Textbook on Conditions Associated with the Western Diet

Low sugar population, health testing, book reviews
On sugars basics 2-B-1

Low sugar population, health testing, book reviews


LSP the evidence that they don’t get CAWD:  

Combine with 1-B-LSP intro

  1. Mystery:   This book is about solving why those populations on a low sugar diet (LSPs) have a different set of illnesses.  It is about what has been known since 1982 called conditions associated with the western diet (CAWD), and before that as conditions of civilization, and prior as conditions of affluence.  It arrives at the cause, fructose, and how through fructosylation (fructation) it damages the mitochondria (MTD), and when consumed significantly above what cellular repair system can repair, the altered functions of the cells throughout the body increase the risks for all the CAWD, and especially among the elderly in what is known as age related conditions. 

    Since the seminal work by Burkett and Trowel in 1981, the science solving that mystery has made an incontrovertible case against fructose.  The second of 6 Sections is on sugars.  The third section is on the mitochondria, which fructose “modifies” through the Trojan horses of proteins and polyunsaturated fats (PUFAs):  it bonds to them in a process of fructation (also labeled fructosylation) in the cytosol, and some of those damaged molecules are transported into the mitochondria a topic in Section 3, which is devoted to the mitochondria and its altered performance, most significantly is the reduced production of ATP, the causal factor for insulin resistance (IR) in the liver.  Section 4 names what I considered the most significant changes the damage goods cause operating through a diminished production of ATP and other chemicals produced by the mitochondria.  On the big demon list is a reduced production of collagen, sensitivity to uric acid, and a reduced rate of autophagy (RRA).  RRA explains why low sugar populations are resistant to, for example the effect of cigarettes (the degree correlates to the percentage of those who life-long limit their sugar to under 24 grams a day (WHO’s dietary recommendation for sugar intake for women).  Section 5 is on those conditions that are called age related health conditions but are more accurately called conditions associated with the western diet (CAWD) since they are nearly unknown among the low sugar populations (LSPs).  Thus by Section 4 is set out the cause for our health disaster, and the association between mitochondrial dysfunction (MTDD) and the conditions, the topic for section 5.  And since most readers would be interested in what to do repair our fructose damage mitochondria and the consequences there from, as a Benthamite (utilitarian) I am morally obligated to write a Section 6 on what to do.  Simply limiting sugar to 24 grams a day will only very slow promote healing among adults, much quicker among children, and at a moderate rate among young adults.  There are ways to double and quadruple that rate, and this is what Section 6 is about. 

    Oh, and as a Benthamite I am also obligated to set the record straight concerning tobacco science and its consequence.  Thus many bromides [truths that on the shelf of time are stable] that are engraved in textbooks and taught by key opinion leaders (KOLs) and their dupes; these bromides will be dumped into my acid bath of basic science.  The foundation of this book, and thus the bath is to piece together into a sold fabric the pieces of science that answer the basic questions of why we get what are now as conditions associated with the western diet, and the LSPs don’t get them.  The test is the modus operandi, the why is this happening.  Why do we get cancer, and they don’t?  Why is fructose very different than glucose?  Why does the LSPs mitochondria outperform the mitochondria of the HSPs?  Why does this difference effect health, and how?   The answers are there is journal articles, thousands of journal articles, many of them tangent, and a few seminal covering a large area of research.  I let the journal speak. 

    This is more than solving a mystery, it is also about wellness.  The amount of harmful bromide spread as healthful upon the minds of physicians, dieticians, and the public by KOLS and their dupes, has created is exposed then in Section 6, there is what to do that promotes healing. 


2.  CAWD        I am not the first to see the association of MTD dysfunction and CAWD:  A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's diseaseepilepsymigraine headaches, strokes, neuropathic painParkinson's diseaseataxiatransient ischemic attackcardiomyopathycoronary artery disease, chronic fatigue syndromefibromyalgiaretinitis pigmentosadiabeteshepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction—link 2007 .

Insulin resistance is a result of two complimentary effects, ones is that the damage to MTD causes both reduced size of MTD and reduced absorption of and metabolism of glucose (and presumable fructose and galactose which are also metabolized in MTD.  A 2006 study found among other things:  glycogen synthesis was decreased by over 50% in patients with type 2 diabetes.  That study also found consistent with population studies that the children of diabetics have similar reduction in metabolism of glucose:  Further analysis has found that the reduction in mitochondrial function in the insulin-resistant offspring can be mostly attributed to reductions in mitochondrial density.”  This finding is supported by another which measured the size of MTD of three groups of 10 each, lean, slightly obese and t2d.


3.   Biomarkers of LSPs:  What is normal biomarkers for those on the western diet, isn’t for LSPs on a paleo diet         

TABLE 2 Electron microscopy measurements of mitochondria size in vastus lateralis skeletal muscle from lean and obese nondiabetic volunteers and type 2 diabetic subjects


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


Population -----   



Women -



SBP----   -

DBP-- ----


DBP -----



























Table 3:  Systolic blood pressure and diastolic blood pressure in Yanomamo Indians 69.     

