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Weight Loss and the Microbiome

September 16, 2017 7:10 pm / 4 Comments on Weight Loss and the Microbiome

1450 words

Last month I argued that there was more to weight loss than CI/CO. One of the culprits is a virus called Ad-36. Obese people are more likely to have Ad-36 antibodies in comparison to lean people, which implies that they have/had the virus and could be a part of the underlying cause of obesity. However, a paper was recently published that your stool can predict whether or not you can lose weight. This is due to how certain bacteria in the gut respond to different macronutrients ingested into the body.

ScienceDaily published an article a few days ago titled Your stools reveal whether you can lose weight. In the article, they describe the diets of the cohort, which followed 31 people, some followed the New Nordic Diet (NND), while others followed the Average Danish Diet (ADD) (Hjorth et al, 2017; I can’t find this study!! I’ll definitely edit this article after I read the full paper when it is available). So 31 people ate the NDD for 26 weeks, and lost 3.5 kg (7.72 pounds for those of us who use freedom numbers) while those who ate the ADD lost an average of 1.7 kg (3.75 pounds for those of us who use freedom numbers). So there was a 1.8 kg difference in pounds lost between the two diets. Why?

Here’s the thing: when people were divided by their microbiota, those who had a higher proportion of Prevotella to Bacteriodoites lost 3.5 more kg (7.72 pounds) in 26 weeks when they ate the NND in comparison to the ADD. Those who had a lower proportion of Prevotella to Bacteriodoites lost no additional weight on the NND. Overall, they say, about 50 percent of the population would benefit from the NND, while the rest of the population should diet and exercise until new measures are found.

The New Danish Diet is composed of grains, fruits, and vegetables. The diet worked for one-half of the population, but not for the other. The researchers state that people should try other diets and to exercise for weight loss while they study other measures. This is important to note: the same diet did not induce weight loss in a population; the culprit here is the individual microbiome.

Now that those Bacteroidotes have come up again, this quote from Allana Collen’s 2014 book 10% Human: How Your Body’s Microbes Hold the Key to Health and Happiness:

But before we get too excited about the potential for a cure for obesity, we need to know how it all works. What are these microbes doing that make us fat? Just as before, the microbiotas in Turnbaugh’s obese mice contained more Firmicutes and fewer Bacteroidetes, and they somehow seemed to enable the mice to extract more energy from their food. This detail undermines one of the core tenets of the obesity equation. Counting ‘calories-in’ is not as simple as keeping track of what a person eats. More accurately, it is the energy content of what a person absorbs. Turnbaugh calculated that the mice with the obese microbiota were collecting 2 per cent more calories from their food. For every 100 calories the lean mice extracted, the obese mice squeezed out 102.

Not much, perhaps, but over the course of a year or more, it adds up. Let’s take a woman of average height. 5 foot 4 inches, who weights 62 kg (9st 11 lb) and a healthy Body Mass Index (BMI: weight (kg) /(height (m)^2) of 23.5. She consumes 2000 calories per day, but with an ‘obese’ microbiota, her extra 2 per cent calorie extraction adds 40 more calories each day. Without expending extra energy, those further 40 calories per day should translate, in theory at least, to a 1.9 kg weight gain over a year. In ten years, that’s 19 kg, taking her weight to 81 kg (12 st 11 lb) and her BMI to an obese 30.7. All because of just 2 percent extra calories extracted from her food by her gut bacteria.

This corresponds with the NND/ADD study on weight loss… This proves that there is more than the simplistic CI/CO to weight loss, and that an individual’s microbiome/physiology definitely does matter in regards to weight loss. Clearly, to understand the population-wide problem of obesity we must understand the intricate relationship between the microbiome/brain/gut/body relationship and how it interacts with what we eat. Because evidence is mounting that the individual’s microbiome houses the key to weight loss/gain.

Exercise does not induce weight loss. A brand new RCT (randomized controlled trial) showed that in a cohort of children who were made to do HIIT (high-intensity interval training) did show better cardiorespiratory fitness, but there were no concomitant reductions in adiposity and bio blood markers (Dias et al, 2017). What this tells me is that people should exercise for health and that ‘high’ that comes along with it; if people exercise for weight loss they will be highly disappointed. Note, I am NOT saying to not exericse, I’m only saying to not have any unrealistic expectations that cardio will induce it, it won’t!

