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The Ecology of Overnutrition

How Excessive Prosperity Alienate Friends and Attract Enemies

When you get more than your fair share of anything, biology puts a big target on your back to compensate.

In the previous section of this chapter I laid out the foundational arguments for why I believe that diseases connected to over-nutrition can’t be explained through mechanisms where nutrients are assumed to behave like toxins, and that in order to arrive at the right conclusion we need to put the problem into an ecological context.

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Because of our nature as holobionts, we are essentially walking planets or eco-systems where our individual endogenous cell-population is in minority even to fractions of our commensal microbial community, such as if “we” went to war with “them” we would actually be outnumbered, according to current estimates by about 1.3:1 when only counting bacteria, and depending on when we last emptied our bowels.1) If we added up the total number of microbes including fungi, viruses and phages this ratio would also probably be several orders of magnitude higher, and counting the ratio of human to microbial genes we are not only outnumbered but also out-gunned at an estimated ratio of 100:1.2) We would also have to consider the possibility of divided loyalties among our own, since some of our cellular organelles and a large part of the genes in our own DNA have a microbial origin.3) All these things considered, our chances of winning a war don’t look so good and if we don’t feel like going against the odds, betting everything on shear mass and size, it is probably in our best interest to avoid conflict and instead seek to keep peace, and to do that from a place of inferiority we need to be experts at managing relationships.

Relationships between organisms and between organisms and their environment are what defines ecology and they seem to function according to the same principles regardless of the level of analysis. For example what determines wether certain organisms make friends and form mutualistic coalitions or if they instead enters a state of conflict are roughly the same things weather you’re studying exclusively human relationships, or relationships between other organisms in varying environments, either from a distance or from behind a loupe or a microscope. This is because relationships between individual genetic replicators such as cells and viruses, which can both be considered to be the smallest units of analysis in biology, are what has formed the foundation for all existing forms of life, and since multicellular life builds on unicellular life this means that the will and behaviour of individuals cell must be sufficiently congruent with groups of cells, and then groups of cells with other groups, all being subjected to the same laws of nature and natural selection. Hence our behaviour both as individuals and groups is just a scaled up version of what goes on at a micro-level, so to a large part we act like giant cellular genetic replicators (consistent with Richard Dawkins “selfish gene-theory”). This consistency across all levels of magnification can then help us to decipher the practical meaning and significance of biological and ecological phenomenons that are observed at a micro-level, which are otherwise very difficult to interpret.

Unsurprisingly, for the same reason that deers clusters around meadows and humans around grocery-stores, restaurants and refrigerators, the majority of the microbes residing on our body-surfaces are located to the gastrointestinal tract, which is also mirrored by current estimations that about 70 % of our total population of immune-cells also take up residence there.5) This is why our dietary habits, trough mechanisms of both nutrition and immunology, are critical factors influencing the relationship we have with our commensal colonisers, which in turn are what determines our health as holobionts as we shall se further on in this section.

Gnotobiotic Studies

The easiest way to demonstrate how our relationships with microbes factors into the mechanisms that connects over-nutrition with pathology is by showing what happens if we try to factor them out. This have been done many times in studies where the commensal microbiome of test-animals is eliminated or reduced through sterile methods of fetal delivery or by antibiotic treatment respectively which then enables us to study the effects of different nutritional interventions without ecology interfering, or at least not interfering as much. These types of models are often called gnotobiotic, which means that the degree of microbial interference is more ore less known and/or controlled for. Most studies of this sort show that while normal mice fed an obesogenic diet gains both body- and liver-fat and become insulin resistant, mice that lack a commensal microbiome (to the degree in which this is possible), which are often referred to as being germ-free (GF), remain weight-stable without developing metabolic symptoms despite eating an identical diet and a similar amount of calories.6) Some studies also show that GF-mice voluntarily consume less of a diet that is provided ad-libitum when compared to colonised controls who gained weight and became insulin resistant while the GF-mice remained weight-stable and insulin-sensitive.7) Together this seems to suggest that nutrition is more effectively regulated in the GF state. Not only in terms of appetite, but also through postprandial mechanisms and as a result GF animals carry about 40% less body-fat compared with their colonised counterparts.8) 9)