Age years --------

Men -----------

















50 +




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

Men 25-39




Women 25-39



3.9 vs 5.7

3.5 vs 6.85

3.55 vs 7.65


3.5 vs 6.2

3.85 vs 3.9

3.8 vs 7.25


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

Men  <40


60 +


Women < 40


60 +

1.7 vs 3.4

3.5 vs 5.2

3.7 vs 7.2


5.95 vs 11.4

3.2 vs 14.1

3.95 vs 19.1


Figure 4 Fasting plasma leptin (ng/mL) in Ache Indians versus American marathon runners.83   Ache (Axe people) are indigenous hunter-gatherers of eastern Paraguay.






Systematic recording of dietary intake while living in the forest entirely off wild foods suggests that about 80% of their energy in the diet comes from meat, 10% from palm starch and hearts, 10% from insect larva and honey, and 1% from fruits. Total energy intake is approximately 2700 kcal per person daily.[1] 


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







Average American








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 insulin resistance, fitness is the best marker for health/longevity——link to senior runners.   


Cardiovascular fitness is of all measurement the best predictor health and quality of life.   So why is there so a difference in all of this markers for health of LSPs and HSPs.  Figure 1 and 4 contain the answer, IR.  Children on the western diet develop IR.  Many by comparison to the LSPs are born with IR.  A mother with IR pass on through fetal environment IR. Her elevated glucose causes cellular responses that affect the number of receptors for the transport of glucose into cells and other cellular functions.  It is a fetal adaptation to the dietary environment the child will be exposed to.  These changes on a cellular level or further established by the frequently consumption of excessive sugar.  What I predict is that at some point, even with physical training and change of diet, obtaining the levels of insulin and leptin in figures 1 & 4 will not be possible.  My guess would be by the 25th year—could well be in the teen years. 


4.  Defective mitochondria:  What is driving the damage to the mitochondria.  The literature finds 3 causes:  oxidative stress from the reactive chemical created in metabolism, in addition there is the role of uric acid produced during the metabolism of fructose in the mitochondria, there is fructosylation, and with damage to the mitochondria the repair systems of the mitochondria are not functioning at optimal levels.  Evidence from defective mitochondria comes from lower use of oxygen and smaller size in those with type 2 diabetes--at 2005, 2006.   A reduced basal ADP-stimulated and maximal mitochondrial respiratory capacity underlies the reduction in in vivo mitochondrial function, independent of mitochondrial content [number of mitochondria].  A reduced capacity at both the level of the electron transport chain and phosphorylation system underlies this impaired mitochondrial capacity [less ATP molecules]”--at 2008.   As maintained those with IR in the liver which is caused by the high fructose diet will develop in the liver and later in other tissues defective mitochondria similar the diabetic but to a lesser degree.  This will causes a decrease in the production of ATP through the Krebs cycle, and as a consequence an increase in cellular and serum glucose.  In the liver and conversion rate of glucose to glycogen and the production of ATP has decrease due to defective mitochondria and the effects of inflammation caused by a fatty liver, thus slowing the utilization of glucose and raising serum glucose, the hallmark of IRsee 2008 and 2011.  Cells throughout the body already load with glucose become resistant to the uptake of more glucose as the liver’s functions decline. Through a feedback mechanism these body cells become resistant to the uptake of more glucose. Added to this is the Crabtree effect:  a high level of glucose down regulates glucose metabolism (inhibition of respiration), “that effect was strongly antagonized by fructose 1,6-bisphosphate (F16bp). . . .  as able to inhibit mitochondrial respiration. . .” [2] This combination of factors explains the development of insulin resistance in tissues besides the liver.

Fructose has a very low insulin index because over 95% is taken to the liver by the hepatic portal vein where it is phosphorylated there thus making it incapable of passing out of the liver like glucose--Wiki.  invisible to insulin by being taken from the serum on first pass from the small intestines via the hepatic portal vein to the liver.  This explains why fructose though invisible to insulin, has a glycemic index (which measures glucose uptake from foods) of fructose is between 19 to 23, while glucose is rated at 100, and sucrose at 60 (thus not 50).   The rise in insulin is because of the slower uptake of glucose through the GLUT-5 transport system into the hepatocytes.

          “Perturbations in the regulation of glucose and lipid metabolism are both involved in the insulin resistance in skeletal muscle in obesity and type 2 diabetes (2,3). Previously, our laboratory (30) as well as others (31) have observed that the severity of skeletal muscle insulin resistance in type 2 diabetes and obesity is related to diminished activity of oxidative enzymes. In addition, accumulation of triglycerides in skeletal muscle is also correlated with the severity of insulin resistance and with diminished oxidative enzyme activity in these disorders(23) [not causal] . . . The mitochondria area was reduced by ~35% in type 2 diabetes and obesity.” at 2002.  Size and shape of mitochondria are strong associated with compromised functioning of the mitochondria—see for example the work of Nobel Laureate Otto Warburg.  Research is needed to find out if this change also occurs with IR.


