Home | On the good life | Book outline by chapters and subheadings | Letter on book project sharing | 1B-low fructose-avoids conditions associeted with western diet | 2:1 The basic on sugar, and related topics | 2:6 Rancid Unsaturated fatty acids in cell membranes | 2:7 THE FAT STORY. History and Science | 3-1 Mitochondrdial structures and maintenance | 6:1 AUTOPHAGY, repair, replace, recycle, and defense systems | 6:2 HORMONAL HEALTH | 6:3 Diet basics: Energy restriction, keto, and fasting diets | 6:4 type-2 diabetes diet versus drugs

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1B-low fructose-avoids conditions associeted with western diet


1:1 Low sugar populations, the evidence that they don’t get Conditions Associated with Western Diet (CAWD).  http://healthfully.org/rbook/id2.html  12/13/2020


A chart on the cost of infirmities caused by the western diet.  It is caused by an industry that profits through manufactured food, and others that profit from illness.  They are fulfilling their fiduciary obligation of maximization.


https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/2012/nejm_2012.366.issue-11/nejmp1200478/20130726/images/img_xlarge/nejmp1200478_f1.jpeg


 1. Two worlds: The paleo peoples’ natural foes are parasites, including worms, virus, bacteria, fungi, larva, parameciums, and other life forms that have evolved to live off a mammalian host.  Civilized humans developed conditions not found (or rarely) in the natural world, including obesity, diabetes, atherosclerosis, arthritis, cancer.  dementia, psychiatric conditions, osteoporosis, osteoarthritis, strokes, heart attack, stroke, and others.  This book is about why that happens including the major downstream-pathogenic changes caused by excess fructose causing a reduction in the production of ATP by the mitochondria.  It is pieced together from the relevant-current science.    


A slight decline in the average length of stay was more than offset by a 50% increase in the number of admissions per 1000 population.  The industry's 31% increase in the number of beds per 1000 population. . . . The number of active physicians in the United States increased by a factor of approximately four between 1950 and 2009.  There has been a large increase in the number of specialists and an even larger increase in the number of specialties and subspecialties, from a few dozen 50 years ago to more than 150 now. . . . The number of hospitalists has grown rapidly, from no more than 1000 15 years ago to 7000 10 years ago to approximately 30,000 in 2011, according to physician-economist David Meltzer of the  University of Chicago.[1] [The once common community hospitals are now corporate hospitals.]


https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/2012/nejm_2012.366.issue-11/nejmp1200478/20130726/images/img_xlarge/nejmp1200478_f2.jpeg


Why are we so much sicker than in the 1950?  Why is the average period of infirmity 16.7 years?  Adjust the current longevity figures for the reduction in cigarette smokers (46 to 16%),[2] lower death rate among those under 20, reduced toxic exposures in the work places, the under regulated uses of pernicious chemicals, the infectious conditions that were among the top 10 causes of death.  Adjusting for these, there is a decline in quality of life and longevity.  Why isn’t the average age of death near 90?  This technical book will answer that question.    


Why aren’t the paleo peoples on traditional diet having our chronic health problems?[3]  What is causing the health decline of the civilized populations?  Why weren’t the poor peoples in western societies before the 1850s having what once was caused conditions of affluence? 


            This technical book pieces together the journal evidence on how we damage the mitochondria by excess fructose, and other causes, followed by their cellular & unhealthful effects.  It also corrects the tobacco science.  Please rise above your social conditioning to evaluate the evidence.


In 1958, per capita health expenditures were $134. This may seem astonishingly small, but it actually includes everything, inclusive of care paid for by government or private health insurers. A worker earning the average wage in 1958 ($1.98) would have had to work 118 hours—nearly 15 days--to cover this expense. By 2012, per capita health spending had climbed to $8,953.  At the average wage, a typical worker would have to work 467 hours—about 58 days. . . . On a per worker basis, total U.S. health spending this year will amount to $21,280, which would require an average-paid worker 1,108 hours of work to finance (and even more when taxes are taken into account).[4] 


This book is about CAWD (conditions associated with the western diet—the label used by Dennis Burkitt and Trowell, 1981).  There is a chorus of professors and others that pulled away the marketing curtain of sugar is just empty calories.  The history of science on cigarettes is repeated:  the warnings of the 1920s were repeated by a chorus for 4 decades, but marketing, big bucks, and regulatory capture won.  Cigarettes are still on the market, and cereals that have 40% of calories from sugar, which are heavily marketed to the youths.  Under 5% of physicians know that excess fructose is a slow poison comparable to ethanol.  Marketing of cigarettes works, and Apple Jack is 2nd, Captain Crunch 3rd, and Reese’s Puff’s 5th sales in 2017[5].  Section 2 covers how excess fructose damages the mitochondria, 3 is on the mitochondria, 4 is on major causes for CAWD, and 5 is the conditions. 