Effects on Digestion and Absorption

The resistance shown by GF animals to develop common symptoms of metabolic dysfunction in response to over-nutrition is often thought to manifest because of impaired digestive efficiency, that it is just a result of less nutrients being available when digestion is not aided by microbes. This fits within the common perspective, but makes very little sense when considering that most of the diet-variants used to induce metabolic disease and obesity are hyper-refined, with the “active” ingredients that cause metabolic symptoms consisting mostly of disaccharides and triglycerides which are sufficiently processed by endogenous enzymes (which have also been shown to be present in comparable levels in GF and normal animals) to become available to the enterocytes for absorption.10)

Similar Capacity to Digest and Absorb Refined Diets

The most common form of carbohydrate in obesogenic rodent-diets is sucrose, and the enzyme that digests this molecule into absorbable glucose and fructose is actually present in higher levels in GF animals compared with colonised controls.11) While no data is available on fructose, the capacity for glucose absorption has been show to be normal in GF mice, and it also adapt (at least to some extent) reciprocally to increased dietary levels when animals are provided ad-libitum access to a liquid glucose-solution.12) Similarly, GF animals also seem to have a normal capacity for lipid-absorption in response to a large triglyceride bolus.14) However when studied for a period of a few weeks GF-mice do display inferior lipid-absorption compared with colonised mice, but this has been shown to be paralleled by a decrease in food-intake which is suggestive of an altered set point for negative feedback-regulation through increased satiety that also overrides the hedonic stimulus from the diet causing cessation of feeding, and if this truly was a consequence of a defect in digestion/absorption we would instead expect to see the reverse trend with an increase in food-intake in order to compensate.15) Regarding protein-metabolism, GF-mice actually have increased levels of proteolytic enzymes in their guts, presumably as a compensatory mechanism for lacking microbial digestive aid, but although they seem to assimilate less nitrogen from their diets compared with colonized controls, they have proven to be in relative positive nitrogen-balance, suggesting adequacy of diet and a lower turnover of endogenous amino-acids 16)

How Organisms Respond to Impaired Digestion

To get a sense of what happens when digestion is truly insufficient to an organism, and the subsequent behavioural consequences, we can turn to studies where the synthesis, release or function of bile-acids and digestive enzymes are inhibited. Mutant mice that lack the receptor for cholecystokinin (CCK), a hormone that triggers the release of bile and pancreatic enzymes into the small intestine show severely impaired digestion which is associated with a hyperphagic response leading to a 35% increase in food-intake and a similar increase in body-weight.18) Interestingly this impaired digestion also gave them symptoms consistent with type-2 diabetes mellitus (DM2). Similar results on food-intake are also observed when selectively blocking pancreatic enzymes and depending on the enzyme that is inhibited this also seem to affect food-preference away from the reciprocal macronutrient.19) 20) Insufficient secretion of pancreatic enzymes is actually often clinically termed type 3c diabetes (DM3c) as it has been shown to cause the same cardiovascular sequelae as type-1 diabetes (DM1) mellitus and DM2. This seems very counterintuitive at first glance, and even more so when considering that this impairment might actually precede endocrine pancreatic insufficiency, and that signs of co-morbid DM3c is found in about 40% of patients with DM1 and in 30% of those with DM2.21) A similar degree of hyperphagia as was shown in CCK-mutant mice is also displayed in GF mice relative to colonised mice but only when consuming a regular chow-diet (rich in polysaccharides), which results in a 30% higher level of food-intake without affecting bodyweight, but when consuming an obesogenic diet the reverse trend is instead observed with GF mice consuming less food and also excreting about 40% more fecal fat.23) This goes to prove the point that both apetite and postprandial regulation of nutrition is highly responsive to micro-ecological factors.