Fig. 3.

Decline in skeletal muscle mitochondrial function with aging humans[3]


[1] Wiki, 12/18 Ache https://en.wikipedia.org/wiki/Ach%C3%A9.  The article’s discussion of their diet puzzles on why the men prefer to hunt rather than gather food for which coconuts are plentiful and supplies 25% more energy per hour of labor than hunting.  I aver that hunting reduces boredom more than gathering foods such as coconuts.  Given this it explains why another article finds that the average for hunter-gatherers is 60% of calories from animals and insects.  

[2] Kelley, David, Jing He, et al Oct 2002, Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes

[3] Kevin Short, Maureen Bigelow, et al, April 2005, Decline in skeletal muscle mitochondrial function with aging humans



Review of Burkett & Trowell   -- include  WESTERN DISEASES: THEIR EMERGENCE AND PREVENTION. By H.C. Trowell and D.P. Burkett

Burkitt. Cambridge, MA, Harvard University Press, 1981. 456 pp. $40.00.


During travels through developing and industrialized countries in the West Pacific, Far East, and Central America, I often wondered about the state of health of these peoples and those in similar countries around the world. I was especially curious about the prevalence of chronic non-infectious diseases and how these were related to culture, environment, diet, and personal health practices. Furthermore, I was intrigued about the extent to which Western acculturation directly or indirectly

affected health. These questions are now answered on a global basis in this book edited by two eminent physicians, H.C. Trowell and D.P. Burkitt. I applaud their efforts and those of the contributors in presenting current information on this timely and significant aspect of international health and epidemiology.  As is succinctly stated in their preface, "this book attempts to discuss the commoner diseases of civilization." In essence, these diseases are ones felt by the editors

to be characteristic of modern Western industrialized societies: metabolic and cardiovascular diseases (e.g., coronary artery disease, hypertension, diabetes mellitus, cerebrovascular disorders); intestinal diseases (e.g., appendicitis, diverticular disease, cancer, hemorrhoids, polyps, constipation); and a variety of others, including

nephrolithiasis, gout, pernicious anemia, thyrotoxicosis, and breast and lung cancer. 


The major chapters in the book study several specific populations from all corners of the earth. They are collected in sections under the concepts of hunter-gatherers, peasant-agriculturists, migrants and mixed ethnic groups, and the Far East. The people described include Inuit Eskimos, Australian aborigines, Pacific Island groups, South African populations, Hawaiian ethnic groups, and the population of Taiwan and China.  The chapters are thorough and well-written, with numerous and current references. The 34 contributors, of whom the majority are physicians, have had extensive experience living and working with these populations. In each chapter, discussions cover population demographics, cultural aspects of the diet, and important studies on disease-specific morbidity and mortality data. A common thread running through all of the chapters is the role of diet (carbohydrate, fat, fiber, and protein components) and known health risk factors (smoking, sedentary living, alcohol consumption,

stress concomitants, and individual susceptibility) as associated factors in the epidemiology of these diseases. Topics are presented in an informative manner for the reader to consider, without biased "breast-beating" over conjectured dogmas. Another section of chapters is concerned with the international epidemiology and environmental aspects of certain important diseases, including multiple sclerosis,

cancer, and the arthritides. The current state of the art in the treatment and prevention of cardiovascular diseases, intestinal disorders, and diabetes mellitus is also examined. There are only two shortcomings of this book, but they are inherent in its design and do not detract from its purpose. In some instances, the available orbidity and data are limited and are not able to be broken down into specific rates, i.e., by age group. Second, the subject of psychiatric diseases is not covered; however, this would entail a separate text.


Western Diseases: Their Emergence and Prevention stands on its own merits as a welcomed and necessary reference for those involved in the fields of international health and epidemiology. I also highly recommend this book to anyone who anticipates working in the fields of overseas health care or exploration medicine. 



Department of Epidemiology and Public Health

Yale University School of Medicine


The Burden of Prudence – Industrialisation and Disease

Thomas McKeown


Hugh Trowell and Denis Burkitt are a distinguished physician and surgeon who have spent most of their professional lives in Africa; with T.L. Cleave and G.D. Campbell, they have probably contributed more than anyone else to our understanding of the relation between the health problems of developed and developing countries. In Western Diseases they bring together reports by 34 contributors, who describe their experience of changes in the pattern of disease in several countries as Westernisation occurs. There are four main lines of evidence, which the editors admit are not all equally secure. 1. Until recently many of the non-communicable diseases now predominant in the West were uncommon or absent in hunter-gatherers and peasant agriculturists. 2. When these populations change from their traditional ways of life to those of the developed countries, they begin to exhibit the Western pattern of disease. 3. The incidence of some of the diseases has declined in Western populations which have reversed certain features of their lifestyle to bring it closer to that of peasant agriculturists. 4. Of the multiple influences responsible for the Western pattern of disease, dietary changes are probably the most important.

The full text of this book review is only available to subscribers of the London Review of Books.


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