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5) Obesity and diet: “Obesity
is a chronic health problem. It is the major factor
for type II diabetes, cardiovascular disease. It is also
associated with cancer, osteoarthritis, liver
disease, sleep apnea, depression and other medical conditions that
affect mortality and morbidity” Wiki. The
official rate of 36% is based on the CDC
phone survey, a method that grossly underestimates. "Asking someone how
much they weigh is probably the second worst question behind how much money
they make… From past research, we know that women tend to under-report their
weight, and men tend to over-report their height, Wiki. And
it is worse: the 6.3 % of the population
who are morbidly obese (BMI above 40) are not included in with the 36% in the
category of obesity--see. “The
consumption of sweet soda and fruit
drinks has more than doubled since the 1970s… drinking sugary drinks was
affecting genes that regulate weight and increased the genetic predisposition
of a person to gain weight…. giving to children and adolescents calorie-free
drinks like mineral water or soft drinks sweetened with artificial sweeteners
resulted in weight loss” Wiki. Other studies have shown that in just 2
weeks a diet consisting of 25% of calories from sugar resulted in insulin
resistance--watch the CBC
program on sugar. The
full impact of
the increase in sugar takes years to develop, since obesity is a defect in the
fat storage mechanism from hyperinsulinemia (high insulin), and this take years
to decades to manifest (see #s 8, 9, 18, 19).
What follow mainly centers upon the regulatory system that control
metabolism and appetite, and thus weight, physical energy, and the results of
these homeostatic systems malfunctioning as a consequence of the Western
diet.
6) Biological controls for
weight gain: Gary Taubes- (book
list, at p. 112-125) convincing argues that the sedentary lifestyle is not a
cause of obesity but a result of the biological process that causes the
increase in adiposity. He argues that just like the biological mechanisms which
set height and hair distribution, there is one for weight. Gary uses animal examples of hippo, elephant,
blue whale, and squirrels prior to hibernation as illustration of this
mechanism. Insulin has the greatest
regulatory function, though over a dozen hormones and enzymes are involved. When hormones set weight to obese, they
control not just the rate of conversion of carbohydrates to fat and the storage
of fat, but also the rate of metabolism and appetite. Thus not only does
obesity through the load of extra weight diminish capacity for an active
lifestyle, but obesity affects the hormonal mechanisms driving weight gain also
zaps the energy needed to be active.
Those who are very active are so because of hormones and heredity.
Obesity is not a result of over eating, but of excessive fat storage.
“Consuming excess calories does not cause us to grow fatter, any more than it
causes a child to grow taller. Expending
more energy than we consume does not lead to long-term weight loss; it leads to
hunger” Tabues-1 454. Taubes
also argues
that to control weight long term
requires resetting the hormonal mechanism so that a lower percentage of fat is
stored and appetite diminished. This
explains why over 90% of people who after a diet fail to long-term maintain
their weight loss, their weight control mechanism has not been reset.
To reset the mechanism requires a low sugar,
low carb diet with the source of energy replaced by fats. The sex hormones are also extensive involved. Taubes 1 (page 373-4) writes of the
experiments by George Wade on rats which the controlling effects of estradiol. Taubes2 ends the discussion by pointing out
the all the other mechanisms such as growth are tightly controlled by hormones,
why should we expect fat storage to be different? A similar view is expressed by Prof.
Lustig.
7)
Leptin A high
level of leptin decreases appetite through signaling the
brain; leptin resistance entails a defect in the signaling and thus causes
weight gain. “Administration of leptin
to rodents decreases food intake and increases energy expenditure.
In contrast to starvation, weight loss after
peripheral or central leptin administration is restricted to adipose tissue “Physiology. The same results have been obtained with
patients with leptin deficiency. “Leptin
(Greek meaning "thin")
is a 16-kD adipokine that plays a key
role in regulating energy intake and expenditure, including appetite and hunger, metabolism, and behavior. It is one of
the most important adipose-derived
hormones. This hormone circulates
in and acts on the hypothalamus to
regulate food intake and energy expenditure. When fat mass falls, serum leptin
levels fall stimulating appetite and suppressing energy expenditure until fat
mass is restored. This hormone
circulates in and acts on the hypothalamus to regulate food intake and energy
expenditure. Leptin acts on receptors in the
hypothalamus of the brain, where it inhibits
appetite. This appetite
inhibition is long-term, in contrast to the rapid inhibition of eating by cholecystokinin (CCK)
and the slower suppression of
hunger between meals mediated by PYY3-36. Leptin signals the brain that the body has
had enough to eat, producing a feeling of satiety. In humans, low circulating serum leptin has
been associated with cognitive changes associated with anorexia, depression,
HIV, and the development
of Alzheimer's disease. Yet another proposed mechanism involves
the phenomenon known as leptin resistance. Leptin is a hormone that regulates long-term
energy balance in many mammals. An important role of leptin is long-term
inhibition of appetite in response to formation of body fat. This mechanism is
known to be disrupted in many obese individuals: even though their leptin
levels are commonly elevated, this does not result in reduction of appetite and
caloric intake. Leptin resistance can be triggered in rats by ad libitum
consumption of energy-dense, highly palatable foods over a period of several
days.[36] Chronic
consumption of fructose in rats ultimately results in
leptin resistance (however, this has only been demonstrated in a diet where
fructose provided 60% of calories; the
actual consumption by humans in a typical Western diet is several
times lower. Once leptin signaling has been
disrupted, the individual becomes prone to further overeating, weight gain, and
insulin resistance” Wiki.
“Dieters who
lose weight, particularly those with an overabundance of fat cells, experience
a drop in levels of circulating leptin. This drop causes reversible decreases
in thyroid activity, sympathetic tone, and energy expenditure in skeletal
muscle, and increases in muscle efficiency and parasympathetic tone. The result
is that a person who has lost weight below their
natural body fat set-point has a lower basal metabolic rate than an
individual at the same weight who is of that natural weight; these changes are
leptin-mediated, homeostatic responses meant to reduce energy expenditure and
promote weight regain as a result of fat cells being shrunken below normal
size. Many of these changes are reversed by peripheral administration of
recombinant leptin to restore pre-diet levels…. Studies on leptin cerebrospinal fluid (CSF)
levels provide evidence for the reduction in leptin
crossing the BBB [-brain barrier] and reaching obesity-relevant targets, such
as the hypothalamus, in obese people. It
is likely that the leptin resistance in these individuals is due to a post
leptin-receptor deficit, similar to the post-insulin receptor defect seen in
type-2diabetes “ Wiki. Adipose tissues produce
a hormone, adiponectin, which provides the mechanism for regulating the amount of
adipose tissue including effecting glucose flux, lipid catabolism, protection
from endothelial dysfunction (factor in atherogenesis), insulin sensitivity
weight loss, control of energy metabolism, reduction of TNF-alpha. Obesity is associated with decreased
adiponectin. Another major regulatory
hormone is Ghrelin which is similar to leptin in extent of regulatory
functions. Ghrelin is produced in the gastrointestinal track and has sites of
action in the pancreas, nervous system, reproductive system and immune systems.
It, like leptin, helps regulate metabolism and hunger. Having covered briefly
ghrelin and adiponectin, for simplicity their roles are dropped out of the
analysis along with others. The purpose
is to see the forest and understand the processes, not to present a description
of each important species of tree. Leptin
regulation in part is influence by insulin, and both are the main cause for
obesity, and like insulin, leptin has many other roles.[1] Dr. Lustig, in his
Fat Chance, p. 47
states: No matter the mechanism,
insulin
blocks leptin signaling both in rodents and in humans… In the brain insulin
causes leptin resistance and “brain starvation.” In summary, IR entails high
level of insulin and that among functions of
insulin is the down regulation of leptin, which thereby results in an increase
in the drive to eat (what is called hunger) and reduction in satiation upon
eating.
8) Insulin
and glucagon in glucose regulation: “The Isle of Langerhans in the pancreas produces the hormones
glucagon, insulin and amylin, somatostatin, and pancreatic polypeptides, all of
which play a role in the regulation of glucose-glycogen levels. Glucagon and insulin play major roles in the
regulation of cellular glucose-glycogen levels.
“Glucagon raises glucose levels by promoting gluceogensis & glycogenolysis. Its effect is opposite that of insulin, which lowers glucose
levels. The pancreas releases glucagon when
glucose levels fall too low. Glucagon causes the liver to convert stored glycogen polymers into glucose, which is released into the stream. As these stores become
depleted, glucagon then encourages the liver and kidney to synthesize
additional glucose by gluconeogenesis.
Glucagon turns off glycolysis in the
liver [the production of ATP], causing glycolytic
intermediates to be shuttled to gluconeogenesis. High
glucose levels stimulate the release of
insulin” Wiki. “Insulin causes cells in the skeletal muscles, and fat tissue to absorb glucose from the [for metabolism]. Insulin stops the use of fat as an energy
source by inhibiting the release of glucagon.
Insulin is provided within the body in a constant proportion to remove
excess glucose from the, which otherwise would be toxic. When glucose levels
fall below a certain level, the body begins to use stored sugar as an energy
source through glycogenolysis, which breaks down the glycogen stored
in the liver and muscles into glucose, which can then be utilized as an energy
source.[2] When control of insulin
levels fails, diabetes mellitus can
result. Patients
with type-2 diabetes are insulin resistant [or fail to produce sufficient
insulin, see discussion below on variations in T2D]. Over 40% of those with Type-2diabetes require
insulin as part of their diabetes management plan” Wiki. “Insulin
causes esterification of fatty acids–-forces adipose tissue to make
fats (i.e.,
triglycerides) from fatty acid esters and thereby forces its storage and its
lack the reverse” Wiki.
9) Insulin resistance
(IR): Insulin is promoted by a number of mechanisms describe throughout
this paper. These include glycation by
fructose in the liver, non-alcoholic fatty liver disease, insulin resistance in
the liver, reduce secretion in the adipose tissue of adiponectin (a process
associated with obesity), and by prolonged elevated serum insulin level. High
level of insulin from a high carb diet
reduces the responsiveness of insulin receptors on cell walls. With lower response
there is high serum
glucose. The pancreas thus secrets even
more insulin to lower the serum glucose to a safe target level. This high insulin
promotes fat storage and
thus obesity. It also reduces the
production of leptin which affect the process that controls the body’s set
“normal weight” through increased appetite and if necessary reducing metabolism
to maintain that higher weight. Most of
the adverse health consequences of high serum glucose results from its affect
upon adhesion factors joining cells and damage through glycation. Insulin resistance
promotes glycation through
the higher level of serum sugars for a longer period of time.[3]
When the glucose and fructose levels are high, glycation damages the proteins
on the cell wall (endothelial cells) lining the arteries. Overtime the reactive
sugars, carbon
monoxide, and various drugs can significantly compromise the endothelial cells’
functions. This can cause endothelial
dysfunction. IR is a risk factor
for ischemic events, because it increases by
higher level of circulating sugars glycation which damages the endothelial
cells. So damaged there is an increased probability
of leakage of plaque from the tunica intima into the blood stream.[4] Since insulin upregulates leptin, IR
increases serum leptin, which can
develop into leptin resistance. “Leptin resistance
can be triggered in
rats by ad libitum [at ones pleasure]
consumption of energy-dense, highly palatable foods [sugar and starches] over a
period of several days…. IR
stimulates the formation of new fatty tissue and accelerates weight gain. Obesity
should therefore not be regarded as a
pathology or disease, but rather as the normal, physiologic response to
sustained caloric surplus… Sedentary
lifestyle increases the likelihood of development of insulin resistance.
It's been
estimated that each 500 kcal/week increment in physical activity related energy
expenditure reduces the lifetime risk of type-2 diabetes by 6%. A different study found that
vigorous exercise at least once a week reduced the risk of type-2 diabetes in
women by 33%” Wiki. Exercise lowers serum glucose. In Science 2003 a study confirmed an age
association with IR in that
there is among the elderly approximately a
40% reduction in oxidative and phosphorylation activity in the
mitochondria; viz., the person with IR,
his mitochondria clears glucose at a
slower rate. A further complication is that adipose tissue
through reduced production of adiponectin causes insulin resistance. With obesity
the production of adiponectin
decreases. “This
effect results from increased expression of molecules involved in both
fatty-acid combustion and energy dissipation in muscle. Moreover, insulin
resistance in lipoatrophic mice was completely reversed by the
combination of physiological doses of adiponectin[5]
and leptin, but only
partially by either adiponectin or leptin alone” at 2001 and 2002, also 1989.
10) High-fructose diet role
in causing Insulin resistance (IR) and
other consequences: On Pages 123-24 of Fat Chance by Dr. Robert Lustig is
listed “the unique metabolism of fructose can induce each of the phenomena
associated with metabolic syndrome.”
Fructose which is only metabolized in the liver in several ways starts
the process leading to IR and MeS. Dr.
Lustig lists them. 1) Fructose when
metabolized in the liver depletes the liver’s store of ATP[6]. Among its affects is the accumulation of
uric acid which increases blood pressure and causes gout. 2)
Fructose is metabolized in the mitochondria of the liver where it
produces an excess of acetyl-CoA which leaves the mitochondria. 3)
This acetyl-CoA is converted to fat within the liver, which causes
non-alcoholic fatty liver disease (NAFLD,
see #15 below). 4) Fructose
activates an enzyme in the liver that leads liver insulin resistance. To this
I would add that glucose is stored as
glycogen, and that this process is impaired through damage cause by
fructose. Reduced production of glycogen
entail elevated serum glucose and thus increased insulin, one way liver
dysfunction promotes IR. 5) This
insulin resistance in the liver causes
a rise in the level of serum glucose. 6)
This higher level of glucose in the causes the pancreas to release more insulin. 6)
This higher level of insulin increases fat
storage (width gain). 7) Leptin level is lowered in response to higher insulin,
and this sends a message to the hypothalamus in the brain to increase hunger. 8)
Fructose as a reactive chemical damages proteins
at 7.5 times the rate of glucose through the Maillard reaction, moreover since
there is much more in the liver as site of metabolism then the measured serum
level, the rate of liver damage is highest.
