Plantains and Resistant Starch-Rich Foods Have More Health Benefits Than Just Keeping You Regular

Why do you need more plantains in your life, you ask?  Not only are they delicious, but they also contain a specific type of dietary fiber called resistant starch (RS).  RS has been a hot topic in research lately because it may protect against colon cancer, diabetes, and even help with weight management.  Additionally, RS provides food for your gut microbes, which in turn benefits your digestive tract.  In this post, I’ll tell you about what foods contain RS as well as leave you with a recipe so that you can add more plantains to your life.

Most people know to eat fiber when they are constipated, but what is fiber exactly?  Dietary fiber constitutes a family of compounds that originate from plants and are not digested by humans.  In 2002, the US Institute of Medicine added “functional fiber” to this family to designate the roughage that has health benefits in humans (1).  RS is not broken down in the stomach and absorbed in the small intestine, but instead it is fermented by the gut microbes in your colon.  The resulting compounds play a variety of beneficial roles, including providing energy to the cells that line your intestines.  Therefore RS is considered a type of functional fiber.  

There are five different types of resistant starch that differ by their 3-dimensional structures and/or their origin.  Most of the RS are created by nature and are found in starchy foods such as cereal grains or seeds (type 1), uncooked potatoes and green bananas (type 2), and cooked and cooled starches like rice (type 3).   Type 4 RS is artificially made by a chemical reaction and is mainly found in processed foods.  The last type of RS (type 5) is also au naturel, and is formed when fats stick to starch molecules to form complexes.  Below you will find a table summarizing the different types of RS and their common food sources.

           Microbial degradation of RS in your colon produces a number of compounds including gases (think farts) and short chain fatty acids (SCFAs).  The SCFAs acetate, proprionate, butyrate and valerate are used as fuel by your intestinal epithelial cells (2).  These compounds can influence the pH of the gut and thereby affect which microbes are present, as not all bacteria tolerate acid equally (3).  Only specific types of bacteria can degrade RS, so consuming this fiber also selects for the species that contain the proper enzymes.  By eating foods with RS, you are not only creating an environment that is preferential to specific beneficial bacteria, but these microbes will turn the fiber into molecules that help your gut.

Research has shown that the bacterial fermentation products of RS may help to protect against colorectal cancer.  Most of these studies used animal models or cells grown in a test tube to try to understand the mechanism of protection.  For example, the SCFA butyrate has antitumor properties in cell culture studies (4).  Although fewer studies have been performed in humans, scientists recently determined that RS supplementation to a diet high in red meat reduced markers of colorectal cancer (5).  Further research is needed in order to better understand how RS may protect against colon cancer, but the evidence is mounting that this functional fiber plays a role in maintaining colonic health.

RS may mitigate some of the risk factors associated with diabetes, and particularly type 2 diabetes.  Foods high in resistant starch often have a low glycemic index, meaning that they do not significantly elevate your blood glucose level.  This property is particularly important for people with type 2 diabetes because their disease inhibits their bodies’ ability to uptake glucose into their cells and therefore they should not consume foods that release large amounts of glucose.  Consuming foods high in RS may also help to reduce blood glucose levels in subsequent meals, as shown by a study in which consumption of high-amylose starch at breakfast reduced the glycemic response after eating a lunch with readably digestible starches (6). Therefore the benefits of eating foods high in RS may last beyond the meal in which it was consumed.

Even if you aren’t worried about colon cancer or diabetes, RS may help with weight management, which is a common goal in our society.  RS has a lower energy density than that of other carbohydrates and therefore when substituted into a diet, results in less calorie consumption.  Eating RS may make people feel more full, however, the evidence supporting this hypothesis is not very clear.  For example, one study fed its participants 25 g of type 3 resistant starch with breakfast and found no impact on calorie intake or satiety for the rest of the day (7).  In contrast, another group fed lean and overweight men and women either 20 or 30 g of a mixture of type 1, type 2, and viscous fiber in a smoothie with breakfast and found that the 30 g dose improved satiety until after lunchtime and decreased food intake at dinner (8).  Perhaps the differences in these results are due to the fact that different types of resistant starches were used.  Nonetheless, adding RS to your diet will benefit your health, but may not necessarily help you lose weight.