Nutrient-Deficits Can Cause “Sterile Obesity”

Since hyperphagia and also weight-gain can be triggered by insufficient digestion in normally colonised animals, presumably by creating a relative nutrient deficit then it could also be predicted that if GF mice were given a diet that rendered them deficient in critical nutrients this would in turn also render them susceptible to become obese if indeed the capacity for digestion and absorption is not truly a limiting factor. Conveniently, this has been demonstrated by study using two almost identical experimental diets, differing only in the source of dietary fat which was lard in the first diet and and palm-oil in the other, and the GF mice only became obese when consuming the latter diet. Palm-oil has a similar chemical composition as lard but it is critically low in cholesterol. Cholesterol is a non-essential nutrient, but when an animal is devoid of intestinal microbes less cholesterol is recycled back from bile in the intestinal lumen which is instead lost with feces and hence this renders them relatively cholesterol-deficient, necessitating increased rates of endogenous synthesis which is very metabolically expensive.25)

The Mechanism Mediating Obesity-Resistance in Response to High-Fat Diets

Regarding the mechanism behind the reduced levels of lipid-absorption (when it is observed in GF animals) some studies have published results that seem to suggest that this is at least partly the result of endogenously induced inhibition of digestion by desensitisation of CCK-action, and that this mechanism is disinhibited when heat-killed bacteria are co-administered with the diet.27) The anti-obesogenic effect of the germ-free state has also been shown to manifest in studies where absorption seems to be equal, measured as the amount of fecal calories excreted and excess energy is then burned of using thermogenic functions of perhaps futile nutrient-cycling-pathways.28) 29) Together this suggests that activated feedback-loops and postprandial compensatory mechanisms are responsible for the resistance to metabolic symptoms in GF animals, and that they may be overridden by signals of microbial competition showing that this resistance is indeed a function, not a defect.

Germ-Free Intestinal Histology is Suboptimal, but does Not Reflect Partial Starvation

Another interesting observation is that the hypertrophic and hypercellular intestinal phenotype that is seen with both over-feeding, caloric restriction and metabolic disease (discussed in the previous section) is not observed in GF mice which instead display the opposite phenotype with reduced cellularity and a thinning of the intestinal wall.30) The only active anatomical compensation that GF-mice seems to apply for their relatively less efficient digestion and absorption (disregarding the enlargement of the cecum, which is more a consequence of rather than an active compensation for decreased digestive efficiency 32) is minor increase in the length of the small and large intestines which is seen to progress in relation to increases in food intake triggered by successively lowered ambient temperatures (which necessitates an increased energetic turnover). However, there was no difference in the increase of (ad-libitum) food-intake between GF-mice and controls with different thermal conditions, indicating that GF-mice were able to sufficiently compensate for its relatively less efficient level of nutrient-assimilation.


Taken together, the data presented above suggests that the anti-obesogenic effect of the GF state in response to hyper-refined diets is the result of homeostatic regulation through both pre- and post-absorptive mechanisms rather than because of a true impairment in digestion and absorption that they cannot overcome.

The Therapeutic Effect of Hypo-caloric Diets, Fasting and Gastric Bypass Depend in Part on the Microbiome

Another argument against the notion of nutrient-toxicity being the mechanism by which diet cause metabolic disease is the observation that even the most commonly used therapeutic method for metabolic disease which is caloric restriction, don’t seam to work according to the toxicology-principle and the effect on body-weight and metabolic parameters are shown to be modulated by the gut-microbiome.33) Similar results have also been observed with intermittent fasting where weight-loss and transition to a more favourable metabolic profile occurs without a reduction in total caloric intake, both effects being dependent on the gut-microbiome.34) Studies on gastric bypass have shown that the effect of the procedure on weight-loss and metabolic parameters cannot be solely explained by reduced caloric intake or impaired digestion and has been shown to be transferable from obese human patients to germ-free mice. Mice who receive microbiome-transplants from pre-operative patients have been shown to gain more weight and presents a worse metabolic profile compared with those receiving transplants from post-operative patients independent of dietary quantity. 35)

Nutritional Physiology is Adapted for Competition

An intriguing thought is that the increased fecal energy-waste often displayed by GF animals when consuming refined diets is that it might be a voluntary action as a consequence of diminished competition for nutrients at the intestinal border which limits the need for their quick removal from the small-intestinal lumen. Both intake and absorption could then be better calibrated with the true nutritional needs of the host without also having to account for the potential danger in letting certain microbes grow too virulent on ingested and left-over nutrients. This can be compared to how nutrition works in a larger ecological scale, like if a predator repeatedly leave parts of his kills for later he risks having it taken by scavengers, causing them to increase in numbers over time which then complicates his existence further. It is hence more advantageous for him to stretch the borders of his appetite and (more) safely store the excess in his stomach and then as body-fat, but this would not be necessary in the absence of such competition. Viewing the problems associated with over-nutrition form this perspective, perhaps we can make more sense of the apparent paradox presented in the previous section, why the active processes of nutrient-absorption are enhanced rather than inhibited in nutritional states leading to metabolic disease.

