By Julita Baker, PHD

In part one of “The Microbiome and Health” series, we learned what a microbiome is, the collection of microorganisms that inhabit our digestive system, and discovered how we initially acquire our individual microbiome. We learned that our initial exposure happens at birth, and that we then build on this bacterial ecosystem with increased exposure to different foods, environments, people, and lifestyle factors. We also learned that our microbiome is linked to almost every part of our health.

 So, what is it about these little critters that’s so important? Has our microbiome changed over evolution? And, which parts of health and disease do our microbes influence exactly (and why is that important)? That is what we are going to focus on here, in part II.

Why the microbiome is important

Symbiosis. 

We co-evolved with these microorganisms. Our health is dependent on them. Their health is dependent on us (and what we eat and are exposed to). 

For example, germ free mice (mice born in a completely sterile environment and hence no exposure to bacteria) don’t have a properly developed immune system. Now, clearly we can’t replicate a sterile environment like this in humans (or can we? How would that even be possible?), but we do know that our microbiomes help to develop our immune system. 

These microbes help in everything from our physiological systems such as glucose regulation, to helping us make more vitamins and minerals, to even determining what kind of psychological state we will be in (here’s one example: Specific microbiome linked with depression)

But, let’s focus on one aspect: glucose management, which is a critical part of our everyday life.

We know managing our glucose is important. Diseases such as obesity, prediabetes, type 2 diabetes, non alcoholic fatty liver disease (NAFLD), are all associated with chronically impaired glucose control. So having balanced glucose is key. 

One of the best examples of how important the microbiome is in glucose homeostasis is a study that was done a few years ago by David Zeevi and colleagues from Tel Aviv University. 

Zeevi examined the postprandial (after eating the food) glucose responses of different foods in 800 individuals (this large number is important in a study, because the more people you can examine, the more statistical power the study has). 

What Zeevi found was that a carbohydrate type and amount did not necessarily equate to the same glucose responses in different people (glucose responses that we might expect). What does that mean?

One person eating a banana and having a low glucose response, did not necessarily mean someone else had a low glucose response. Similarly, a person eating a cookie and having a high glucose reading, did not mean their neighbor would have the same high response. That person might in fact have a LOW reading following consumption of that cookie! 

Even more interestingly, researchers found that this response was dependent on the types of microbes living in each person’s digestive system. 

So the unique bacteria in your body, and in your gut, may directly influence whether you’ll have a high or low glucose reading after eating different foods! 

What does this mean for our health? 

So, what does it mean that different people will see different glucose readings after they eat the same foods as someone else? How can knowing this help us make more educated nutritional choices? 

1. Since we have very individual glucose responses what may be a “high glycemic food” for one person may not be for another. So, this research directly puts into question the idea of “high” or “low” glycemic foods and, therefore, their healthy/unhealthy attributes.

2. The amount of carbohydrates you eat does not necessarily equate to a high glucose response. So the idea of “glycemic load, which is the estimate of how much a specific food will raise your blood glucose after consumption, may be inaccurate. Glycemic load would suggest that the amount of carbohydrates is more important to increasing blood glucose levels than the specific carbohydrate you consume. So, once you know what carbohydrates work for you and your individual physiology, go ahead and have another piece of that potato or a second serving of that rice. Just consuming more won’t necessarily increase your glucose response.

3. There is no ONE diet that is right for everyone. We need individualization and personalization to reach better health. Individualization and personalization can be achieved through better understanding your own unique biomarkers and responses to the foods you eat, your environment and the activity level you keep.

    

200,000 year old co-evolution

So, the way your body responds to the foods you eat, is one example of how our microbiome contributes to our health. But, are they always helpful? Can these tiny little microbes also hurt us?

Species-rich ecosystem is needed for better health

Think about the microbes in your gut as an ecosystem; a rainforest. With optimal health, the rainforest is lush, it’s dense, it’s green, and all of the organisms within work together to keep it alive and flourishing. When you have great diversity in this ecosystem, with lots of the right species, they all support each other in a symbiotic relationship and help each other thrive.

This species-rich gut ecosystem is stronger against environmental influences (say you eat a bad piece of chicken, for example), because the “good” microbes in this metaphorically “lush” and “green” ecosystem can compensate for the possible negative effects of “bad” bacteria that make us sick (1).

Compare this to an ecosystem that is barren, doesn’t have many species of bacteria, and doesn’t have diversity in different microbes. Imagine a landscape with nothing.

This “barren” landscape, with lower bacterial diversity, and lower amounts of healthy strains of microbes, is typically associated with disease states. 

For example, decreased bacterial diversity has been observed in people with inflammatory bowel disease, arthritis, type 1 and type 2 diabetes, eczema, celiac disease, obesity, and arterial stiffness, compared to healthy controls (4). And, there are many, many other examples of how much our microbiome influences health and disease.

Why is this decrease in diversity and healthy strains happening? 

According to Justin and Erica Sonnenburg, researchers from Stanford University, 4 factors have changed in our society that may have contributed to this decrease in healthy strains and decrease in healthy diversity:

1. Consumption of processed foods 

2. Antibiotic use

3. C-sections 

4. Decreases in breast feeding

While these four points are not a comprehensive list, they do account for the main differences. And fixing even just one of these to attain better health is a definite possibility. But how exactly do we do that? What do we eat? What environments do we expose ourselves to? And, what lifestyle factors do we incorporate to integrate healthy strains of bacteria and get rid of bad ones?

In part three of this series, we will discuss how exactly we can do that. How we can flourish these optimal strains and great diversity of microbes to create this “lush” bacterial ecosystem.

References:

1. https://www.amazon.com/Good-Gut-Taking-Control-Long-term-ebook/dp/B00OZ0TOV2

2. J. Yang et al., “Landscapes of bacterial and metabolic signatures and their interaction in major depressive disorders,” Science Advances, 6:eaba8555, 2020.

3. https://www.sciencedirect.com/science/article/pii/S0092867415014816.  David Zeevi, Tal Korem, Niv Zmora, David Israeli, Daphna Rothschild, Adina Weinberger, Orly Ben-Yacov, Dar Lador, Tali Avnit-Sagi, Maya Lotan-Pompan, Jotham Suez, Jemal Ali Mahdi, Elad Matot, Gal Malka, Noa Kosower, Michal Rein, Gili Zilberman-Schapira, Lenka Dohnalová, Meirav Pevsner-Fischer, Rony Bikovsky, Zamir Halpern, Eran Elinav, Eran Segal. Personalized Nutrition by Prediction of Glycemic Responses, Cell, Volume 163, Issue 5, 2015, Pages 1079-1094

4. https://www.bmj.com/content/361/bmj.k2179. Valdes Ana M, Walter Jens, Segal Eran, Spector Tim D. Role of the gut microbiota in nutrition and health BMJ 2018; 361 :k2179

5. https://sonnenburglab.stanford.edu/