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Book on fructose, mitochondria, and the sickest of mammals
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Sickness growth and Burkitt & Trowell's seminal book
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2. Two worlds There is grandeur in the way the pieces causing
the CAWD pandemic fit together.
From
the
book I am writing Why Humans Are the Sickest of Mammals. I start
with the rising cost of the illness
care industries, then chapter 2 is on the health of paleo peoples—a contrast to
those on the high fructose western diet.
The average period of infirmity averages over 16 years—a British Medical
Journal article, 2020. Yes, sucrose is
the MAJOR cause! Fructose in excess
causes insulin resistance and damages the mitochondria (our motor that makes
ATP, our fuel). The sum total of
reaction from fructation[1]
is over 50 times more damaging than glucose. Fructose when bonded to proteins
forms readily dicarbonyls & methylglyoxal.
We all have friends and family infirmed
and some have died from cancer, heart failure, strokes, dementia, diabetes,
suicide, and polypharmacy. These
conditions are virtually unknown among the populations which were on a low
sugar diet. Our economic, medical-sickness,
media, corporate, and government systems puts profits before people
From book I am writing:
With
the development of European imperialism, physician in those colonies reported
that native people did get the conditions of the affluent Europeans. Starting
in the 20th centuries
book appeared noting the difference. There
were reports of the two worlds of illness.
Imperialism brought with the European masters of large areas of the
world, both civilized and primitive, and with the rulers came physicians,
hospitals, and missionaries. Those who wrote of causes, most blamed refined
carbohydrates. Peter (Thomas) Cleave
(1906-1983) with C. Campbell of the UK blame just sugar with
compelling evidence Coronary Thrombosis and the Saccharine Disease,
in 1966, . Gary Taubes’ Case
Against Sugar (2016), covers in a chapter the literature, which I use
below.[2]
AFRICA: Forty-one years after [Dr.
Albert] Schweitzer’s [1913][3]
arrival, and a year and a half after he received the Nobel Peace Prize for
missionary work, Schweitzer encountered his first case of appendicitis among
African natives. “On my arrival in
Gabon,’ he wrote, “I was astonished to encounter no case of cancer…. I cannot,
of course, say positively that there were no cancers at all, but, like other
frontier doctors, I can only say that if any cases existed, they must have been
quite rare” [4]
Fouche,
for instance, district surgeon of the Orange Free State in South Africa,
reported in the BMJ in 1923 that he had spent six years at a hospital that
served fourteen thousand natives. “I
never saw a single case of gastric or duodenal ulcer, colitis, appendicitis, or
cancer in any form in a native, although diseases were frequent seen among the
white or European populations (Supra P 90).
When Trowell arrived in Kenya, he would later write, hypertension and
diabetes were absent. The native
populations were also as thin as “ancient Egyptians, despite consuming relatively
high-fat diets and suffering no shortage of food.” By the 1950s
obese Africans were a common
sight in the cities and towns. In 1956
Trowell himself reported what he believed to be the first diagnosis of coronary
heart disease in a black African, an obese High court Judge who had spent two
decades living (and thus eating) in England.
By the 1960s, hypertension was as common among black Africans as it was
in any other population in the Western world. When Trowell returned to East
Africa in 1970,
“the towns were full of obese Africans and there was a large diabetic clinic in
every city. The twin diseases were born
about the same time and are now growing together” (Supra P 228-9).
ESKIMOS:
“The most striking is
cancer,”‘ ‘noted Hutton based on eleven years in Labrador’, “I have not seen or
heard of a case of malignant growth in Eskimo.” ‘He also observed no asthma
and, like Schweitzer, no appendicitis, with the sole exception of a young
Eskimo who had been “living on a settler‘s dietary.’ “As
late as 1952, malignant cancer among the
Inuit was still deemed sufficiently rate that physicians working in northern
Canada, as in Africa earlier in the century, would publish single cases reports
in medical journal”... (Supra P 257). Hutton
observed that the Eskimos who had adopted the settlers’ diet tended to suffer
more from scurvy, were “less robust, and endured fatigue less easily, and their
children are puny and feeble” (Supra 90).