The Ecological Role of Adiposity


The ability to store fat is not only critical to survival in scenarios of scarcity, it is also directly necessary for effective nutrient-assimilation in normal conditions. This was demonstrated in a study where mutant test-animals were generated that lacked the ability to form adipose-tissue which rendered them extraordinarily metabolically inflexible, and when provided ad-libitum access to a standard chow-diet they were only able to assimilate about 45% of ingested calories, losing the rest to feces and urine compared with control-animals who assimilated 75%.37) Because of this, control-animals only needed to consume about 30% the amount of food compared to what was consumed by mutant animals. Importantly, fecal energy-density was not different between the two groups and hence the ability to increase adiposity could be considered an adaptation to enable increased nutrient assimilation-efficiency which would in turn provide an advantage in a competitive environment such as a cage full of hungry rats and in their normally colonised gastrointestinal tracts.38) In support of the notion that the presence of intestinal microbes can provide a cue to the body as to increase its nutrient assimilation-efficiency by increasing adiposity, studies in GF animals have shown that when they are conventionalised by microbes they rapidly gain body-fat even on a normal diet despite also reducing their feed-consumption by 30%. Even just signals of microbial presence seems to be enough as a study using mice that where injected with bacterial danger-molecules (to the degree that these were present in the circulation of mice fed an obesogenic diet) showed that they developed a similar degree of adiposity on a control-diet as animals that were fed an obesogenic diet.39) Data from a separate experiment in the same study also showed that the obesogenic effect of a high-fat diet was severely blunted when test-animals were deficient in a receptor that initiates anti-microbial immune-responses which bring us to the next important function of adipose-tissue.

An Alarm-fitted Security-System

Like in all other areas of life quick accumulation of wealth doesn’t make you rich unless you can also hold on to it which is why we tend put our salaries in the bank rather than in our wallets. Since adipose-tissue stores large amounts of what is the most dense energy-currency found in biology it also needs to have some of the same properties as a bank, which in addition to being a large space that can store funds also needs to be able to keep the funds safe from intruders, hence both banks and adipose-tissue need to be equipped with an alarm-system, preferably one that is also directly connected with on-call law-enforcers as to avoid being robbed. Consistent with this analogy, adipose tissues seems to posses a very high capacity for transmitting the biological equivalent of an alarm-signal, which is production of inflammatory cytokines, in response to serological signs of a security-breach.40) To this end, adipocytes can switch to an immunological phenotype where they start to take on the functions of antigen presenting-cells which is cytologically characterised by severe cellular hypertrophy which in turn is a typical finding in obese adipose tissue correlating with metabolic dysfunction.42) There are several lines of evidence suggesting a high level of synergism as well as mutualism between adipocytes and immune-cells and that they often work as functional units in both repair- and defence-mechanisms, analogous to the intimate relationship between banks and maintenance- and security-contractors.44) The adipocyte-initiated inflammatory alarm-signal potently attracts immunological reinforcement to the tissue which together form an immunological barricade that protects against microbial intruders, which is a notion supported by the fact that lipodystrophy have been shown to severely blunt the body’s ability to mount an immune-response and that an obese and insulin-resistant phenotype is (counterintuitively) associated with increased survival in incident sepsis.47) In human obesity more than 40% of the total number of cells in adipose-tissue samples can be immune-cells, compared with figures below 10% in lean subjects, framing obesity as a state of enhanced immunological activity or readiness rather than just being the result of overconsumption, and mechanistically this has been shown to be an adaptive response to changed gut-ecology in animal-studies.55) Interestingly, the high-alertness and reactivity of adipose-tissue to signs of microbial threats also seems to have been exploited by the body as a mechanism to protect sensitive structures such as the heart and synovial joints from infectious attack. This is evident by the presence of seemingly strategically placed fat-pads that act like filters at the tissue-vascular interface, and these fat-pads also show a similar inflammatory phenotype as obese adipose-tissue in diseases such as cardiomyopathy and osteoarthritis respectively, which could explain why these adipose-tissue depots are preserved even in extreme starvation while subcutaneous depots are depleted.57)