The serum level over 2 hours from a 75 gm bolus of sucrose is twice that
of glucose. 9) Two experiments on young
healthy subjects comparing the effects of 1000 kcal of extra fructose to that
of 1000 gm of glucose. At 9 weeks out
there was a 25% greater insulin insensitivity in the fructose group, at
1980, and
2005 and, in
rats[7], also. 10) This effect of fructose damaging the liver
contributes to the association of a high fructose diet with cancer, Alzheimer’s
disease, and other age related conditions.
As prof. Lustig puts it:
“Fructose isn’t the only cause of obesity, but it is the primary cause
of chronic metabolic diseases which kills . . . slowly. Fructose can fry your
liver and cause all the
same diseases as alcohol [on
point 2013]. We know we must limit our
ethanol consumption or face the consequences.
But sugar flies under the radar” Lustig supra 125. Population studies
also shed light. The Chinese and Japanese traditional diet is
high in the refined carbohydrate white rice, yet T2D is just 1 percent. With
the introduction of the Western diet with its sugar laden beverages, the rate of
obesity has shot up in Japan to over 20 percent, at. Since the traditional
Japanese diet is high in carbs, yet obesity, CVD, and diabetes is very low, this
demonstrates the role of fructose, not glucose in pathology.
11) High sugar diet:
The disaccharide
sucrose is the principle sugar which is readily converted during digestion into
glucose and fructose. High fructose corn
syrup (HFCS) found only in process
foods is cheaper and sweeter than sucrose. It is made from corn starch which
is pure
glucose by an enzymatic process developed in Japan and became a commercial
success in the 1980s. It usually
consists of 55% fructose and 43% glucose, thus HFCS’s effect is similar to
sucrose. Being water soluble and readily
hydrolyzed, HFCS and sucrose are rapidly cleared from the stomach as
monosaccharides. Both sucrose and HFCS are readily absorbed by the duodenum. Glucose stimulates the
production of insulin which causes cells to absorb the
glucose for metabolism and to store fat, while fructose is transported directly
to the liver for metabolism. The
duration and amount of insulin follow consumption of sugar, starches, and other
sources of glucose has major health consequences. A chain of
interconnected conditions arise from decades-long elevation in glucose in the serum
and of fructose in the liver. Metabolic
syndrome, insulin resistance, obesity, and fatty live are results of
fructose-initiated damage to the liver, and other causes. The liver can synthesize glucose from certain
amino acids, lactate, and glycerol. The
liver can break down glycogen into glucose, and convert glucose to glycogen
which it can store. Sugars
cause oxidative
and glycation damage to the liver which diminish its functions.
“Fructose has a reaction
constant 7.5 times as
high as that of glucose in its non-enzymatic reaction with protein in vitro” at 1988;
moreover their graphs shows over a 3 hour period following ingestion of 75
grams of sucrose twice the serum level of fructose, thereby resulting in 15
times the amount of fructose. Both
sugars
attach to proteins and lipid in a process called glycation by the Millard
reaction. Thus fructose in theory
causes
damage at 15 times the rate of glucose—no in vivo studies have been performed
for confirmation. In
Hippocampus 2008: “Here, we used functional
and structural assays to
characterize the effects of excessive caloric intake on the hippocampus, a
brain region important for learning and memory.
We conclude that a high-caloric diet reduces
hippocampal synaptic plasticity and impairs cognitive function, possibly
through BDNF-mediated effects on dendritic spines.” High
sugar diet causes fatty liver and metabolic syndrome; this is supported both
by population
studies and laboratory research (# 17 below).
High sugar diet is linked to tooth decay insulin intolerance, gout,
obesity, diabetes, CVD, Alzheimer’s
disease, cognitive decline, and many other age-related chronic conditions. Since
fructose is only metabolized in the
liver, the liver is particularly prone to damage through glycation. This liver
damage among other things causes IR in the liver.
A high level of serum glucose raises the
insulin level, to which over decades the muscles and other cells become
resistant to the insulin, thus causing even more insulin resistance. A high
carb diet in itself is not
sufficient. As pointed out at the end of
#10, the traditional high carb Japanese diet had both a low rate of obesity and
T2D.
Add the Sugars from sodas and manufactured foods of the Western diet,
and it has all changed. The high
sugar/fructose diet is a health disaster.
12) Fructose, the differences from glucose: “Unlike glucose, which is metabolized widely in
the body, fructose is metabolized almost completely in the liver in humans,
where it is directed toward replenishment of liver glycogen and triglyceride synthesis.[8] Fructose is also not metabolized in
insulin-sensitive peripheral tissues. Fructose is selectively taken up and
almost completely metabolized by liver hepatocytes,
while much of
dietary glucose passes through the liver where it is metabolized in skeletal
muscle to CO2, H2O and ATP” Wiki. “Fructose
is often recommended for diabetics because it does not
trigger the production of insulin by pancreatic β cells, probably because β
cells have low levels of GLUT5 [transport system into pancreas] although
its net effect is debated. Fructose has
a very
low glycemic index of 19 ħ 2, compared with 100 for glucose and 68 ħ 5 for
sucrose [for glycemic index table at article on carbohydrates].
Fructose is also seventy-three percent sweeter than sucrose. Compared with
consumption of high glucose beverages, drinking high-fructose beverages with
meals results in lower circulating insulin and leptin levels, and higher ghrelin levels after the meal. Since leptin and insulin decrease
appetite and ghrelin
increases appetite, some researchers suspect that eating large amounts of
fructose increases the likelihood of weight gain” Wiki.
“Since fructose consumption has been hypothesized to be a cause of insulin resistance, obesity, …
and, leading to metabolic syndrome. In preliminary research, fructose
consumption was correlated with obesity. A study in mice showed that a high
fructose intakes increases adiposity.
While a few other tissues (e.g., sperm
cells and some intestinal
cells) do use fructose directly, fructose is metabolized primarily in the
liver. A preliminary human study
indicated that fructose may influence metabolic activity or flow in brain regions regulating satiety ("fullness"), and so may promote overeating.
Excessive fructose consumption may contribute to the development
of non-alcoholic fatty liver
disease [#15 below]” Wiki. Typical findings: “For effects of high
fructose diet include: “Fructose
is more lipogenic than glucose or starches, and usually causes greater
elevations in triglycerides and sometimes cholesterol than other
carbohydrates. Dietary fructose has
resulted in increases in serum pressure, uric acid, and lactic acid. People
who are hypertensive,
hyperinsulinemia, hypertriglyceridinemia[9],
non-insulin-dependent diabetes, or postmenopausal women are more susceptible to these
adverse effects of dietary fructose
than healthy young subjects.” “[Evidence]
suggest that
fructose stimulates triglyceride production but impairs triglyceride removal,
whereas glucose stimulates both of them" Wiki, relying on 1996. In Fructose, weight gain
and insulin resistance
syndrome, 2002
journal article states: “Because
leptin production is regulated by insulin responses to meals [and fructose
doesn’t stimulate insulin production], fructose consumption also reduces
circulating leptin concentrations. The combined effects of lowered circulating
leptin and insulin in individuals who consume diets that are high in dietary
fructose could therefore increase the likelihood of weight gain and its
associated metabolic sequelae [injury].” The
rise in CVD and obesity results from its dietary increase. USDA chart: The
per-capita yearly consumption of sweeteners was 109 lbs. in 1950 and 152 lbs.
in 2000. The USDA states: “The food consumption in 1970 was 2275 calories
and in 2000 was 2,750 calories per person per day, 475 calories above the 1970
level.” Though
both glucose and
fructose are about equally efficient at producing ATP (the body’s energy
source), fructose rate of glycation is “7.5 times higher than glucose” (at). Adjusting for its higher
serum level and
longer duration, the in vivo rate is 15 times that of glucose. In addition fructose
has a greater role than
glucose in causing obesity, IR, MeS,
and NAFLD. The role in fructose
leading to insulin resistance entails collateral damage
to the immune system, and as a consequence an association with
atherosclerosis. Pathogens within the tunica intima of
the arteries is the leading cause of AS
and thus CVD. Fructose’s
negative effect upon the immune system explains in part why
those with T2D have twice the risk
of heart attack (AMI).[10]
“Increasing experimental evidence indicates that
several
factors that influence metabolism also play a role in the regulation of immune
responses” at. Though I have relied upon
Wikipedia as a source, those with a financial interest spin Wikipedia articles
to downplay the role of fructose and promote the cholesterol–fat myths. Thus
I have turned to other sources on diet
and journal articles to counter the pharma and food manufacturers’ tobacco-science
distortions. The statement repeatedly
made by Prof. Robert Lustig (see Video Library) that fructose is poison and should be
regulated like alcohol is supported by the evidence. A 2013 nutritional
journal article is titled Fructose is alcohol without the Buzz; both are metabolized the
same way in
the liver and are equally toxic to the liver—thus proving Dr. Lustig’s fructose
is poison claim.
13) Sugar
addiction: “The
hedonic pathway comprises a neural conduit between two brain areas: the ventral tegmental
area (VTA) and the nucleus accumbens (NA also known as the reward center)…
Pleasure occurs when the VTA signals the NA to release dopamine, a
neurotransmitter…. When the released dopamine binds to its specific dopamine D3
receptor in the NA, the sense of pleasure is experienced. Sugars are also key
players in the hedonic
pathway, modulating reward to response to meals. In normal circumstances, after
you’ve eaten a
sufficient amount, leptin sends a signal to the VTA to suppress the release of
dopamine, thereby reducing the reward of food…. If you feed a rodent a
palatable food (e.g., a high-fat, high-sugar food such as cookie dough), the
animal experiences reward because dopamine is released from VTA and binds to D3
receptor in the NA…. Dopamine stimulation in the NA reinforces the intake of
drugs or alcohol and also of food…. After you’ve eaten a sufficient amount,
leptin sends a signal to the VTA to suppress the release of dopamine, thereby
reducing the reward of food. That’s what
obesity is: leptin resistance.
What about insulin, leptin’s
accomplice? Normally, people are
sufficiently sensitive to insulin.
Insulin’s job is to clear dopamine from the synapses…. Thus the rise in
insulin that occurs during a meal blunts the reward of further food intake. This
acts as a servo-mechanism built into the
hedonic pathway to prevent overfeeding.
Insulin resistance leads to leptin resistance in the VTA, contributing
to increased caloric intake by preventing dopamine clearance from the NA. Increase
pleasure is then derived from food
when energy stores are full…. Thus, the combination of high fat along with high
sugar is likely to be more addictive than high fat alone. All the criteria for
sugar addiction have
been demonstrated in rodent models.
Evolutionary, sweetness was the signal to our ancestors that something
was safe to eat“, Prof. Robert Lustig, Fat
Chance 2013, p 50-56. If you doubt the sugar addiction theory, try
cutting your sugar intake to 24 grams a day (6 teaspoons). Use the food labels
to determine sugar
content and USDA Handbook for the bulk foods (mainly fruits, vegetables). I
tried it, and though fairly good at
eliminating sugar added products, I keep nibbling on apples, bananas, raisins,
and grapefruit juice. I have eliminated the sugar added at the source, the
grocery store, but not those on the shelf at home; they simply aren’t getting
replaced, and the worse of them have been trashed. Secondly observe the behavior
of children
between the ages of 3 and 6, most crave sugar added products, and let their
parents in the super market know it. “When the nucleus accumbens
is excessively activated by sweet food or
powerful drugs, says Bartley Hoeble of Princeton, ‘it can lead to abuse and
even addiction. When this system is
underactive, signs of depression ensure.
Rats can be easily addicted to sugar,’ according to Hoebel, ‘and will
demonstrate the physical symptoms of opiate withdrawal when forced to
abstain.’ [This] implies that the
addiction can be overcome with sufficient time, effort, and motivation, which
is not the case with hunger itself…. Avoiding carbohydrates will lower insulin
levels even in the obese, and so ameliorate the hyperinsulinemia that causes
the carbohydrate craving itself. ‘After a
year to eighteen months the appetite is normalized and the craving for sweets
is lost’, said James
Sidbury, Jr. about the effects on
children of his carbohydrate-restricted diet.”
Taubes 446.
14) The breakdown of the regulatory system for serum glucose and weight
control: it is a 4 step process that
begins with a high sugar and refined carbohydrate diet. This results in fructose damaging the liver in ways that result in insulin
resistance in the liver and also to produce non-alcoholic fatty liver disease (NAFLD).
This causes both insulin and leptin resistance. Damage to the pancreas
beta cells will cause T2D.
At the same time weight is gained.
And with drug treatment resistance develops
which result in injections of insulin. The weight gained through insulin
results in an increase in adipose tissue, which produces hormones that are
resistant to calorie restricted diets that include carbs. The weight regulatory much of which is in the
adipose tissue is resistant to reduction in adipose tissue.
15) Fetal environment IR, T2D, and obesity: “Insulin
is a gateway hormone affecting
others whereby the overproduction of insulin plays a key role in the
process. Beside the question of
predisposition to obesity based on genes, there is also the fetal
insulin-glucose load from the mother. In
the near-term fetus, high glucose level result in increased production of
insulin by the fetus and increase in the isle of Langhorne cells which produce
insulin. These changes predispose
the
person to an increased sensitivity to sucrose.