If physicians and dieticians have the right answers, then why is their diet causing a health disaster?  If we have miracle treatments, then why does the average period of major infirmity average over 16 years?  The wrong model fail explains the costs and failure of diets.


This section 1 is a comparison of 2 worlds LSPs and HSPS (low sugar populations and high sugar populations).  Learn why normal for those on the western diet is not good enough.  What I have put together is the Rosetta stone of the biological glyphs and translated them a story about fructose in the endoplasmic reticulum glycating unsaturated fats and proteins that are transported to the mitochondria.  You are with Vasco Nunez de Balboa’s crew in 1513 crossing the Isthmus of Panama to viewing the Pacific Ocean, and arrive during the storm of illness.


I offer you a guide with the best of 2020 biological science through Panama.  Pl ease rise above your social conditioning to let your rational module of your brain view the Pacific Ocean and know of fructose. So that you can understand the causes of western conditions. 


 This book is a product of 16 years of full-time studies of the journals, one-fourth of which are posted at healthfully.org/rg.[6]   I also stand upon the shoulders of dozens of books (see appendix) and hundreds of lectures and documentaries (/rh.id4).  My charts through Panama to the Pacific of infirmities is adjusted for the tobacco science generated by industries that profit from sugar addiction and illness. 


Living in a senior community, everyone around me is wounded.  The few who are not hobbled or scared don’t know what is lurking inside.  A brother of mine, Peter, who was physically fit, worked out several times a week, of normal weight, died this June (2020) at the age of 64 of colon cancer—it took 4 years.   My other brother Allen at 71 years has been averaging 70 pounds excess fat for the last 30 years—he gave up trying to lose it.   Only 2 out of 190 residents where I live run.  I, at the age of 77, run 60 to 80 miles a month, but I don’t know what is lurking in me (I ate the western diet for 71 years).  None of us have the biomarkers in the range of the low sugar populations (1:2).  As Professor Staffan Lindeberg, who studied the Kitavans off of New Guinea said in a lecture 2015, Normal is not good enough--referring to western standards for biomarkers (1:2).  He was a leading advocate of the paleo diet, was very lean, and in 2016 he died of pancreatic cancer.  In his case being better than normal was not good enough.   


You are about to look at two worlds, and find out why those on the western diet are so chronically sick—we are the sickest of mammals.  The charts of the sea of sickness are on these pages.  The voyage to knowing our place for the first time starts here; welcome aboard.   


 


2.     The 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 as conditions associated with the western diet (CAWD), and before that as conditions of civilization[7], and prior as conditions of affluence.  The book is on its major cause, excess fructose, and how through fructosylation (fructation) damages the mitochondria (MTD).  When consumed significantly above what cellular repair system can fix, the altered functions of the cells throughout the body increase the risks for all of the CAWD, and especially among the elderly because of the natural decline in the MTD’s production of the energy molecule ATP, which runs 95% of the chemical processes in the body. 


 



Adenosine triphosphate


 


          At 20 the average healthy, fit person produces daily 120 pounds of ATP (adenosine triphosphate) from mainly the metabolism of fats and carbohydrates.  Though there are only 0.2 moles of ATP (2 ounces, 54.6 grams, mole weight 273 gm), it is recycled in a few seconds.  The P in ATP stands for phosphate, the phosphate ion, PO4, with 3 extra electrons 3(PO4-1).  The phosphate ion supplies the energy for the chemical reactions in the body by ATP losing one of its 3 phosphates to form ADP (adenosine diphosphate). 


The energy used by human cells in an adult requires the hydrolysis of 100 to 150 moles of ATP daily, which is around 50 to 75 kg. A human will typically use up his or her body weight of ATP over the course of the day. Each equivalent of ATP is recycled 1000–1500 times during a single day (100 / 0.2 = 500).[8] 


          In the cytosol of the cell carbohydrates and fats are converted into pyruvate and acetyl CoA which are transported into the mitochondria.  The Krebs cycle (also called the citric acid cycle) in the mitochondria through the catabolism of pyruvate and acetyl CoA supplies the energy which restores the phosphate ion back onto the ADP (adenosine diphosphate) to produce ATP again—a process using the electron chain transport to supply the energy for what is called oxidation phosphorylation.  Most of the ATP is shipped out of the MTD into the cytosol,[9] organelles, and nucleus to supply the energy for cellular functions.  Stripped of the phosphate, the ADP is then transported to the nearest MTD (of which the typical active cell has over 100 of them per cell) for restoration of the phosphate. 