The Inherent Dangers of Dietary Fat-Absorption

Since dietary lipids are among the few macro-nutrients that are absorbed by enterocytes using endocytosis, this provides a convenient opportunity for intestinal microbes to enter the body, which they are of course already exploiting.59) If they manage to survive inside enterocytes they could then potentially highjack host lipid transport-mechanisms to reach distant tissues. Fortunately the body has evolved a clever mechanism to prevent this where microbial antigens are continually integrated into the lipid transport-vesicles, the chylomicrons, which then instead of entering the blood-stream goes together into the lymphatic system, which is totally devoid of erythrocytes and therefore also of iron (a common growth-limiting metal for microbes), and is instead full of antigen-presenting cells and lymphocytes.60) In this way the body stays one step ahead by priming the immune-system depending on what kind of microbes that are currently residing in the gut.61)

If microbes were to gain entry to the enterocyte or the intercellular spaces, there is another security-issue involved with the absorption of fat, and that is the transport of the lipid-filled chylomicrons across the basal-membrane of the intestinal wall over to the lymphatic lacteals. Because of the large size of chylomicrons and that the basal-membrane is a very dense acellular structure (and hence unable to allow diffusion nor perform transcytosis), and to preserve the integrity of the chylomicron the basal-membrane needs to be temporarily broken to allow passage. This is orchestrated by mast-cells co-localised with the enterocytes in the intestinal mucosa that upon stimulation by dietary fats starts to secrete a substance called histamine, which in turn increases vascular permeability and subsequent fluid-accumulation and recruitment of immune-cells. The increased fluid accumulation serves to facilitate the transport of the chylomicrons and the movement of recruited immune-cells, and the latter then proceed to punch holes in the basal-membrane, creating a temporary defect in the intestinal barrier (preferably) lasting just long enough to allow passage of the chylomicrons after which the holes are sealed again by endogenous repair-mechanisms. This phenomenon has been shown to be dependent on the size of absorbed fatty acids, and is more pronounced in response to lipids with longer carbon-chains as those with shorter ones does not require chylomicron-mediated transport. Released histamine is then degraded by an endogenous enzyme released into the lymph by the enterocytes as not to allow it to cause a systemic compromise of the bodys other barriers.62)

The risks involved with the absorption-process of dietary fat and the resulting precautions taken by the body could perhaps explain the “inflammatory potential” of commonly applied high-fat diets in experimental settings, and same as why a bank that has to move an increasing amount of funds must reciprocally tighten up security, a person who consumes a lot of nutrients must also have an enhanced activation of their immune-system, which could explain the dose-dependent association between total fat-mass and markers of systemic inflammation (which largely come from adipose-tissue), and why inflammation tends to decrease after surgical removal of fat-mass, perhaps at the expense of immunity in the short term.63) One could also predict that the inflammatory potential of a diet high in fat would also depend on the microbiological context, i.e. what microbes that are currently residing in the gut (which depend on nutrients other than fat as well as other dietary and non-dietary factors), and also, continuing with the bank-metaphor, that an increase in traffic of easily accessible funds will also directly attract both dedicated and opportunistic criminals; pathogens, which will also undoubtedly try their best to get more control of this process, creating a potentially vicious circle that can perhaps only be broken by lowering the amount of wealth in transit.