Fortunately predisposed does not mean beyond cure. Additional evidence comes from that the fact
that over the last twenty-five years, birth weight has increased worldwide, by
as much as 200 grams (half a pound)… it is likely that maternal weight gain is
translated into fetal body fat; the more weight the mother gains during
pregnancy the great the birth of the newborn, and the more fat cells early on,
the greater the risk later on” Lustig 76.
“The number of fat cells is determined before you are born” Lustig
77. Over-nourished infants are
predisposed to obesity if their mother developed gestational diabetes.
The picture is complicated by the fact that
undernourished fetuses are also predisposed to obesity. “Newborns in Pune, India versus those born in
London demonstrated that, despite the fact those new born in India weighed 700
grams less at birth, their insulin levels were markedly elevated… the
India-born babies demonstrated increased adiposity four times higher insulin,
and two times higher leptin levels than their London-born counterpart… they
were predestined to develop obesity and metabolic syndrome” Lustig 79. “Worse yet premature babies also manifest
insulin resistance… enormously high risk for metabolic syndrome in childhood or
in adulthood” Lustig 79-80. Clearly
fetal environment affects risk factors.
Most significant is the drift towards overweight and obese mothers: given its causal relationship to the next
generation of overweight mothers, we are evolving to a fat species.
16) Role of genetics:
“A large number of genes
increase the sensitivity to a high carbohydrate study. We identified four loci containing variants that confer
type-2diabetes
risk, in addition to confirming the known association with the TCF7L2 gene. These loci
include a non-synonymous
polymorphism in the zinc transporter SKC30A8, which is expressed exclusively in
insulin-producing  -cells, and two linkage disequilibrium blocks that contain genes
potentially involved in -cell development or function (IDE–KIF11–HHEX and EXT2–ALX4).
These associations explain a substantial portion of disease risk and constitute
proof of principle for the genome-wide approach to the elucidation of complex
genetic traits" at Nature 2007. For
over 99% the populace these
genes are merely a risk factor dependent upon environment (high fructose diet),
thus obesity is rare among hunter-gatherers.
17)
Non-alcoholic fatty liver disease (NAFLD) and its extreme form NASH: “A recent
study using the National Health and Nutrition Examination Survey
(NHANES) found a 30% prevalence of NAFLD
in the United States between 2011
and 2012. NAFLD is related to insulin
resistance and
the metabolic
syndrome. Most patients with NAFLD have few or
no symptoms. Patients may complain of fatigue, malaise,
and
dull right-upper-quadrant abdominal discomfort.
Mild jaundice may
be noticed although this is rare. More commonly NAFLD is diagnosed following
abnormal liver function
tests during
routine
tests. Soft drinks have
been linked to NAFLD due
to high concentrations of fructose[11],
which may be present either in high-fructose
corn syrup or,
in similar
quantities, as a metabolite of sucrose.
The
quantity of fructose delivered by soft drinks may cause increased deposition of
fat in the abdomen”
Wiki. “Non-alcoholic fatty liver disease (NAFLD) is the term
for a wide range of conditions caused by a build-up of fat within the
liver cells. It is usually seen in people who are overweight or obese. NAFLD is
related to insulin resistance and the metabolic syndrome and may respond to
exercise, diet change, and weight loss.
It is a spectrum disease, and at the low end of NAFLD, few have symptoms.
Some patients complain of fatigue and malaise. A healthy liver should contain little
or no fat. Most people with NAFLD
only carry small amounts of fat in their liver, which doesn't usually cause any
symptoms. This early form of the disease is known as simple fatty liver, or steatosis.
(“Steatosis” is also used to refered to the
disease condition NASH, see below.) Simple fatty liver is very common in the UK,
reflecting the number of people who are obese or overweight. It is one
of the most common forms of
liver disease, with an estimated 25-30% people in the UK having early
forms of NAFLD”
NHS. “It
is difficult to distinguish alcoholic FLD from NFLD, and both
show micro-vesicular and macro-vesicular
fatty changes at different
stages. Fatty change represents the intra-cytoserumtic accumulation of triglycerides
(neutral
fats). At the beginning, the hepatocytes
present small fat vacuoles (liposomes) around the nucleus (micro-vesicular
fatty change). In this stage,
liver cells are filled with multiple fat droplets that do not displace the
centrally located nucleus. In the late stages, the size of the vacuoles
increases, pushing the nucleus to the periphery of the cell, thus giving
characteristic signet ring appearance (macro-vesicular fatty change). Large vacuoles may coalesce and produce fatty cysts, which
are irreversible lesions. Defects in fatty acid
metabolism are
responsible for pathogenesis of FLD,
which may be due to imbalance in energy consumption and its combustion, resulting
in lipid storage, or can be a consequence of peripheral
resistance to insulin, whereby the
transport of fatty acids from adipose
tissue to the liver is increased.
Impairment or inhibition of receptor molecules (PPAR-α, PPAR-γ and SREBP1) that
control the enzymes responsible for the oxidation and synthesis of fatty acids
appears to contribute to fat accumulation. On the other hand, nonalcoholic FLD
may begin as excess of unmetabolised energy in liver cells. Hepatic steatosis [fat build up in liver] is
considered reversible and to some
extent non-progressive if the underlying cause is reduced or removed. FLD
is observed in up to 75% of obese people, 35% of whom progressing to NAFLD”
Wiki. A
liver can remain fatty without disturbing liver function, but by varying
mechanisms and possible insults to the liver may also progress to become
non-alcoholic steatohepatitis (NASH),
a state in which steatosis is combined with inflammation and
fibrosis (steatohepatitis).
Non-alcoholic
steatohepatitis (NASH)
is
the most extreme form of NAFLD, and
is regarded as a major cause of cirrhosis of
the liver of unknown cause. NASH
is a progressive disease: over a
10-year period, up to 20% of patients with NASH
will develop cirrhosis of
the liver, and 10% will suffer death related to liver
disease.[8] Cigarette smoking is not associated with an
increased risk of developing NASH.
The exact cause of NAFLD is still
unknown [business-spin leaving out the role of fructose]. However, both obesity and
insulin
resistance probably
play a
strong role in the disease process. The exact reasons and mechanisms by which
the disease progresses from one stage to the next are not known. One debated
mechanism proposes a "second
hit", or further injury, enough to cause change that leads from hepatic
steatosis to hepatic inflammation. Oxidative stress,
hormonal imbalances, and mitochondrial abnormalities
are potential causes for this "second hit" phenomenon. Common findings are elevated liver enzymes and
a liver ultrasound showing
steatosis[12]”
Wiki. “Steatosis suggests that the accumulation of
fat due to fructose metabolism causes a disruption of those functions of the
liver affecting serum insulin level.
High serum insulin is defined as insulin resistance. The association
of NAFLD with obesity (70-90% of the obese have NAFLD at)
is
strong evidence for the role of insulin and fructose[13] So too is NAFLD associated with
glycation, at 2008. For example, “bariatric surgery patients show
an improvement in NASH symptoms [the
extreme form of NAFLD] in around 80%
of patients” journal and
Wiki. The fructose conversion to fat in the liver
accumulates not only in visible clumps in the liver (which when extensive
develops into clinical cirrhosis of the liver) but also with droplets of fat
within hepatic cells. The liver
goes from about 3 pound to about 5 pounds with NAFLD.
17B)
NASH, Non-alcoholic steatohepatitis: “is the most extreme form of NAFLD
and is regarded as a major cause
of cirrhosis of the liver of unknown causes” Wiki. Weight gain is accelerated as fat content of
the liver progress and the effects of IR
worsen. Thus 60 to 70% of the obese have
NAFLD and have progressed to 18.5% NASH,
while of the morbidly obese (BMI
> 40) 91% have NAFLD of which 29% have NASH—see. “NASH is a progressive disease: over a 10-year period, up to 20% of
patients with NASH will develop cirrhosis of the liver, and 10% will suffer death related to liver disease.” [For
cause] one debated mechanism proposes a
"second hit", or further injury, enough to cause change that leads
from hepatic steatosis to hepatic inflammation. Oxidative
stress, hormonal imbalances, and mitochondrial abnormalities are
potential causes for this ‘second hit’ phenomenon” Wiki. For reasons still being investigated,
inflammation in the liver is associated with the conversion of NAFLD to NASH and cirrhosis. Definitive
diagnosis of NASH requires a liver biopsy with over 60% of a hepatocytes weight
consisting of fat. On one biopsy 24% of those with NAFLD are missed. [This is because] “histologic lesions of NASH are unevenly
distributed throughout the liver parenchyma; therefore, sampling error of liver
biopsy can result in substantial misdiagnosis and staging inaccuracies”—see. Though both caloric restriction (<1500
calories/d, and carb restriction ( < 20gm/d) produced lower hepatic
triglycerides and weight loss, the low carb diet produced significantly
superior results at 2011.
Given the 95% long-term failure rate of energy restriction, the benefits
are but short-term and thus carb restriction is the preferred therapeutic
approach.
18) Fructose and non-alcoholic fatty liver disease (NAFLD): Fructose
brings about this condition in much the
same way as alcohol: ethanol is
metabolized in the liver and used in the production of fatty acids, the same for
fructose.[14] Insulin in the liver causes the hepatocytes
to burn glucose and store the fat that they are producing from fructose. This
accumulation of fat will modify
metabolic processes outside the liver, which will result in IR.
Over many years the high
fructose diet will cause sufficient fat for a diagnosis of NAFLD, which afflicts
30% of the adult population. Moreover, glycation by fructose
in the liver occurs
at rate 15 times that of glucose when consumed in equal portions (see #12), and. This random latching on to proteins in the
liver cause more havoc with liver functions, and can progress to a point where
it shows up on liver
function tests. “The degradation of the metabolic
processes in the liver
entails a decrease in energy and subsequent related emotional problems such as
depression. The close parallel in
fructose metabolism results in metabolic consequences which resemble those from
alcoholism. Given the many
functions of the liver, a healthy liver has numerous varied benefits” Wiki. In Gastroenterology “soft drink consumption is
the most common risk factor for fatty infiltration of the liver in patients
without classic risk factors” like
finding,
and.
The
role of sugar is found in hundreds of journal article on NAFLD. “Fructose It’s
Alcohol Without the
Buzz” (the title of a 2013
journal article) describes the similarity to alcohol caused liver damage. This parallel
to alcohol has been used by Dr.
Lustig and others.
19) Role of insulin in
developing insulin resistance: Liver damage through fructose
metabolism in
the liver is associated with NAFLD
though the conversion of fructose to fat.
Though the exact cause of the gradual process of developing insulin
resistance in the liver is not known, in the aetiology of bodily insulin
resistance, liver insulin resistance comes first. This order of events is supported by the
observation concerning hepatitis C, an infection of the liver:
“The extra insulin resistance caused
by Hepatitis C apparently
brings on diabetes at 35 or 40, instead of 65 or 70…. Eventually, type-2diabetes or latent autoimmune diabetes occurs when
glucose levels become higher throughout the day as the resistance increases and
compensatory insulin secretion fails.
The elevated insulin levels also have additional effects (see insulin) that cause further abnormal biological effects throughout
the body” Wiki. The body has developed a system for preventing
IR; it secretes insulin in cycles
of
3 to 6 minutes. However, the body
has
not evolved a way to handle the high sugar-carbohydrate Western diet.
Elevated insulin from the Western diet is a
direct cause of IR by decreasing
the
response of the insulin receptors on the surface of muscle and adipose
cells. Strong evidence for
this comes
from bariatric surgery, which results in fasting following the operation as the
stomach heals. Within 1 week 90%
of
patients are cured of T2D and IR, thus showing that insulin is the
main direct cause and not the quantity of adipose tissue is the cause of IR—at 2006, also see #23 for discussion of bariatric surgery.
19b) The role of
refined carbohydrates in develop IR and MeS. The spike in glucose and thus insulin
from refined
carbohydrates elevates insulin and will with a steady diet cause IR as stated above. However,
the influence of corporate bucks has
kept out the role of refined carbs. Pharma
makes too much treating diabetes and the comorbidities from IR
to implicate carbohydrates and thus
insulin. “There was no mention
that
carbohydrates might be responsible for the causing or exacerbating either
metabolic syndrome or the combination of low HDL, high triglycerides, and
small, dense LDL,… In the now established version of the alternative
hypothesis—that metabolic syndrome leads to heart disease—the carbohydrates
that had always been considered the causative agent had been officially
rendered harmless. They had been
removed
from the equation of nutrition and chronic disease, despite the decades of
research and observations suggesting the critical causal role they played.”
Gary Taubes, Good Calories,
Bad Calories, 2005, p183. And it gets worse the fix gets blamed as the
cause: the doubling of the risk
of MI
for those with T2D is blamed on
low-carb diet with its increased saturated fats. “Traditional restriction of carbohydrate
intake in persons with diabetes and thus an increased intake of fat, usually
saturated” quoting the 1988 Surgeon General’s Report, supra 186. This is the
logic that led the American Diabetes Association, from the early 1970s to
recommend that diabetics eat more carbohydrates rather than less, despite a
complete absence of clinical trials that might demonstrate the benefits of so…”
supra 186-7.
20) Role of adipose tissue in
developing
insulin resistance and obesity: The accumulation of fat within the hepatocytes
(liver cells) in addition to clump of fat in the liver adversely affects liver
functions and intra cellular fat in the pancreas causes T2D. Having once been
thought of as merely containers for fat storage, in the last 3 decades adipose
(fat) tissue has been shown to produce a number of hormones.