In a 460-page report entitled Physiological
and medical Observations Among the Indians of Southwestern United States and
Northern Mexico, (1908) Ales
Hrdlicka described his observations from 6 expeditions he had
undertaken.[5] “Malignant disease, he said, if they exist at
all—that they do would be difficult to doubt—must be extremely rare…. Ales Hrdlicka
considered the possibility, which [Ancel] Keys would raise fifty years later,
that these Native Americans were by chronic disease unaffected because their
life expectancy was relatively short: he
rejected it because evidence suggested that they lived as long as or longer
than the local whites.[6] Chas M. Buchannan, for instance, practiced
fifteen years among two thousand Indians with an average life expectancy of
fifty-five to sixty years and saw only one case of cancer. Henry E. Goodrich,
practicing for thirteen
years among thirty-five hundred Indians, saw a single case. [7]
ISLANDS: In
Fiji, in 1900, among 120,000 aborigines,
Melanesians, Polynesians, and ‘Indian coolies,’ there were only two recorded
deaths from malignant tumors (Taubes P 93).
United States cancer: In the United States
the proportional number of cancer deaths rose dramatically in the latter part
of the nineteenth century: in New York
from thirty-two per thousand deaths in 1864 to sixty-seven in 1900...
thirty-seven in Philadelphia (Supra P 93).
Cancer: The very concept of
diseases of civilization begins with cancer.
“In 1844 Stanislas Tanchou, a French physician, a veteran of Napoleon’s
army and a knight of Napoleon’s Legion of Honor, reported on his assessment of
death registries throughout Europe, concluding that cancer was more common in
cities than in rural areas and that its incidence was increasing throughout the
Continent. He acknowledged that cancer
was an ancient disease, perhaps always present but, ‘like insanity it seems to
increase with the progress of civilization’,” (Supra P 253). Tanchou
was the first to poll distant and out
of the way physicians on conditions, and they responded they were rare. In 1902,
the British government founded the
Cancer Research Fund to work with the Royal College of Physicians and the Royal
College of Surgeons in investigating “all matters connected with, or bearing
on, the causes, preventions, and treatment of Cancer and Malignant Diseases-(Supra
P 253). Within months, the letters and
specimens began to arrive [from around the British Empire.] “There
is a general unanimity of opinion in
favor of the idea that cancer is a rare disease among the aboriginal tribes, a
. R. U. Moffat wrote about Kenya and Uganda… and yet had seen only “one
undoubted case of cancer: a breast
cancer in a Swahili woman living in Mombasa” [a city on the coast of Kenya;
thus, not a rural native] (Supra P 254).
Hoffman published his seven-hundred-plus-page report Mortality
from Cancer Throughout the World in 1915. He concluded that “too
many ‘qualified medical
observers’ were making this same observation—the relative absence of cancer in
aboriginal and indigenous populations—and doing so in far too many locations
around the globe to all it to be explained away” (Supra P 255). Albert
Schweitzer began working at a hospital
in equatorial lowlands of West Africa in 1913... “astonished to encounter no
cases of cancer’ among the thousands of native patients he saw each year. However,
as ‘the native [took to] living more
and more after the manner of the whites,’ he wrote, cancer in his patient
population became ever more frequent” (Supra 275). “Canadian physicians
published an analysis of
thirty years of cancer incidence among the Inuit in western and central
Artic. Lung and cervical cancer had
shown a “striking increase” over that time period, they reported, but there
were still “conspicuous deficits” in breast-cancer rates. They could
not find a single case of breast
cancer in an Inuit patient before 1966, and only two cases between 1967 and
1980” (Supra P 257-8). This has all
changed as the Western diet worked its pathologies upon the Inuit. Like too
many aboriginal peoples to adopt the western ethanol and sucrose, they became
the sickest of peoples in the world—a deadly double stress combination.
Graph from the same Forbes, NEJM article supra
SUMMARY:
Most
of these historical observations came from colonial and
missionary physicians like Schweitzer and Hutten, administering to populations
prior and early exposure to western foods.
The new diet inevitable included refined carbohydrates which could be transported
around without spoiling, mainly white flour, sugar, foods made from them, dried
beans, whiskey, and can goods. Then diseases
of civilization or Western diseases
would appear: obesity, diabetes,
cardiovascular disease, stroke, cancers, arthritis, osteoporosis, and other
conditions of affluence. “When any
diseases of civilization appeared, all of them would eventually appear.” This
led investigators to propose that all these diseases had a single common
cause the consumption of easily digestible, refined carbohydrates. A few
including Cleave and Yudkin of the UK
limited cause to sugar, calling it the saccharine disease. This hypothesis
of sugar was rejected in the mid-1970s,
when it could not be reconciled with [Ancel] Key’s hypothesis that fat and
cholesterol were the problem[8]-(Supra
P 91).