Impairing Intestinal Glucose-Transport Cause Fatal Diarrhoea

There is an easy way to study the effects of over-nutrition that occur independently from increased serum-levels of nutrients, and that is to recreate such conditions only at the intestinal level by using experimental strategies that inhibit absorption. As stated in the previous section, mutations that affect the functionality of the intestinal glucose-importer SGLT1 are fatal, but interestingly only when the test-animals are fed a sucrose-rich diet, and studies have shown that they not only survive but thrive when no or low amounts of carbohydrate is present in the diet, and that absorption of a large glucose bolus is merely slowed, not reduced.65) Consistently with the hypothesis put forth in this section, the cause of death in animals with mutant SGLT-1 fed a high carbohydrate diet has been shown to be dehydration, not starvation, as a consequence of diarrhoea caused by an increased amount of glucose being available to intestinal bacteria and the same effect has been observed in pharmacological studies on SGLT-1 inhibitors and also as a side-effect after resection of the superior small intestine.66) In light of these observation, we can make more sense of why the body seem to be very quick about increasing absorption-capacity in anticipation of a large nutrient load, and indeed having a competitive edge over luminal microbes seem to be an important factor for survival. In further support of the notion that nutrient-absorption adapts to a competitive environment, studies have also shown that when competitions diminishes such as when the microbiome is eliminated/reduced, gut-levels of SGLT1 plummets, and upon re-colonisation it gradually returns towards to normal. The effect of microbes on nutrient transporters are dependant on the type of bacteria, and some cause a decrease in SGLT1 and instead cause an up-regulation of GLUT2.67) However, like previously discussed, the presence of intestinal microbes is not a prerequisite to efficient absorption of glucose and a study has shown that when provided ad-libitum access to a liquid glucose-solution the level of intestinal SGLT1-expression and hence glucose transport in GF animals can both match and surpass their wild-type littermates.68)

Conflicting Evidence

There are studies showing that when using selective genetic breeds in certain dietary scenarios even germ-free can display a phenotype consistent with metabolic disease. This cast doubt over the facts presented in the previous paragraphs and also over the general hypothesis that microbes are an essential link between over-nutrition and pathology. Two very recent studies in particular give robust criticism to this idea. The first one showed that an obesogenic diet caused an increase in body-weight, plasma cholesterol, fasting and postprandial glycemia in both conventional and GF mice.69) However, even though the proportional increase was similar, when the absolute values are compared GF mice display numbers similar to conventional mice fed the control diet, and a larger dose of glucose had to be used in GF-animals in order to produce a comparable increase in glycemia. Also, neither group showed an elevation of cytokines related to the inflammatory response, which is thought to be the mechanisms by with over-nutrition manifests the more concrete pathological features of metabolic disease such as atherosclerosis. This observation also support the notion that weight-gain and insulin resistance are not pathognomonic to disease, even though they are often closely associated with it. However, in a second study that was recently published the researchers did manage to cause the expression of an almost identical patho-metabolic phenotype in both GF and wild-type mice fed an obesogenic diet, and they also found signs of elevated inflammation in adipose-tissue.70) results are in sharp contrast with an earlier study that used an almost identical methodology which showed resistance to diet-induced metabolic symptoms in GF mice which raises the question about who got it right?71) Since methods of generating, keeping and testing for sterility in these animal models are imperfect, there is always a risk of contamination that may or may not be detectable and hence there is an overarching risk of statistical errors. Another major complicating factor is that elimination of live microbes is not sufficient to control for microbially mediated effects as studies have shown that infusion with abiotic microbial or endogenous danger-molecules can cause a practically identical obese and metabolic phenotype in mice fed a normal diet compared with mice fed an obesogenic diet.72) The experimental diet used in both of the before-mentioned studies that showed contrasting findings despite very homogenous study-designs contained large amounts of casein, which is a protein derived from milk and it has been shown to commonly be contaminated with large amounts of non-viable (hence non-culturable) bacteria that sometimes manage to grow and proliferate during the production-process.73) Unfortunately neither study used molecular detection-methods to control for this, so we still don’t know if these inconsistencies presented are because of false-positive or false-negative findings, and hence not if gut micro-ecology truly is the sole link between diet and metabolic disease.

Summary – Why Relationships Matter

The large part of the data I have presented above argues that micro-ecology is the causal mediator between over-nutrition and metabolic disease, however there are also some conflicting evidence and more research is therefore definitely needed in order to draw a more firm conclusion on this very complicated issue. Even though the literature is somewhat divided, I believe that the hypothesis put forth in this section makes the most sense since it abides by the same principles as similar phenomenons that are observable in other areas of ecology while the conventional explanation of nutrient-toxicity hardly make it past logic reasoning based on basic physiology.