“In recent years, been recognized as a major endocrine organ,[1] as it produces hormones such as leptin, estrogen, resistin, and the cytokineTNFα” Wiki.
These hormones control among other things metabolism, appetite, weight,
and fat distribution. The reduced secretion of adiponectin by
adipose tissue has been shown in conjunction with reduced leptin as causes of IR—see #7-9 above. “In
the fat cells of obese individuals, there
is increased production of metabolism modulators, such as glycerol, hormones,
and pro-inflammatory cytokines, leading to the development of insulin resistance.” Wiki. With obesity through
decreased leptin there is an increase in appetite and a lower rate of
metabolism and this lower rate entail a higher blood glucose level and thus
damage through glycation. Obesity
is a
marker for a malfunctioning glucose-leptin-insulin regulatory system--80% of
those with T2D are obese. High carb diet contributes to obesity by
stimulating insulin production. “Fat
production in adipocytes is strongly stimulated by insulin. By controlling the
activity of the pyruvate dehydrogenase and the acetyl-CoA carboxylase enzymes, insulin promotes unsaturated fatty acid synthesis.
It also promotes glucose uptake and induces SREBF1, which activates the transcription of genes that stimulate
lipogenesis” Wiki. Adipose
tissue produces estriol, which is an antagonist (suppresses) of estradiol.
Estradiol causes fat to be stored in the buttocks,
thighs, and hips in women. Following
menopause when estradiol declines the fat migrates to the abdomen, which is
strongly associated with MIs (heart attacks). In these ways through estriol synthesis is
women obesity is associated with health issues seen with a decline in estradiol
following menopause. See HRT for the benefits and tobacco science
pharma uses.
HbA1c (glycated hemoglobin) is a measure of
the amount of glycation that occurs
during the life of a red-blood cell over the previous 90 days which is
indicative of the management of serum glucose, and thus a test for diabetes. Note: all these values for diabetes have been
lowered in the last decade so as to increase the number treated.
21) Treating pre-diabetics e 2 common forms
of type-2-diabetes: Most cases of T2D have low serum insulin. For all types of T2D, as
stated when
describing NAFLD (# 16 & 17)
and
the associated IR, It all starts with insulin resistance in the
liver through the action of fructose.
About 20% of glucose metabolism occurs in the liver and all of fructose
metabolism. Eventually due to the
action
of insulin excess cellular fat accumulates in the beta cells of the pancreas
and the insulin production sharply declines resulting in symptomatic
hyperglycemia. However, in pharma’s
push
to sell drugs, some who are predi
Unlike
type 1 diabetes that is a result of autoimmune destruction of the beta cells, T2D can be reversed through diet. T2D
can also be managed with drugs other than insulin. A second more acute form of T2D
develops when tolerance develops to
those drugs, and insulin must be administered.
Because of the action of insulin on fat storage, glucose conversion to
fat, and its action upon leptin which increases appetite about 80% of those who
are obese have T2D. With the addition of insulin, for most the
rate of weight gain increases as does the comorbidity rates.
22) Latent Autoimmune Diabetes of Adults
(LADA): Of those
diagnosed with
T2D about 5%, are not obese and appear to have adult onset
type-1 diabetes, which is commonly mistakenly treated as T2D.[15]
“The concept
of LADA was first introduced in
1993…. It is estimated that more than 50% of persons
diagnosed as
having non-obesity-related type-2
diabetes may actually have LADA…
Not
all people having LADA are thin or
skinny, however—there are overweight individuals with LADA who are misdiagnosed
because of their weight” Wiki. “It is clear that type-2 diabetes
is not a single disorder but is rather a syndrome of great heterogeneity… When diabetes
is associated
with obesity, the disease usually seems to be caused by insulin resistance plus an impaired
ability
of the pancreas to compensate for the resistance. The present data suggest
that non-obese diabetic [LADA]
elderly male subjects form another subgroup of the disease
where peripheral insulin
action is normal and the insulin secretory defect is the major cause of the disease….
In non-obese hyperglycaemic subjects, however, there was
no evidence
of peripheral insulin resistance…
only a marked secretory defect involving both the first-and second-phase
response” Diabetologia,
1991 at 486. Though it has since ancient times been known
that dietary management is an effective treatment at reducing morbidity and
mortality, because of damage to the pancreas, with LADA for most neither alternate
day fasting diet or bariatric surgery (see #31) will be curative.
LADA
occurs in 5-10% of those diagnosed with T2D.
Possible some subset will be cured
as
the islets
of
Langerhans
beta cells in the pancreas regenerate. Unfortunately
the literature is sparse.
[1] “In the periphery
leptin is a modulator of energy expenditure, modulator between fetal and
maternal metabolism, permissive factor in puberty, activator of immune cells,
activator of beta islet cells, and a growth factor. Further, it interacts with
other hormones and energy regulators: insulin, glucagon, insulin-like growth
factor, growth hormone, glucocorticoids, cytokines, and metabolites... Leptin affect bone metabolism…. Factors that acutely affect leptin levels are
also factors that influence other markers of inflammation, e.g., testosterone,
sleep, emotional stress, caloric restriction, and body fat levels. While it is
well-established that leptin is involved in the regulation of the inflammatory
response, it has been further theorized that leptin's role as an inflammatory
marker is to respond specifically to adipose-derived inflammatory cytokines” Wiki. Cytokines
are a broad class of compounds including the interleukins which play important
immune system roles. Elevated levels
of
cytokines are associated with an assortment of pathological conditions.
[2] “Although
other cells can use other fuels (most
prominently fatty acids), neurons depend on glucose as a source of energy in the
non-starving human. They do not require insulin to absorb glucose, unlike
muscle and adipose tissue, and they have very small internal stores of
glycogen. Glycogen stored in liver cells (unlike glycogen stored in muscle
cells) can be converted to glucose, and released into the blood when glucose
from digestion is low or absent, and the glycerol backbone in triglycerides can also be used to
produce glucose” Wiki.
[3]
Resistance is common when a hormone is at a stead peak state. The body adjust to this high level to reduce
its affect. To prevent this the
pancreas
release insulin every 3 to 6 minutes, for graph. This tolerance is similar
to tolerance to alcohol, where with repeated usage a greater dose is required
for inebriation.
[4]
This is quite different than the way pharma frames the discussion of CVD—see endothelial dysfunction.
A series of articles expose the tobacco
science taught by KOLs—see http://healthfully.org/rh/id1.html,
id2, rl/id5,
rl/id8, rl/id9, rl/id5, rl/id10.
[5]
Adiponectin is a hormone secreted by adipose tissue which modulates a number of
metabolic processes including glucose regulation and fatty acid oxidation.
Its level increases during energy
restriction.
[6] ATP,
Adenosine triphosphate the body’s energy molecule: is a nucleoside
triphosphate used in cells as a coenzyme. It is often called the "molecular unit of currency" of intracellular energy transfer. ATP
transports chemical
energy within cells for metabolism. It is one of the end products of photophosphorylation, cellular respiration, and fermentation and used by enzymes and structural proteins in many cellular processes, including biosynthetic reactions, motility, and cell division. It’s depletion plays a major role in death during heart
attack and from congestive heart failure, since ATP is the molecule which is
the energy source used by the heart.
Statins, for example, deplete the ATP supply by 40%, thus pharma doesn’t
test their statins on those with congestive heart failure—though it is often
given to them.
[7] “In summary, fructose but not glucose feeding
led to impaired insulin action in both the liver and peripheral tissues” at 1989.
[8] As
evidence clearly shows (see Aetiology of insulin and leptin resistance
on page 2, which goes over the steps starting with high fructose consumption
--listed at above 50 grams a day) that causes the liver damage which can
ultimately lead to all cases of T2D.
[9]
High levels of triglycerides are good because they are a safer source of energy
than carbs which cause glycation and thus CVD.
[10]
The other casual factor is that diabetes promotes a reduction in cellular
adhesion, which facilitates the leaking of plaque from within artery
walls. This reduction in adhesion
which
promotes the leaking of erythrocytes (red blood cells) from capillaries which
causes blindness, kidney failure,
and
gangrene in legs.
[11] Those
who claim the high-fat diet is the cause of NAFD are doing
tobacco science.
It is based on a rat model—for example-see. However, though not vegetarians--like rabbits
used for cholesterol myth--their diet is relative to man low in fats.
Eskimos who ate a high fat low carb diet, yet
have a very low rate of NAFLD & CVD. NAFLD
is associated with the high carb-fructose Western diet.
[12] “In cellular pathology, steatosis (also
called fatty change, fatty degeneration or adipose
degeneration) is the process describing the abnormal retention of lipids within a cell. It reflects an impairment of
the normal processes of synthesis and elimination of triglyceride fat. Excess lipid
accumulates in vesicles that displace the cytoplasm. When the vesicles are
large enough to distort the nucleus, the condition is known
as macrovesicular steatosis; otherwise, the condition is known as microvesicular
steatosis. While not particularly detrimental to the cell in mild cases,
large accumulations can disrupt cell constituents, and in severe cases the cell
may even burst. Mo direct is that “Short-term high fat feeding in rats results
specifically in hepatic fat accumulation…caused a ~3-fold increase in liver
triglycerides and total fatty acyl-CoA content without any significant increase
in visceral or skeletal muscle fat content [parallels human development of NAFD
for those who are not obese]… suppression of endogenous glucose production by
insulin was diminished and insulin-stimulated peripheral glucose disposal [IR]… In conclusion, these data
supported the hypothesis hepatic steatosis leads to hepatic insulin
resistance…” at 2004.
[13]
The role of fructose as the starting point for
the progress to IR, NAFLD, MeS, and,T2D is based
upon strong evidence, yet Wikipedia on
NAFLD, merely sates that it is “due
to other causes than excessive alcohol use” and one sentence on fructose in the
context of soft drinks: “Soft drinks have
been linked to NAFLD due to high concentrations of fructose, which may be present either in high-fructose corn syrup or,
in similar quantities, as a metabolite of sucrose. The quantity of fructose delivered by
soft drinks may cause increased deposition of fat in the abdomen.[6][7]” But is not merely soft drinks as a source of
fructose, but the excessive amount of sugar and refined carbs in the Western
diet, all sources. The foot print of corporations is found throughout
Wikipedia.
[14] American Association for the
study of Liver Disease, 2013:“Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver
disease in adults and children. A number of genetic and environmental factors
are known to predispose individuals to NAFLD.
Certain dietary sugars, particularly fructose, are suspected to contribute to
the development of NAFLD and its
progression. The increasing quantity of fructose in the diet comes from sugar
additives (most commonly sucrose and high fructose corn syrup) in beverages and
processed foods. Substantial links have been demonstrated between increased
fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing
evidence suggests that fructose contributes to the development and severity of NAFLD. In human studies, fructose is
associated with increasing hepatic fat, inflammation, and possibly fibrosis.
Whether fructose alone can cause NAFLD
or if it serves only as a contributor when consumed excessively in the setting
of insulin resistance, positive energy balance, and sedentary lifestyle is
unknown. Sufficient evidence exists to support clinical recommendations that
fructose intake be limited through decreasing foods and drinks high in added
(fructose-containing) sugars.” Pharma
has drugs for NAFLD.
[15] Type 1 diabetes
is caused by the immune-mediated destruction of islet insulin-secreting
β-cells. This chronic destructive process is associated with both cellular and
humoral immune changes in the peripheral blood that can be detected months or
even years before the onset of clinical diabetes. Throughout this prediabetic
period, metabolic changes, including altered glucose tolerance and reduced
insulin secretion, deteriorate at variable rates and eventually result in
clinical diabetes. A fraction of individuals with humoral immunological changes
have clinical diabetes that initially is not insulin-requiring. The onset of
diabetes in these patients is usually in adult life, and because their diabetes
is at least initially not insulin-requiring, they appear clinically to be
affected by type 2 diabetes. Such patients probably have the same disease
process as patients with type 1 diabetes in that they have similar HLA genetic
susceptibility as well as autoantibodies to islet antigens, low insulin
secretion, and a higher rate of progression to insulin dependency. These
patients are defined as being affected by an autoimmune type of diabetes not
requiring insulin at diagnosis, which is also named latent autoimmune diabetes
of the adult (LADA)” ADA 2001, full.
23) Bad pharma and type-2 diabetes: Like so
much that occurs in today’s medicine, what is sold as beneficial isn’t best for
the patient. It is corporate tobacco
ethic producing tobacco science which is used to promote junk treatments. The common pattern
used by pharma is to identify a surrogate endpoint; in this case high serum
glucose, claim that this surrogate endpoint is strongly associated with
pathologies (serum glucose at a very high level), treat the surrogate endpoint
with drugs. Clinical trials are designed
to sell the product. Once give FDA
approval, pharma next expands the market by doing more tobacco science to
provide “evidence” for benefits to a much larger population including an
asymptomatic population with modestly elevated serum glucose. At the same time
treatment choices counter to
pharma’s financial interest are both attacked by tobacco science and
downplayed. Thus over example through
education in diet can often reverse the need for medications. “Only 13%
of diabetics are instructed by
their physician and 25 percent of those instructed by dietitians showed a sound
knowledge of their dietary requirements” at. Failure to follow
a strict diet hastens the rate of decline resulting in more drugs. Finally insulin
is added. All of these drugs have under-reported side
effects. Moreover, there is the additive
effect, where by multiple drugs, often in unexpected ways overload various
bodily organs such as the kidney or affect catalytic process such as cytochrome P450 and thereby produce unexpected side effects.
