Western Civilization Abstracts 2

© 2012

Glucose intolerance associated with early-life exposure to maternal cafeteria feeding is dependent upon post-weaning diet

            (Akyol, McMullen et al. 2012) Download

In addition to being a risk factor for adverse outcomes of pregnancy, maternal obesity may play a role in determining the long-term disease patterns observed in the resulting offspring, with metabolic and dietary factors directly programming fetal development. The present study evaluated the potential for feeding rats an obesogenic cafeteria diet (O) pre-pregnancy, during pregnancy, during lactation and for the offspring post-weaning, to programme glucose tolerance. Early-life exposure to an O diet had no significant effect on offspring food intake. Early-life programming associated with O feeding to induce maternal obesity was associated with reduced adiposity in offspring weaned onto low-fat chow. Adult offspring exposed to an O diet in early life and weaned on a chow diet had low fasting glucose and insulin concentrations and appeared to be more sensitive to insulin during an intraperitoneal glucose tolerance test. When weaned on an O diet, male offspring were more prone to glucose intolerance than females. On the basis of the area under the glucose curve, maternal O feeding at any point from pre-mating to lactation was associated with impaired glucose tolerance. The mechanism for this was not identified, although increased hepatic expression of Akt2 may have indicated disturbance of insulin signalling pathways. The observations in the present study confirm that maternal overnutrition and obesity during pregnancy are risk factors for metabolic disturbance in the resulting offspring. Although the effects on glucose homeostasis were independent of offspring adiposity, the programming of a glucose-intolerant phenotype was only observed when offspring were weaned on a diet that induced greater fat deposition.

Some diseases characteristic of modern western civilization. A possible common causative factor

            (Burkitt 1973) Download

The effects of a cafeteria diet on insulin production and clearance in rats

            (Castell-Auvi, Cedo et al. 2011) Download

The aim of the present study was to determine the effects of a cafeteria diet on the function and apoptosis of the pancreas, and the activity and expression of the insulin-degrading enzyme (IDE). Female Wistar rats were fed either with a cafeteria diet or a control diet for 17 weeks, and blood and tissues were then collected for analysis. The cafeteria diet-treated rats had higher plasma insulin and C-peptide levels (P < 0.05), showing increased insulin secretion by the pancreas. Insulin protein and gene expression levels were higher in the pancreas of obese rats, as was its transcriptional controller, pancreatic duodenal homeobox 1 (P < 0.05). Feeding a cafeteria diet down-regulated the gene expression of the anti-apoptotic marker B-cell/lymphoma 2 (BCL2), and up-regulated the protein levels of BCL2-associated X protein, a pro-apoptotic marker (P < 0.05). The cafeteria diet caused lipid accumulation in the pancreas and modified the expression of key genes that control lipid metabolism. To assay whether insulin clearance was also modified, we checked the activity of the IDE, one of the enzymes responsible for insulin clearance. We found increased liver IDE activity (P < 0.05) in the cafeteria diet-fed animals, which could, in part, be due to an up-regulation of its gene expression. Conversely, IDE gene expression was unmodified in the kidney and adipose tissue; although when the adipose tissue weight was considered, the insulin clearance potential was higher in the cafeteria diet-treated rats. In conclusion, treatment with a cafeteria diet for 17 weeks in rats mimicked a pre-diabetic state, with ectopic lipid accumulation in the pancreas, and increased the IDE-mediated insulin clearance capability.

Acne vulgaris: a disease of Western civilization

            (Cordain, Lindeberg et al. 2002) Download

BACKGROUND: In westernized societies, acne vulgaris is a nearly universal skin disease afflicting 79% to 95% of the adolescent population. In men and women older than 25 years, 40% to 54% have some degree of facial acne, and clinical facial acne persists into middle age in 12% of women and 3% of men. Epidemiological evidence suggests that acne incidence rates are considerably lower in nonwesternized societies. Herein we report the prevalence of acne in 2 nonwesternized populations: the Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Additionally, we analyze how elements in nonwesternized environments may influence the development of acne. OBSERVATIONS: Of 1200 Kitavan subjects examined (including 300 aged 15-25 years), no case of acne (grade 1 with multiple comedones or grades 2-4) was observed. Of 115 Ache subjects examined (including 15 aged 15-25 years) over 843 days, no case of active acne (grades 1-4) was observed. CONCLUSIONS: The astonishing difference in acne incidence rates between nonwesternized and fully modernized societies cannot be solely attributed to genetic differences among populations but likely results from differing environmental factors. Identification of these factors may be useful in the treatment of acne in Western populations.

