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- The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease
- Western pattern diet
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The dietary pattern that characterizes the Western diet is strongly associated with obesity and related metabolic diseases, but biological mechanisms supporting these associations remain largely unknown. We argue that the Western diet promotes inflammation that arises from both structural and behavioral changes in the resident microbiome. The environment created in the gut by ultra-processed foods, a hallmark of the Western diet, is an evolutionarily unique selection ground for microbes that can promote diverse forms of inflammatory disease.
Recognizing the importance of the microbiome in the development of diet-related disease has implications for future research, public dietary advice as well as food production practices. Research into food patterns suggests that whole foods are a common denominator of diets associated with a low level of diet-related disease.
Hence, by studying how ultra-processing changes the properties of whole foods and how these foods affect the gut microbiome, more useful dietary guidelines can be made. Innovations in food production should be focusing on enabling health in the super-organism of man and microbe, and stronger regulation of potentially hazardous components of food products is warranted.
The share of whole versus ultra-processed foods is a dietary factor that has traditionally been given minor attention in nutritional science. However, a growing body of epidemiological research supports the idea that ultra-processed foods are detrimental to human health.
Classification of foods according to processing has, among others, been reviewed by Monteiro and co-workers in the NOVA classification, where foodstuffs are grouped into categories according to the extent and purpose of processing applied to them [ 1 ].
Also, it is safe to conclude that ultra-processed foods are one major hallmark of the Western diet. In high-income countries, ultra-processed foods are now dominating the food supply, and they are rapidly gaining ground in growing economies [ 5 ]. Transnational food and beverage corporations are increasingly targeting low income countries, strategically using pricing and availability to increase consumption of ultra-processed foods at the expense of traditional foods [ 6 ].
Individuals consuming large amounts of these types of foods are at greater risk of being obese than people who consume relatively little [ 7 , 8 , 9 ], and the availability of ultra-processed foods is positively associated with the prevalence of obesity [ 10 , 11 ]. Also, the dietary share of ultra-processed foods determines the nutritional quality of diets in several populations [ 12 , 13 , 14 ].
Associations with adverse health effects in humans are also present when looking at food groups. For instance, although a high intake of meat in general is associated with an increased risk for several health outcomes [ 15 , 16 , 17 , 18 , 19 ], processed meat shows a much stronger association [ 20 , 21 , 22 , 23 ].
Intake of whole grains is associated with a reduced risk of several non-communicable diseases, as opposed to refined grains [ 24 , 25 ]. A study on fish intake reported adverse effects on markers of metabolic syndrome from processed fish, whereas whole fish seems to be protective [ 26 ].
These studies indicate that by studying how processed foods and whole foods affect human physiology and metabolism differently, we can shed light on the mechanisms of the adverse effects of the Western diet.
Nutrition researchers have tended to focus their attention on characteristics of the Western diet such as the energy density and the addition of fat, sugar and salt. We argue that other factors introduced during food processing can have an equally important effect by promoting inflammation-related processes through diet—microbiome—host interactions. The microbiota composition can change rapidly upon dietary changes [ 27 ] and contribute to negative health effects, as evidenced by microbe transplant studies in rodents.
Such changes can include dysbiosis and microbiota encroachment, leading to inflammation and metabolic disturbances [ 28 , 29 , 30 ]. However, a change in microbiota composition is not a prerequisite for changes in function. Dietary factors that alter the metabolic behavior of the microbes already present can also have a large impact. Gut bacteria adjust their metabolism according to both the substances produced by other microbes and the nutrient supply, which may produce effects that influence metabolic and inflammatory pathways in the human body [ 31 ].
For instance, both human and animal studies have demonstrated that pathogens, pathobionts and other members of the microbiome can respond to a change in their environment e. Major changes in the diet and subsequent changes in microbiota can, at least to some extent, be reversed within the same generation.
However, recent studies in rodents have demonstrated that the loss of microbiota diversity due to dietary changes can be transferred to later generations, with progressive loss of diversity [ 35 ].
