of non-coffee drinkers who did not receive the caffeine.  However, they also found that people who consume little or no caffeine on a regular basis did not get a boost in alertness either.  This differs from other studies and could be because of self-report and current estimations of foodstuffs/beverages with caffeine, or compliance issues- indeed they found salivary caffeine concentrations to differ quite dramatically compared to other studies with similar consumption classifications.  They also explored some interesting genotype relationships with caffeine and anxiety, though consumption seems relatively unaffected by susceptibility to anxiety and habituation brings tolerance to these effects.  One of the associated SNPs, ADORA2A (adenosine A2A receptor gene) rs5751876, is one that I can lookup from my own 23andme data, I can see that I am (C;T), suggesting a reduced risk for anxiety to caffeine compared to (T;T).  There were several other SNPs on ADORA2A that were linked to anxiety as well.  The other major symptom besides low alertness with caffeine withdrawal is headache.

So if you’ll excuse me i’m off to refill my cup- the headache isn’t gone yet.

Reference

1. McCusker RR, Goldberger BA, & Cone EJ (2003). Caffeine content of specialty coffees. Journal of analytical toxicology, 27 (7), 520-2 PMID: 14607010

2. Hackett J, Telepchak MJ, & Coyer MJ (2008). Analysis of total caffeine and other xanthines in specialty coffees using mixed mode solid-phase extraction and liquid chromatography-diode-array detection after microwave digestion. Journal of analytical toxicology, 32 (8), 695-701 PMID: 19007523

3. Rogers PJ, Hohoff C, Heatherley SV, Mullings EL, Maxfield PJ, Evershed RP, Deckert J, & Nutt DJ (2010). Association of the anxiogenic and alerting effects of caffeine with ADORA2A and ADORA1 polymorphisms and habitual level of caffeine consumption. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 35 (9), 1973-83 PMID: 20520601

Empirical evidence backs up what most of us knew all along.

The absurd “toning” shoes that companies are now making a pretty penny (it’s a $17 billion a year industry already!) with that promise to tone various parts of the body or burn more calories compared to regular shoes are debunked by a couple independent studies at UW-La Cross.  They tested energy expenditure, muscle activation in a number of different muscles, heart rate, VO2, and RPE (rating of perceived exertion) between regular running shoes (New Balance) and several “toning” brands: Sketchers Shape-ups, MBT, and Reebok EasyTone and apparently found no statistical significance between them.

Read about the results of the studies here, as well as articles with quotes from the authors in blogs on the WSJ and Time.

It should be noted that these 2 studies are not yet published in peer-reviewed journals.  The studies are also small in nature, however data should come before commercial claims do, and so far there is no credible supporting evidence – “studies” from the shoe companies I am unable to find in peer-reviewed journals.

PyschologyToday.com published an article yesterday titled “Why Changing Somebody’s Mind, or Yours, is Hard to Do.”  I maintain that understanding human behavior is under-appreciated when trying to relay nutritional messages to others, so periodically i’ll update with articles like this.  Knowing why people resist new information can be used to take a new approach, and hopefully become more self-aware of bias tendencies as well.

The article is worth the quick read; it discusses theories of self-affirmation and cultural cognition.  The research on self-affirmation suggests we often block factual information as a protective mechanism (to protect self and group identity could be a fitness advantage) when it challenges self integrity.  However some studies suggest that you can limit these defense mechanisms by doing something to get the person/people to self-affirm (remind them of their integrity, feel good) prior to presenting information.  Cultural cognition suggests that we mold our perspectives to groups that we identify best with.  This increases the group strength and influence and makes us feel good with acceptance.  When threats of opposing opinions confront us, we are respond with irrationality.  This is obvious when pondering political and scientific topics.

In a perfect world, only experts would share opinions and those who are not would adjust their perspectives accordingly.  Unfortunately, our human tendencies create for a messy reality of quackery and misinformation, while the true evidence remains elusive except from a small percentage of the population.  We are not wired to be objective and maintaining objectivity is something that takes training/practice and a certain level of intelligence/mindfulness.

Why is this important to nutrition?

There are some studies relevant to health that show people who complete a self-affirmation are more accepting of information.  There are a couple examples here and here.