These consequences polypharmacy are often treated with more drugs.
Organizations that set out treatment guidelines such as the NIH and American Heart Association knowingly
use this tobacco science to expand the drug market. Our corporatist government
promotes the
regulatory façade. And it gets worse.
: Pharma following the standard
pattern of
expanding the market for its drugs has through their KOLs (key opinion leaders)
expanded late 2014 the disease
population by lower its surrogate markers high serum glucose and glycation of
hemoglobin (HAC1) and thereby include a population without symptoms. The sales
pitch is that its drugs lower the
risk of morbidity and mortality associated with elevated glucose.[1] The 2014 article by John
S. Yudkin Jr. in the British Medical Journal goes over the new standards and
their consequences. Over half of those placed on drugs for
elevated glucose, shouldn’t. Moreover
this elevation of glucose is a
natural part of aging. The cure for T2D
is a very low carbohydrate diet with alternate day fasting (see #30). Instead
doctors educated by pharma fail to warn their patient about refined carbs. Instead
of a cure, billions are spent on
drugs that only slow the progression of T2D.
For a person who develops T2D at the age of 50, their life is
shortened an average of 7-10 years—their mortality rate has doubled. And
it gets worse the dietary recommendation
is a low-fat diet, thus high carbs, the Western diet. And they hold that fructose,
because of its
low glycemic index, is a safe sweetener.
The dietary switch to carbohydrates has been convincing shown not to prevent
cardiovascular disease
(as claimed) but to promote
it. This
dietary switch is made worse by recommending the replacement of saturated fats
with polyunsaturated fats which like carbohydrates promote atherosclerosis. (Note
at the end of this paper are a list of
quality documentaries and University of California Television programs and some
lectures by Dr.
Jason Fung which confirm the key points here made
on diet and its effects upon T2D, NAFLD,
insulin resistance, leptin resistance, obesity, etc.). What can be said
about bad pharma failing to
act in the public interest equally applies to food manufacturers. What follows
is a discussion of the good and
bad fats; to lump them together is good marketing science, and more tobacco science.
  cis-2-butene—both-CH3
are on same side; with trans-fat they are on different sides of the carbon
chain, and thus form a straight carbon chain—above left.
24) Polyunsaturated too much omega 6 fatty
acids: one of the 2-major health issues
is that most plant source
of fats is high in polyunsaturated fats, one is rancidification (section below)
the other is that they have about 20 times as much omega 6 (N-6) fatty acids
to omega-3 (N-3).
Tree nuts are not high in polyunsaturated fats. They include avocado,
olive, coconut, almond,
and thus are not rich in the bad polyunsaturated N-6. The paleo-diet main
source of fat came from animals—very few societies consumed significant
quantities of grains and nuts. “Many
experimental studies have provided evidence that incorporation of alternative
fatty acids into tissues may modify inflammatory and immune reactions and that
omega-3 fatty acids in particular are potent therapeutic agents for inflammatory
diseases… When humans ingest fish or fish
oil, the EPA
and DHA from the diet partially replace the omega-6
fatty acids, especially AA, in the membranes of probably all cells, but
especially in the membranes of platelets, erythrocytes, neutrophils, monocytes,
and liver cells. Inflammation plays
an important role in both the initiation of atherosclerosis and the development
of atherothrombotic events” 2002
Biomed.
In other words, the high amount of N-6 blocks
most of the conversion of N-3 to anti-inflammatory agents. “Excess omega−6 fatty acids from vegetable oils interfere with
the health benefits of omega−3 fats, in part because they compete for the same
rate-limiting enzymes. A high
proportion of omega−6 to omega−3 fat in the diet shifts the physiological state
in the tissues toward the pathogenesis of many diseases: prothrombotic,
pro-inflammatory and pro-constrictive. A
ratio of 2–3/1 omega 6 to omega 3 helped reduce inflammation in patients with
rheumatoid arthritis
A ratio of
5/1 had a beneficial effect on patients with asthma but a 10/1 ratio had a
negative effect. A ratio of 2.5/1 reduced rectal cell proliferation in
patients with colorectal cancer, whereas a ratio of 4/1 had no effect” Wiki. Paleo diet
has a ratio of N-3 to N-6 is less
than
1 to 4; the Western diet ratio is 1 to 15 or greater. Thus it is wise to avoid
corn, canola, sunflowers, and soya oils. Olive
and palm oils are low in
polyunsaturated fats, even lower are animal fats.
25) Polyunsaturated fats are subject
to rancidification: “is the hydrolysis and/or autoxidation of fats into short-chain aldehydes and ketones which are objectionable in taste and odor. Hydrolytic rancidity refers to the odor that develops when triglycerides are hydrolyzed and free fatty acids are released to
form free
tatty acids and salts of free fatty acids.
Oxidation primarily occurs with unsaturated fats. Microbial rancidity refers to a process in which microorganisms,
such
as bacteria or molds, use their enzymes such as lipases to break down fat.[2] Rancidification can produce
potentially toxic compounds
associated with long-term harmful health effects concerning advanced aging,
neurological disorders, heart disease, and cancer. A combination of
water-soluble and fat-soluble antioxidants is ideal” Wiki. “Lipid peroxidation refers
to the oxidative degradation
of lipids. It is the process in which free radicals "steal" electrons from the
lipids in cell membranes, resulting in cell damage. It most often affects polyunsaturated fatty acids, because they contain multiple double
bonds in between which lie methylene bridges (-CH2-) that possess
especially reactive hydrogens.
If not terminated fast enough, there will be damage to the cell membrane, which consists mainly
of lipids. In addition, end-products
of lipid peroxidation
may be mutagenic and carcinogenic. For
instance, the end-product malondialdehyde reacts
with deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts to them, primarily M1G” Wiki.
The detailed 2010
article Pathological Aspects of Lipid Peroxidation list aging, Alzheimer’s disease, Parkinson’s disease,
amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), atherosclerosis (and
thus CVD and other related
conditions), pre-eclampsia (pregnancy disorder affecting about 4%), diabetes,
renal diseases, chronic lymphedema (also
known as lymphatic obstruction, causing swelling by compromised lymphatic
system), hepatic diseases including liver IR,
NAFLD, NASH (#16), exacerbating
hepatitis C and cirrhosis of the liver, and a causal factor for cancers. The
various authors of each section of this
in-depth article describe the process by which the lipid peroxidation causes
pathology. The role of oxidation of fats
and cholesterol within the artery walls as being atherogenic is clearly made in
that article. The effects of
rancidification in the body are beyond dispute.
Also contributing are dietary sources of rancid oils. “The
possibility that the body fats might undergo a similar kind of degradation is
still largely ignored—perhaps
because the irregular irreversible pattern of this type of process seems at
odds with the enzyme-controlled reversible pathways of traditional
biochemistry. Yet work with mitochondria and other biological preparations has
shown that the processes commonly grouped together as " degeneration
", " fatigue ", and " ageing " (none of which have a
basis in classical enzymology) develop in close parallel with evidence of Rancidification”
at 1969. The source can either be dietary rancid fats
or in vivo oxidation—in vivo causing the greatest issues. Now let us follow
the chain of events
concerning IR and CVD.
Rancid fats contribute to liver dysfunction NAFLD and IR by
accumulating in the liver in a form that the liver can’t dispose of. Similarly
they contribute to atherosclerosis
and CVD by being in a form with the
muscle cells in the tunica intima (muscular layer) of the artery walls cannot
uptake and metabolized these rancid fats.
The macrophages in the tunica intima similarly can’t dispose of the
rancid fats. Thus like trans-fats (see
section below) rancid fats contribute to CVD
and atherosclerosis. “Accumulating evidence suggests
that oxidized
fats and lipid oxidation products in the diet can contribute to the
pathogenesis of atherosclerosis” at 2002, and 1998. Non-enzymatic oxidation
causes the failure of
the body to dispose of them; they accumulate like those of the unnatural,
man-made trans-fats.
26) Trans-fats: Beside polyunsaturated
fats being subjected to in vivo
oxidation, they are commercially catalytically hydrogenated to prevent
oxidation and improve properties: they retain flavors of the products baked and
deep fried than unsaturated fats, and being a solid like lard produced products
with a superior texture to the polyunsaturated fats. And follow the dollar: hydrogenated polyunsaturated fats are much
cheaper than natural saturated fats.
During hydrogenation of the double bonds in polyunsaturated fats, an
assortment of cis-and-trans bonding occurs.
In this way trans-fats are preferentially created over cis-fats because
of their lower energy of reaction. Not
found in nature but in trace amounts, we lack an enzyme to metabolize trans-fats. “The
daily intake of about 5 g of trans-fat (1.5 teaspoons) is
associated with a 25 percent increase in the risk of ischemic heart disease” NEJM, at. “Trans-fats are found only in trace amounts
in meat and dairy products. Their major
source is in food
production: liquid cis-unsaturated
fats such as vegetable oils are hydrogenated to produce saturated fats, which
have more desirable physical properties[3]
[namely, flavorful baked and fried
foods, longer shelf life, and at half the
price of animal fats and cheaper than palm and olive oils]. Trans-fats are a contaminant introduced by a side
reaction on the catalyst in partial hydrogenation of vegetable oils. However,
partial hydrogenation reconfigures
most of the double bonds that do not become chemically saturated, twisting them
so that the hydrogen atoms end up on different sides of the chain. This type of
configuration is called trans, from the Latin, meaning "across".[39] The trans configuration is the lower energy form, and is
favored when catalytically equilibrated as a side reaction in hydrogenation” Wiki. In 1975, 5.6 billion Ib. of hydrogenated
vegetable oil were produced in the United States, which is an average of 28
Ib/year/person (113)” ARN
1984. This amounts to 35 grams per
day. Based on population studies and
clinical trials, trans-fats are blamed for high levels of cholesterol, lower the
good HDL, and as a major cause of CVD,
but it is their effect upon prostaglandins that is the way they cause CVD and
MI. This is more pharma spin. An
experiment on rats using feed high in
trans-fats and HFCS was able in 16 weeks to produce in the rats NASH, IR, MeS, and T2D trans fed rats, 2008. Thus trans-fats and as
discussed in #s 24-25 the polyunsaturated fats are driving along with fructose the
association of CVD with diet--not
the cholesterol and saturated fats. The
abnormal and thus lacking a bio-pathway for disposal trans and rancid fats and
excess fructose are the main villains. But
as pointed out in the section on the Mediterranean
diet,
complex population studies are like data mining, where you dig determines what
you find. Far better are laboratory
animal and in vitro experiments.
27) Laboratory evidence that trans-fats
cause CVD: Pharma’s KOLs (key opinion leaders)
push the cholesterol myth: “trans-fats increases the risk of coronary heart disease by raising levels of the lipoprotein LDL (so-called "bad cholesterol") and lowering levels
of the lipoprotein HDL ("good cholesterol") “ Wiki. “It
is now well known that the hydrogenation process and particularly the formation
of trans-fatty acids has led to increases in serum cholesterol concentrations
whereas LA [linoleic acid] in its regular state in oil is associated with a
reduced serum cholesterol concentration” Biomed. This has been confirmed with high trans-fat in clinical experiment on volunteers.
But it has been shown (see part 2) that pharma
pushes the high LDL, high total cholesterol,
and high-fat diet as causes of CVD
for to promote drug sales
of their statins. What follows are from articles which explain
the damaging cellular effects of transfats.
In a 2006 review
article on trans-fats:
“Because of their effects on the
metabolism of gamma-linoleic and arachidonic acid, ingestion of trans-fatty
acids can affect the metabolism of prostaglandin and other eicosanoids and may
alter platelet aggregation and vascular function. In addition incorporation
of trans-isomers
into membrane phospholipids may influence the physical properties of the
membrane as well as the activities of the membrane-associated enzymes…. Effect
collagen induce platelet aggregation.…
inhibit activities of Na+ , K+-ATPase
and adenylate cyclase and reduce density of B-adrenergic receptors in rat heart
membranes [raise blood pressure]…. Recent evidence indicates that trans-fats promote
inflammation…. Increased tumor
necrosis factor (TNF) system, levels of interleukin-6 and C-reactive protein….
Several studies suggest that trans-fats cause endothelial dysfunction [affects
wall of arteries and other tissues]… soluble vascular-cell adhesion
factor…reflected by reduction in
brachial artery flow-mediated vasodilation by 29 percent [raises blood
pressure], as compared with intake of saturated fats. Other effects include
consumption of
trans-fats reduced the activity of serum paroxonase, an enzyme that is closely
associated with HDL cholesterol, and impaired the postprandial activity of
tissue plasminogen activator. Trans-fats
appear to affect lipid metabolism through several pathways….” The
same finding with much greater detail is
in the 1984 thorough review
by the Department of Agriculture.
Several epidemiological studies found a significant association of
trans-fats with CDV and MI, including
those studies which
controlled for contravening variables.[4] As previously stated LDL and high total
cholesterol are bystanders.
Pro-inflammatory effects of pathogen colonies within the artery walls has
been incontrovertible
demonstrated to be major
cause
of CVD. Given
the clear association in dozens of population studies and clinical trials of
trans-fats to CVD, governments have responded to this health hazard created by
the food industry. With the body of
experimentation upon rats revealing the mechanism, the deleterious effects of
trans-fats has been established, the principle one being it effect upon
blocking the conversion of the essential omega-3 fatty acid, at. For more on trans-fats see Part 4.
The smoking gun lines with the fact that trans-fats exert a
pro-inflammatory effect, and the inflammatory processes in artery walls in
response to damaged LDL causes atherogenesis.
