Extract by JK

file:///C:/Users/Lab%20User/Downloads/RRCC-16919-the-western-diet-and-lifestyle-and-diseases-of-civilization_030811.pdf   Open access article published in 2017

The western diet and lifestyle and diseases of civilization

Pedro Carrera-Bastos1 Maelan Fontes-villalba1 James H O’Keefe2 Staffan Lindeberg1 Loren Cordain3

Abstract: It is increasingly recognized that certain fundamental changes in diet and lifestyle that occurred after the Neolithic Revolution, and especially after the Industrial Revolution and the Modern Age, are too recent, on an evolutionary time scale, for the human genome to have completely adapted. This mismatch between our ancient physiology and the western diet and lifestyle underlies many so-called diseases of civilization, including coronary heart disease, obesity, hypertension, type 2 diabetes, epithelial cell cancers, autoimmune disease, and osteoporosis, which are rare or virtually absent in hunter–gatherers and other non-westernized populations. It is therefore proposed that the adoption of diet and lifestyle that mimic the beneficial characteristics of the preagricultural environment is an effective strategy to reduce the risk of chronic degenerative diseases. Keywords: Paleolithic, hunter–gatherers, Agricultural Revolution, modern diet, western lifestyle and diseases.

Wouldn’t copy from PDF  --  recreated by jk

Table 1  Historical milestones in human generations  ^{14, 63-65}

Table 2 Systolic blood pressure (SBP) and diastolic blood pressure (DBP) at age 40–60 years in hunter–gatherers and horticulturalists (mm Hg) ^26,67–69

Table 3:  Systolic blood pressure and diastolic blood

 pressure in Yanomamo  Indians ⁶⁹.

Figure 1, Fasting plasma insulin (IU/mL) in Kitava horticulturaists (first number) versus healthy Swedes (second number).⁷⁴  Transposed from graph by JK

Figure 3,  Fasting plasma leptin (ng/mL) in Kitava hoticultalists versus healthy Swedes. ⁹²

Figure 5:  Waist circumference (cm)/height (m) in Kitava horticulturalists versus healthy sweeds:  Kitava 45.8 versus 53.2 men; women 45.9 versus 51.7

Figure 7,  Maximum oxygen consumption in various populations (mL/kg/min). ⁶⁷

Note, JK:  the IKung are desert dwellers in South Africa and the Warao live in costal Jungle regions of Northern South America all of which the temperature limits physical excursion; while the Lapps and Eskimos for most of the year can’t breathe deeply.  The Maasai live on the plains of Kenyan and Tanzania.  The Lufas I couldn’t find a reference to, the link #97 to the  abstract didn’t reference oxygen consumption, and the full article is not available for free.  Oxygen consumption is associated with, cardiovascular fitness.  After lack of insulin resistance, fitness is the 2^nd best marker for health/longevity—link to senior runners.     