Online, it may be more difficult to utilize this technique.  Health articles never start in a way that would result in a self-affirmation- it would be quite strange.  It may be one big limitation to the ability of print/internet to change the poor state of nutritional information.  In fact, it could promote people to find websites that are not evidence-based.  This is probably happening, though it may be difficult to gauge which other human tendencies also lead people to poor nutritional sources.

It is sometimes quite evident when political and value frameworks are used to interpret health research.  Cultural cognition may help to explain why there seem to be relationships between the recent paleo-nutrition movement and libertarianism, for example.  A few of them are anthropogenic global warming denialists as well (a survey would be interesting to see what percentage are), even when there is strong science suggesting otherwise.  There are certainly obvious shared belief systems by the main people and it seems their followers are like this as well.  While I certainly think that nutrition needs an evolutionary framework, some of the paleo bloggers take it to a different level by creating their own lifestyle culture based on selective information.  While the idea of paleo nutrition is seemingly good (preliminary research is mostly supportive, and getting people to eat whole foods is great), I do question the objectivity in some of the conclusions they draw and some of the principle assumptions that they stand on.  More on this in later posts.  My point now is simply to highlight these interesting relationships.

Conclusion

We need to be wary of provoking immediate emotional reactions on and offline when discussing nutritional topics, which can be a difficult task.  Self-affirmation can be used as a tool to improve the efficacy of information dissemination, and cultural cognition suggests why people tend to form perceptions depending on group conformance and not necessarily an accurate surveying of the evidence.

Recently I wrote about a study on organic vs synthetic pesticides on sustainability, which suggested that organic pesticides are not always more efficacious against pests nor as selective (not killing natural enemies of pests) than synthetic pesticides.

Earlier this month a study was published on a related area: organic farming on natural enemy evenness.  Different farming techniques can alter the balance of the natural enemy species’ and cause a reduction to only a select few species.  Existing evidence suggests this may limit the ability to control pest populations.

Natural enemy diversity includes richness (number) and evenness (abundance of species).  The latter has not been studied as well as the former.  The authors analyzed survey data from Washington potato fields and found no significant impact on richness from different pest-management techniques, but organic fields were more even on the distributions of natural enemy species compared to conventional fields, which were ruled by largely 1 species.  To extend the findings to other crops, they performed a meta-analysis on 38 studies and found that organic farms had greater evenness in organic fields.

However, as I count on the graph below, counting individual increases or decreases when going from conventional to organic reveals approximately 50/50 split; it seems that the magnitude of evenness on organic farms is sometimes much greater.  This could be for several reasons.  The studies that they analyzed had 40 predator and 8 insect pathogens, 23 crops, in 16 different countries.

So there are a lot of different variables to consider here (as goes with meta-analyses), and perhaps sub-analyses with different groups would show advantages for conventional with some crops or species or areas.  But in general, the data suggest organic currently has the advantage.

Next, they performed field enclosure tests to see if natural enemy evenness suppressed pests.  They setup 42 predator-pathogen evenness combinations (7 predators and pathogens) based on the previous potato field survey data with total densities remaining equal (richness constant).

They found that increasing evenness in predators and pathogens increased plant biomass.  Plant mass correlates with potato tuber yield, suggesting that yield is also increased when evenness is increased.  More evenness also increased pest (potato beetle) mortality.  Predator and pathogen evenness were additive in these findings.  Also, they found that natural enemy species better survived when evenness was greater (a little competition is good).

I particularly liked the way they visually presented these results, here they are:

a. lighter shading = higher plant weight with increasing evenness; the plane angle suggests both pathogen and predator evenness are independently related to plant weight:

b. darker shading as both evenness axis increase means fewer beetles:

c. this shows that more natural enemies survived when predator (but not pathogen) evenness was greater:

The authors discuss the findings of this study, that pest densities were ~18% lower and plant mass 35% larger, which could mean that a greater evenness with organic farming could offset the losses in yield from reduced pesticide use.  They note that field enclosure experiments have limitations though, and state a need for more studies.

They suggest that organic farming may improve evenness through (generally) reduced usage of broad-spectrum (non-selective) pesticides.  The study I recently discussed suggests that organic pesticides are not always more selective against pests compared to natural enemy species over synthetics.  Perhaps the development of more selective pesticides will give the best of both worlds: an increased evenness seen with organic farming and an even greater yield characteristic (in general) of conventional farms.