“Because the presence of inflammation is an independent risk factor for
atherosclerosis… the production of interleukin-6 and TNF-a by
cultured mononuclear cells was greater after one month…” NEJM—see also,
a 2006 summary article. Through fat
accumulation, trans-fats cause a fatty liver and thus promote NAFLD--at
2008.
“It seems that a strong relationship exists between the consumption of TFA in
the oxidized oils and lipid peroxidation and non-alcoholic fatty liver disease
(NAFLD)” at 2011. Based on lab and population studies, assiduously
avoid artificially produced trans-fats[5].
28) What are the regulations:
Official response has been prohibiting
trans-fats in a number of countries, but not the U.S. “According
to the FDA, the average American consumes
5.8 grams of trans-fat per day (2.6% of energy intake). This is government
figure is low because
trans fatty acids that are part of mono- and diglyceride [bound with glycerol]
are not required to be listed on the ingredients label as making contributions
to calorie count or trans fatty acid content.
Trans-fats in the form of
monoglycerides and diglycerides are not considered fats by the FDA, though upon
absorption from digestive track they yield trans-fats. Another gap in calculation
is that trans-fat
levels of less than 0.5 grams per serving are listed as 0 grams
trans-fat on the food label. There
is no requirement to list trans-fats
on institutional food packaging; thus bulk purchasers such as schools,
hospitals, [restaurants], and cafeterias are unable to evaluate the trans-fat
content of commercial food items [nor is there an incentive to spend more
for trans-free foods]” Wiki. The major
source of trans-fats in the U.S. is
in fried foods from restaurants, and this source is not included in US
dietary figures for trans-fats. A number of countries
have
simplified the process of controlling trans-fatty acids by banning them,
starting with Denmark in 2003 and now also Iceland, Sweden, Switzerland . “Spain
… no significant levels of trans-fats
were found in any of the anaylsed products, regardless of brand of origin” at Bakery. The regulations might make a difference,
because death rate per 100,000 2011 from coronary heart disease is 80.5 US, 55.9
for Denmark, for Spain
43, Switzerland 52, Japan 31, Israel 46, Italy 51, Greece 60, U.K. 69, and
France 29, source LeDuc Media. And France consumes the highest rate of
saturated fats. The highest rate of
obesity and diabetes is in the US, which corresponds to the highest consumption
of fructose. Let us not become distracted
by what could
by the minor causes such as fats when the elephant in the kitchen are refined
carbs and sugars. The weakness of lab
work on fats make the case,[6]
we need to look at the Western high carb diet. However
the manufactured food industry and fast-food restaurants prefer unsaturated
fats because they are about half the price, and they prefer hydrogenated fats
because they taste better and have a longer shelf life; thus another example of
what Prof. Ben Goldacre calls “pretend regulatory fixes”. The zero trans-fats on food label is
deceptive for 2 reasons, at up to 0.5 grams per portion the entry is 0, and
since no one is checking food content; there is an incentive to manufacture the
dietary numbers on product labels. It is
like having a speed limit for Freeways but no traffic cops enforcing the
limit.
29) Saturated fats are good for you: We have
all heard repeatedly that saturated fats are bad: they cause CVD by clogging
blood vessels. This claim is accepted as proven, yet “a meta-analysis of 21
studies considered
the effects of saturated fat intake and
found that Intake of saturated fat was not associated with an increased risk of
coronary heart disease, stroke, and cardiovascular disease" Wiki. Though this fat myth was stated in #12, I need to repeat this along with the myth
that dietary cholesterol also promotes CVD.
This too is false; the chorus of professors and doctors who expose these myths
are not given space in the corporate press or time on corporate television—the
exception is Australia Broadcast Corporation. Compelling
evidence shows that the high refined carb-fructose diet has resulted in the
current health disaster, and that carbs should be replaced with saturated fats and
monounsaturated fats,
because polyunsaturated fats promote through omega 6-fatty acids (N6) their affect
negative effect upon
the immune system that increases age related diseases, and also through
rancidification. The Paleolithic diet
had a ration of N6 to N3 of under 4 to
1, with the Western diet the ratio is 16 to 1.
Excess omega−6 fatty acids from vegetable
oils interfere with the health benefits of omega−3 fats, in part because they
compete for the same rate-limiting enzymes.
Through
this negative affect upon omega-3 fatty acids which omega-6 fatty action
competitively blocks its action; also when rancid, polyunsaturated fat through
oxidation, has an affect comparable to that of transfats in promoting
cardiovascular disease. Prof. Donald
Miller, MD presents the compilation to an audience of physicians the evidence
which shows that saturated fats are good for you--on YouTube; watch it if in
doubt. France of the developed countries
has the highest consumption of fats and saturated fats has the lows death rate
of developed nations from CVD—and it
ain’t because of red wine. France also has of the developed western countries
the lowest consumption of sugars; 27 kg per person per year as reported for
2000 by the CEDUS—at
p122, from the book, The Rise of
Obesity in Europe. The control group
in the rat experiment
(#26 above) has a human equivalent in the
French who eat no trans-fats and low fructose diet.
30)
Managing T2D, obesity, NAFLD, IR and MeS with diet: Diet has been used to
manage the intractable
type-1 and type-2 diabetes since the ancient Greeks (see Hippocrates). The rise
in frequency with the Western diet
and that there are now 5 categories of drugs used to manage serum glucose
entail that pharma has expanded the guidelines to include a much larger
population. This section just deals with those who are managed by just oral
medications; section #32 for those who are also on insulin. Extreme low-carb
Atkins type diets are
successful. Several small dietary trials
have been done in hospitals which produced results within 2 weeks. One on 10
obese patients with T2D establishes the benefits of
diet. All 10 patients were obese, 7 with
hypertension, 5 dyslipidemia, and 2 with coronary artery disease. To set baseline,
the first week consisted of
normal diet and thus included foods from fast-food establishment, the next two weeks
they followed an Atkins diet with 21 g of carbohydrates per day and all the
protein and fat they wanted. Patients on
Atkins diet spontaneously reduced their mean energy intake from 3,111 to
2164/day. Diabetes medications were adjusted according to their improvements. In
just two weeks their body weight decreased by 2.02 kg to an average of 112.41
kg, but after adjusting for water loss the mean change was 1.65 kg. Hemoglobin
A1c (HA1c) decreased from 7.3% to
6.8%, insulin sensitive improved by 75%,
and mean serum triglyceride and cholesterol levels decreased 35% and 10%
respectively (more proof that saturated fats don’t promote
hypercholesterolemia) at
p. 19. Another
trial of 6 months using a ketogenic diet cured NAFLD in 4 of the 5
participants, and the mean weight loss was an average of 28 lbs.[7] Other similar experiments have confirmed
reduced rate of metabolism when on a diet and the effects of high sucrose diet
upon IR. The extremely low-carb
diet work and should
be followed by those whose T2D
hasn’t progressed to the stage of requiring insulin.
31) Why drugs fail: T2D
is caused by diet, and it is reversible through diet. There are three strong
indications of this is
the cure for T2D. One, for over 90%
of those undergoing bariatric surgery they are cured before significant weight
loss. Second, that prior to insulin both
type1 and type 2 diabetes were managed with diet. The low-carb diet was used
to manage serum
glucose; see for example, Sir William Osler, The
Principles and Practice of Medicine, 7th Ed. 1909, p420. Third,
is that Dr. Fung has cured many of his T2D
patients with ADF. As Dr. Jason Fung clearly
explains the problem is not glucose but insulin. As stated repeated insulin causes fat storage, which leads to
obesity and fat in the insulin producing cells in the pancreas which eventually
causes a decline in insulin product that results on high serum glucose
resulting in T2D. Insulin through
leptin regulation increases
hunger. What is needed is not more
insulin or increased insulin sensitivity, but less insulin. The two mainstays
of diabetes medication
don’t lower insulin. Metformin type drugs
decreases hyperglycemia
primarily by suppressing glucose production by the liver (hepatic gluconeogenesis), though action in the mitochondria, and
metformin increase peripheral insulin sensitivity, and decreases the absorption
of glucose from the intestinal track.
The "average" person with type 2 diabetes has three times the
normal rate of gluconeogenesis; metformin treatment reduces this by over
one-third” Wiki. “The other leading
type of diabetic drugs is the sulfonylureas.
They bind ATP in a process which increases the secretion of insulin, and
they limit glucose production in the liver” Wiki.
Binding glucose is not a fix, nor more than binding fats which some weight loss
medications do. This is because the
glucose (and fat) go the intestines where the bacterial flora their digest
these carbs; and this result in gas, intestinal pain, diarrhea, and other side
effects. The best solution is to go on a
very low-carb diet—something pharma and food manufactures oppose. Moreover
when serum sugar is managed by
drugs, there is no reduction in cardiovascular events are death but instead for
most types of drugs is increased, and the tighter the management the greater
the morbidity. Doctors should be
recommending as first line the extreme low-carb diet.
32) Bariatric surgery cures T2D
and MeS: There are major health
benefits for the
morbidly obese (BMI over 40). Study of 232 patients who had either bariatric
surgery or none, the mortality rate in the surgery group was 1%, in those
without treatment 4.5% per year. Mean
glucose level in the surgery group fell for 187 to 140 mg/dl. The surgery group
needing medical management
of glucose fell from 31.8% to 8.6 and the non-treatment group increased from
56.4% to 87.5%, 1997. Dr. Jason Fung states
that 90% of those who undergo bariatric surgery
are cured of T2D. “Series with long-term follow-up show that
gastric bypass and biliopancreatic diversion achieve durable normal levels of serum
glucose, serum insulin, and glycosylated hemoglobin in 80% to 100% of severely
obese diabetic patients, usually within days after surgery” 2002. On point is a study that
used blood tests designed to measure improved function of beta cells in
pancreas and insulin sensitivity. All
ten subjects tested at end of 1 week following bariatric surgery and all 10
were cured of T2D. The study showed
that the cure was a result
of fasting rather than weight loss--2006.[8] “Among the panoply of obesity-related co-morbidities that are ameliorated
by bariatric surgery, perhaps the most impressive and scientifically
interesting is the rapid, dependable resolution of type 2 diabetes. Numerous
studies, including a meta-analysis of 22,094 patients, confirm that 83% to 86%
of patients with diabetes experience complete remission of their disease after
Roux-en-Y gastric bypass (RYGB)…. After biliopancreatic diversion (BPD), the
remission rate is greater than 95%,”at. “Most
reported series show that return to
euglycemia and normal insulin levels occur within days after surgery, long
before there is any significant weight loss. 15,24,25 In
1995, Pories et al 24 reported
the results of GBP in a series of
608 morbidly obese patients. Preoperatively, 146 patients were diabetic (type
2) and 152 had impaired glucose tolerance. GBP achieved normal levels of serum
glucose, insulin, and glycosylated hemoglobin in 83% of diabetic patients and
in 98.7% of patients with impaired glucose tolerance within 4 months after
surgery, without the need for any diabetic medication or special diet, and
before any weight reduction occurred” at. “Immediately
after bariatric surgery, the patient is restricted to a clear liquid diet,
which includes foods such as clear broth, diluted fruit juices or sugar-free
drinks and gelatin desserts. This diet is continued until the gastrointestinal
tract has recovered somewhat from the surgery. The next stage provides a
blended or pureed sugar-free diet for at least two weeks. This may consist of
high protein, liquid or soft foods such as protein shakes, soft meats, and dairy
products. Foods high in carbohydrates are usually avoided when possible during
the initial weight loss period.
Post-surgery overeating is curbed because exceeding the capacity of the
stomach causes nausea and vomiting” Wiki. The evidence clearly shows that fasting--not
weight loss--cures T2D. Fasting
entails very low serum insulin, and this permits the body to burn the fat with
hepatic liver and beta pancreatic cells.
The latter restores insulin production.
As stated earlier those with T2D,[9]
have a decline in insulin production.
33)
The diabetes cure fasting diet for insulin dependent T2D: Similar in effect
to bariatric surgery is
fasting. The alternate-day fasting
regime as proposed by Dr.
Jason Fung has proven success.
Fung’s diet incorporates on the off-fasting
day the low-carb diet (actually low insulin diet). Dr. Fung refers to a 6-month
study which
compared intermittent fasting (IER) to
conventional reduced energy diet (CER)—both
groups consumed the same number of calories. The IER
group significantly outperformed the CER
group as to weight loss by 15% and insulin sensitive—at 2011. Unfortunately
this diet was not low carb, which is part of Dr. Fung’s low insulin diet.
Dr. Fung explains the dynamic of intermittent
fasting with his low insulin diet. Fasting
for obese patients is easy since their body merely switches to burning fat and
hunger is only moderate. Restoration of
insulin sensitivity, thus lower serum, entails increased metabolism of fat and
lower leptin thus less hunger. Also on
his diet there isn’t the reduction in metabolism that develops with the
low-calorie diet, thus increased weight loss, and avoids the yo-yo effect of
ordinary diets. My own proposal would be
to go on a program like the one recommended by Dr. Richard Bernstein; a very low carbohydrate
diet[10], which “was the standard
treatment for diabetes throughout the 19th century” Wiki. The
low-carb diet should also be low
insulin, thus small meals and frequent small snacks. Since insulin is part of
a complex regulatory
system and all foods produce an insulin response (see table on Insulin Index at
end of this paper), those on 3 or more diabetic drugs and or insulin should
take an aggressive dietary approach of alternate-day fasting. If compliance
with the very-low carb diet
proves difficult, then start out with three changes. One, small meals to keep
the insulin level low (most foods will cause some rise in insulin). Two, substitute
resistant starches and increase vegetables.