Cafeteria diet-induced obesity is associated with a low spontaneous growth hormone secretion and normal plasma insulin-like growth factor-I concentrations

            (De Schepper, Smitz et al. 1998) Download

Pituitary growth hormone (GH) secretion has been shown to be blunted in human and animal obesity. With respect to human obesity, cafeteria diet-induced obesity might be an appropriate model to study spontaneous GH secretion. In 6 cafeteria diet-overfed obese male Wistar rats and 6 control rats with chronically implanted catheters, GH levels were measured every 15 min over 6 h by standard RIA. A significantly lower GH secretion, reflected by the integrated GH concentration, was found in the obese rats (median 16.46, [range 10.55-19.13] ng/ml x 6 h vs 35.63 [range 21.90-41.50] ng/ml x 6 h, P < 0.05). The GH secretion in the obese rats was significantly negatively correlated with the body fat percentage, assessed by dual X-ray absorptiometry (Rho = -0.95, P < 0.05). Median plasma insulin-like growth factor-I (IGF-I) concentration was comparable between the two groups, while the median insulin concentration was significantly higher in the obese group (1.95 [range 1.76-3.55] ng/ml vs 1.21 [range 0.86-2.13] ng/ml, P < 0.05). No significant correlation existed between GH secretion and the plasma insulin concentration. In conclusion, cafeteria diet-induced obesity is associated with a low spontaneous GH secretion and normal plasma IGF-I concentration. The hyperinsulinemia present in this model probably explains the normal IGF-I concentrations, but not the GH hyposecretion.

The Dynamics of Devaluation: The Spiritual Disease of Civilization

            (Glasberg 2010)         Download

The presentation seeks to identify a major spiritual sickness that is not only widespread but also kept out of public discourse or seriously minimized in terms of its scope and destructive effects. Most religious traditions derive much of their power by giving 'believers' a sense of personal and/or collective worth, where worth may be associated with a feeling of positive valuation. However, as religious traditions decline in the wake of a materialist science or as they become corrupted by developing false forms of valuation, Western, if not world, civilization becomes ever more threatened by the disease of devaluation. In this context, the study will attempt three things: (1) to identify the manifestations or symptoms of devaluation as a disease of the soul; (2) to place these symptoms in a kind of historical context; and (3) to develop some effective healing strategies that may serve to counter, not only the symptoms but also the root causes of the disease of devaluation. In particular, it will be argued that false forms of valuation need to be identified so that public discourse can minimize the possibilities of these taking root and leading to one of the tragedies of our time: that is, the gaining of a kind of substitute value by the devaluing of some other group.

Agrarian diet and diseases of affluence--do evolutionary novel dietary lectins cause leptin resistance?

            (Jonsson, Olsson et al. 2005) Download

BACKGROUND: The global pattern of varying prevalence of diseases of affluence, such as obesity, cardiovascular disease and diabetes, suggests that some environmental factor specific to agrarian societies could initiate these diseases. PRESENTATION OF THE HYPOTHESIS: We propose that a cereal-based diet could be such an environmental factor. Through previous studies in archaeology and molecular evolution we conclude that humans and the human leptin system are not specifically adapted to a cereal-based diet, and that leptin resistance associated with diseases of affluence could be a sign of insufficient adaptation to such a diet. We further propose lectins as a cereal constituent with sufficient properties to cause leptin resistance, either through effects on metabolism central to the proper functions of the leptin system, and/or directly through binding to human leptin or human leptin receptor, thereby affecting the function. TESTING THE HYPOTHESIS: Dietary interventions should compare effects of agrarian and non-agrarian diets on incidence of diseases of affluence, related risk factors and leptin resistance. A non-significant (p = 0.10) increase of cardiovascular mortality was noted in patients advised to eat more whole-grain cereals. Our lab conducted a study on 24 domestic pigs in which a cereal-free hunter-gatherer diet promoted significantly higher insulin sensitivity, lower diastolic blood pressure and lower C-reactive protein as compared to a cereal-based swine feed. Testing should also evaluate the effects of grass lectins on the leptin system in vivo by diet interventions, and in vitro in various leptin and leptin receptor models. Our group currently conducts such studies. IMPLICATIONS OF THE HYPOTHESIS: If an agrarian diet initiates diseases of affluence it should be possible to identify the responsible constituents and modify or remove them so as to make an agrarian diet healthier.