Bjornara et al (2016) showed that, when the NND was compared to the ADD, there was better adherence to the NND when compared to the ADD. Poulskin et al (2015) showed that the NND provided higher satisfaction, and body weight reduction with higher compliance with the NND and with physical activity (I disagree there, see above).

This study is important for our understanding of weight loss for the population as a whole. More recent evidence has shown that our microbiome and body clock work together to ‘pack on the pounds‘. This recent study found that the microbiome “regulate[s] lipid (fat) uptake and storage by hacking into and changing the function of the circadian clocks in the cells that line the gut.” The individual microbiome could induce weight gain, especially when they consume a Western diet, which of course is full of fat and sugar. One of the most important things they noticed is that mice without a microbiome fared much better on a high-fat diet.

The microbiome ‘talks’ to the gut lining. Germ-free mice were genetically unable to make NFIL3 in the cell lining of the gut. So germ-free mice lack a microbiome and lower than average production of NFIL3, meaning they take up and store fewer lipids than those with a microbiome.

So the main point about this study is the circadian rhythm. The body’s circadian clock recognizes the day/night system, which of course are linked to feeding times, which turn the body’s metabolism on and off. Cells are not directly exposed to light, but they capture light cues from visual and nervous systems, which then regulates gene expression. The gut’s circadian clock then regulates the expression of NFIL3 and the lipid metabolic machinery which is controlled NFIL3. So this study shows how the microbiome interacts with and impacts metabolism. This could also, as the authors state, explain how and why people who work nights and have shift-work disorder and the concurrent metabolic syndromes that come along with it.

In regards to the microbiome and weight loss, it is poorly understood at the moment (Conlon and Bird, 2015), though a recent systematic review showed that restrictive diets and bariatric surgery “reduce microbial abundance and promote changes in microbial composition that could have long-term detrimental effects on the colon.” They further state that “prebiotics might restore a healthy microbiome and reduce body fat“(Segenfrado et al, 2017). Wolf and Lorenz (2012) show that using “good” probiotic bacteria may induce changes in the obese phenotype. Bik (2015) states that learning more about the microbiome, dysbiosis (Carding et al, 2015), and how the microbiome interacts with our metabolism, brain, and physiology, then we can better treat those with obesity due to the dysbiosis of the microbiome. Clark et al (2012) show how the mechanisms behind the microbiota and obesity.

Weight loss is, clearly, more than CI/CO, and once we understand other mechanisms of weight loss/gain/regulation then we can better treat people with these metabolic syndromes that weirdly are all linked to each other. Diets affect the diversity of the microbiome, the diversity of the microbiome already there though, may need other macro/micro splits in order to show differing weight loss, in the case of the NND and ADD study reviewed above. Changes in weight do change the diversity of the microbiome of an individual, however, the heritable component of the microbiome may mean that some people need to eat different foods compared to others who have a different microbiome. Over time, new studies will show how and why the macro/micronutrient content matters for weight loss/gain.

Clearly, reducing the complex physiological process of weight gain/loss to numbers and ignoring the physiological process and how the microbiome induces weight gain/loss and works together with our other body’s cells. As the science grows here we will have a much greater understanding of our body’s weight loss mechanisms. Once we do that, then we can better help people with this disease.

Is Obesity Caused by a Virus?

August 12, 2017 10:33 pm / 6 Comments on Is Obesity Caused by a Virus?

2150 words

I’ve recently taken a large interest in the human microbiome and parasites and their relationship with how we behave. There are certain parasites that can and do have an effect on human behavior, and they also reduce or increase certain microbes, some of which are important for normal functioning. What I’m going to write may seem weird and counter-intuitive to the CI/CO (calories in/calories out) model, but once you understand how the diversity in the human mirobiome matters for energy acquisiton, then you’ll begin to understand how the microbiome contributes to the exploding obesity rate in the first world.