    

           So what foods contain resistant starch, you ask?  Check out the following table to find out:

           On a family trip to Belize last year,  I discovered a meal that is both high in resistant starch and delicious!  At a quaint outdoor cafe in Placencia, we were served the breakfast of the day: beans, rice, fried plantains, and two eggs.  If you were feeling spicy, you could sprinkle on one of their habanero hot sauces.  It was amazingly simple, but very satisfying and delicious.  I have been recreating the dish at home to stir memories of the Caribbean.  Here’s the recipe to try it out for yourself:

Beans & Rice with Fried Plantains and Eggs

Makes enough for 4-6 people

Ingredients

1 can black beans rinsed and drained (you can use any beans you desire)

2 c cooked rice (white or brown) and if you’re feeling fancy, add tomatoes and spices to your rice while cooking

2 very ripe plantains (to the point that they are almost completely black in color)

2 eggs/person

Several tbsp of your favorite cooking oil

Peel the plantains and slice them roughly ¼ inch thick.  Heat several tbsp of oil in a large skillet over medium low heat.  When the oil is warm, place the plantain slices in the skillet.  After several minutes, check to see whether they have browned.  If so, flip and cook until browned on the second side.  The plantains are properly cooked when they start to take on a translucent tint.  Remove the slices from the pan.  Repeat until all of the plantains are cooked.  Heat another few tbsp of oil in the skillet and add the beans and cooked rice.  Stir occasionally, and cook the beans and rice until heated through, then add the plantains back to the pan.  Turn heat to low until the food is ready to eat.

    In a separate apparatus, cook 2 eggs/person in your favorite fashion - scrambled, fried, over easy, etc.  

    Plate the eggs on top of the rice, beans, and plantain mixture.  Serve with your favorite hot sauce (preferably one of Marie Sharp’s Belizean products).  Enjoy!

References and Further Reading

1. “7 Dietary, Functional, and Total Fiber”. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). Washington, DC: The National Academies Press, 2005.
2. Macfarlane S, Macfarlane GT. Regulation of short-chain fatty acid production. 2003. Proc Nutr Soc 62:67–72
3. Lewis SJ, Heaton KW. Increasing butyrate concentration in the distal colon by accelerating intestinal transit. 1997. Gut 2:245-51
4. Fung KY, et al. A review of the potential mechanisms for the lowering of colorectal oncogenesis by butyrate. 2012. Br J Nutr 5:820-31
5. Humphreys KJ, et al. Dietary manipulation of oncogenic microRNA expression in human rectal mucosa: a randomized trial. 2014 Cancer Prev Res (Phila) 8:786-95
6. Brighenti F, et al. Colonic fermentation of indigestible carbohydrates contributes to the second-meal effect. 2006. Am J Clin Nutr 4:817-22
7. Klosterbuer AS, et al. Resistant starch and pullulan reduce postprandial glucose, insulin, and GLP-1, but have no effect on satiety in healthy humans. 2012. J Agric Food Chem 48:11928-34
8. Harrold J, et al. Satiety effects of a whole-grain fibre composite ingredient: reduced food intake and appetite ratings. 2014.  Food Funct 10:2574-81
9. Murphy MM, et al. Resistant starch intakes in the United States. 2008. J Am Diet Assoc 108:67–78.

Nice Review Papers on Resistant Starch  

Birt DF, et al. Resistant starch: promise for improving human health. 2013. Adv Nutr. 4:587-601. 

Raigond P, et al. Resistant starch in food: a review.  2014. J Sci Food Agric. doi: 10.1002/jsfa.6966

Do your food choices affect your gut microbes?