Tying It All Together

Probably the least controversial statement that can be made about diets that have been shown to cause metabolic disease is that they are commonly hyper-refined, and that included nutrients therefore hardly even need to be processed and digested by the consumer in order to be absorbed. Contrastingly the diets that are associated with health seem to be rich in more complex nutrients that make optimal use of the digestive machinery of the consumer and also that of its symbiotic microbes. Since we are complex holobionts, freedom from microbial colonisers is utopic, and probably even dystopic if we knew the true consequences.76) By adapting the choices we make with regards to diet (and other integrated life-style factors) we can at least influence the level of conflict and resistance we face on a daily basis by favouring colonisation by either friendly or hostiles microbes. Since a refined diet makes symbiotically inclined microbes obsolete and instead creates a competitive landscape where our endogenous cell-populations are pitted against microbial parasites that thrive on the very same nutrients as they do, there are only three options going forward in such a scenario. The first one is for the body to become a superior competitor, which then necessitates an obese phenotype, and this would be equivalent to what is usually termed “metabolically healthy obesity” which is however still associated with a small increased risk of cardiovascular disease compared to lean and metabolically healthy subjects.77) The second option is to try to get what we need and then play defence, which necessitates a powerful immunological phenotype because of the larger parasitic threat compared with the first scenario, and this would be analogous to what happens in lean diabetics. The third option is a combination of the previous two, which seems to be a fair representation of what goes on in most cases of metabolic disease.

Integrating Nutrient-Deficiencies

From the perspective put forth in this section we can also integrate the effect of nutrient-deficiency into the pathophysiological model since this will impair defensive capabilities and therefore incite opportunism and hostility from previously peaceful colonisers. As previously described, a state of nutrient-deficiency might also create an environment that attracts parasites by the excess generated by attempted compensation through increased consumption of foods rich in other nutrients that are not deficient. Under-nutrition would then have the potential to incite and initiate similar pathological phenotypic expressions in the host-organism as over-nutrition which is a notion that is supported by the J-shaped association between BMI and cardiovascular-disease, and the fact that DM2 occurs even in people that are underweight which represents about 3-4% of total DM2 in some populations.78)

Nutrition Both Regulates and is Regulated by Birth-Rates

What foods we eat were previously unanimously determined by the local ecosystem in which we made a living, and the amounts were in turn kept in check by the ecological relationship between our population and the populations of the species that constituted our food-supply, and our food-supplies food-supplies and so on. The amount of food that is available controls female fertility and hence birth-rates, and in turn birth-rates (which is obviously more complex than just involving nutrition) then determines how much food is available to the individuals of the tribe, hence over time this puts populations and individuals in balance with the yields of the local ecosystem more or less involuntarily and unconsciously.81) The practical problem that then presents itself is that if we want to keep existing in an arena of seemingly infinite abundance (and effective birth-control) such as modern society, we need to carefully consider what foods we use to constitute our daily diet and we also need to fine-tune our intake-level according to a logical estimate of our daily needs and also simultaneously suppress our innate subconscious desire for totalitarianism as genetic replicators, which is something we are intrinsically bad at doing, humans as well as all other living beings. This easily explains the failure of scientific advancements and harsh public-health policies in reversing the increasing prevalence of metabolic disease, because we are in conflict with what are perhaps the most ancient drivers of all genetically based life, and we might hence have severely underestimated the challenge.

In Closing

In order to thrive as holobionts in a competitive ecosystem, we need to be good at equitable distribution of resources among our members. We also need to be careful about what signals we put out to potential recruits, and a growing budget increasingly attract players which aims align more with their respective individual needs rather than the goal and purpose of the team. Hence, if we want to approach something that could be defined as “optimal health” in a holobiotic sense, we voluntarily need seek cooperative relationships with our commensal colonisers. However, a prerequisite for this is resignation of some of our current riches, a life lived closer to the borders of our true needs as organisms. Such a life wont change the numerical disadvantage we face from microbes as holobionts, nor will it abolish the fundamental ecological realty of competition, but what will happen is that we will increasingly attract players with more of a cooperative play-style which beats being surrounded by enemies, if we have to pick, which we all do.


In the modern world, selection of species appropriate foods with at least some level of voluntary restriction on quantity are two non-negotiable ingredients of a healthy diet because besides from providing adequate nutrition this fosters beneficial micro-ecological relationships and hence lowers the parasitic pressure on the host, which in turn lowers our risk of metabolic disease.


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