Introduction:  The physical activity, sleep, sun exposure, and dietary needs of every living organism (including humans) are genetically determined. This is why it is being increasingly recognized in the scientific literature, especially after Eaton and Konner’s1 seminal publication in 1985, that the profound changes in diet and lifestyle that occurred after the Neolithic Revolution (and more so after the Industrial Revolution and the Modern Age) are too recent on an evolutionary time scale for the human genome to have fully adapted.1–27 In fact, despite various alleles being targets of selection since the Agricultural Revolution,28–42 most of the human genome comprises genes selected during the Paleolithic Era43 in Africa,43–59 a period that lasted from about 2.5 million years ago to 11,000 years ago.14 Indeed, anthropological and genetic studies suggest that all human beings living in Europe, Asia, Oceania, and the Americas share a common African Homo sapiens ancestor.47–57 This concept is corroborated by data showing that there is less genetic diversity throughout the world’s non-African population than there is within Africa itself.44–46,53,57,58 Moreover, many of the selective pressures underlying these post-agriculture alleles were not induced by changes in sleep, exercise, and diet but rather by pathogens, fatal diseases, and harsh environments,28–31,37–39 with a few key exceptions.41,42 One of those exceptions pertains to alleles of the LCT gene (which codes for the enzyme lactasephlorizin hydrolase [LPH]) that give rise to the phenotype of adult lactase persistence (ALP).60 These LPH-encoding alleles were initially selected in populations with a long history of milk and dairying, such as north-western Europeans and some sub-Saharan African and Bedouin pastoralists. Today, ALP occurs in about 35% of the world’s population.60 The impetus for these genetic changes was not to increase longevity and resistance to chronic degenerative diseases but rather to increase the probability of survival and reproductive success.27,61,62 Occasionally, mutations that had positive survival and reproductive value sometimes also caused adverse health effects in the postreproductive years.4,27,61,62 Furthermore, single gene mutations, although relevant for physicians when treating an individual patient, are imperfect models to prevent chronic degenerative diseases whose clinical symptoms normally affect the post-reproductive years and involve numerous genes.61 Importantly, 11,000 years represent approximately 366 human generations,63 which comprise only 0.5% of the history of the genus Homo (Table 1).14,63–65 Indeed, the Industrial Revolution and the Modern Age, which mark the beginning of the western lifestyle, represent only seven and four human generations, respectively (Table 1),14,63–65 and were marked by rapid, radical, and still ongoing changes in lifestyle and diet,14,65 coupled with improved public health measures that greatly reduced mortality in the prereproductive years (and hence largely eliminated impaired reproductive fitness as a selection pressure).62,66 As such, it is highly unlikely that genetic adaptations that allow us to thrive on a western diet and lifestyle have occurred.

Health status of pre-agriculture traditional populations: The idea that modern Homo sapiens are still adapted to an ancestral environment is reinforced by data showing that hunter–gatherers, and other populations minimally affected by modern habits, exhibit superior health markers, body composition, and physical fitness compared with industrialized populations, including:

1. Low blood pressure in hunter–gatherers and horticulturalists (Table 2)26,67–69 when compared with current optimal values defined by health institutions (120 mm Hg and 80 mm Hg for systolic blood pressure and diastolic blood pressure, respectively)70

2. Lack of association between blood pressure and age in hunter–gatherers (Table 3)69 and horticulturalists68 compared with in North Americans and Swedes26,68,70

3. Persisting excellent insulin sensitivity among middle-aged and older individuals in non-westernized traditional populations that maintain their ancestral lifestyle26,71–81

4. Lower fasting plasma insulin concentrations and higher insulin sensitivity (measured by the Homeostatic Model Assessment [HOMA] index) in the horticulturalists of Kitava (Papua New Guinea) compared with in healthy Swedes (Figures 1 and 2, respectively)74

5. Lower fasting plasma leptin in the horticulturalists of Kitava and the Ache hunter–gatherer Indians of Paraguay compared with in healthy Swedes82 (Figure 3) and North American male distance runners83 (Figure 4), respectively

6. Lower body mass index (BMI) in hunter–gatherers, traditional pastoralists, and horticulturalists26 compared with in westerners.26,84 For instance, as observed by Lindeberg,26 in Kitava, 87% of men and 93% of women aged 40–60 years had a BMI below 22 kg/m2 and not a single individual in this age group was overweight or obese26

9. Greater maximum oxygen consumption (VO2 max) in hunter–gatherers and traditional pastoralists compared with in average Americans67 (Figure 7)

10. Better visual acuity in hunter–gatherers and other traditional populations minimally affected by western habits compared with in industrialized populations85

11. Better bone health markers in hunter–gatherers compared with in western populations and even traditional agriculturalists26,86–98

12. Lower fracture rates in non-westernized populations compared with in western populations. 26,96–99

Another line of evidence supporting the superior health markers of hunter–gatherers and other traditional populations comes from the historical records of explorers, adventurers, and frontiersmen, which invariably described the populations they encountered as being healthy, lean, fit, and free of the signs of chronic degenerative diseases.26  But perhaps even more important than these observations are the medical and anthropological reports showing a low incidence of chronic degenerative diseases such as metabolic syndrome and type 2 diabetes, 26,67,73,74,100 cardiovascular disease (CVD), 26,65,67,68,100–112 cancer, 26,67,113–118 acne,119 and even myopia 85 in hunter–gatherers, traditional pastoralists, and horticulturalists compared with in western population s26,65,67,85,100,108,109,113,114,119,120 and even ancient Egyptians, 67,114,121–123 and medieval Europeans.