Reference

Crowder DW, Northfield TD, Strand MR, & Snyder WE (2010). Organic agriculture promotes evenness and natural pest control. Nature, 466 (7302), 109-12 PMID: 20596021

I watched the annual Nathan’s July Fourth Hot Dog Eating Contest this year, in which the champ Joey Chesnut consumed 54 hot dogs and buns (over 28,ooo kcal) in 10 minutes.  Some observations:

The majority of the eaters appeared to be thin (some very) in good shape.  I know little about how these people “train” for eating competitions, but I suspect (as the study below suggests) it is mostly a practice of extreme self-control.  It is tempting to speculate that the personality types necessary for competitive eating may preclude a normal self-assessment (psychological issues), though this could probably be said about many sports.  In other words, is competitive eating a disorder?  Some prominent eaters are noted to have obsessive exercise tendences (including bodybuilding which may suggest body-image problems and control issues), which are seen in other disorders.   But these are all non-qualified opinions and not yet based in science.

I have never heard of any warnings to health of competitive eating, which is increasing in popularity, in the media.  There is a very vague IFOCE (the main international organization that holds contests and rankings) safety page but there is no information on potential health risks of competitive eating.  This seems to be because we don’t know much yet.

But I did recall a paper (open access) on a study from 2007 that should be highlighted.  Their preliminary results and warning on the lack of science should be noted:

To our knowledge, no cases of gastric perforation, Boerhaave’s syndrome, or Mallory-Weiss tear have been reported as a sequela of competitive speed eating. On the other hand, we know of no studies on the short- or long-term effects of speed eating on its competitors. Nor are there any data in the literature about the science of speed eating and how its competitors are able to consume such enormous quantities of food in such short periods of time.

They took one of the top IFOCE ranked eaters and one control subject and did a few tests.

It seems like speed eaters have to some degrees both a birth given ability to eat and develop it further with training, in which there are a number of methods.  They note that eaters often use water loading to expand the stomach without the need for calories.  They caution potential adverse effects of this such as hypothermia, water intoxication, and cerebral edema.  Two water load tests were done on the subjects: WL5 (drinking water at own pace for 5-minutes or until sated) and a WL100 (water consumed at 100mL/min until sated.  The speed eater outperformed the control subject in both tests: 4.5 Liters vs less than 2 L respectively for the WL5 (was stopped before 2 minutes) and 2.4 L vs 2 L respectively for the WL100 (stopped before sated).  With a solid-phase nuclear gastric emptying scan (involves consuming a radioactive meal to follow where it goes), they found that at 2 hours, the speed eater emptied only 25% of the meal from the stomach at 2 hours vs 75% for the control.  This suggests that this speed eater (possibly all are like this but it needs to be tested) has an increased ability to store water in the stomach rather than an increased ability to empty it into the intestines. 

 The next test for the subjects was to eat as many hot dogs as possible during a 12 minute period, and this was tracked by fluoroscopy.  This produced some very cool images of the stomach filling as each ate (check the full text to see them).  The control subject consumed 7 hot dogs before he was uncomfortably full.  The fluoroscopic images showed no distention and little dilatation of the stomach and there was no outward difference in the appearance of his abdomen.  The speed eater, unlike the control showed mild distention and decreased peristalsis prior to eating.  He consumed 36 hot dogs in 10 minutes, and fluoroscopic images showed distention with little/no peristalsis.  They noted that the eater stated that he felt no sensation of satiety/fullness/bloating/discomfort, but because of “a small theoretic risk of gastric performation,” the test was ended with 2 minutes left.  The abdomen was extremely protruded.  This eater described a gradual flattening of the abdomen over several days after competitions, and during that time he consumed nothing.

Interestingly, the authors make comparisons to professional athletes in other sports after interviews with the speed eater:

…In effect, he was slowly able to overcome the usual checks and balances associated with eating by exercising extraordinary will power and self-discipline during his training, consuming more and more food when others wouldn’t be able to swallow another bite without feeling sick (as our control subject did). Only as a result of this prolonged and intensive training process was the speed eater gradually able to adapt his stomach until it could withstand the rigors and stresses of competitive speed eating. In that sense, a world-class speed eater requires the same level of will power, self-discipline, and commitment as any professional athletes honing their skills in gymnastics, track, or other athletic endeavors.

Even more interesting, is a comparison to:

…a predatory carnivore that periodically gorges itself on its kills, ingesting massive amounts of food for sustenance until it captures another prey days or even weeks later.