While chewing, do you ever stop to think about how the food you are consuming will affect your body?  Its probably more likely that you notice its aroma, flavor or texture.  Perhaps after the meal you register that you feel satiated, full, or even uncomfortably full.   I have always loved to eat -- growing up dinner was a time to connect with my family.  As an adult, I enjoy exploring new foods, for the sake of savoring the flavor of the food, and also how it makes me feel both physically and emotionally.  After becoming aware of the trillions of bacteria that live in my gut, I added a new dimension to my thoughts on eating -- will my microbes enjoy the food that I give them?  This realization led me to question how my food choices affect my microbial populations.  Do they change after every meal?  Or after a dramatic shift in dietary habits?  The answer, it turns out, is a combination of both of these options.

As I discussed in my last post, our guts are dominated by two main groups of bacteria - Bacteriodetes and Firmicutes, with smaller populations of Actinobacteria and Proteobacteria.  These larger populations of bacteria tend to vary little in a person over time.  For instance, my gut contains 71.5% Bacteriodes (from the phylum Bacteriodetes) and it is unlikely that any other group of bacteria will be able to outcompete these dominant microbes and take over.  Therefore researchers tend to refer to these abundant bacteria as our core microbiota, as they are common in many different people.

At roughly the age of 2, our gut microbial population resembles what it will look like for the rest of our lives in that we obtain our core microbes.  The makeup of our microbiota is defined by a number of factors - including our genes, environment, and diet. The factor that we possibly have the most control over is the food we put in our mouths.  Data is collecting that our microbial counterparts affect our health in both positive and negative manners.  Therefore when we think about “healthy” eating we should really expand our view to include how our food will affect our gut microbiota.  

A number of studies have shown that our core microbial populations are relatively stable over time despite changes in diet and season (a small sampling: 1-4).  For example, Wu et al asked participants about their short term (24 hour) and long term (1 year) diets to assess their average nutrient intake and then correlated this information with their measured populations of gut microbes (1).  They found that long term diet was associated with the type of core bacteria present: people who consumed more animal products had higher levels of Bacteriodes (phylum Bacteriodetes), whereas people ate more carbohydrates contained enriched Prevotella (phylum Bacteriodetes).  Another study followed the Hutterites, a traditional community, and how their gut microbiome changed with the seasons over the course of one year (2).   Davenport et al chose this population to remove the environment as a variable, as the Hutterites live on communal farms and share meals.  The authors found that the gut microbiome varied more between individuals than in a specific individual over time, suggesting that a person’s microbial population is relatively stable despite seasonal differences in food consumption.  These studies suggest that our long term dietary habits, for example how much fiber and fat we consume, are primarily responsible for shaping our personal microbial ecology.

Despite our long term gut microbiome stability, changes in dietary habits can result in rapid (albeit not drastic) effects on our microbial populations.  For instance, the Hutterite population mentioned above had a more diverse microbiota in the winter than in the summer.  This result is surprising as the main difference in the diet between these seasons was the consumption of more fresh produce in the summer, and the availability of fresh fruits and vegetables would lead to a more diverse diet and logically a more diverse microbiota.  However, these authors observed the opposite effect.  They postulated that the carbohydrate fermenting bacteria might dominate the gut ecosystem when the community consumes the summer diet.

Wu et al also assessed the short term effects of diet on the gut microbiota, albeit on a very small sample size.  They isolated 10 people in a hospital and gave them either a high fat/low fiber or low fat/high fiber diet for 10 days, monitoring their gut microbes along the way.  After 24 hours, all of the subjects’ microbiomes changed regardless of which diet they consumed!  However, the changes observed were significant within an individual, but not large enough to say change one person’s microbiota into another’s.

Another study tested how shifting from an omnivore to a strictly plant- or animal-based diet affected an individual’s gut microbial population (5).  David et al found that the switch to a wholly animal-based diet more dramatically changed the gut microbes than ingesting  only plant-based foods. Interestingly, this change occurred within the first 24 hours of consuming only animal products.  This same study also determined whether bacteria associated with plant- and animal-based foods are transferred to the human gut.  The researchers found bacteria associated with fermented foods (cheese and salami) or with genes derived from chloroplasts (plant organelles) in the feces of both the animal- and plant-eating subjects, with the type of genes observed corresponding to the respective dietary source.  This finding suggests that you can obtain probiotics (or their genes) from fermented foods.   However, this study did not address whether these bacteria will permanently colonize the human gut.