Counter arguments:

It has been argued that traditional populations may have been genetically protected against the chronic degenerative diseases that occur in industrialized countries, yet when non-westernized individuals adopt a more contemporary lifestyle, their risk for chronic degenerative diseases is similar or even increased compared with modern populations. 26,67,78–80,108,109,124–144 Further, when they return to their original traditional lifestyle, many disease markers or symptoms return to normal. 81, 145 ….  These studies also indicate that few or no genetic adaptations have occurred to protect any population from chronic diseases that are elicited by modern diet and lifestyles. Indeed, two different individuals when exposed to the same modern environment (e.g., western diet, physical inactivity, insufficient and inadequate sleep, chronic psychological stress, insufficient or excessive sun exposure, use of recreational drugs, smoking, pollution) will probably express a suboptimal phenotype.27,65,146,147/ ….

Anti-nutrient content and inflammatory potential

Warning this section is based on pharma’s putative causes, which causes the researchers to study the signs that appear from insulin resistance, the damage from uric acid to kidney and endothelial cells, the under production and/or production of defective collagen, and fructosylation .  The starting point is a high fructose diet whose toxic effects are magnified by the amount of starch (glucose) and the load place on the liver by regular consumption of ethanol.   Pharma is in the business of treating illness.  To fulfill its fiduciary obligation it actively does tobacco science to promote useless and harmful drugs and to oppose the use of effective drugs, diet and supplements.  The long lists signs instead of major causes generates an even longer list of useless drugs.  The list creates cognitive dissonance and thereby buries the obvious cause and thereby reduce the percentage of healthy people.   