The reason not covered by
Taubes but others was that at the corporate level several industries (farming,
food manufactures, tobacco, fast foods, and pharma) wanted to blame the lipids
(cholesterol and saturated fats) for the rise in cardiovascular disease--other
conditions of
affluence were ignored.
Pharma had been treating, staring
in
the 60s, hypercholesterolemia with a drug that blocked dietary cholesterol, the
food manufactures were hawking refined carbs especially sugar and vegetable
oils, big farming had fields mainly of corn, wheat, rapeseed, safflower, and
sugar cane, and fast food wanted cheap grains v s. Meats and dairy poultry lacked
sufficient
support. Corporate “influence” trumped
science and succeeded in changing dietary recommendations. Ignoring cigarettes
and sugar, governments
around the world adopted cholesterol and animal fats as the main cause for
cardiovascular disease. Corporate media,
physicians, and dietician soon were in line with their recommendations, though
the studies and research supporting the
lipid theory were all flawed.
Thomas Cleave wrote, “I don’t hold
the cholesterol view for a moment.
Mankind has been eating saturated fats for hundreds of thousands of
years. For a modern disease to be
related to an old-fashioned food is the most ludicrous things I have every
heard in my life. If anybody
tells me that eating fat was the cause of coronary disease, I should look at
them in amazement. But when it comes to
the dreadful sweet things that are served up… that is a very difference
proposition.” Dollars trumped science
and humans are social animals. With religious glasses few see beyond the
beliefs of the common herd seeded by KOLs[9],
media, and physicians. Fewer dig through
the literature to uncover the scientific fraud used for marketing, and if they
do, they are denied the media platform.
We are a social animal not a scientific Sherlock Holmes searching for
the evidence-based solutions—most lack the training and the media pours
cognitive dissonance into their ears. When
government, media, and industries speak, we go to war, in this case a war on
saturated fats and cholesterol. Dollar
ethics shout and science is buried by tobacco science. We are the sickest of
mammal—by miles.
[1] Fructation (fructosylation) is the non-enzymatic bond of
fructose inside a cell and also the additional bonding of products of the
original reaction, such was dicarbonyls formed from fructose. Dicarbonyls are
50,000 more reactive than
fructose.
[3] Ludwig Philipp Albert Schweitzer (1875-1965)
was an Alsatian-German Polymath, theologian, Lutheran minister organist,
musicologist, writer, humanitarian, philosopher and physician. He received the
1952 Nobel Peace Prize, and
an essay of his was included in my high school literature book. At his own expense he established in 1913 a
hospital 200 miles upstream of Cape Lopez in Gabon Africa. Thousand came to
his hospital for years. There were period of being in Europe raising
money for setting up a new hospital with more staff.
[4] Gary Taubes, The case against Suga ,(2016)
P 257
[5]
This work, of Berkitt and Trowel all 454
pages is available on the internet.
[6]
Hrdlicka, Ales Commission, from his 213-4m, with parts from Taubes
[8] The
McGovern Select Committee on Nutrition and Human Needs also known as the McGovern
Commission was another example of dollar politic. It scopes was to both
to focus on the ever-rising
rate of heart disease and to make recommendations as to human needs and
national nutritional policy and to give the appearance of a consensus of
science as to the cause, while behind closed doors it was decided to support
corporate big agriculture, food manufactures, tobacco, and pharma, and the
commission did. The commission relied
upon Ancel Keys and others that were scientists for hire. The commission ignored
the evidence which
clearly favored the evidence against sugar, rancid fats, and supported
saturated fats. The role of tobacco as a
cause was not broached, even though the excess deaths were higher for
cardiovascular disease than for all cancers for a person who smokes long-term a
pack a day, and over 45% of adults smoked. The results were a reduction in fats
and an
increase in sugar for low-fats foods. This is one example in the endless lists of evidence supporting that we
have elected a corporatist state—money talks.
[9]
Key Opinion Leaders, similar to scientists for higher, advocates for
industry rising to the top of the medical field because of pharma. They are
minions in the systems which have
made us the sickest of mammals in our neoliberalism corporate honor system.