Three, gradually reduce sugars. The
Use of two metabolic pathways results in
the mitochondria over producing acetyl-CoA; so warns Prof. Lustig MD in Fat
Chance, p. 108[11]. Click on link for the details on healthful diet divided into 6 parts; for choices of foods the section at length, for 6 pages summation with the 2nd
and 3rd sections devoted to food selection. I
recommend the YouTube lectures by Dr. Jason
Fung which explains
T2D
and how to reverse
T2D with diet. He explains how
pharma treats glucose instead of the cause excessive insulin. The drugs
pharma offers do not stop its progression. T2D
shortens life an average of 7 years.
[1] For a
number of these medications there is no net long-term
patient benefit for the population of those with moderate symptoms when
compared to a low carb diet. This is
strong reason to conclude that there are no positive major health benefits for
those without symptoms. The net
benefit
claims are based upon pharma’s
clinical
trial, well below the standard of sound science. What is true of psychotropic drugs is true of
other classes (click on Positive Bias) for these results are consistent
with pharma’s business model.
[2]
This affect by bacteria is one of the causes for atherosclerosis.
Bacteria are found in the tunica media (muscle
of artery walls) and are a major cause for CVD.
Another example of pharma distorting the beliefs about CVD—for confirmation of infectious
agent role. Thus
the toxins from
bacteria damage both the LDL and its fatty acid content.
[3] Desirable properties of not being subject to
oxidation (they lack a double bond unsaturated fats), which improves flavor,
and they “melt at a desirable temperature (30-40° C)” Wiki.
Removing trans-fats following hydrogenation of vegetable oil adds to its
cost. Thus for flavor, shelf-life,
and
price hydrogenated vegetable oils are commercially valued.
[4] A well designed
study in Boston looked at the
dietary intake of 239 hospital patients with their first MI were matched to 282
control subjects. A questionnaire was
used to estimate dietary intake of trans-fats, and adjustments were made for
contravening variable. “Relative
risk
for the highest quintile, 2.44.”
Trans-fats constituted 1.6% of daily energy intake. The highest quintiles consumed twice the
daily intake of the lowest. “The
association could not be explained by other established risk factors.”
[5] Trans-isomers of fatty acids constitute about
5% to 6% of dietary fat in the average US diet, mostly derived from partial
hydrogenation of vegetable oils…. Typical margarines in
the US market range from 10% to 30% of
total fat… more than 10% of total fat are also frequent in cookies, crackers,
breads, pastries, and French-fried potatoes” at AHA.
[6] There are just two studies using a Google
Scholar search of the literature. One
population wing of the Nurses’ Health Study found a clear association after controlling
for confounding variables of transfats with CHD (coronary
heart disease).
The other was trial using rats of 4 cohorts (6 in each): trans-fat +
HFCS, lard + HFCS, trans-fat, and control (without t forced sedentary lifestyle). The
combo of HFCS and trans-fat had had the
greatest weight gain, and liver weight gain, but there was no indication as the
CHD (possible by deliberate
omission). Liver
damage is not a proven surrogate for CHD.
The lack of an animal study is telling.
[7]
That one participant showed 0 lbs. loss, this makes me believe that this person
didn’t comply with the diet, and was the one who’s
NAFLD
wasn’t cured. The diet was
on the honor
system. Possible the person only
complied a couple days prior to monthly testing.
[8] Those who
undergo bariatric surgery undergo
fasting. “The oral glucose load,
together with the circulating levels of intestinal incretins and adipocytokines
has been studied in 10 diabetic morbidly obese subjects before and shortly
after biliopancreatic diversion (BPD) [bariatric surgery]to avoid the weight loss
interference. Diabetes disappeared 1 week after BPD, while insulin sensitivity
(32.96 ħ 4.3 to 65.73 ħ 3.22 μmol · kg fat-free mass−1 ·
min−1at
1 week and to 64.73 ħ 3.42 μmol · kg fat-free
mass−1 ·
min−1 at
4
weeks; P <
0.0001) was fully
normalized. Fasting insulin secretion
rate (148.16 ħ 20.07 to 70.0.2 ħ 8.14 and 83.24 ħ 8.28 pmol/min per m2; P < 0.01) and total insulin output
(43.76 ħ 4.07 to 25.48 ħ 1.69 and 30.50 ħ 4.71 nmol/m2; P < 0.05) dramatically decreased,
while a significant improvement in β-cell glucose sensitivity was observed,” 2006.
[9] Pharma, of course, wants to treat those who are
merely IR, who show up on the HAc1
test with or fasting glucose tolerance test as IR. The guideline has recently
been changed from just manage through exercise and diet to also including the
use of drugs.
·
[10]
The
Bernstein diet: The allowed carbohydrate amounts are a maximum
of 6 grams
for breakfast, 12 grams for lunch, & 12 grams for dinner.
·
Avoiding all foods with added sugar
or honey such as desserts, candies, and pastries; all foods made from grains
and grain flours such as breads, cereals, pasta, and rice; all starchy
vegetables such as potatoes, corn, carrots, peas, tomatoes, and beans; all
fresh or preserved fruits and fruit juices; all dairy products except for butter,
cream, and fermented cheeses.
·
The patient takes responsibility for
blood sugar control including blood glucose testing up to 8 times per day.
·
Target blood glucose levels that are
nearly constant for the entire day.
·
Weight loss for obese people with type
2 diabetes.
·
Exercise for all those with type 2
diabetes.
·
Basal and bolus dosing for insulin users.
[11] The evidence
support this aspect of the
Western diet contributing to its unhealthy consequences is supported by
population studies. As for the role
of
Acetyl-CoA, a search of Googlescholar failed to find confirmation of its role,
and his book lacks a reference.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
34) 4 Diets for health, moderate weight loss,
obesity, severe T2D and morbid obesity: DIETS -- 10/23/15
1) Healthy diet: For those in good health
and
normal weight. The goal is to keep serum
fructose & insulin low, thus avoid added sugar & easily digestible
starches. Small meals, with fiber,
fats,
and proteins along with increased physical excursion keeps serum glucose and
thus insulin low. Low rate of glycation
requires very low fructose (see section 5, #4).
At least 2 days a week keep carbs to under 25% of total calories; for an
average male and women that would be 600 and 500 calories which is 170 and 143
grams respectively. The jk short fast at least once weekly
promotes a healthy liver.
2) Weight loss diet of less
than 20%: Daily the jk short fast and 20% calories from
carbs or less. If progress is slow, then add the New
Atkins Diet. Very low carbs with fasting cleanses the
liver to cure NAFLD[1],
IR, MeS, and T2D.
3) T2D diet on one drug, &/or
obesity: Daily JK
short fast and
the new
Atkins type diet. Monitor plasma
glucose so as to reduce dependence on drugs.
If after 6 month this hasn’t cured T2D
then replace the JK short fast with
full alternate-day fasting. Watch Dr. Janson Fung explain the issues
on insulin
and
diabetes and alternate
day fasting diet.[2]
4) Severe
T2D and morbid obesity: Follow a
very low carb diet with alternate-day
fasting. T2D is a progressive disease treated
with drugs to lower glucose,
then more drugs, & then insulin injections.
It is caused by diet and can be cured by diet.
The fast following bariatric surgery cures
over 80% of T2D in the first few
weeks, before major weight loss.
JK short fast: go on a 16 hour fast (7 PM
until 11:00 AM) or longer, thus extending the beneficial nighttime fat burning
production of ATP (the energy
molecule) to midday. At night because of
not eating there is low glucose and thus insulin is not secreted by the
pancreas. The body then metabolizes fat
for energy (ATP). If hunger becomes
an issue than eat a small
handful of nuts, green vegetables, or low-carb power bar to kill pangs; the
effect of a small portion on insulin production is minimal. (Another version
of the fast is to consume
just 20% of calories, all low carbs; thus if on a non-fasting day you eat 2,500
calories, then on the fasting day just 500 calories. Choose whichever fast has
the best
compliance.) Always select low net-carb
snacks.
Atkins maintenance phase: Once weight target is reached, the
daily intake of carbs is increased by 10 grams per week to find the level where
weight is gained, then drop below that level.
Continue to limit refined carbs and foods with high glycemic index to
small portions, limits sweets with fructose, and use the JK short fast to maintain
a healthy liver. Set up a routine of vigorous
exercise since it is a general health tonic and mood elevator.
Healthful
food choices 10/23/15
|
Increase
|
Decrease
|
Avoid
|
|
Saturated and
monounsaturated fats (animal
fats, lard, & butter are best, followed by palm kernel, coconut, and
olive oils), fiber, leafy vegetables, egg, peanuts, , fish, free ranging
beef, nuts, whole milk dairy products including cheese, plain yogurt, and
cottage cheese, breakfast protein mix, whole grain products[3],
beans,
|
Meats &
poultry unless free ranging[4],
large portions of fruits especially melons, bananas, grapes, raisins, and
dates[5].
60 grams of protein male, 45 female daily ideal.
|
Fructose, sugar
added foods[6],
fruit juices,[7],polyunsaturated
and transfats, vegetable oil [8],
refined carbohydrates, whole wheat4, large portions of carbs and
fruit, potatoes, rice, instant breakfast cereals.
|
|
Vinegar,[9]
high fiber cereal,[10], tomatoes juice, Karo corn syrup or
sorbitol as sweeteners.
|
Fried foods
(unless high in saturated fat),
large portions of food with high glycemic index,
|
Lunch meats
unless cooked[11],
all GMOs12, corn[12],
soy products,[13]
most crackers, chain restaurants.
|
Sugars
without fructose:
barley
malt, corn syrup, corn syrup solids,
dextran, dextrose, diastatic malt,
diatase, ethyl maltol, galactose,
glucose, glucose solids, lactose, malt syrup, maltodextrin, maltose, & rice syrup. For extensive foods recommendations use Fat
Chance, pages 199-205 by Prof. Robert
Lustig.
35) Healthful choices: What is beneficial
for senior as listed at Diets,
supplements & drugs is all the more so for
diabetics because of their higher risks. Of special merit is high dose aspirin
(325 mgs with meals). From the paper on aspirin: “Diabetes treatment of
type 2 (T2D) with high dose aspirin or other salicylates has a positive
effect upon obesity and diet induced insulin resistance; thus by improving the function of insulin
it lowers serum glucose level through improved in glucose metabolism. Increased inflammation
of diabetics is
associated with morbidities for which aspirin is a treatment.” Given the positive
effect upon
insulin resistance and glucose management, a reasonable inference would be that
aspirin reduces the risk of developing T2D and the related NAFLD
and IR. This benefit has been long known: “Administration
of salicylates was shown over a century ago to lower glucose levels in patients
with diabetes.” A review of the research
on aspirin provides compelling evidence for its daily usage and is proof of the
power of pharma to direct medical practice to maximize their profits.
Aspirin benefits are detailed in hundreds of
journal articles summation,
history and uses, cancer prevention, prevention of atherosclerosis and thus
CVD and hypertension. There are two concise papers on what to
eat. The longer one has related
topics,
at id8. I highly recommend a
careful reading and adopting the recommendations. There is a list of supplements including
CoQ10, Vitamin C (both are effective antioxidants, one fat soluble and the
other water soluble), omega-3 fish oil, and the sex hormones (estradiol with progesterone, and testosterone) for the elderly in
sufficient
dose. Read
the papers on these
hormones carefully so as to avoid pharma’s less than ideal products.
Pharm is against all of these because they
prevent diseases; thus pharma does tobacco science to education the physicians
and warn the public.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
APPENDIX
Diet-Food
Basics
Adipocytes
(lipocytes)
fat cells compose adipose
tissue & secrete hormones resistin, adiponectin, leptin and Apelin.
ATP, Adenosine
TriPhosphate (adenosine
with 3 phosphate molecules (PO4) attached), transfers chemical energy within
the cell through the loss of one or two of its phosphate groups.
ATP
goes from a high state of energy to a low state. The main way ATP goes back
to the high state of energy is through absorbing
energy from the metabolism of carbohydrates or fats in the mitochondria, where
ATP is restored to three phosphate
group. ATP provides the energy driving over 90% of the biosynthesis
processes in the body, such as in the production of hormones, of proteins, and
thousands of other compounds. ATP is used to make muscle fibers
contract and in intercellular active transport of large molecules.
Carbohydrate
(carb): fiber, fructose,
glucose-glycogen, starch, sucrose (net
carbs is total carbs minus fiber):
Fiber, vegetable fiber, roughage, the
carbohydrate component not broken down by digestive
enzymes, but some is by gut bacteria.
Fiber has more than ten sugar units.
It lowers the insulin spike when consumed with refined carbs.
Fructose (fruit sugar) a
monosaccharide found in fruits. Main
sources are the disaccharide sucrose, fruits, and high fructose corn syrup.
It is metabolized in the liver into either
glucose or fat. Fructose is converted to fat in the liver,
where when insulin is high is stored there, which can cause IR and NAFLD. Also fructose is 7.5
more reactive then glucose. Through
the process
of glycation fructose damages
the liver and causes our
chronic age-related diseases.
Glucose
a monosaccharide is the main energy
storage molecule for plants; in animals it is stored as long chain called glycogen. Glucose is as one half
of the disaccharide
sucrose, and is also obtained from the hydrolysis of starches which are long
chains of glucose molecules--also from sucrose.
Glucose and fat are the main sources for production of ATP
Starch is long
chains of glucose units. This
polysaccharide is produced mostly by green plants for energy storage.
Sucrose, table
sugar, is the disaccharide consisting of fructose
and glucose and is produced
mainly by plants.