Alterations in gut microbiotica220 and increased intestinal permeability221 are possible causes of low-grade chronic inflammation. Indeed, when the intestinal barrier is disrupted, it allows increased passage of gut luminal antigens derived from food, bacteria, and viruses221 into peripheral circulation (endotoxemia222). One particular antigen, lipopolysaccharide (LPS), from Gram-negative bacteria, is routinely used in animal experiments to induce acute immune stimulation.223 When LPS binds Toll-like receptor (TLR)4, it triggers the release of nuclear factor kappa-B (NF-kb) dimers that translocate into the cell nucleus, where they bind to DNA target sites, thereby inducing the expression of genes that code for various inflammatory enzymes, cytokines and chemokines, cell adhesion molecules, antiapoptotic and angiogenesis proteins, inducible nitric oxide synthase, and matrix-degrading enzymes224 that are involved in the atherosclerosis process.19,166,222,224 Moreover, these pro-inflammatory cytokines may disrupt insulin signaling, promoting insulin resistance.164 So a chronic low-grade endo-toxemia may lead to low-grade chronic inflammation,222 which is at the root of various disorders.160,165–167,222,224,225 In this regard, recent evidence shows that certain western foods (dairy cream, butter, egg muffins, sausage muffins, hash browns, and sugar) allow increased passage of luminal antigens into peripheral circulation, leading to TLR2 and TLR4 activation.222,226–228 Interestingly, one study found that these events were prevented by a high intake of orange juice (perhaps because it contains flavonoids with reactive oxygen species [ROS] and inflammation-suppressive activities, such as naringenin and hesperidin),228 which opens the possibility that other fruit and vegetables may elicit similar effects. Some factors contributing to increased intestinal permeability include nonsteroidal anti-inflammatory drugs,221 antacids,221 changes in gut microbiota,221 alcohol,229 lectins,221 saponins,230–235 and gliadin.236 It was recently found that gliadin, a prolamine in wheat (which is a novel food in the human diet in evolutionary terms65), increases gut permeability by means of zonulin production in the gut enterocytes.236 Zonulin causes disruption of the tight junction proteins that maintain the gut barrier function and leads to increased gut permeability.237 In addition, gliadin (which is resistant to heat and digestive enzymes154) is able to interact with gut-associated lymphoid tissue, stimulating the innate immune system in celiac and nonceliac individuals (whereas the adaptive immune response is exclusive of celiac patients).238,239 Gliadin may increase found in beans) are rapidly transported across the gut wall into systemic circulation of animals,221 and tomato and peanut lectins have been found in systemic circulation in humans following consumption of tomato juice and roasted peanuts, respectively.249,251 These findings might be important, as virtually every cell in the body and every extracellular substance can be bound by lectins because of their ability to bind glycosylated structures.154 Of note, in vitro data have shown that WGA can bind insulin and leptin receptors,154,252 which could theoretically elicit insulin and leptin resistance.26,100,154 Moreover, lectins from lentils, kidney beans, peas, and wheat potently increase the production of inflammatory cytokines (interleukin [IL]-12, IL-2, and interferon γ) in cell cultures,253 and WGA also stimulates production of tumor necrosis factor (TNF)-α and IL-1β in vitro.254 Furthermore, WGA and PHA induce the production of metalloproteinases (MMPs) in leukocytes,255,256 and WGA directly causes the activation of platelets and potently increases their aggregation.257 This may be relevant because rupture of the fibrous cap and formation of the blood clot, which is mediated by MMPs and platelets, is a crucial mechanism involved in thrombus production. In this regard and although these chain of events have not to our knowledge been examined in vivo, it should be mentioned that peanut oil has unexpectedly been shown to be highly atherogenic in rats, rabbits, and primates,258 and reduction of its lectin content decreases its atherogenicity.258 Interestingly, one of the very few human-controlled dietary intervention trials with hard endpoints, DART (Diet And Reinfarction Trial), found a tendency toward increased cardiovascular mortality in the group advised to eat more fiber, the majority of which was derived from cereal grains.259 Of relevance is that this nonsignificant effect became statistically significant after adjustment for possible confounding factors (such as medication and health state).260 Another class of antinutrients that may increase intestinal permeability in humans and hence endotoxemia are saponins, which are present in some cereal grains, legumes, quillaja, alfalfa sprouts, and solanaceous plants such as potatoes and green tomatoes.230–235 These steroid glycosides or triterpenoids are formed by a sugar compound (glucuronic acid, glucose, or galactose, among others) and an aglycone (nonsugar molecule) portion.230,231 By binding the cholesterol molecule on gut cell membranes, the aglycone portion disrupts the gut barrier and increases intestinal permeability.231 Unfortunately, the effects of lectins and saponins on intestinal permeability, endotoxemia, and inflammation have been poorly studied in humans to allow us to draw significant conclusions. Novel food processing procedures, such as extreme heating, irradiation, ionization, pasteurization, and sterilization, may also promote low-grade chronic inflammation by leading to the nonenzymatic glycation and oxidation of proteins and lipids in common consumed foods.261 This complex and heterogeneous group of compounds, called advanced glycation end products (AGEs) and advanced lipid oxidation end products (ALEs), once partially absorbed into the systemic circulation may have deleterious health effects261 by direct modification of proteins and lipids262,263 (such as LDL glycation and oxidation, for instance) and perhaps also indirectly via the receptor for AGEs (RAGE).261,262 Of relevance to chronic degenerative diseases is the possible interaction of AGEs and ALEs with RAGE, which may activate several intracellular signal transduction pathways that lead to various downstream events, such as the activation of NF-kb and activator protein-1 transcription factors,261,262 which increases the expression of endothelin-1, angiotensin II, adhesion molecules, inflammatory cytokines, and plasmin activator inhibitor-1.261,262 Indeed, in diabetic patients, a high AGE intake was associated with higher levels of C-reactive protein (CRP), TNF-α, and vascular cell adhesion molecule (VCAM-1).261 In contrast, low-AGE diets reduce serum AGE levels, as well as markers of inflammation and vascular dysfunction (CRP, TNF-α, and VCAM-1) in diabetic and renal failure patients.261,262 The effects of dietary AGEs and ALEs are obviously more pronounced in diabetics (who present an enhanced formation of endogenous AGEs due to hyperglycemia)261 and kidney failure patients (who have an impairment of AGE renal excretion).261 Nevertheless, in a cross-sectional study of healthy subjects of different ages, dietary AGE intake was an independent determinant of high-sensitivity CRP and of circulating AGEs, which, in turn, were associated with endogenous lipid peroxidation and HOMA index.263 AGE and ALE content in food is greatly influenced by processing and cooking conditions, including temperature, time, and moisture.264 Consequently, the avoidance of processed foods and the use of steaming, poaching, boiling, and stewing as the main cooking methods, instead of frying, broiling, and grilling, may be a sensible way to decrease the formation of these compounds.261,264 Of interest, tobacco, by being processed in the presence of reducing sugars, represents another source of exogenous AGEs.262 Indeed, circulating AGE levels have been found to be significantly higher in smokers than in nonsmokers.265