          With age the functionality of the MTD declines and its excess capacity in each cell declines, the production rate of ATP declines.  Every process in the cell, since they run on ATP, they too decline.  For example, collagen is replaced at a slower rate, thereby increasing the percentage of inferior collage.  Repair systems such as through the antioxidants function at a lower rate; and thus, all things go well below the youthful peak.  This aging process on a cellular level is accelerated on the western diet; ergo, the conditions associated with the western diet; thus, the age-related conditions. 


 


3.  A view of the charts (CAWD book):  Since the seminal work Western Diseases:  Their Emergence and Prevention by Burkitt and Trowell in 1981, a survey by 21 contributors in 19 countries, a chapter each population, in  solution to the CAWD has been solved.  Burkitt and Trowel like many others thought it was caused by REFINED carbohydrates, some by lipids, and some by sugar (topics that we be developed in other chapters).  The science showing that fructose was different was based on a few feeding experiments.  Since then the physical differences between fructose and glucose have been worked-out,[10] which explains the results of the feeding experiments. Beyond that in this book you shall learn how fructose, a slow poison, functions to be the major cause of CAWD—mystery solved. 


The second of 6 Sections is on sugars.  The third section is on the mitochondria, which does more than make ATP.  A key point is that fructose “modifies” through the Trojan-horses, proteins and polyunsaturated fats (PUFAs):  fructose bonds non-enzymatically to amino acids in proteins in the process of fructation (a term I prefer over fructosylation[11]) in the endoplasmic reticulum, and some of those damaged molecules are transported into the mitochondria (3:3).  It also bonds to unsaturated fats, which undergoes further reactions and contributes to the rancidification.  Some of the consequences are also in section 3.   Most significant is the reduced production of ATP, the causal factor for insulin resistance (IR) in the liver.  Section 4 covers the science of what I considered the most significant changes caused by the 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, IR, and a reduced rate of autophagy (RRA).  Down stream there are major contributors such as excessive lipid droplets, fatty liver, kidney and pancreas, endothelial dysfunction.  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 and 36 for men).  Section 5 is on those conditions that are called age related health conditions but are more accurately called CAWD, since they are nearly unknown among the low sugar populations (LSPs) and some of the conditions manifest their ugly head such as fatty liver, diabetes, and obesity in school-age children.  Section 4 set out the major cause for our health disaster, and the association between mitochondrial dysfunction (MTDD) and the conditions, in section 5 are many of the examples.  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 slow promote healing among adults, much quicker among children, and at a moderate rate among young adults.  There are ways to over double the rate of autophagy 9self-healing) in Section 6. 


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] 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 mixed with contrary evidence.  The function of this bath is to wash way the crapolla and bring out the colors of the patch-work quilt that covers our western health disaster and answer the question of why there are two sets of conditions, ours and the LSPs. 


The book repeated presents the modus operandi, the why it is 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?  How does this difference effect health?   The answers are there is journal articles, thousands of journal articles, many of them tangental, and a few seminal covering a large area of research.  I let the journal speak. I am the patchwork quilt maker. 




[1] Fuchs, Victor, March 2012, in NEJM, Major Trends in the U.S. Health Economy since 1950

[2] A pack a day smoker shortens their life 7 to 10 years in matched studies.  Major causes ischemic events and cancer. 

[3] “Chronic illness now is responsible for more than 80 per cent of all deaths and for an even higher fraction of cases of total disability.  Fries, James, July 1980, NEJM, Aging, natural death, and the compression of morbidity. 

[4] Conover, Chris, Forbes, Dec 2012, The cost of health care 1958 vs 2012.

[5] Burrows, Dan, in Kiplinger, Oct 2018,  America-s-most-popular-breakfast-cereals

[6]  At the website are pasted over 3-thousand journal articles and links to them. Links are in articles I wrote covering topics over 50 topics.  A lot can be done in 16 years.   Each section page such as on HRT has an index of other topics with links thereto; and there is an internal Google search engine on each section page.  Google search includes also the other website skeptically.org.

[7] Also called diseases of affluence.  I, contrary to common usage, use condition for illnesses that aren’t contagious, and  diseases for contagious illness.  Gout and most cancers (exception Burkitt’s lymphoma) are not contagious.  

[8]  Wikipedia (Wiki), adenosine triphosphate, Oct 2020  10000 X 54.6 = 54,600 gm/454 = 120 lbs.    

[9] Cytosol in Eukaryotic cells, it is the intracellular fluid contained within the cell membrane--the liquid found inside cells.

[10] The two sugars are optical isomers.  See #4 below for brief summary

[11] Fructation follows the form of glycation, and should be used since the processes are identical.  Each term naming the sugar bonding non-enzymatically.   However, current uses extends glycation to all sugars while suggesting to the reading that it is only glucose.  Pharma is very happy treating glucose, and thereby blaming glucose for what is done by fructose; moreover, LabCorp’s measurement of fasting glucose and HbA1C doesn’t distinguish the bonding by fructose.