Even though the types of core bacteria might not change in your gut much over the long term, what they are doing can be directly modified by the food you eat.  Bacteria are highly adaptable and can swap genes with each other.  For example, a recent study showed that the gut bacteria of Japanese individuals gained the ability to breakdown seaweed.  The genes responsible for this activity were transmitted from marine bacteria that live on seaweed (6) (a benefit of eating raw food!).  In other words, the gut microbes of these people adapted to a diet that includes raw seaweed by sharing genes with the organisms that consume seaweed in the ocean.  So by consuming more raw and fermented foods, you may be transferring genes to your gut microbes to help you break down the ingredients of the respective fermented food.  So the next time you eat sauerkraut, think about how you may be enabling your gut microbes to more efficiently break down cabbage.

So what is the take home message from all of these studies?  Your diet affects which microbes colonize your gut and these microbes have the potential to modulate your health.  In the short term, the microbial populations are constantly shifting in response to your daily food intake.  Changing your microbes in the long term, however, would probably require a lifestyle change - eg becoming a carnivore, vegetarian or vegan.  So next time you decide what to eat for dinner, stop and think about how your food might affect your microbes.  What do they like to eat, you ask?  Stay tuned for the next post….

References

1.  Wu, G. D. et al. Linking long-term dietary patterns with gut microbial enterotypes. 2011

Science 334: 105–108

2.  Davenport, E.R. et al. Seasonal variation in human gut microbiome composition. 2014. PLOS ONE 9: e90731

3.  Louis, P. et al. Understanding the effects of diet on bacterial metabolism in the large intestine.  2007. J. App. Microbiol. 102: 1197-208

4.  Faith, J.J. et al. The long-term stability of the human gut microbiota. 2013. Science 341: 1237439

5.  David, L.A. et al. Diet rapidly and reproducibly alters the human gut microbiome. 2014. Nature. 505: 559-563

6. Hehemann, J.-H. et al. Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. 2010 Nature 464: 908– 912

What can you learn from your poo?

I delivered the bad news to my husband on Christmas morning, “Oh no! You have the bad gut microbes!”  Back in June, we sent stool samples to the American Gut project, and we happened to receive our results just in time for the holidays.  My proclamation stemmed from my knowledge of several high profile scientific papers, which found that a higher ratio of a specific group of bacteria correlates with obesity (1-3).  Kevin’s gut is dominated by these same bacteria.  Upon further reading, however, I discovered another more comprehensive study of lean and obese people that found no signature pattern of gut microbes (4).  I realized that although it is incredibly interesting to learn which microbes live inside of us, this science is still too young to jump to any definitive conclusions.  Determining which bacteria inhabit our bodies is the first step in understanding how these organisms influence our health, and  participating in studies such as American Gut will help to collect information such that in the future we may be able to make health recommendations based on our microbial populations.

        Gut microbes?  By now you may have heard that bacteria living on your body outnumber your own cells 10 to 1.  These bacteria both eat and excrete as part of their daily routine, so it is not difficult to imagine that these single-celled organisms affect our bodies’ physiology.  Currently, the microbes on our skin, in our mouths, genitalia, and guts are being characterized in hopes to better understand how they influence our health (for example, the Human Microbiome Project).  Most of these scientific studies focus on identifying which bacteria live on us.  With this information in hand, researchers can further analyze these microbes to determine their metabolic potential.  After cataloging who lives on us, the next questions involve categorizing what these bacteria are capable of metabolizing -- what molecules are they releasing, and how do these compounds affect our health?  But logically, we must first begin to understand “who” before we can most effectively answer “what” they are doing.