Glycemic load, fiber, and fructose

During the Paleolithic period, most of the carbohydrate (CHO) sources were wild fruit, berries, vegetables (typically presenting low glycemic index [GI]26), and sometimes tubers, with cereal and honey intake being scarce.14,26,65 Today, most CHO come from processed foods such as refined sugars and refined cereal grains.65 Even whole grains possess a higher glycemic load (GL) than does most unprocessed fruit and vegetables.65 The GL takes into account both the GI and the amount of CHO in a given serving of a food. It is estimated that the GL of Paleolithic diets was significantly lower than the GL of western diets.65 This observation is relevant because chronic adoption of a high-GL diet may lead to hyperglycemia and hyperinsulinemia,266 which may contribute to dyslipidemia (elevated serum triglycerides, small-dense LDL-C, and reduced high-density lipoprotein [HDL]-C),266 hypertension,267 elevated plasma uric acid, 267 and insulin resistance,266 the primary metabolic defect in metabolic syndrome.266 Moreover, by eliciting postprandial hyperglycemia, it may increase oxidative stress, proinflammatory cytokines, protein glycation, and procoagulant activity, thereby adversely affecting endothelial function, among other pathophysiological effects.266,268–270 Indeed, a recent meta-analysis of 37 prospective cohort studies suggests that diets with a high GI, high GL, or both may increase the risk of type 2 diabetes, heart disease, and gallbladder disease.270 Furthermore, intervention studies show that a low GL diet may be an effective strategy for overweight and obesity271,272 and confer better glucose, insulin, lipoprotein, and inflammatory cytokine profiles in overweight and type 2 diabetes patients.268 Finally, the chronic adoption of a high GL diet may lead to a number of hormonal changes (such as elevated insulin-like growth factor-1 [IGF-1]/insulin-like growth factor binding protein-3 [IGFBP-3] ratio and increased ovarian and testicular androgen synthesis, coupled with decreased sex hormone-binding globulin hepatic synthesis) that ultimately may result in polycystic ovary syndrome, epithelial cell cancers, acne, and juvenile myopia, among other diseases.85,119,266,273 Another nutritional change is fiber intake. Most Paleolithic diets had more fiber (.30 g/d), generally from fruit and vegetables,65 than did the typical western diet, where most of the fiber derives from cereal grains.65 Fruit and vegetables have, on a calorie per calorie basis, two and eight times more fiber than do whole grains.65 In addition, fruit and vegetables typically contain soluble fiber, whereas much fiber in cereal grains is of the insoluble type.26 