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2B-1:2-Western
diseases, the evidence of 2 worlds 5/13/22 good
CAWD conditions associated
with the Western diet CHD Coronary heart disease CVD cardiovascular disease
HSP high sugar population LSP low sugar population MTD mitochondria
t2d type 2 diabetes
Chapter 2:
Diseases of the Western diet: 1.
Introduction 2. Why we got the wrong
a 3. The historical evidence and beliefs on
sugar and carbs affecting health 4. The
literature on conditions of affluence
5. Books on conditions of affluence
6 The authors of the seminal work on CAWD 7. Seminal book, Western
Diseases: Their Emergence and Prevention 8. The reception, a review I skip to #7 the Burkitt & Trowel book
7. Seminal
book, Western Diseases: Their Emergence and Prevention: by Doctors Burkitt and Trowell in 1981; it is a 456 page survey by
34 contributors in 19 countries providing 27 articles on 21 populations that
aren’t on the western diet. Combined the
authors taught medicine for over half a century in East Africa and had
travelled widely visiting hospitals on 5 continents. In this major synthesis
of cross-cultural research, 34 distinguished
scientists and physicians wrote on 25 common metabolic and degenerative
diseases characteristic of all advanced Western nations and Europeans living in
the country where the contributors practiced medicine. They noted the lack of
those conditions of
natives in these underdeveloped countries; viz., among both hunter-gatherers
and peasant agriculturalists. It was a survey of populations
who didn’t or didn’t or until
recently eat refined carbohydrates.
Their survey establishes the difference in condition between LSPs and
HSPs and added more conditions to the list by Cleave. There is a limit on the
comparison, the more recent data was polluted by contravening variables. All of the articles,
there was no controlling for fructose, cigarettes, ethanol, and working
conditions such as in mines. There was
no attempt to separate those on a traditional diet as farmers, from those not
on a traditional diet. Working
conditions has over the centuries been horrific, worse than in Europe in the 19th
century.[1]
The table of content of Western Diseases: Their
Emergence and Prevention
Contributors
v foreword
ix Preface
xii
Part I
Emergence of
Western diseases in sub-Saharal Africans
1 Hypertensions,
obesity,
diabetes mellitus and coronary
heart disease
3
2 Surgical
diseases of
the large bowel and other related
Diseases
33
Part II
Environmental
factors of certain diseases
3
Gallstones
47
4
Renal stone
60
5
Multiple sclerosis
71
6
Arthritides in negroid
peoples of southern Africa
83
7
Cancer
93
Part III Hunter-gatherers
8
Eskimos (Inuit)
113
9
North American Indians
129
10
Amerindians of Brazil
138
11
Australian Aborigines
154
Part IV
Peasant
agriculturalists
12
Papua New Guinea
171
13
Uganda West Nile
district
188
14
Zimbabwe
194
15
Pacific Islands of
Nauru Tuvalu and Western Samoa 204
Part V
Migrants and mixed
ethnic groups
16
New Zealand, Maori and Pacific
Polynesians
227
17
Israeli Migrants:,
268
18
South African Black, Indian and
Coloured Populations
285
19
Hawaii ethnic groups
319
Part VI
Far East
20
Japan
327
21
Taiwan and China,
352
VII Regression of certain
Western Diseases
22. Diabetes mellitus
373
23 Hypertension, hyperlipidaemia,
angina and
coronary heart 392
24 Hypertension and angina
411
25 Haemorrhoids, diverticular
disease and deep
vein thrombosis 421
Part VIII
Summary
26 Contributors’ reports
427
27 Treatment and prevention:
a note on
autoimmune disease in Sub Saharal Africans
436
Index
445
Below
are my
2016 notes on their book; it covers most of their chapters:
1 Hypertension,
obesity, diabetes mellitus and coronary disease—Hugh Trowell:
Groups with
low blood pressure and not effected by age; 30 ethnic groups have been
identified (1920-1940). After 40 years
levels actually feel to average of 105/60 mm/HG in 97 men aged more than 60
years. There is much essential hypertension nowadays. First case of hypertension
reported in 1941.
During that period there were 56 cardiovascular deaths, but no manifestation of
essential hypertension or ischaemic heart disease, both of which were common in
European and Indian persons. Eighty-nine
Africans displayed advanced atherosclerosis of the aorta, but the coronary
arteries had been spared. There were 150
European qualified doctors in Kenya, Uganda and Tanganyika. Stress is normal
in these people: fear of evil spirits, dread
charms, burning of hut by personal enemies, high murder rate, and early
deaths. Hunter-gathers obtain most of
their food in 2-3 hours work a day.