I never considered an evolutionary explanation before this.

Eaters seem to lose the ability to sense satiety with the dramatic alterations in gastric physiology.  However, many competitors are very fit and not overweight.  The authors noted that this man had to practice extreme self-discipline and willpower by measuring portions instead of relying on satiety signals.  But competitive eating is a relatively new “sport,” and competitors are young.  If they lose their self-control with age, their risk of obesity may be much higher than the general population.  I would also add that contents are often highly processed junk foods which may not provide sufficient micronutrient intakes.  Also of concern is that their stomaches may be permanently damaged by losing the ability to shrink to a normal size, the ability to peristalse or emptying solid food.  This could lead to neasea, vomiting, and the need for gastric surgery.  The authors suggest IFOCE perform follow ups in their athletes to assess risks. 

This WSJ blog about the study includes quotes from the authors that show they don’t think the risk of injury is as great as other sports, though.  As I quoted from the study before, no health problems have apparently been formally reported yet.  But it certainly deserves further study, and eaters should be aware of the evidence – or in this case lack of study to this point.

Reference

Levine MS, Spencer G, Alavi A, & Metz DC (2007). Competitive speed eating: truth and consequences. AJR. American journal of roentgenology, 189 (3), 681-6 PMID: 17715117

I posted previously about 2 studies that suggest dietary nitrate enhances some measures of performance.  Another by one of the same groups (Bailey et al.) reproduces these findings and further explores mechanisms.

For a background of the existing speculated mechanisms, see the last post.  This study used a different technique: Phosphorus-31 magnetic resonance spectroscopy (³¹P-MRS), which assesses muscle metabolism noninvasively.  They chose this to examine muscle phosphocreatine (PCr) concentration, ADP concentration, and pH, along with pulmonary VO2 dynamics (reflects oxygen consumption), to estimate total ATP turnover rates and which fuel sources contributed at what extent from PCr hydrolysis, glycolysis, and oxidative phosphorylation.  They speculated that nitrate would reduce the O2 cost of exercise like established previously, but intramuscular PCr degradation would also reduce, suggesting phosphate cost of force production would also decrease, without a pH change.  Because of a sparing effect of PCr concentration, high-intensity exercise should be prolonged.

7 healthy males were asked like the other studies to refrain from high nitrate foods during the study.  After some initial baseline testing which established work rates, they were randomly assigned, in a double-blind, crossover fashion, 6 days of 5.1 mmol/day nitrate (0.5 liter organic beetroot juice; same product as previous study) or a placebo (low-calorie black-currant juice cordial with negligible nitrate).  There was again a 10-day washout between the periods.  The authors noted that this study was performed before their first study was published, so the subjects did not know then that beetroot juice might be ergogenic.

On days 4 and 5 of 6 of the supplementation periods, step exercise tests from baseline to low and high-intensity work rates tested VO2 dynamics and muscle activity.  Day 4 included a high-intensity rate until failure.   EMG data among others (e.g. blood pressure) were taken as well.

On day 6, the testing protocol from day 4 was repeated while undergoing ³¹P-MRS.

The subjects reported beeturia and red stools corroborating other studies (a good sign they were consuming it as well I suppose).

Subjects consuming the beetroot juice had greater nitrite concentrations, as expected, as well as a significantly lower average systolic blood pressure. 

For both low and high-intensity exercises, muscle activity as measured by iEMG were not different between groups, nor was heart rate after exercise. 

Low-intensity exercise (knee extension)

Like the previous studies show, this one also found that the nitrate group had a 25% reduction in the increase in pulmonary VO2 from rest to low-intensity, and VO2 and the end of exercise was reduced. Resting was not different.  End of exercise CO2 production (VCO2) was not different. VE (pulmonary ventilation) was not different, suggesting along with heart rate that nitrate exerts its effects only on the skeletal muscle, not from an indrect reduction of energy cost of cardiorespiratory processes.  Resting energy expenditure had a small but insignificant increase in the nitrate group, which may suggest a shift in substrate utilization toward more carbohydrate use through NO-mediated glucose uptake in the skeletal muscle cells, but this will have to be further studied.  Work efficiency was also greater in the nitrate group. 

The nitrate group had a 36% reduction in the amplitude of PCr degradation, and phospate concentration accumulation was reduced by 21%.  The amplitude of ADP concentration was reduced, while pH was not different between the groups.