One of the books I’ve been reading about the human microbiome is 10% Human: How Your Body’s Microbes Hold the Key to Health and Happiness. P.h.D. in evolutionary biology Alanna Collen outlines how the microbiome has an effect on our health and how we behave. Though one of the most intriquing things I’ve read in the book so far is how there is a relationship with microbiome diversity, obesity and a virus.

Collen (2014: 69) writes:

But before we get too excited about the potential for a cure for obesity, we need to know how it all works. What are these microbes doing that make us fat? Just as before, the microbiotas in Turnbaugh’s obese mice contained more Firmicutes and fewer Bacteroidetes, and they somehow seemed to enable the mice to extract more energy from their food. This detail undermines one of the core tenets of the obesity equation. Counting ‘calories-in’ is not as simple as keeping track of what a person eats. More accurately, it is the energy content of what a person absorbs. Turnbaugh calculated that the mice with the obese microbiota were collecting 2 per cent more calories from their food. For every 100 calories the lean mice extracted, the obese mice squeezed out 102.

Not much, perhaps, but over the course of a year or more, it adds up. Let’s take a woman of average height. 5 foot 4 inches, who weights 62 kg (9st 11 lb) and a healthy Body Mass Index (BMI: weight (kg) /(height (m)^2) of 23.5. She consumes 2000 calories per day, but with an ‘obese’ microbiota, her extra 2 per cent calorie extraction adds 40 more calories each day. Without expending extra energy, those further 40 calories per day should translate, in theory at least, to a 1.9 kg weight gain over a year. In ten years, that’s 19 kg, taking her weight to 81 kg (12 st 11 lb) and her BMI to an obese 30.7. All because of just 2 percent extra calories extracted from her food by her gut bacteria.

Turnbaugh et al (2006) showed that differing microbiota contributes to differing amounts of weight gain. The obese microbiome does have a greater capacity to extract more energy out of the same amount of food in comparison to the lean microbiome. This implies that obese people would extract more energy eating the same food as a lean person—even if the so-called true caloric value on the package from a caloriometer says otherwise. How much energy we absorb from the food we consume comes down to genes, but not the genes you get from your parents; it matters which genes are turned on or off. Our microbes also control some of our genes to suit their own needs—driving us to do things that would benefit them.

Gut microbiota does influence gene expression (Krautkramer et al, 2016). This is something that behavioral geneticists and psychologists need to look into when attempting to explain human behavior, but that’s for another day. Fact of the matter is, where the energy that’s broken down from the food by the microbiome goes is dictated by genes; the expression of which is controlled by the microbiome. Certain microbiota have the ability to turn up production in certain genes that encourage more energy to be stored inside of the adipocite (Collen, 2014: 72). So the ‘obese’ microbiota, mentioned previously, has the ability to upregulate genes that control fat storage, forcing the body to extract more energy out of what is eaten.

Indian doctor Nikhil Dhurandhar set out to find out why he couldn’t cure his patients of obesity, they kept coming back to him again and again uncured. At the time, an infectious virus was wiping out chickens in India. Dhurandhar had family and friends who were veteraniarians who told him that the infected chickens were fat—with enlarged livers, shrunken thymus glands and a lot of fat. Dhurandhar then took chickens and injected them with the virus that supposedly induced the weight gain in the infected chickens, and discovered that the chickens injected with the virus were fatter than the chickens who were not injected with it (Collen, 2014: 56).

Dhurandhar, though, couldn’t continue his research into other causes for obesity in India, so he decided to relocate his family to America, as well as studing the underlying science behinnd obesity. He couldn’t find work in any labs in order to test his hypothesis that a virus was responsible for obesity, but right before he was about to give up and go back home, nutrional scientist Richard Atkinson offered him a job in his lab. Though, of course, they were not allowed to ship the chicken virus to America “since it might cause obesity after all” (Collen, 2014: 75), so they had to experiment with another virus, and that virus was called adenovirus 36—Ad-36 (Dhurandhar et al, 1997; Atkinson et al, 2005; Pasarica et al, 2006; Gabbert et al, 2010; Vander Wal et al, 2013; Berger et al, 2014; Pontiero and Gnessi, 2015; Zamrazilova et al. 2015).