Also, a Western diet could lead to a permanent loss of bacteria important to microbiome function [ 36 ] and possibly induce inheritable metabolic changes via the epigenome [ 37 ]. In sum, the environment created in the gut by ultra-processed foods could be an evolutionarily unique selection ground for microbes with behaviors that promote diverse forms of inflammation-related disease.
Throughout the human evolution, nutrients had to be released from cells with a few exceptions, such as nutrients in milk, honey and eggs to be available for uptake by the enterocytes. However, in a Western diet, a large share of the energy is provided by acellular nutrients ; a term coined by Ian Spreadbury [ 38 ]. Acellular nutrients, i. The share of cellular nutrients that become accessible during digestion in the gut differs from food to food, depending on the nature of the food matrix and processing that alters the properties of the outer cell [ 39 ].
Animal cells lack cell walls, and their phospholipid membranes are efficiently hydrolyzed by human digestive enzymes, liberating the cell content into the gut lumen [ 43 ]. Processing of animal foods e. Plant cells have cell walls consisting mainly of fibre [ 45 ], making the contents of intact plant cells less available for uptake in the small intestine.
During mastication, some plant cells are ruptured, and the macromolecules inside become available for hydrolyzation by human digestive enzymes in the gut. The release of nutrients from ruptured cells is dispersed along a large part of the small intestine, and, depending on the particle size and the food matrix, a fraction of the cellular nutrients will not be released at all, passing through the small intestine [ 41 , 42 ].
Nutrients in intact plant cells reaching the colon will become available to fibre-degrading bacteria that hydrolyze the cell walls of the intact cells. Food processing that leads to breakage of cell walls affects the nutrient availability in the small intestine. Where whole grains of, for instance, wheat contain all of their nutrients in cells, grains that are milled to whole meal flour will contain a mixture of intact and ruptured cells, as milling of plant seeds causes a substantial portion of the cells to rupture [ 39 ].
Further refining of the seed contents will leave less of the cells intact, and, in white flour, a large share of the nutrients is acellular. Although milling was also used by pre-agricultural humans, the level of consumption of refined acellular macronutrients from milled grains during the last centuries, and especially the last five decades, is by far unprecedented in a historical context.
The production of modern, ultra-processed foods also highly relies on extracted oils and starches for use as ingredients in food products. Extraction of oils and starches from seed crops renders all the nutrients acellular.
The possible impact of this increased accessibility has received little attention as of today, but the unarguable large shift in the nutrient accessibility cannot be discounted in terms of possible health impacts in light of the new knowledge of the microbiome.
Increased amounts of readily accessible acellular nutrients in a Western diet might facilitate increased growth potential as well as altered composition and metabolism of the gut microbiota.
These effects could propagate further down the digestive system. Accordingly, Turnbaugh and co-workers found that a Western diet high in simple sugars caused a dramatic loss of microbial diversity in mice, coinciding with a bloom in bacteria capable of metabolizing such sugars, which are normally not present in the distal colon [ 30 ].
Territory expansion signaling could translate to increased production of virulence factors, which could damage the host directly or via increased amounts of microbes or microbial products entering the bloodstream or the intestinal wall. Indeed, increased amounts of microbes and microbial by-products, originating from the gut, are found in patients with lifestyle diseases [ 47 , 48 ]. Also, the duodenal microbiota differs in composition and function in normal weight as compared to obese people, providing an indication that the small intestinal microbiota is a discrete determinant of body fat mass amount, and that manipulating the duodenal microbiota, for example through diet changes, could affect fat mass [ 49 ].
Further, research has shown that, for instance, starch from grain based foods [ 40 ] and fructose from sugary drinks [ 50 ] can exceed the carbohydrate absorption capacity of the small intestine in humans and mice, respectively, providing easily accessible growth substrates for the bacteria in the distal small intestine as well as in the colon. Cellular plant foods are likely to affect the gut microbiota in a different way.
As a substantial amount of cells from whole plant foods will enter the colon in an intact state [ 41 ], this could favor the growth of bacteria that degrade fibre and produce beneficial metabolites e. We argue that the increase in small intestinal nutrient availability from acellular, compared to cellular, foods could prove to be one decisive factor for the microbiota-mediated effects of the diet, and that the protective effects from whole plant foods on several health outcomes could be partly explained by favoring the growth of beneficial fibre-degrading bacteria in the colon.
