Book on fructose mitochondria and the sickest of mammals
1B-low fructose-avoids conditions associeted with western diet
Low sugar populations, the evidence that they don’t get Conditions Associated with Western Diet (CAWD).
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.
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
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.
[The once common community hospitals are now corporate hospitals.]
are we so much sicker than in the 1950? Why is the average period of infirmity
years? Adjust the current longevity
figures for the reduction in cigarette smokers (46 to 16%), 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
Why aren’t the paleo peoples on traditional
diet having our chronic health problems? What is causing the health decline
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
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).
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
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. 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. 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
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, 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.
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,
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 =
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,
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.
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,
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
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)
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.
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.
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.
 Fuchs, Victor, March 2012, in NEJM,
Major Trends in the U.S. Health Economy
pack a day smoker shortens their life 7 to 10 years in matched studies. Major
causes ischemic events and cancer.
 Conover, Chris, Forbes, Dec 2012, The cost of health care 1958 vs 2012.
Burrows, Dan, in Kiplinger, Oct 2018,
 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
Also called diseases of affluence. I, contrary to common usage,
for illnesses that aren’t contagious, and diseases for contagious
illness. Gout and most cancers (exception Burkitt’s
lymphoma) are not contagious.
 Wikipedia (Wiki), adenosine triphosphate,
Oct 2020 10000 X 54.6 = 54,600 gm/454 =
in Eukaryotic cells, it is the intracellular fluid contained within the cell
membrane--the liquid found inside cells.
The two sugars are optical isomers. See #4
below for brief summary
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, 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
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
Since only 5% of the MTD proteins are made by the MTD, the
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
This is the link to which fructose and at lesser rate glucose
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.
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
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 IR—see
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
. .”  This
combination of factors explains the development of insulin resistance in
tissues besides the liver.
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
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 disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic
attack, cardiomyopathy, coronary artery disease, chronic fatigue
syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis 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 .
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
7. The voyage:
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.
 Fructose is a net 20 times in a cell
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
 Kelley, David, Jing He, et al Oct 2002, Dysfunction of Mitochondria
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.
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
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.
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
Yale University School of Medicine
Enter supporting content here
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.