Atkinson and Dhurandhar injected one group of chickens with the virus and had one control group. The infected chickens did indeed grow fatter than the ones who were not infected. However, there was a problem. Atkinson and Dhurandhar could not outright infect humans with Ad-36 and test them, so they did the next best thing: they tested their blood for Ad-36 antibodies. 30 percent of obese testees ended up having Ad-36 antibodies whereas only 11 percent of the lean testees had it (Collen, 2014: 77).

So, clearly, Ad-36 meddles with the body’s energy storage system. But we currently don’t know how much this virus contributes to the epidemic. This throws the CI/CO theory of obesity into dissarray, proving that stating that obesity is a ‘lifestyle disease’ is extremely reductionist and that other factors strongly influence the disease.

On the mechanisms of exactly how Ad-36 influences obesity:

The mechanism in which Ad-36 induces obesity is understood to be due to the viral gene, E4orf1, which infects the nucleus of host cells. E4orf1 turns on lipogenic (fat producing) enzymes and differentiation factors that cause increased triglyceride storage and differentiation of new adipocytes (fat cells) from pre-existing stem cells in fat tissue.

We can see that there is a large variation in how much energy is absorbed by looking at one overfeeding study. Bouchard et al (1990) fed 12 pairs of identical twins 1000 kcal a day over their TDEE, 6 days per week for 100 days. Each man ate about 84,000 kcal more than their bodies needed to maintain their previous weight. This should have translated over to exactly 24 pounds for each individual man in the study, but this did not turn out to be the case. Quoting Collen (2014: 78):

For starters, even the average amount the men gained was far less than maths dictates that it should have been, at 18 lb. But the individual gains betray the real failings of applying a mathematical rule to weight loss. The man who gained the least managed only 9 lb — just over a third of the predicted amount. And the twin who gained the most put on 29 lb — even more than expected. These values aren’t ’24 lb, more or less’, they are so far wide of the mark that using it even as a guide is purposeless.

This shows that, obviously, the composition of the individual microbiome contributes to how much energy is broken down in the food after it is consumed.

One of the most prominent microbes that shows a lean/obese difference is one called Akkermansia micinphilia. The less Akkermensia one has, the more likely they are to be obese. Akkermansia comprise about 4 percent of the whole microbiome in lean people, but they’re almost no where to be found in obese people. Akkermansia lives on the mucus lining of the stomach, which prevents the Akkermansia from crossing over into the blood. Further, people with a low amount of this bacterium are also more likely to have a thinner mucus layer in the gut and more lipopolysaccharides in the blood (Schneeberger et al, 2015). This one species of microbiota is responsible for dialing up gene activity which prevents LPS from crossing into the blood along with more mucus to live on. This is one example of the trillions of the bacteria in our microbiome’s ability to upregulate the expression of genes for their own benefit.

Everard et al (2013) showed that by supplementing the diets of a group of mice with Akkermensia, LPS levels dropped, their fat cells began creating new cells and their weight dropped. They conclude that the cause of the weight gain in the mice was due to increased LPS production which forced the fat cell to intake more energy and not use it.

There is evidence that obesity spreads in the same way that an epidemic does. Christakis and Fowler (2007) followed over 12000 people from 1971 to 2003. Their main conclusion was that the main predictor of weight gain for an individual was whether or not their closest loved one had become obese. One’s chance of becoming obese increased by a staggering 171 percent if they had a close friend who had become obese in the 32 year time period, whereas among twins, if one twin became obese there was a 40 percent chance that the co-twin would become obese and if one spouse became obese, the chance the other would become obese was 37 percent. This effect also did not hold for neighbors, so something else must be going in (i.e., it’s not the quality of the food in the neighborhood). Of course when obesogenic environments are spoken of, the main culprits are the spread of fast food restaurants and the like. But in regards to this study, that doesn’t seem to explain the shockingly high chance that people have to become obese if their closest loved ones did. What does?