          In my quest to figure out who lives on me, I joined the American Gut project.  This study is interested in determining how your diet influences your microbial population.  Therefore before you send in your sample, you are instructed to keep a food journal for at least a week, which details everything you consume.  On the day you ship your sample, you fill out a detailed questionnaire including your daily percentage of calories from carbohydrates, protein, and fat as well as how many different species of plants you eat in any given week.  Several months later, you receive a poster in the mail that summarizes your results. 

    Here are some of the highlights of my gut microbes:

Humans are colonized by four main groups of bacteria - predominately Bacteriodetes and Firmicutes, with smaller populations of Actinobacteria and Proteobacteria.  These groups are referred to as phyla. If you remember from biology, all living organisms can be organized according to how closely they are related.  As you move down the scale of kingdom, phylum, class, order, family, genus, and species, the more genetically similar two living beings are.  For example, plants and animals are in different kingdoms, whereas humans share the same family with chimps, gorillas, and orangutans.  The plot above shows that my gut microbiota is dominated by the phylum Bacteriodetes.  In contrast, my husband contains mostly Firmicutes, which was surprising to me because we live together and eat basically the same food.  I also convinced my grandmother to participate in the study.  Interestingly, her gut is colonized with predominately Bacteriodetes, like me, which suggests that genetics may play a role in shaping our gut ecology.

        My most abundant microbe (71.5%!) is a subgroup of Bacteriodetes, the genus Bacteriodes.   This result is consistent with the finding by Wu et al. that consumption of saturated fat and animal protein increases these microbes (5).  I do not eat mammals, but I do consume plenty of dairy products, which are full of these nutrients.  This same study also showed that the genus Prevotella (phylum Bacteriodetes) is associated with diets rich in plant material and fiber, which unfortunately were not present in my stool despite the fact that I eat a lot of vegetables.  Bacteriodes, however, can also break down plant starches.  This example shows that although it is helpful to know which microbes live on me, it would be even more useful to know what metabolic functions my microbes possess and furthermore what my Bacteriodes are actually eating and excreting inside of my gut.

       Switching gears to some of my bacteria in different groups, my gut contains Faecalibacterium (phylum Firmicutes), whose presence is inversely correlated with gut inflammation, which is good (6). I also have an enriched population of Sutterella, which belong to the order Burkholderiales (phlyum Proteobacteria).  These bacteria may be enhanced on a diet that is high in cruciferous vegetables (broccoli, cauliflower, cabbage, etc) (7), which I do eat a lot of.  If specific vegetables enrich bacterial populations in our guts,  how stable is our gut ecology?  Does it change after every meal?  Or only after a dramatic shift in dietary habits?

        Diet influences our bacterial populations because what we put in our mouth ultimately selects for the type of bacteria that will thrive in our guts.  Nutrients that are not absorbed by our bodies provide fuel for our gut microbes.  Can we change our microbial landscape by changing our diet?  I’ll go into more detail on this topic next time, so stay tuned.

References:

1.  Ley RE, Bäckhed F, Turnbaugh P, Lozupone CA, Knight RD, et al. Obesity alters gut microbial ecology. 2005. Proceedings of the National Academy of Sciences, 102: 11070–11075.

2.  Ley RE, Turnbaugh PJ, Klein S, Gordon JI, et al. Microbial ecology: human gut microbes associated with obesity. 2006. Nature 444: 1022–1023.

3.  Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, et al. A core gut microbiome in obese and lean twins. 2009. Nature 457: 480–484.

4.  Finucane MM, Sharpton TJ, Laurent TJ, Pollard KS. A taxonomic signature of obesity in the microbiome? Getting to the guts of the matter. 2014 PLoS One 9:e84689

5.  Wu, G. D. et al. Linking long-term dietary patterns with gut microbial enterotypes. 2011

Science 334: 105–108

6. Willing, B. P. et al. A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes. 2010. Gastroenterology 139: 1844–1854

7.  Li, Fei; Hullar, Meredith A. J.; Schwarz, Yvonne; Lampe, Johanna W. Human Gut Bacterial Communities Are Altered by Addition of Cruciferous Vegetables to a Controlled Fruit- and Vegetable-Free Diet. 2009. Journal of Nutrition 139: 1685-1691