Sugar!

    

          This New Year, I resolved to eat less refined sugar. If you have been paying attention to the news lately, you may have heard that sugar is our new enemy, supplanting fat.  Sugar has been implicated in the obesity epidemic and the rise of type 2 diabetes diagnoses, and also may negatively affect cardiovascular health.  What are the main sources of sugar in our diets and how can we reduce our sugar intake?  Read on to find out the low down on sugar and also a recipe for those special occasions when you are really craving something sweet.

 Many foods naturally contain sugars.  For example, fructose, the sweetest of the sugars, is found in many types of fruit, and lactose is abundant in dairy products.  A well-balanced, healthy diet can include both fruit and milk products.  Where we get into trouble with sugar is when its supplemented in foods.  Added sweeteners amount to roughly 22 teaspoons (or 350 calories) of extra sugar per day for the average American according to the USDA’s Economic Research Service.   These calories provide no nutrients besides energy to your body.   When energy is not presently needed, it is stored for later use, and thus consuming excess sugar over time leads to weight gain.   

Processed foods are the most common source of added sugar for the average American.  Food manufacturers have figured out that sweetening their products makes them more delectable and stimulates our brain reward systems to keep us coming back for more.  Added sugar sneaks into foods like pizza, bread, soup, fruit juice, spaghetti sauce, hot dogs, ketchup, salad dressing, flavored yogurts, mayonnaise, and even peanut butter.  The food’s ingredient list will not necessarily use the word “sugar,” but instead a more disguised term.  If you are concerned about your added sugar intake, here is a list of ingredients to look for:

Agave nectar	Evaporated cane juice	Maltose
Brown sugar	Fructose	Malt syrup
Cane sugar	Fruit juice concentrates	Maple syrup
Corn sweetener	Glucose	Molasses
Corn syrup	High fructose corn syrup	Raw sugar
Crystalline fructose	Honey	Sucrose
Dextrose	Invert sugar	Syrup

Perhaps the most notorious of the list above is high fructose corn syrup (HFCS).  HFCS is a liquid sweetener added to many foods and in particular soft drinks.  HFCS has replaced sucrose (table sugar) as the food industry’s sweetener of choice due to its liquid properties that make it extremely amenable to adding to processed foods.  Furthermore HFCS is derived from corn, a crop abundantly produced in the American Midwest.  In contrast, sucrose is isolated from tropical plants that are imported into the US.  Sugar cane and beets are the common sources of sucrose, whereas HFCS is made by enzymatically treating corn syrup to increase its fructose content.  In 2004, Bray et al. hypothesized that the increased use of HFCS in foods was linked to the rise of obesity in the US.  This article sparked a heated debate over the use of this sweetener, which has resulted in a vehement backlash against HFCS.  Many food companies have switched back to sucrose, and even the Corn Refiners Association tried to change the name of HFCS to “corn sugar,’ but the FDA denied their petition.  Is HFCS really worse for us than sucrose?

Despite the fact that HFCS and sucrose have different origins, they both contain roughly 50:50 glucose to fructose, although HFCS additionally contains water and some larger sugars. Of the two main components, glucose is the most ubiquitous (natural) form of sugar that is used in numerous cell types for energy in organisms ranging from bacteria to humans. The breakdown of fructose also produces energy, but in humans is mainly localized in the liver.  In addition to providing energy, fructose and glucose can be converted to molecules that store energy, or are eventually used to form amino acids (the building blocks of proteins) and fats.  Fructose metabolism bypasses some of the regulatory controls that are applied to glucose, which may lead to an increase in triglycerides (fats) released into the bloodstream.  This observation has led scientists to hypothesize that increased fructose consumption may contribute to obesity, among other diseases.  However, the role of fructose in the development of obesity, diabetes, cardiovascular disease, and fatty liver disease is a topic of considerable debate in the scientific community (see review papers in the references).  Many of the studies that support these findings have been criticized for using extreme fructose doses, animal models that do not translate well to human metabolism, or are based on epidemiological studies that show association, but not direct causation.  Given that HFCS and sucrose both contain a considerable amount of fructose, they should be consumed in moderation until the role of fructose in human health is further elucidated.

         It is not surprising that sugar is the newest scapegoat for our health problems.  In the 1980s, fat was demonized, which resulted in adding sugar to low- and nonfat foods in order to make them more palatable.  In another few decades, another food will likely be singled out.   The lesson we need to learn is that biochemistry is extremely complicated.  No matter how hard we wish that there was a single magic solution to all of our weight and health problems, our bodies are too complex for it to be that simple.  Instead, maybe we should follow Michael Pollan’s advice in Food Rules: An Eater’s Manual, “Eat food.  Not too much.  Mostly plants.”  A balanced, primarily plant-based diet combined with exercise has proven to help many people improve their health.  The hardest part is changing our habits, precisely what a good proportion of Americans pledge to do every New Year.  So here’s to sticking to New Year’s resolutions!

However, I know myself. I will not be able to completely eliminate refined sugar from my diet.  In this respect, Rules 60 and 64 in Pollan’s book are also applicable, “60. Treat treats as treats.” and “64.  Break the rules once in a while.”  Pollan argues that if you are craving a “special occasion food,” like dessert, you should make it yourself as you would be unlikely to bake a cake or cookies every day, but you could easily buy them at the store.  And if you are really craving sugar, then eat it!  When I want to satisfy my sweet tooth, I like to make my sister Jill’s chocolate chip cookies, for which you will find the recipe below.  Be warned, once you start eating them, its difficult to stop!

Jill’s Chocolate Chip Cookies

Makes 12-24 cookies, depending on how large you make them.

1 stick unsalted butter

⅓ c brown sugar

⅓ c white sugar

1 egg

½ tsp vanilla

1 ¼ c flour

½ tsp baking soda

pinch of salt

chocolate chips

love (Jill says its the secret ingredient)

Preheat oven to 375 deg F.  

In a large bowl, mix the butter and sugars until fluffy (a wooden spoon works well).  Add the egg and vanilla and stir until just combined.  Then add the flour, baking soda, and pinch of salt.  Mix until all of the dry ingredients are just about incorporated, and then add chocolate chips to your liking.  If you want fluffier cookies, place the dough in the refrigerator for about 15 minutes.  Roll the dough into quarter-sized balls and bake for 10 minutes, or until golden brown.  Cool on a wire rack and enjoy!

Further Reading

Reviews of Sucrose and Fructose and Their Effects on Human Health

Sun SZ and Empie MW. Fructose metabolism in humans - what isotopic tracer studies tell us. Nutr Metab (Lond) 2012. 9: 89.

Rippe JM.   The metabolic and endocrine response and health implications of consuming sugar-sweetened beverages: findings from recent randomized controlled trials. Adv Nutr 2013. 4: 677-686

 

White JS. Challenging the fructose hypothesis: new perspectives on fructose consumption and metabolism. Adv Nutr 2013. 4: 246-256

van Buul VJ, Tappy L, Brouns FJPH. Misconceptions about fructose-containing sugars and their role in the obesity epidemic. Nutr Res Rev 2014. 27: 119-130

White JS. Straight talk about high-fructose corn syrup: what it is and what it ain't. Am J Clin Nutr 2008. 88: 17165-17215

Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010. 90: 23-46

 

Nice Article on Sugar in The Atlantic

Hamblin J. "Being happy with sugar." The Atlantic 05 Jun. 2014

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