There are, of course, the same old explanations such as sharing food, but by looking at it from a microbiome point of view, it can be seen that the microbiome can and does contribute to adult obesity—due in part to the effect on different viruses’ effects on our energy storage system, as described above. But I believe that introducing the hypothesis that we share microbes with eachother, which also drive obesity, should be an alternate or complimentary explanation.

As you can see, the closer one is with another person who becomes obese, the higher chance they have of also becoming obese. Close friends (and obviously couples) spend a lot of time around each other, in the same house, eating the same foods, using the same bathrooms, etc. Is it really an ‘out there’ to suggest that something like this may also contribute to the obesity epidemic? When taking into account some of the evidence reviewed here, I don’t think that such a hypothesis should be so easily discarded.

In sum, reducing obesity just to CI/CO is clearly erroneous, as it leaves out a whole slew of other explanatory theories/factors. Clearly, our microbiome has an effect on how much energy we extract from our food after we consume it. Certain viruses—such as Ad-36, an avian virus—influence the body’s energy storage, forcing the body to create no new fat cells as well as overcrowding the fat cells currently in the body with fat. That viruses and our diet can influence our microbiome—along with our microbiome influencing our diet—definitely needs to be studied more.

One good correlate of the microbiomes’/virsuses’ role in human obesity is that the closer one is to one who becomes obese, the more likely it is that the other person in the relationship will become obese. And since the chance increases the closer one is to who became obese, the explanation of gut microbes and how they break down our food and store energy becomes even more relevant. The trillions of bacteria in our guts may control our appetites (Norris, Molina, and Gewirtz, 2013; Alcock, Maley, and Atkipis, 2014), and do control our social behaviors (Foster, 2013; Galland, 2014).

So, clearly, to understand human behavior we must understand the gut microbiome and how it interacts with the brain and out behaviors and how and why it leads to obesity. Ad-36 is a great start with quite a bit of research into it; I await more research into how our microbiome and parasites/viruses control our behavior because the study of human behavior should now include the microbiome and parasites/viruses, since they have such a huge effect on eachother and us—their hosts—as a whole.

Microbial Intelligence and Intelligent Physiology

July 13, 2017 6:52 am / 3 Comments on Microbial Intelligence and Intelligent Physiology

1100 words

When organisms that we don’t normally signify as ‘intelligent’ do, indeed, show ‘intelligent’ behavior, our definition of the word—what we call ‘intelligent’ behavior—needs to be reevaluated. Bacteria and other microbes can certainly respond to cues from their environments and communicate with each other. So if bacteria can respond to environmental stimulus by having plastic behavior, then they do show a semblance of ‘intelligence’. Just because bacteria don’t talk doesn’t mean that they are not ‘intelligent’ in their own right.

Bacteria respond to cues from their environment, just like any other intelligent organism. That means that they have behavioral plasticity, the ability to change their behavior based on what occurs in their environments. Bacteria have been shown to exhibit behaviors we would call ‘intelligent’, i.e., acquiring information, storage, processing, use of information, perception, learning, memory, and decision-making (Lyon, 2015). It is proposed that “bacteria use their intracellular flexibility, involving signal transduction networks and genomic plasticity, to collectively maintain linguistic communication: self and shared interpretations of chemical cues, exchange of chemical messages (semantic) and dialogues (pragmatic)” (Jacob et al, 2004).

Clearly, bacteria can and do adapt at the phenotypic level, not only the genotypic level as some have asserted in the past. Using this definition of intelligence, that is, being able to perceive, process and integrate information about the state of the environment to change the organism’s behavior is intelligent behavior (Pinto and Mascher, 2016), all organisms, from bacteria to humans and in between are intelligent. If bacteria do show evidence of behavioral plasticity—and they do—then we must look at them as intelligent creatures, as well as come to the realization that all biological organisms are, in their own right, intelligent. Intelligence is not only for any ‘higher’ organisms; so-called ‘lower’ organisms do show behavioral plasticity, meaning they know what is occurring in their environment. Is that not intelligent?

Any organism that can immediately act in a different way when its environment changes can, in my opinion, be said to be intelligent. All biological organisms have this ability to ‘go off of their genetic coding’, if you will, and change their behavior to match what is currently going on in their environment. Furthermore, the number and fraction of single transduction genes can be used as a measure of ‘bacterial IQ’ (Sirota-Mahdi et al, 2010).