Here are the estimated ATP-derived fuel sources (white bars = nitrate group, grey = placebo).  Reductions in total ATP, oxidative phosphorylation-derived ATP, and PCr-derived ATP were statistically significant:

High-intensity exercise (knee extension)

Primary component VO2 amplitude had a tendency to be lower in the nitrate group, which is in contrast to the previous study with cycling.  This may be related to the intensity, specific exercise, or body positioning.  The amplitude of the slow component was reduced by 52%.  End of exercise VCO2 were not different.  Work efficiency was greater in the nitrate group.

The concentration of PCr slow component amplitude was reduced by 59% in the nitrate group.

Here are the estimated ATP-derived fuel sources (white bars = nitrate group, grey = placebo).  Reductions in total ATP, oxidative phosphorylation-derived ATP, and PCr-derived ATP were statistically significant (consistent with the low-intensity group):

Exercise Tolerance

There was a 25% increased time to failure in the nitrate group in the exercise tolerance tests (nitrate: 734 +/- 109 seconds vs. placebo: 586 +/- 80 seconds), with all 7 subjects improving.  This tended to be correlated to the PCr concentration remaining.

Conclusions

Again, nitrate reduced the oxygen cost of exercise (at both exercise intensities), but this study found that PCr degradation is also reduced during both low and high-intensity exercise without a change in muscle pH.  Total ATP was also reduced with nitrate.  These are consistent with the previous hypothesis that nitrate improves the efficiency of exercise through reducing the ATP cost of producing force.  The tolerance of high-intensity exercise may be maintained by the preservation of PCr concentrations by nitrate, supported by other research.

Regarding the ATP determinations, the authors note that these estimations use a number of assumptions and may be subject to error, but along with a reduction in the VO2 suggests that PCr and oxidative metabolism contributions were reduced, suggesting an increased efficiency in force production rather than an increased mitochondrial P/O ratio (ATP synthesis at a given oxygen consumption). 

Interestingly, they also note that evidence of altitude training improving submaximal endurance efficiency may support these results as people living at high altitudes have much greater concentrations of nitric oxide products, including nitrite, so this might reduce their energy cost of activity.

In all, much of this study corroborated their other, and it will be interesting to see what they look at next.

A final note: in the last post I noted a study on creatine supplementation that changed oxygen uptake kinetics.  I failed to notice the lead author Andrew Jones from that one is also involved in these studies.  With brief overviews the designs are very similar to these 2 nitrate studies (the first used cycling, and this used knee-extensor).  Creatine has been well established to be an ergogen, it seems it and nitrate may have some overlap in their mechanism.  I may investigate this in a future post and email Dr. Jones for his thoughts.

Cautious Interpretations

This is the 3rd study showing dietary nitrate may effect markers or tests of endurance performance.  However, each study is very small in subject numbers and requires replication in different contexts as well as larger studies.  Also, as stated in the other post, it remains to be directly tested if dietary nitrate can improve time to failure at submaximal exercise (e.g. long distance endurance), and the real world implications of improving time to failure at severe exercise is probably limited.  As noted by the authors, if the goal is sprinting (going from one point to another as fast as possible), the improvement would likely be much smaller.

Nevertheless, this is interesting stuff and important in a number of ways.

Reference

Bailey SJ, Fulford J, Vanhatalo A, Winyard PG, Blackwell JR, Dimenna FJ, Wilkerson DP, Benjamin N, & Jones AM (2010). Dietary nitrate supplementation enhances muscle contractile efficiency during knee-extensor exercise in humans. Journal of applied physiology (Bethesda, Md. : 1985) PMID: 20466802

As pointed out by Marion Nestle yesterday, the scientific review process and conclusions for the 2010 Dietary Guidelines are available online at the Nutrition Evidence Library, and it looks like a great resource to bookmark.

It displays the information in the following organizational format:

• Systematic review questions - Questions formulated by the Committee.
• Conclusion statements - Concise statements that answer the questions based on the Committee’s review of the evidence.
• Evidence summaries - Synthesis of the articles included in the NEL evidence-based systematic review, including evidence summary paragraphs for each article considered in the review and a summary overview table.
• Search plan and results - A description of the search parameters and selection criteria used to identify peer-reviewed literature related to the topic of interest. Additionally, the final list of articles included in the review is provided, along with the articles excluded from the review with reasons for exclusion.
• Worksheets – Comprehensive, templated evidence worksheets which summarize key evidence from each study and document the methodological appraisal of the study quality.