Paleolithic diets as a model for prevention and treatment of Western disease

         (Lindeberg 2012) Download

OBJECTIVES: To explore the possibility that a paleolithic-like diet can be used in the prevention of age-related degenerative Western disease. METHODS: Literature review of African Paleolithic foods in relation to recent evidence of healthy nutrition. RESULTS AND DISCUSSION: Available evidence lends weak support in favor and little against the notion that lean meat, fish, vegetables, tubers, and fruit can be effective in the prevention and treatment of common Western diseases. There are no obvious risks with avoiding dairy products, margarine, oils, refined sugar, and cereal grains, which provide 70% or more of the dietary intake in northern European populations. If stroke, coronary heart disease, type 2 diabetes, and cancer are preventable by dietary changes, an ancestral-like diet may provide an appropriate template.

Traditional non-Western diets

         (Lipski 2010) Download

In traditional cultures, balancing health with a balanced lifestyle was a core belief. The diseases of modern civilization were rare. Indigenous people have patterns of illness very different from Western civilization; yet, they rapidly develop diseases once exposed to Western foods and lifestyles. Food and medicine were interwoven. All cultures used special or functional foods to prevent disease. Food could be used at different times either as food or medicine. Foods, cultivation, and cooking methods maximized community health and well-being. With methods passed down through generations, cooking processes were utilized that enhanced mineral and nutrient bioavailability. This article focuses on what researchers observed about the food traditions of indigenous people, their disease patterns, the use of specific foods, and the environmental factors that affect people who still eat traditional foods.

Lifestyle variables, non-traditional cardiovascular risk factors, and the metabolic syndrome in an Aboriginal Canadian population

            (Liu, Young et al. 2006) Download

OBJECTIVE: To examine lifestyle factors associated with metabolic syndrome (MetS) and to explore the relationships between MetS and non-traditional cardiovascular disease risk factors [adiponectin, leptin, C-reactive protein (CRP), interleukin-6 (IL-6), and serum amyloid A (SAA)] in an isolated Aboriginal Canadian community. RESEARCH METHODS AND PROCEDURES: Data were obtained from 360 non-diabetic adults participating in a population-based study of Aboriginal Canadians. Fasting samples were drawn for glucose, insulin, lipids, adiponectin, leptin, CRP, IL-6, and SAA. Percentage body fat was measured using bioelectrical impedance analysis. Past year physical activity and fitness level were assessed. MetS was diagnosed according to the criteria of the National Cholesterol Education Program, the World Health Organization, and the International Diabetes Federation. RESULTS: The results showed that older age, higher percentage body fat, and lower fitness levels were associated with increased odds of MetS regardless of MetS definition and subject gender. Past year physical activity was independently related with the World Health Organization-MetS in male subjects. Subjects with MetS had significantly higher leptin, CRP, IL-6, and SAA levels and lower adiponectin levels; however, only adiponectin remained significantly low after adjustment for age and percentage body fat. DISCUSSION: The study showed that higher percentage body fat and lower physical activity and fitness were associated with a higher prevalence of MetS in this Aboriginal community and that hypoadiponectinemia was independently associated with MetS.

A Western-type diet attenuates pulmonary hypertension with heart failure and cardiac cachexia in rats

            (Lourenco, Vasques-Novoa et al. 2011) Download

Western-type diets (WD) constitute risk factors for disease but may have distinct effects in heart failure (HF) with cardiac cachexia (CC). We evaluated hemodynamic, metabolic, and inflammatory effects of short-term WD intake in pulmonary hypertension (PH) with CC. Male Wistar rats randomly received 60 mg . kg(-1) monocrotaline (M) or vehicle (C) and consumed either a 5.4-kcal . g(-1) WD (35% animal fat, 35% simple carbohydrate, 20% protein, 0.4% Na(+)) or a 2.9-kcal . g(-1) (3% vegetable fat, 60% complex carbohydrate, 16% protein, 0.25% Na(+)) normal diet (ND) for 5 wk. Mortality, energy intake, body weight (BW), metabolism, hemodynamics, histology, apoptosis, gene expression, transcription factors, and plasma cytokines were evaluated. Compared with the C-ND group, the M-ND group had PH, HF, and mortality that were significantly attenuated in M-WD. The extent of myocardial remodeling and apoptosis was higher in M-ND than in C-ND but lower in M-WD than in M-ND, while conversely, energy intake, BW, cholesterol, and TG plasma concentrations were lower in M-ND than in C-ND but higher in M-WD than in M-ND. M-ND had increased myocardial NF-kappaB transcription factor activity, endothelin-1, and cytokine overexpression and higher circulating cytokine concentrations than C-ND, which were lower in M-WD than in M-ND. PPARalpha activity, however, was lower in M-ND, but not in M-WD, compared with the respective C groups. WD attenuated PH and CC, ameliorating survival, myocardial function, metabolism, and inflammation, through transcription factor modulation, suggesting a beneficial role in CC.

