While most readers would  have a reasonable idea about what kind of food constitutes a Cafeteria-style diet, few would be aware that it is actually a fast-evolving scientific construct used for clinical research into common metabolic diseases. In fact, a lot of our current evidence-based research is founded on clinical trials involving lab-rats such as pedigree Wistar or Sprague Dawley rats, which are fed a variety of controlled pelletised diets called ‘rat chow’.

Interestingly, a recent paper published in the journal Obesity, posed the question whether or not these pellets actually produce robust models for understanding human metabolic syndrome. With an out-of-control epidemic of obesity, diabetes, heart disease and cancer, there has never been a better time to consider the relevance of scientific models based on rat chow.

This particular paper is the product of a collaborative effort by several experts in departments of Nutrition, Physiology, Biophysics, Metabolism, Pharmacology, Cellular Integrative Physiology and Cancer Biology, at various American Universities. This paper, however, avoids the well-trodden ground arising from researching individual nutrients, which leads to the kind of seemingly  ineffective general advice we are all familiar with, such as to avoid saturated fat, lower salt intake, and increase the consumption of fibre. In this case, the scientists set out to duplicate real urban conditions where ‘American children consume up to 25% of calories from snacks.’¹

These children are, in increasing numbers, developing fatty liver disease which is a condition formerly only found in hard-core alcoholics. The cause is attributed largely to the escalating consumption of high-fructose corn syrup, which is present in all snack foods, bottled juices, soft drinks and confectionary, and may also be found in rat chow. Rat chow is of course an industrial food, formulated to contain the usual essential fats, refined carbohydrates and proteins necessary to sustain life in a rat community; nevertheless, the authors considered it inadequate as a diet for the purposes of studying the effect of real supermarket foods.

The method chosen for this piece of research was to give a group of Wistar rats a two week acclimatisation period while being fed a standard rat chow (SC). They were then separated into four groups: standard chow (SC) control; high-fat chow (HFD); low-fat chow (LFD); and a standard diet with ad libitum access to snack foods (CAF). This last experimental group was given three different snack foods per day to browse from, consisting of biscuits, cheese, cereals, crackers, processed meat, fruit loops, cocoa puffs, hot dogs, muffins, Doritos, cake and so on.

The clinical investigations included blood measures, glucose tolerance test, and tissue pathology (pancreas, liver, epididymal white adipose tissue, brown adipose tissue).  What the scientists found after 15 weeks was that the CAF rats gained almost double the weight of the SC controls, whereas LFD and HFD rats showed only intermediate weight gain. At seven weeks, blood sugar homeostasis was relatively normal in all groups, but insulin was nearly double in CAF and HFD rats, indicating a state of pre-diabetes. At 15 weeks, however, the CAF rats demonstrated overt hyperglycaemia as is observed in diabetes. The CAF also induced elevations in both white and brown adipose mass, macrophage infiltration and inflammation far in excess of the HFD rats. Furthermore, the CAF diet produced fatty liver and liver inflammation as we see in human children.

The scientists were naturally pleased with the results of their pioneering work: ‘Taken together, we have demonstrated in a comparative study that the CAF is a more robust model of metabolic syndrome than lard-based HFD and that the rapid-onset of weight gain, obesity, multiorgan dysfunctions and pathologies observed in the CAF model more closely reflect the modern human condition of early onset obesity. The CAF diet, while labor intensive and “untraditional,” may be the best model to emulate modern human obesity trends.’

Since this landmark study in 2011 there has been an explosion in this kind of research. For example, in a recent experiment using a community of Wistar rats fed a CAF diet for 12 weeks, the scientists demonstrated that such dietary changes ‘were accompanied by a significant decrease in gut bacterial diversity, decreased Firmicutes and an increase in Actinobacteria and Proteobacteria abundances, which were concomitant with increased endotoxaemia.’²

This discovery accompanies other interesting research findings concerning the type of alterations the CAF diet induces in fat metabolism, with a fourfold increase in lipogenesis added to earlier findings. These were an increased ‘body fat mass, plasma triacylglycerol (TAG) and insulin levels, glucose uptake by white and brown adipose tissues, as well as the sympathetic activity to both adipose tissues.’³ The blood also showed an increase in the presence of toxic advanced glycation end-products while the kidneys showed obvious inflammation.⁴

Cognitive function is also evidently impaired by a Cafeteria-style diet, especially in juvenile rats. These rats exhibit anxiety, depression and poor memory. Neuroplastic and functional changes in key areas of the brain are also responsible for alteration in eating behaviour and satiety mechanisms, while microglial activation and neuro-inflammation are evident.^5–7

Finally, the type of diet scientists use in a trial can introduce non-dietary variables which are not traditionally taken into account in results; however, these may, in fact, markedly influence obesity, dysbiosis, heart disease, blood sugar regulation, inflammation, oxidative stress and other outcome measures. For instance, realistic Cafeteria-style diets contain metabolically active additives such as preservatives, colours, flavours, pesticides and herbicides which are known to be obesogenic, diabetogenic or carcinogenic. Real urban cafeteria diets are also deficient in important vitamins and minerals necessary for homeostasis.⁸

There is hope, however, for the vast populations of urban dwellers who today subsist on ultra-processed convenience foods, when a supply of black, green, red, or white tea is found to offset some of the harm of a Cafeteria-style diet. Apparently the well-known anti-inflammatory and antioxidant constituents present in tea are still potent at a ‘1% dose’. ⁹

References:

1.    Sampey BP, Vanhoose AM, Winfield HM, et al. Cafeteria diet is a robust model of human metabolic syndrome with liver and adipose inflammation: comparison to high-fat diet. Obes Silver Spring Md 2011;19:1109–17.

2.    Del Bas JM, Guirro M, Boqué N, et al. Alterations in gut microbiota associated with a cafeteria diet and the physiological consequences in the host. Int J Obes 2005 2018;42:746–54.

3.    de Melo AF, Moreira CCL, Sales CF, et al. Increase in liver cytosolic lipases activities and VLDL-TAG secretion rate do not prevent the non-alcoholic fatty liver disease in cafeteria diet-fed rats. Biochimie 2018;150:16–22.

4.    Navarro MEL, Santos KCD, Nascimento AF do, et al. Renal inflammatory and oxidative and metabolic changes after 6 weeks of cafeteria diet in rats. J Bras Nefrol Orgao Of Soc Bras E Lat-Am Nefrol 2016;38:9–14.

5.    Ferreira A, Castro JP, Andrade JP, Dulce Madeira M, Cardoso A. Cafeteria-diet effects on cognitive functions, anxiety, fear response and neurogenesis in the juvenile rat. Neurobiol Learn Mem 2018;155:197–207.

6.    Gutiérrez-Martos M, Girard B, Mendonça-Netto S, et al. Cafeteria diet induces neuroplastic modifications in the nucleus accumbens mediated by microglia activation. Addict Biol 2018;23:735–49.

7.    Parkes SL, Furlong TM, Naneix F. Commentary: Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning. Front Psychol 2015;6:536.

8.    Bortolin RC, Vargas AR, Gasparotto J, et al. A new animal diet based on human Western diet is a robust diet-induced obesity model: comparison to high-fat and cafeteria diets in term of metabolic and gut microbiota disruption. Int J Obes 2005 2018;42:525–34.

9.    Soares MB, Ramalho JB, Izaguirry AP, et al. Comparative effect of Camellia sinensis teas on object recognition test deficit and metabolic changes induced by cafeteria diet. Nutr Neurosci 2017;1–10.