This may all be relevant because dietary fiber, in particular soluble fiber, increases satiety,274,275 reduces postprandial free fatty acids,275 and contributes to better glycemic control (perhaps through a glucagon-like peptide-1 effect).275 Furthermore, dietary fiber appears to play an important role in intestinal health, as suggested by Higginson and Oettlé276 in the 1960s. They observed that in Africa, where “a large amount of roughage is consumed”, colon cancer and constipation were rare, whereas they were common diseases in western countries. This was also observed by Calder et al,277 who reported that a shift from rural to urban living and at the same time from a traditional to a westerndiet (containing a low amount of fiber) and lifestyle in Kenya was associated with diverticulitis and colon carcinoma. Today, there is an increasing recognition and understanding of the complex role that fiber plays in maintaining intestinal health that goes beyond the “traditional” increased bulk and stool frequency effect. For instance, dietary fiber fermentation in human intestine produces short-chain fatty acids, mainly acetic acid, propionic acid, and butyric acid,278 which exert several beneficial effects on the intestinal tract. For instance, butyrate and propionate, by inhibition of histone deacetylase, are able to block the generation of dendritic cells (DCs) from bone marrow stem cells, thereby inhibiting the inflammatory response mediated by DCs.279 Also, butyrate controls the assembly of epithelial cell tight junctions, leading to decreased intestinal permeability,280 which may be central to many inflammatory diseases, as explained previously. Even more relevant, butyrate reduces bacterial translocation into peripheral circulation independently of intestinal permeability,281 most likely through decreased NF-kB activation.281 Although whole grains are increasingly being recommended, in part to increase fiber intake, given its potential adverse effects already discussed, it would perhaps be prudent that most of the dietary fiber came from fruit and vegetables. Perhaps even more important, the introduction of refined sugars and, more recently, of high fructose corn syrup (HFCS), has increased fructose intake to unprecedented high levels.65,135 Mounting evidence suggests that this dietary shift may be an important player in obesity, insulin resistance, dyslipidemia, gout, hypertension, kidney disease, and nonalcoholic fatty liver disease.65,135,266,282,283 Although fruit is a natural source of fructose, it also contains vitamin C, which offsets some of the adverse effects of fructose,135 and various other nutrients, as well as fiber. As such, consuming unprocessed fruit is not equivalent to consuming pure fructose, sucrose, or HFCS. The simple fact that fructose presents a low GI,266 but yet because of its unique metabolism135,266 may have numerous adverse effects, combined with the fact that cereal grains and isolated sugars are the primary high-GL foods in the western diet,65 suggests that the historical focus on the GI and GL is incomplete and has to account for fructose and, perhaps more important, the food source of CHO. Another food group that was not part of Paleolithic diets but is considered a staple today is dairy.65 Milk, yoghurt, and some lactose-containing cheeses, despite having a low GL, elicit a very high insulin response.284–288 The implications of these findings are not entirely known, because the epidemiological evidence is conflicting regarding the association of milk and dairy, insulin resistance, and metabolic syndrome,289–294 but a small dietary intervention study in young boys observed an increase of 103% and 75% in fasting plasma insulin concentrations and relative insulin resistance, respectively, after 7 days on a high-milk diet.288 Furthermore, epidemiologic and intervention studies in children and adults demonstrate that cow’s milk significantly increases plasma levels of IGF-1 and, perhaps more important, the IGF-1/IGFBP-3 ratio.295  Moreover, milk contains various hormones and growth factors296–300 that may have relevant implications for chronic degenerative diseases. Indeed, epidemiologic evidence suggests that milk may be implicated in acne273,300 and epithelial cell cancers,295 particularly prostate cancer.300 Most of these adverse effects are more likely to manifest in the post-reproductive years and, as such, would not negatively affect the selection of ALP-associated alleles. Indeed, as indicated previously, genes that are important for early reproductive success can be selected despite potentially detrimental effects subsequent to their continued expression in later life,301 which is why ALP should not be viewed as genetic protection against potential adverse effects derived from long-term dairy intake. It should be mentioned that reactive monosaccharides such as glucose and especially galactose (from dairy)302 and fructose303 (which are much more reactive than glucose)302,303 lead to AGE production and accumulate intra- and extracellularly.303 Moreover, chronic hyperglycemia is a well-known accelerator of endogenous AGE production.261 In this regard, the chronic consumption of a high intake of sucrose, fructose, and galactose and/or the adoption of a high GL diet may significantly contribute to the formation of AGEs.

It can therefore be concluded that an increase in diet’s GL and insulinotropic potential, coupled with a higher fructose (and possibly galactose) intake and a reduction in vitamin C and dietary fiber consumption, may be another cause of the high incidence and prevalence in industrialized countries of epithelial cell cancers, obesity, metabolic syndrome, gout, CHD, acne, myopia, and various gastrointestinal problems, including constipation, irritable bowel syndrome, and diverticulitis.