Animals supplied 25-35% of their food.
Seven percent of the I Kung African Bushmen were over 65 years of age,
but all were slim (1977). Diet in rural
Wales energy percentages: 1870 4% sugar,
1977 17% sugar and in their diet, cholesterol tripled, fiber dropped 68%, and
fat increased 59%, starch dropped 50%, protein remained at 11%. There was a
rarity of glucosuria in Africans
in the 1930s, all admitted to hospitals were tested, one nurse maid living with
European employers had sugar in her urine.
In 1977 one hospital in Kenya report 137 cases of diabetes. In 1937 that
hospital reported no CHD in the
first thousand Kenyan autopsies. In
South Africa by 1977 1-2% of death attributed to CHD, author assumes that the
factor causing it must be present since childhood.
2 Surgical
diseases of the large bowel and other related diseases—Denis Burkitt
All papers
prior to 1940 indicate a rarity of appendicitis in sub Saharal Africa. Similar
finding for hiatus hernia as too
colon cancer and diverticular disease of the colon.
PART II Environmental factors
of certain diseases
3 Gallstones—Kenneth
Heaton (coauthor
with Burkitt and Trowell in
their 1973 book): not of sufficient
interest, used to support hypercholesteremia.
4 Renal stone: others observed that
both protein and glucose can increase the rate of urinary calcium excretion and
Lemann et al (1969) noted that the glucose effect was exaggerated by calcium
stone formers. Sucrose added supplements
to a standard diet increase the frequency and magnitude of diurnal peaks of
urinary calcium concentration in a majority of subjects. Urinary oxalate excretion
is increased
concomitantly so that the formation product of calcium oxalate. Kang et al.
(1977) observed… that the
ingestion of sucrose by laboratory animals resulted in urinary excretion in a
diffuse interpapillary glomerulosclerosis[2]
and that urinary excretion of N-acetyl-beta-d-glucosaminidase,[3] an
indicator of renal tubularly damage, P 64.
6 Arthritides
[arthritis] in negroid peoples of southern Africa: like other
chapters, low than growing rate.
5
Multiple sclerosis: various theories, one is that the
exposure to
a slow viral agent must occur before the age of 15 for most cases, there are
other progressive diseases which cause the degeneration of the human brain,
such as Kuru, & Cruetzfeld-Jakob are possible diseases causes, P 74. Experiments
show it to be transferrable
agent, e.g., 4 out of 7 scientists developed MS from handling patients’ blood
work.
7
Cancer: Vitamin A reduces risk of cancer, lung
and stomach, p 104. Overall, quite
disappointing,
Part III Hunter-gatherers
8 Eskimos: means raw meat eater. Menarche now 2 years early than 100 years ago,
p 121. Eating raw meat preserves the
little vitamin C in it. They eat from
the stomach of caribou and rabbits the greens; it is their source of vitamin C. They
chew spongy bone for the calcium.
9 North
American Indians: Nothing new
to add.
10
Amerindians of Brazilian:
40 observed, there
were
CVD, no obesity, no diabetes or pre-diabetic levels of serum glucose, 2 skin
cancer, 2 gynaecological cancers, and a
4year old with undifferentiated testicular cancer.
11 Australian aborigines: not suitable because of refined flour and
sugar.
Part IV
Peasant
agriculturalists
12
Papua New Guinea,
agriculture, sweet potatoes, (Ipomoea
Batatas), some 24 varieties are
grown in the clan’s territory, takes about 10 months to mature. Taro is
limited (Colocasia esculenta),
introduced in the last two generations. Most
tribes consume over 90% sweet potato, non-tuberous vegetables was under
5%. A similar heavy dependence on a
single vegetable staple has been reported in other highland tribes. Chemical
composition of the sweet potato
varied widely. Protein from 1 to 1.9%
wet weight, fiber 1.25 to 3%, and calories from 112 to 155 kcal/100 edible
portion. Male daily intake 2,300 kcal,
females 1,770 kcal. Males consumed 25 g
protein, females 20 daily & and fibre was 25 and 20 g respectively. Very
low intake of protein, fats, and refined
carbs and a high intake of complex carbs.
Population increases of 2.7% per years, birth rate of 42/1000, and death
rate of 15/1000 for Murapin population.