The number of studies that have directly addressed how acellular versus cellular foods affect physiology is limited. To advance this field further there is a need for detailed investigation into how acellular and cellular meals and diets affect the microbiome in the gastrointestinal tract. The number of food additives approved for use by the industry has been soaring over the last few decades [ 51 ].
The risk assessment conducted prior to the approval of such substances does generally not include effects on the microbiome [ 51 ], but recent studies have indicated that additives can induce microbiota-mediated adverse effects in the host Table 1.
This is not an exhaustive list. Examples are chosen based on a crude assessment of relevance to issues discussed in this paper dosages administered are below or correspond to ADI levels, or are meant to mimic estimated intake levels in humans.
The increasing use of emulsifiers in food production, e. However, several studies have reported altered microbiota composition and gut inflammation in rodents fed commonly used emulsifiers [ 29 , 54 , 55 , 56 ].
Recent publications report that emulsifiers can act by increasing virulence factors and thereby the pro-inflammatory potential of the microbiome [ 33 , 34 ], and that this low grade inflammation caused by emulsifiers can promote colon carcinogenesis [ 57 ]. The accumulating data linking selected emulsifiers to gut inflammation should cause concern and call for precautionary action. However, lecithin, a substance of animal and plant tissue, which also acts as an emulsifier, has been suggested as a therapeutic agent in treatment of inflammatory bowel disease, as it could improve the re-establishment of an intact mucosal barrier in humans [ 58 ].
The contradictory effects of different types of emulsifiers underline the importance of thorough testing of every food additive on the gut microbiota before approval. Non-caloric artificial sweeteners NAS have made their way from foul-tasting soft drink alternatives for diabetics, to become the choice of the masses.
These sweeteners have also not been tested for effects on the gut microbiota prior to approval. Effects from rodent studies include altered composition of microbes leading to impaired glucose tolerance [ 28 , 59 , 60 ] as well as increased pro-inflammatory potential [ 61 , 62 ] and liver inflammation [ 61 ].
NAS-induced alterations in the microbiota composition leading to adverse metabolic outcomes should give rise to concern, especially because the demand for NAS-containing products are increasing, and persons suffering from metabolic disorders could be more likely to choose such products for health benefits.
Rodent studies demonstrating the disruptive properties of artificial sweeteners on gut microbiota have been criticized for using concentrations corresponding to the acceptable daily intake ADI in humans, thereby exceeding a normal consumption pattern. An observed effect at the ADI level indicates an insufficient safety margin and calls for reassessment. A Western diet can lead to increased levels of endotoxin-producing bacteria in the intestinal tracts of both humans and mice, resulting in metabolic endotoxemia [ 65 , 66 ].
Several studies investigating the effect of major dietary changes on microbiota in mice have utilized so-called high fat diets, and negative changes—including metabolic endotoxemia—are often attributed to the fat content [ 67 ]. However, several other dietary factors could be contributing. An animal study demonstrated that changes in the microbiota leading to intestinal inflammation were caused by a lack of fermentable fibre, and not by the content of fat in the diet [ 68 ].
When mice were fed a diet that induced metabolic endotoxemia, adding a prebiotic improved metabolic marker [ 69 ]. Correspondingly, dietary polyphenols have shown the ability to restore gut barrier integrity [ 66 ], attenuate a number of inflammatory effects of a so-called high fat diet and to induce a healthy microbiota profile in mice when fed together with the high fat diet [ 70 ].
Furthermore, diet-induced inflammation could be mediated partly by the PAMPs pathogen associated molecular patterns produced by microbes in processed foods [ 71 ]. PAMPs, e. When fresh whole foods are prepared for processing, such as mincing meat or dicing vegetables, the increase in surface area and access points favors the conditions for the growth of bacteria.
Clett Erridge has demonstrated that both minimally processed e. As these PAMPs are heat stable, they can be present after heat treatment in food products with seemingly good microbiological quality [ 72 ]. A study of human volunteers reported a reduction in white blood cell count, low density lipoprotein cholesterol, body weight and waist circumference after one week on a diet low in PAMPs, whereas the beneficial changes were reversed by a diet high in PAMPs [ 71 ].