While I haven’t yet looked (and likely won’t post about) at the massive report by the Advisory Committee itself, I browsed through some of this and it looks very thorough and detailed.  Interpretations and which studies were considered could be debated, but it is great to have this information available for reference finding.  Even better is that the evidence in which the Dietary Guidelines is based on is more transparent than ever.

It would seem illogical that organic compounds are all more sustainable than synthetics, or vice versa.  The term “organic” has a health halo, biasing many people toward believing organic growing techniques are best for the environment.  I’ve already covered analyses suggesting that there isn’t enough evidence that suggests organic foods are better for your health, so is the higher cost justified by a lessened environmental impact?  Bahlai et al. just published a paper suggesting that the dichotomous classification of organic and conventional is not optimal for sustainability, we must evaluate pesticides individually.

According to the authors, sustainable agriculture programs put an emphasis on the development of organic and natural insecticides to control pests, with the assumption that they are safer on the environment compared to synthetics.  Public opinion also leans toward this assumption as well.  The various practices (organic, conventional, or integrated) have been studied producing different results on sustainability.  Differences in methodologies, practice classifications, and a number of other variables make it difficult to draw conclusions at this point.  Importantly, they note:

…each system is characterized by a suite of practices which are ideologically, rather than empirically defined, these systems are not mutually exclusive from each other, and vary from region to region depending on regulations. Because of these variations, generalizations about the overall sustainability of one system over another are never universal.

Organic farms do indeed (generally) use pesticides, they just aren’t synthetically made, while conventional farms can use both natural and synthetics.

This study focuses on soybean aphid, which is a major pest in North America.  The investigators chose 4 new “potential reduced risk” insecticides with the Agriculture and Agri-Food Canada, 2 synthetic and 2 natural (certified for organic crops in Canada).  2 synthetic controls (currently used) were also included:

First, lab tests studied toxicity of the pesticides against 2 species that help control aphid populations: Harmonia axyridis and Orius insidiosus, and found that the currently used synthetic pesticides were most toxic to the beneficial species compared to the 4 new ones.  Of these, the 2 organics were more toxic than than the synthetics.

Then, a 2 year, 5 site study examined efficacy and selectivity of target pests.  The organic pesticides had a lower efficacy than the synthetics at 1 and 2 weeks post-treatment.  Selectivity was greatest with both synthetics. Here are the graphs; the mineral oil and beauveria bassiana are the organic pesticides, compared to the new synthetic spirotetramat and flonicamid.

Going back to the first table, the net environmental impact was estimated as an Environmental Impact Quotient (EIQ), which is a ranking that incorporates MSDS data and application rate.  According to the EIQ-FUR (field use), the organic pesticides had a higher (in the case of the mineral oil, much higher) environmental impact compared to synthetics.  The authors mention some controversy about using EIQ compared to other ranking methods, but point out the inverse relationship they found between selectivity and EIQ in this study, supporting its use.

Conclusions

The synthetic pesticides studied here tend to be more sustainable compared to the organics.  The authors clearly favor integrated pest management systems over completely organic techniques:

Carefully designed integrated pest management systems are likely the best strategy for minimizing environmental impact of agriculture: where certified organic systems may reject the technology with the smallest environmental impact based on ideology, IPM maintains the flexibility to incorporate any strategy empirically determined to have the smallest impact.

This sounds most sensible to me:  we should study each pesticide using methods like this rather than making misguided generalizations about sustainability.  Indeed, the authors sum it up nicely:

… we reject the organic-conventional dichotomy and emphasize that, in order to optimize environmental sustainability, individual tactics must be evaluated for their environmental impact in the context of an integrated approach, and that policy decisions must be based on empirical data and objective risk-benefit analysis, not arbitrary classifications.

I do have to question whether measuring only efficacy and selectivity and making conclusions about sustainability is appropriate.  Hopefully future studies will measure other impacts.

Reference

Bahlai, C., Xue, Y., McCreary, C., Schaafsma, A., & Hallett, R. (2010). Choosing Organic Pesticides over Synthetic Pesticides May Not Effectively Mitigate Environmental Risk in Soybeans PLoS ONE, 5 (6) DOI: 10.1371/journal.pone.0011250