Milk--the promoter of chronic Western diseases

            (Melnik 2009) Download

Common chronic diseases of Western societies, such as coronary heart disease, diabetes mellitus, cancer, hypertension, obesity, dementia, and allergic diseases are significantly influenced by dietary habits. Cow's milk and dairy products are nutritional staples in most Western societies. Milk and dairy product consumption is recommended by most nutritional societies because of their beneficial effects for calcium uptake and bone mineralization and as a source of valuable protein. However, the adverse long-term effects of milk and milk protein consumption on human health have been neglected. A hypothesis is presented, showing for the first time that milk protein consumption is an essential adverse environmental factor promoting most chronic diseases of Western societies. Milk protein consumption induces postprandial hyperinsulinaemia and shifts the growth hormone/insulin-like growth factor-1 (IGF-1) axis to permanently increased IGF-1 serum levels. Insulin/IGF-1 signalling is involved in the regulation of fetal growth, T-cell maturation in the thymus, linear growth, pathogenesis of acne, atherosclerosis, diabetes mellitus, obesity, cancer and neurodegenerative diseases, thus affecting most chronic diseases of Western societies. Of special concern is the possibility that milk intake during pregnancy adversely affects the early fetal programming of the IGF-1 axis which will influence health risks later in life. An accumulated body of evidence for the adverse effects of cow's milk consumption from fetal life to childhood, adolescence, adulthood and senescence will be provided which strengthens the presented hypothesis.

Autonomic denervation and the origins of chronic Western diseases

         (Quinn 2010) Download

Many chronic Western diseases result from lifestyles that include refined diets, poor bowel habits, limited physical exercise and suboptimal patterns of childbirth. Western diets result in reduced stool weights, increased bowel transit times and persistent physical efforts during defaecation. Prolonged physical efforts during defaecation and childbirth cause latent, or direct, injuries to branches of the cardiac (thorax), coeliac (abdomen) and hypogastric (pelvis) plexi. Injuries to autonomic nerves result in impaired visceral function including visceral dysmotility, tissue hypoplasia and hyperplasia, increased susceptibility to infection, and, aberrant reinnervation with sensitisation of the central nervous system (CNS). These unrecognised injuries are vulnerable to the long list of causes of autonomic Dysfunction, e.g. stress, alcohol, drugs, infection, trauma, cancer, etc. Specific injuries at different anatomical locations in midline autonomic pathways give rise to a wide range of Western diseases from infancy to old age, through diverse and cumulative mechanisms.

Origins of Western diseases

            (Quinn 2011) Download

Recent gynaecological studies show that childbirth, constipation, trauma and surgery cause injuries to autonomic nerves at different anatomical sites in the female pelvis resulting in endometriosis, adenomyosis and fibroids. Re-growth of abnormal nerves causes allodynic symptoms ('light touch causing pain or discomfort') some years later including vulvodynia, dyspareunia, dysmenorrhea, irritative bladder and bowel symptoms. Further consequences of autonomic denervation include tissue hypoplasia and hyperplasia, visceral dysfunction, susceptibility to infection, alcohol, tobacco and drugs, as well as pain with sensitization of the central nervous system. The 'autonomic denervation' view extrapolates these observations from the female pelvis to the varied anatomy of branches of the cardiac and coeliac plexi to provide primary mechanisms for many forms of Western disease. This account sets out the autonomic denervation view, identifies features of autonomic denervation in extrapelvic organs, and, contrasts it with prior accounts of chronic Western diseases including those of DP Burkitt, PRJ Burch and DP Barker.

Blood-pressure rise with age--a Western disease?

            (Trowell and Burkitt 1981) Download

Colon cancer: a civilization disorder

            (Watson and Collins 2011) Download

Colorectal cancer arises in individuals with acquired or inherited genetic predisposition who are exposed to a range of risk factors. Many of these risk factors are associated with affluent Western societies. More than 95% of colorectal cancers are sporadic, arising in individuals without a significant hereditary risk. Geographic variation in the incidence of colorectal cancer is considerable with a higher incidence observed in the West. Environmental factors contribute substantially to this variation. A number of these risk factors are associated with a Western lifestyle and could be considered a product of 'civilization'. Recently, smoking has been recognized as a risk factor. Energy consumption also influences colorectal cancer risk, with obesity increasing risk and exercise reducing risk. However, the strongest contribution to environmental risk for colorectal cancer is dietary. Consumption of fat, alcohol and red meat is associated with an increased risk. Fresh fruit and vegetables and dietary fibre may be protective. Much has been learnt recently about the molecular pathogenesis of colorectal cancer. Colorectal cancer always arises in the context of genomic instability. There is inactivation of the tumour suppressor genes adenomatous polyposis coli, p53, transforming growth factor-beta, activation of oncogene pathways including K-ras, and activation of the cyclooxygenase-2, epidermal growth factor receptor and vascular endothelial growth factor pathways. The mechanisms by which some environmental factors modify the mutation risk in these pathways have been described.