This, of course, has implications for our intelligent physiology. Since our physiological systems incorporate the intelligent processes of the intelligent cell, then, on a larger scale, our physiology is also intelligent. Our physiology is constantly responding to cues from the environment, attempting to maintain homeostasis. Since our body has a need to stay in homeostasis, then our physiological systems are indeed intelligent in their own right. They incorporate the processes of the intelligent cell; looking at our physiology in this way, we can see how and why these systems are intelligent.

Further, physiologists have been referring to physiological systems as “homeodynamic”, rather than “homeostatic”, seeing chaotic states as healthy “allowing organisms to respond to circumstances that vary rapidly and unpredictably, again balancing variation and optimization of order with impressive harmony” (Richardson, 2012). If our physiological systems can do this, are they not intelligent? Further, according to physiologist Dennis Noble, “Genes … are purely passive. DNA on its own does absolutely nothing until activated by the rest of the system through transcription factors, markers of one kind or another, interactions with the proteins. So on its own, DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” So, as you can see, genes are nothing without the intelligent physiology guiding then. This is only possible with physiological systems, and this begins with the intelligent cell—intelligent microbes.

Some people misunderstand what genes are for and what they do in the body. The gene has long been misunderstood. People don’t understand that genes direct the production of proteins. Since physiological systems—at their core—are run by microbes, then the overall physiological system is itself intelligent. Genes, on their own, are not the masters but the servants. Genes do code for proteins that code for traits, but not under their own direction; they are directed by intelligent systems.

Think of how our gut microbiome co-evolved with us. Knowing what we now know about intelligent cells, we can also say that, by proxy, our microbiome is intelligent as well.

Understanding intelligent cells will lead us to understand intelligent physiology then, in turn, lead us to understand how genes are the servants—not the masters as is commonly asserted—of our traits. Physiology is an intelligent system, and since it is intelligent it can then react to cues from the environment, since it is made up of smaller cells, which make up the larger whole of the intelligent physiological system. These intelligent systems that we have evolved are due to the changeability of our environments in our ancestral past. Our physiology then evolved to be homeodynamic, attempting to maintain certain processes. The ever-changing environment that our genus evolved in is the cause for our homeodynamic intelligent physiology, which begins at the smallest levels of the cell.

The intelligent microbes are the smaller part of the larger whole of the intelligent physiological system. Due to this, we can say that at the smallest levels, we are driven by infinitesimally small microbes, which, in a way, guide our behavior. This can definitely be said for our gut microbiome which evolved with us throughout our evolutionary history. Our microbiome, for instance, had to be intelligent and communicate with each other to maintain our normal functioning. Without these intelligent cells, intelligent physiology would not be possible. Without ever-changing dynamic environments, our intelligent physiology and intelligent cells would have never evolved.

Intelligent physiology evolved due to the constant changeability of the new environments that our ancestors found themselves in. If we would have evolved in, say, more stable, unchanging environments, our physiological systems would have never evolved how they did. These intelligent physiological systems can buffer large ranges of physiological deficiencies. The evolvability of these systems due to the changeability of our ancestral environments is the cause of our amazing physiological intelligence, developmental plasticity, and microbial intelligence.

When you think about conception, when a baby is forming in the womb, it becomes easier to see how our physiological systems are intelligent, and how genes are the slaves—not masters—of our development. Intelligence is already in those little cells, it just needs an intelligent physiology for things to be set into motion. This all goes back to the intelligent cells which make up the larger part of intelligent physiology.

Our View of ‘Intelligence’ Needs to Change

June 12, 2017 6:59 am / 2 Comments on Our View of ‘Intelligence’ Needs to Change

900 words

What is intelligence? How would we define it? Would intelligence be reacting to what occurs in the immediate environment; having the ability to have behavioral plasticity or even communicating with others? Amazingly, bacteria have been found to do both things noted above: They have been found to be able to react to their environment, i.e., have the ability for plastic behavior and they have even been shown to communicate with one another. Hell, even something as simple as a slime mold has been found to navigate a maze to find food. Is that not intelligence?