Conclusion

The adoption of diet and lifestyle that are very different from what shaped the human genome for more than 2 million years is a major factor in the widespread prevalence of chronic degenerative diseases that are epidemic in western countries. This conclusion strongly suggests that focusing on isolated dietary or lifestyle variables is not an appropriate preventive medicine strategy. Indeed, the evolutionary template predicts that optimal gene expression, and ultimately an increase in health span (the number of years in good health), even if it would not affect average life expectancy, will not be achieved by any single dietary or lifestyle change but rather through the combination of several measures, such as regular physical exercise; stress management; sun exposure according to latitude and skin color (in order to maintain plasma 25[OH] D above 45 ng/mL and at the same time avoiding the adverse effects of excessive sun exposure); adequate sleep; avoidance of tobacco smoke; reduced exposure to pollutants, dietary AGEs, ALES, and other Maillard reaction compounds; and the adoption of a diet similar to that followed by Paleolithic hunter–gatherers. Giving support to this notion, four recent human intervention trials18,23,341,342 and one animal trial343 have demonstrated that a diet composed of meat, fish, shellfish, eggs, fresh fruit and vegetables, roots, tubers, nuts, and seeds may be superior to so-called healthy diets such as the Mediterranean diet.341

Paleo theory fails:  1) Fails to name fructose; 2) diets vary greatly so unhealthy fats, easy to digest carbs, weird chemicals theory of pathogenesis has exceptions

Critical of Lindeberg: The study total misses fructose whose harm is increased by the switch to a low- fat diet, thus higher carb/sugar western diet.  Also not mentioned is the eating 6 times a day (grazing on mainly carbs) and lack of fasting.  Instead as causes listed and then a section on high glycemic load.  Another error from this is in the comparison of marathon runners to Kativans, since the runners as a group carb-loaded prior to running and while training, which includes overload on sugar/fructose.  More crap is the mentioning of vitamin D but not C and defective collagen caused by under production in the polyol pathway or hyperuricemia.  Stressed is junk food and lack of activity; however, the traditional societies have low activity—just watch an anthropology film.  Walking in search of food, cooking, preparing foods and socializing are all low intensity activities.  Dairy cannot be a cause since several societies in Africa (Massi) and artic regions (Laps) have dairy as a staple.  Moreover, adjusting for use of tobacco and smoke from cooking and lighting, the conditions prevalent now were rare among the elderly of the 17^th through 19^th centuries, and first decade of the 20^th century.  High up is putative inflammatory nature of our diet which is low in micronutrients, while missing insulin resistance and fructose with its conversion to uric acid and its high rate of glycation that diminishes the production .of collagen.  Other putative causes include:   Regular sun exposure 38,151 (except  for the Inuit, whose very high intake of vitamin D3 from fish and marine mammals158,159 may have rendered the lack of ultraviolet stimulated cutaneous vitamin D synthesis less relevant) • Sleep patterns in synch with the daily variation in light exposure152 • Acute as opposed to chronic stress160 • Regular physical activity, as this was required to obtain food and water, to escape from predators, for social interaction, and to build shelters146,147,153 • Lack of exposure to man-made environmental pollutants160 • Universal fresh (generally unprocessed) food sources as depicted in Table 4.14,64,65,154,155,157.   The article blames refined carbs with their high glycemic load as another possible main cause of insulin resistance and metabolic syndrome, but makes no mention of Lindberg’s study of the Kativans whose carbs for energy is over 70%. Full article is 22 pages and has 343 footnotes.  

Note I have put in bold what is important, and have put my comments in brackets.  At the end our the putative causes for the conditions associated with the western diet (CAWD).  The causes start with the high fructose diet that overwhelms the cellular repair system.  This affects the liver to cause insulin resistance, and once insulin resistant the CAWD are significant increased.  The work of Dr. Joseph Kraft has established that insulin resistance (IR) is by far the major causal factor.  And in the 4 decades since his use of glucose tolerance test which measures serum insulin every 15 minutes over 5 hours following the injection of a bolus of glucose.  The modus operandi has now been sufficiently worked out on how excessive fructose causes IR and how both IR and fructose are the major causes  for CAWD.

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© 2011 Carrera-Bastos et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. Research Reports in Clinical Cardiology 2011:2 15–35 Research Reports in Clinical Cardiology Dovepress submit your manuscript | www.dovepress.com Dovepress 15 Review open access to scientific and medical research Open Access Full Text Article DOI: 10.2147/RRCC.S16919

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