At bottom of this chapter is a review of Burkitt & Trowell's 1981 survey book on conditions associated with the western diet.


4.  How excess sugar causes CAWD:  There is a complexity to life, a complexity that is every increasing with evolution, from the simplest virus to the mammals.  Every step of life has an orchestrated function that promotes survival.  This book is about what has happened because of the consumption at an average of 7 times that of paleo peoples of a slow acting poison, the reactive sugar fructose.  We have not evolved to be fruit eaters.  The systems cannot handle that amount of reactive sugar fructose,[1] no more than our liver can handle the ethanol in a gallon of wine, a quart of rye, or a 24-bottles of beers daily.  Ethanol pernicious effects start with the liver, and from liver dysfunction there are other consequences such as depression, and hemorrhaging veins in the throat.


Fructose also works upon the liver to cause insulin resistance first in the liver than in every biologically active cell.  Fructose also to cause a fatty liver (NAFLD) when in excess by its conversion to fat in the liver.  Insulin has a number of consequences (3:6) including weight gain and diabetes.  But unlike ethanol, fructose also has pathogenic consequences through its effect upon the mitochondria and the organelles called endoplasmic reticulum (ER, 3:4).  The mitochondria (MTD) and the ER function as an interconnected team.  


In every cell in the body there are the organelle rough endoplasmic reticulum (RER) which supplies the MTD with 95% of its proteins.  They are called rough because its surfaces are dotted with ribosomes.  The smooth endoplasmic reticulum (SER) supplies cholesterol and fats.  The ERs supply the These ERs are tethered to the nucleus and also to the MTD. 


For both types of ER, the MTD supplies all of its ATP, the major energy molecule. 


Since only 5% of the MTD proteins are made by the MTD, the other 95% come from the RER as needed through the ribosomes that are that are attached RER.  In a signaling chain the MTD send messengers to the RER for proteins, and the RER to the nucleus.  From the nucleus comes the DNA which are needed for the ribosomes on the surface of the RER.  The ribosomes produce the proteins for the RER and MTD.  Those proteins for the MTD are transported through the RER and the tubules that connect the RER to the MTD. 


This is the link to which fructose and at lesser rate glucose bond to the proteins and unsaturated fatty acids being transported to the MTD, by a non-enzymatic process called glycation. So bonded the substrate’s functions are compromised. The net results of the compromised proteins and unsaturated fatty acids (UFAs) is mitochondrial dysfunction (MTDD).  With MTDD there is reduced production of ATP, thus all cellular systems are adversely affected, including the repair systems.  Fructose is like ethanol but worse, since ethanol’s pathological assault is mainly upon the liver, and from the liver comes a limited set of consequences.  With fructose causing MTDD, the list is much longer:  the conditions associated with the western diet, CAWD.  We are the only vertebrate with years of infirmity, and excess sugar opens that door. 


5.    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 cause 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.

6.  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.

 

7.    The voyage:  This book in 6 sections pieces together the evidence on how fructose causes CAWD.  There is a need for this section #1, since the question of why the difference between the two populations, low sugar populations (LSPs) and high sugar populations (HSPs) has been marginalized over the last 40 years.  C Conditions of affluence has now become a global pandemic and renamed CAWD  Most readers believe that cancer, ischemic events, arthritis, dementia, and on and on are the norm for the seniors and their cats and dogs.  This section is a wakeup call, it is not natural, it is not the norm for old age if they are in a life-long low sugar population, including the wild animals. 

Now you know the answer to CWAD, what follows is the evidence as permitted by current science.  The paleo peoples, next 2 chapters, their bio-measurements are a basic proof that what is normal for lean Swedes is not good enough.  Darwin started with domesticated breeding, I with LSPs.  There is much more in the following 800 pages, read on and be like Balboa seeing the ocean. 




[1]   Fructose is a net 20 times in a cell more reactive than glucose.  Ten-times more reactive because of its structure and double that because glucose is metabolized first before fructose.  For both in the open form they bond to electron rich targets without the guidance of an enzyme in a process called glycation.  This adversely effects the substrate’s function. 

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


Book review of the seminal work by Burkitt and Trowell, physicians who spent a life-time treating natives and Europeans in the British colonies.

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.

MARK L. DEMBERT
Department of Epidemiology and Public Health
Yale University School of Medicine
~~~~~~~~~~~~~~~~~~~~~~~~~

For 5 tables of the biomarkers for paleo peoples http://healthfully.org/rmb/id5.html

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On how daily excessive fructose damages the mitochondria and thus is the main cause for the conditions associated with the Western diet--much, much, more the cause than insulin resistance, type-2 diabetes, and weight gain, all of which are caused by mitochondrial dysfunction, which starts first in the liver.