Ken Richardson, author of the book Genes, Brains, and Human Potential: The Science and Ideology Behind Intelligence writes:

Living things, then, need to be good at registering those statistical patterns across everyday experience and then use them to shape the best response, including (in the cell) what genes to recruit for desired products. This is what intelligence is, and it’s origins coincide with the origins of life itself, and life is intelligence. (Richardson, 2017: 115)

In multicelluar systems, of course, the cells are not just responding to one another, but also collectively to the changing environment outside. That requires an intelligent physiology, as described in chapter 5. However, it is still the statistical structure of the changes that matters and that forms the basis of a living intelligence. Even at this level, closest to the genes, then, the environment is emphatically not a loose collection of independent factors to which the cells respond, in stimulus-response fashion, under gene control. This reality makes the additive statistical models of the behavioral geneticist quite unrealistic. (Richardson, 2017: 120)

Currently, our view of intelligence has an anthropometric lean. But, as I’ve been saying for months now, why should we view humans as a sort of ‘apex’ to evolution? Why should we be the measuring stick? If you really think about it to put us—our brains—at the top of a rank order as ‘the best’ and not recognize what other, smaller supposedly ‘archaic’ forms of life can do, then maybe it’s best to take off our human-centric glasses and look at the whole of the animal kingdom as intelligent—including bacteria, as they show the basic things necessary for what we would call intelligence, i.e., behavioral plasticity.

In this paper published just two months ago, the authors write:

Bacteria are far more intelligent than we can think of. They adopt different survival strategies to make their life comfortable. Researches on bacterial communication to date suggest that bacteria can communicate with each other using chemical signaling molecules as well as using ion channel mediated electrical signaling. (Majumdar and Pal, 2017)

Furthermore, looking at definitions of the term ‘behavior’ from ethology, we can see that bacteria exhibit these behaviors that we have deemed ‘human’ or ‘human-like’:

“Externally visible activity of an animal, in which a coordinated pattern of sensory, motor and associated neural activity responds to changing external or internal conditions” (Beck et al. 1981)

“A response to external and internal stimuli, following integration of sensory, neural, endocrine, and effector components. Behavior has a genetic basis, hence is subject to natural selection, and it commonly can be modified through experience” (Starr and Taggart 1992)

“Observable activity of an organism; anything an organism does that involves action and/or response to stimulation” (Wallace et al. 1991)

“What an animal does” (Raven and Johnson 1989)

Bacteria have been found to fit all of the criteria mentioned above. If organisms can react to how the environment changes, then that organism has—at least a semblance—of intelligence. Bacteria have also been found to be able to learn and they also have memories, so if this is true (and it is), then bacteria are intelligent.

Finally, Westerhoff et al (2014) write that leaving out the terms ‘human’ and our brains as measuring sticks for what is intelligent, that “all forms of life – from microbes to humans – exhibit some or all characteristics consistent with “intelligence.” For people with anthropocentric views of evolution, however, this is a hard pill to swallow. If the data says that bacteria have evidence of ‘cognition’ and an ability to react to outside environmental cues then bacteria have a semblance of intelligence. There is no denying it.

We clearly need to look at intelligence in a different way—one that’s free of any anthropocentric bias—-and if we do, we would recognize numerous species as intelligent that we would never have thought of before since we view ourselves as some sort of ‘apex’ of evolution, that we are supreme on this earth, when the bacteria—the modal bacter—reign supreme and will continue to remain supreme until the Sun explodes. So if bacteria show the ability to communicate with one another and the ability to change their behavior when their environment changes, i.e., that they learn and have ‘memories’ of past events, then maybe it’s time for us to change from our human-centric view of intelligence (which makes a ton of sense; viewing us as an ‘apex’ of evolution makes no sense and doesn’t allow us to appreciate the wide range of variation on earth).

As Gould wrote in Full House, looking at only the right tail we would believe that some sort of ‘progress’ reigns supreme, but looking at the whole sum of variation, we can see that the bacteria are the mode of all life, have been the mode of all life and will remain the mode of all life until the Sun explodes and all life forever perishes from Earth.