Diverticulosis coli: update on a "Western" disease

            (Ye, Losada et al. 2005) Download

Diverticular disease affects upwards of 50% of the population over the age of 60 years in Western countries and is becoming more common as the population ages. Studies from the 1970s and 1980s related its occurrence to the use of low-fiber diets and to the prolonged colonic transit time and increased intraluminal pressure associated with low-volume stools. Pulsion diverticula (pseudodiverticula) emerge through the thickened circular layer of the muscularis propria of the left colon at points of penetration of the vasa recta that supply the submucosa and mucosa. Complications of diverticular disease such as hemorrhage, diverticulitis, peridiverticular abscess, fistula, and perforation are well recognized. More recently, attention has been drawn to the polypoid prolapsing mucosal folds that may develop as the affected segment of bowel (usually the sigmoid) becomes shorter and to changes in the mucosa surrounding the diverticula and in the bowel wall that may result in confusion with ulcerative colitis or Crohn disease (sigmoid colitis-associated diverticulosis [SCAD]). Distinguishing SCAD from these entities is extremely important, and pathologists should be aware of the possibility of overdiagnosing chronic inflammatory bowel disease in biopsies or resection specimens of sigmoid colon with diverticular disease.


Akyol, A., S. McMullen, et al. (2012). "Glucose intolerance associated with early-life exposure to maternal cafeteria feeding is dependent upon post-weaning diet." Br J Nutr 107(7): 964-78.

Burkitt, D. P. (1973). "Some diseases characteristic of modern western civilization. A possible common causative factor." Clin Radiol 24(3): 271-80.

Castell-Auvi, A., L. Cedo, et al. (2011). "The effects of a cafeteria diet on insulin production and clearance in rats." Br J Nutr: 1-8.

Cordain, L., S. Lindeberg, et al. (2002). "Acne vulgaris: a disease of Western civilization." Arch Dermatol 138(12): 1584-90.

De Schepper, J. A., J. P. Smitz, et al. (1998). "Cafeteria diet-induced obesity is associated with a low spontaneous growth hormone secretion and normal plasma insulin-like growth factor-I concentrations." Growth Horm IGF Res 8(5): 397-401.

Glasberg, R. (2010). "The Dynamics of Devaluation: The Spiritual Disease of Civilization." J Relig Health.

Jonsson, T., S. Olsson, et al. (2005). "Agrarian diet and diseases of affluence--do evolutionary novel dietary lectins cause leptin resistance?" BMC Endocr Disord 5: 10.

Lindeberg, S. (2012). "Paleolithic diets as a model for prevention and treatment of Western disease." Am J Hum Biol 24(2): 110-5.

Lipski, E. (2010). "Traditional non-Western diets." Nutr Clin Pract 25(6): 585-93.

Liu, J., T. K. Young, et al. (2006). "Lifestyle variables, non-traditional cardiovascular risk factors, and the metabolic syndrome in an Aboriginal Canadian population." Obesity (Silver Spring) 14(3): 500-8.

Lourenco, A. P., F. Vasques-Novoa, et al. (2011). "A Western-type diet attenuates pulmonary hypertension with heart failure and cardiac cachexia in rats." J Nutr 141(11): 1954-60.

Melnik, B. C. (2009). "Milk--the promoter of chronic Western diseases." Med Hypotheses 72(6): 631-9.

Quinn, M. (2011). "Origins of Western diseases." J R Soc Med 104(11): 449-56.

Quinn, M. J. (2010). "Autonomic denervation and the origins of chronic Western diseases." Med Hypotheses 74(5): 937-44.

Trowell, H. and D. Burkitt (1981). "Blood-pressure rise with age--a Western disease?" Lancet 2(8248): 693-4.

Watson, A. J. and P. D. Collins (2011). "Colon cancer: a civilization disorder." Dig Dis 29(2): 222-8.

Ye, H., M. Losada, et al. (2005). "Diverticulosis coli: update on a "Western" disease." Adv Anat Pathol 12(2): 74-80.