If these effects are corroborated by more studies, then the quality assessment of industrial food products should include analyses for LPS and other toll-like receptor stimulants to avoid inflammatory responses in the host, and improved measures should be taken to limit growth of PAMP-producing bacteria during processing. As the microbiological quality of foods is generally assessed by the presence of live bacteria, the presence of inflammation-inducing bacterial molecules could be a potential food safety issue that has gone under the radar.
Reversely, probiotic or fermented foods could contain beneficial bacterial molecules left in the foods during fermentation. Studies have shown beneficial effects of fermented milk products on metabolic markers in mice [ 74 , 75 , 76 ], also independently of the presence of live probiotic bacteria, either in the product or in the gut of the recipient [ 77 ].
It has been demonstrated in vitro that metabolites from probiotic bacteria are capable of reducing the release of pro-inflammatory cytokines [ 78 , 79 , 80 ]. The exact molecules involved are yet to be identified. We suggest that bacteria-derived molecules in foods are important signals, both to the microbial community in the gut and the immune system of the host, capable of altering microbiota behavior and modulating host inflammatory responses.
Hence, types of processing that generate beneficial or detrimental bacterial molecules in foods could be a relevant addition to the discussion regarding food processing. Many foods undergo extensive heat treatment during preparation that leads to the generation of advanced glycation end products AGEs.
AGEs increase with an increased cooking time, temperature and the absence of moisture [ 81 ].
The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease
The dietary pattern that characterizes the Western diet is strongly associated with obesity and related metabolic diseases, but biological mechanisms supporting these associations remain largely unknown. We argue that the Western diet promotes inflammation that arises from both structural and behavioral changes in the resident microbiome. The environment created in the gut by ultra-processed foods, a hallmark of the Western diet, is an evolutionarily unique selection ground for microbes that can promote diverse forms of inflammatory disease. Recognizing the importance of the microbiome in the development of diet-related disease has implications for future research, public dietary advice as well as food production practices. Research into food patterns suggests that whole foods are a common denominator of diets associated with a low level of diet-related disease. Hence, by studying how ultra-processing changes the properties of whole foods and how these foods affect the gut microbiome, more useful dietary guidelines can be made.
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Western pattern diet
The Western pattern diet WPD is a modern dietary pattern that is generally characterized by high intakes of red meat , processed meat , pre-packaged foods , butter , candy and sweets, fried foods , conventionally-raised animal products, high-fat dairy products , eggs , refined grains , potatoes , corn and high-fructose corn syrup and high-sugar drinks , and low intakes of fruits , vegetables , whole grains , grass-fed animal products, fish , nuts , and seeds. This diet is "rich in red meat, dairy products, processed and artificially sweetened foods, and salt, with minimal intake of fruits, vegetables, fish, legumes, and whole grains. Complex carbohydrates such as starch are believed to be more healthy than sugar , which is frequently consumed in the Standard American Diet. The energy-density of a typical WPD has continuously increased over time.
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Fast food is a type of mass-produced food designed for commercial resale and with a strong priority placed on "speed of service" versus other relevant factors involved in culinary science. Fast food was originally created as a commercial strategy to accommodate the larger numbers of busy commuters, travelers and wage workers who often did not have the time to sit down at a public house or diner and wait for their meal. By making speed of service the priority, this ensured that customers with strictly limited time a commuter stopping to procure dinner to bring home to their family, for example, or an hourly laborer on a short lunch break were not inconvenienced by waiting for their food to be cooked on-the-spot as is expected from a traditional "sit down" restaurant. The fastest form of "fast food" consists of pre-cooked meals kept in readiness for a customer's arrival Boston Market rotisserie chicken , Little Caesars pizza , etc.
Obesity is a medical condition in which excess body fat has accumulated to an extent that it may have a negative effect on health. Obesity has individual, socioeconomic, and environmental causes, including diet, physical activity, automation , urbanization , genetic susceptibility , medications , mental disorders , economic policies , endocrine disorders , and exposure to endocrine-disrupting chemicals. Obesity prevention requires a complex approach, including interventions at community, family, and individual levels.
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