43% of population died before the marriage age—Vines reported an infant
mortality rate for a different population of 127/1000, 12.7%. Subjects of the
present study are typical of
other Papua New Guinea population in that their body weight reaches a maximum
between the age of 20 and 29… 59.8 kg in males and 59.9 for females. By
the seventh decade the average body weight
has decreased by 13.3 kg or 23.percent in the case of women and 13.5 kg or 25
percent in the case of men p.175. Even in Western populations, the lean body
mass in adults falls progressively with advancing age. The contrast is more
marked in the case of
women, females in the present study experienced a weight reduction of 25
percent compared with a loss of 8.5 percent predicted on the basis of Forbes
and Reina’s data (Sinnett et al., 1973; Sinnett 1977a) p. 176.
Malaria:
In the present population malaria was
uncommon. Examination of thick blood
films yielded a parasite rate of lower than 0.4 percent and none of the
subjects had splenic enlargement or anemia…. The low prevalence rate of malaria
is not surprising in view of the high altitude (2,600 m) p 176. Atherosclerosis
is uncommon p 178. No subjects showed evidence of Parkinson’s
disease or of previous cerebrovascular accident p 180. Clezy (1974) drew attention
to the fact that
the rate of colon and rectal cancer was low, reporting a rate per 100,000 being
0.6 for males and 0.2 for females for cancer of the large bowel. By contrast
cancer of the colon and rectum
per 100.000 population as 41.6 in the United States of America
13 Uganda West Nile district:
Millet is the staple grain, similar to wheat
nutritionally. Sugar and salt were
commonly purchased until 4 years ago economic hardship hit. Obesity was rare,
now among the more affluent
is common, especially women. Study based
on one hospital in the West Nile region (the country is divided by the Nile
River). T2d wasn’t diagnosed until the
50s, and ischaemic events are starting to emerge among the Bantu in the
1970s. Stools are large and soft, passed
twice daily, and it is regarded as alarming if a day is missed at 191. Cholesterol
gallstones and ulcers have never
been diagnosed, P 192. “This seeming
peculiar pattern of non-infective disease in the West Nile Ugandans is similar
to that seen formerly in many rural hospitals in the less developed areas of
Africa” at P 192.
14 Zimbabwe
(Rhodesia): Colon and rectum cancers are about 1/10 that
of Europeans, rough estimate, which they attribute to fiber in their diet, p
200, Ulcerative colitis 0 vs 27 for Europeans, comparing 2 hospitals, kidney
stones 54 to 588 p 201. Diverticular disease is a Western disease rarely
encountered in Zimbabwe p 200.
15
Pacific Islands of Nauru, Tuvalu and
Western Samoa: The price paid for civilization has been high
for the people who have enthusiastically embraced our Western lifestyle.
16
New Zealand, Maori and Pacific Polynesians: nothing to add.
17
Israeli Migrants: nothing to add.
18
South African Black, Indian and Coloured Populations: nothing to add.
19
Hawaii ethnic groups: nothing to add.
20
Japan: nothing
to add. The
Japanese prior to the 1600s ate little sugar, then trade with Europe and the
Japanese made confectionaries which were a luxury—Source NKK national TV show
on historical dietary habits, 9/28/18.
21
Twain and China: nothing to add.
End of survey
by JK.
This I held to be sufficient, and thus—though read—I
didn’t take
notes on chapters 16 through 21 and section VII s of their book. That section
was designed to support the
causal factors of low fiber, high cholesterol and salt. All of those population
had a supply of
inexpensive sugar, which I consider the slow acting poison and the major CC for
CAWD. In Section II is on sugar, the
case is made in detail on acting as a slow poison. It is built upon current
science, which was
weak until the beginning of this millennium.
Sugar for them was just another carb without fiber.
[2] Hardening of the glomeruli in the kidney,
also refers to scarring of the kidney’s tiny blood vessels. Glomeruli
filter urea from the blood. Scaring results in protein in the urine;
however, only 15% is from scarring, there are other kidney causes for the
protein.
[3] One of the primary functions of the enzyme
is
to hydrolyze oligosaccharides containing chitin. The enzyme is found in mammals,
fungi
crustaceans, cartilaginous fishes, mollusks, jellyfish, and some bacteria.
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 IR—see
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 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 .
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 ~~~~~~~~~~~~~~~~~~~~~~~~~
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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.
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