Fatty
acids and triglycerides are chains of up to 24 carbon molecules with an organic acid
on the last carbon.
Glycation:
a process where a monosaccharide (simple
sugar) randomly attaches to proteins or lipid; this adversely affects the proteins’
functions. Fructose binding reaction
to
proteins over 2 hours is 14 times that of glucose.
Insulin regulates
other hormones that affect metabolism, appetite, fat and amino acid storage,
blood glucose, etc. It is
produced by the pancreas mainly in response to blood glucose
and causes tissues to absorb
and burn glucose and also to store fat (not burn). Though Pharma has doctors
control elevated glucose with drugs, it is insulin elevated that
produces the comorbidities (negative health
consequences) associated with T2D, thus dietary carbs should be limited.
Insulin
resistance (IR): the condition
of higher than normal serum
insulin to manage glucose due to a diminished response to insulin by various
tissues. IR first occurs
in the
liver cells, and causes fat to accumulate there, which causes NAFLD.
Later the muscle and fat cells develop IR. The pancreas then releases even more
insulin to lower blood glucose. Since
insulin increases fat storage IR causes excess fat storage principle in
the muscles and fat tissue to cause obesity.
Leptin is the
satiety hormone; it causes the brain’s hunger center to suppress appetite,
while ghrelin has the opposite effect.
Leptin is produced by fat cells.
Leptin also regulates metabolism.
Leptin level increase during the night and thus suppresses hunger.
Leptin is responsible for the 20% reduction in metabolism during an energy
restricted diet.
Metabolism in
reference to diet refers to the metabolic conversion of mainly either fat or
carbohydrate into the energy molecule ATP
by the mitochondria. Under conditions of starvation proteins also
can be used to make ATP.
Mitochondria an organelle
function is to produce ATP through
metabolism of fatty acids and glucose.
NAFLD (Non-Alcoholic Fatty Liver Disease): the accumulation of fat by liver cells
sufficient to significantly downgrade their various functions. The NHANES survey 2011 found NAFLD in 30% of adult population—similar % for Europe.
Type-2 diabetes
(T2D): occurs
when the pancreas fails to produce enough insulin to lower glucose to its
normal serum range. This results from IR
and the accumulation of fat in the pancreas, which eventually causes a decline
in insulin.
5.
Setting the Record
Straight on points relevant to diet-- (exposing tobacco science)
High plasma cholesterol causes CVD.
TRUTH: High plasma cholesterol
has not been demonstrated to be a
cause of plaque formation. CVD’s
main cause is infective agents within artery
walls which damage LDL with toxins and cause an immune response by macrophages
that cause atherogenesis. The
cholesterol deposits in the artery walls are a byproduct of the immune
response, as too are calcium crystals, foam cells, triglycerides, and
lymphocytes. Cholesterol is a bystander
not a cause; thus lowering its production with drugs does not prevent AS or heart
attack. Autopsy studies found no relationship between
plasma cholesterol and degree of AS in
those died violent deaths, see. Avoid saturated
fats because they cause CVD by raising the plasma level of
small-dense LDL which is associated with CVD.
TRUTH: Saturated fats don’t
raise cholesterol levels
or small-dense LDL. LDL level is not associated
with CVD (see #1). A meta-analysis of 21
studies on saturated fats, “failed to find an association with CVD, Wiki
and also Wiki. This extends to
all types of fats when “increased from 30 to 50% of total energy,” 2004.
Vegetable
oils are preferred to animal
fats. TRUTH: Vegetable oils are
associated with diseases because they are high in polyunsaturated fats and
become rancid in the body and on the
shelf--1945
and. Some of their
oxidation products are harmful. Second,
they are high in omega-6 fatty acid which blocks
conversion of omega 3 oils to an anti-inflammatory agent. Our Paleolithic ancestor averaged 2 parts
omega-6 to 1 omega-3; today it’s 16 to 1.
Many people wisely take a fish-oil supplement to improve the ratio of
omega-3. Because of its effect on the
immune system and rancidification vegetable oils promote the diseases
involving inflammation, including CVD,
arthritis, and Alzheimer’s disease and other conditions. The more expensive
animal fats are the best source of fat followed by the
palm kernel, coconut, and olive oils which
are high in monounsaturated fats. Sugar (the disaccharide sucrose,
fructose and
glucose), fruit sugar (fructose), and starches (long chains of glucose) are
merely empty calories without nutritive value; viz. harmless sources of energy.
A calorie is a calorie. TRUTH:
sugars and starches (pure glucose) damage tissues. Fructose and glucose
randomly bind to
proteins (in a process called “glycation”) to damages proteins in your cells.
Thus glycation
promotes the degenerative conditions associated with old age: CVD,
atherosclerosis, Alzheimer’s, macular degeneration, et al. Fructose
(fruit sugar) has a glycation rate
of 7-10 times that of glucose. Actual 15
times as great a rate of glycation because of its slower clearance compared to
glucose. Fructose is converted in the
liver to fat which can causes liver dysfunction that progresses to non-alcoholic
fatty liver disease (NAFLD), and
that affects the plasma-glucose
regulatory function of the liver to cause IR. Fructose by minimal
insulin response, it bypasses the appetite regulating system involving leptin
& ghrelin, which causes weight gain.
Fructose stimulates the addiction
center of the brain (see #6 below) to promote sugar addiction. Clearly,
sugars are not harmless empty
calories, nor are starches with high insulin index. The cause of obesity is a sedentary lifestyle
& gluttony. All one needs to do is
eat less and exercise more; viz., burn more calories than one consumes; this is
the common advice given by doctors, dieticians, and accepted as the way to lose
weight. TRUTH: For all mammals
their weight is controlled by
a biological system. The Western diet
with its average of 180 grams of sugars daily causes a fatty liver and IR. Fatty
liver and IR muck up the regulatory
system and thus cause obesity. It
is not gluttony and sloth that causes the
obesity and diabetes pandemics (blaming the victims) but rather the Western
diet which is promoted by food manufacturers and corporatist governments. For the obese, a low-calorie
diet of 75% or less
than normal will result in significant long-term weight loss. Truth The weight regulatory system in an effort to
maintain the set weight will reduce the rate of metabolism approximately 20%
and increase hunger. Eating less simply
results in yo-yo diets. Less than 1% of
obese adults at the end of nine years will obtain normal body weight. To prevent this regain
of weight, the
regulatory system must be reset, and this occurs by going from carb burning
metabolism to fat burning metabolism. by going on an extremely low carb
(ketogenic, Atkins type) diet. Fasting
also promotes fat burning. This type of
diet will eventually result in the burning of fat in the liver and pancreas
which will allow cure IR and thus permit the weight regulatory system to
eventually adjust to a lower weight. Hormone replacement (HRT) will not promote
weight loss. TRUTH: during and following
menopause women experience a precipitous drop in estradiol (the most healthful
and active of the 4 nat ural estrogens).
This drop in estradiol increases LPL which regulates weight, distribution of fat,
and physical activity. “Natural HRT [NHRT, estradiol
plus progesterone] reduces insulin resistance and fasting glucose in women with
diabetes” at. Numerous studies have found similar benefit
for men on testosterone due to its androgen effect which increases metabolism. HRT for men and women poses major health risks
which outweigh their benefits. TRUTH:
natural hormones lower risk for breast and prostate
cancers. Men in the highest group for
testosterone, have the
lowest rate of prostate cancer.
Estradiol moderately lowers the rate of breast cancer. In sufficient
dose NHRT will reset the biological
clock to a younger
age and thereby significantly reduce the risk of most age-related chronic
diseases. Estradiol with progesterone
lowers CVD risk. Testosterone decreases the risk of heart attack.
Current wisdom is based on
pharma’s junk science & tobacco ethics.
Read the section on the WHI study
which exposes NIH’s use of Prempro, the worse HRT. Two lies
about type-2 diabetes: that it is caused by high plasma sugar
therefore drugs are given to lower sugar, and that it is a life-long condition;
viz. it can’t be cured. Truth:
IR is the problem which is cured
by either bariatric surgery or by Dr. Janson
Fung’s dietary treatment of ketogenic diet (low carb
high fat) with alternate day fasting. Pharma is highly regulated by the FD A to
protect the public from the tobacco
ethics used by corporations to fulfill their fiduciary duties. Truth: that there is a revolving door between the
FDA and pharma, and that at the highest levels the FDA is ran by executives
from pharma and their KOLs. For
a summation of the ways in which the
evidence base has been broken—link,
or YouTube Dr. Angell. Our corporatist government enacted the
Prescription Drug User Fee Act of 1992 to make the FDA dependent upon pharma
for over half of its budget. Congress
wants the FDA to serve the pharmaceutical industry. Link to Consumer Report on the FDA. Read Prof. Ben Goldacre’s Bad
Pharma. Doctors know what is best for patients. Truth: the education and sources of for doctors’
information has been manipulated by pharma so as to turn them into drug
pushers. Pharma runs and owns the
results of clinical trials, thus positive bias is the norm--32%. Pharma determines who becomes a KOLs (Key
Opinion Leaders). They are the leads on
clinical trials, write the medical text books, and give continuing education
classes. The information foundation is thus distorted. For an insightful
explanation of how this
has occurred click on link—you need to know. Pharma
and food manufacturers through junk
tobacco science, corporate media, and misinformed doctors causes cognitive dissonance and reliance
on their KOLs. Pharma has framed the
discussions to produce promote the sales of patented drugs. What
has been said about pharma applies to
the manufactured food and tobacco industries—profits before people.
Net
Carbs while on Atkins
ketogenic diet—easy table
by JK
Net Carbs = total carbohydrates
minus fiber
content.
|
Egg
1 = 0.4 grams
Seafood
6 oz. = 0
Meats
6 oz. = 0
Poultry
6 oz. = 0
Oils
6 oz. = 0
|
Dairy
American processed
1 slice 1.5 grams
Cheeses 1 oz. = 0.7
Cottage cheese ½ c = 5
Cream 1 T
= 0.4
Cream cheese 2 T = 1.2
Milk 1 c = 11.7
to 15
Yogurt plain
1 c = 11.6
Greek Yogurt
plain 1 c = 9
|
Raw
Vegetables
Avocado ½ = 2 grams
Bell pepper green ½ c= 2.2
Bell pepper red ½ c =3
Broccoli ½ c = 1
Cabbage shredded ½ c = 1.1
Celery stalk = 1
Cauliflower florets ½ c = 1.4
Cucumber ½ c = 1
|
|
Nuts
Almonds 24 = 2.5
Brazil 6 = 1.4
Cashews 2 T =
5.1
Mixed nuts 2 T = 2
Peanuts 2 T = 1.4
Pecans 1 oz. = 1.2
Walnuts 1 oz. 1.2
|
|
Green beans ½ c = 2
Lettice 1 c = 0.36Olives black 5 = 0.7
Olives green 5 = 0.0
Onion 2 tbs. = 1
Spinach 1 c = 0.2
Squash summer ½ c 2.6
Tomato 1 med = 3.0
Tomato juice 1c = 8
|
|
For
those off
|
the
induction
|
(ketogenic)
phase
|
|
Fruits
Apple med = 8
Banana med = 30
Blueberries ½ c = 9
Dates dried 1 oz = 21
Fig dried med = 6
Grapes 1 c = 26
|
Grapefruit ½ = 9
Melon cantaloupe 1 c = 12
Orange navel med =15
Peach med = 15
Pear med = 20
Strawberry 5 lg = 5
|
Legumes
Black bean home cooked 1 c = 8
Canned baked beans 1c = 36
Kidney home cooked 1c = 11
Pinto bean home cooked = 25
Soybean white 1c =10
|
|
Vegetables not leafy
Beets steamed 1c = 13
Carrots steamed 1c = 8
Corn on cob med steamed 15
Eggplant 1c = 5
|
Olive cured 7 = 1
Onion 1 c = 12
Peas 1 c = 14
Potato med with skin = 26
|
Snow pea ½ c cooked = 2.7
Squash acorn 1 c = 21
Squash zucchini 1c = 3
Sweet potato med = 20
|
To calculate from the food label
simply
subtract fiber from total carbohydrates
On the Atkins website (http://files.atkins.com/1501_CarbCounter_Online.pdf)
is an extensive table of net carbs. For
simplicity the food label on products can be used, simply subtract fiber from
carbohydrates to get an approximate value.
Remember that food manufacturers add sugar to nearly every product plus
many of them have various forms of starch as filler and thickening agent
(starch is pure glucose).
[1] Dr. Fung’s
clinic has documented many cures,
and the fasting that occurs with
bariatric surgery cures T2D in the
first 2 weeks prior to significant weight loss.
T2D, NAFLD and “resolution of NASH in around 80% of
patients”[20] Wiki and.
[2] Watch Dr. Fung explain how the body switches from glucose to
fat burning. Burning excess fat in the
liver to promotes overall metabolic health.
The fructose in the Western diet causes fatty liver. This is caused by
fructose, which causes insulin resistance.
[3] Most whole wheat breads are comparable to
white bread as to glycemic
index (GI) and insulin index (IL) (see
table Part 3), plus they have phytic acid (inositol
hexaphosphate (IP6): “Phytic
acid has a strong binding affinity to
important minerals, such as calcium, iron, and zinc” Wiki that binds to and thus prevents their
absorption. Phytic acid is also in beans, peanuts, soybean, brown rice, oat
meal, corn, and nuts. White flour lacks phytic acid. Sugars are added to mask the rancid taste of
phytic acid. Lustig, Fat
Chance 133.
[4]
Cattle are fed a diet of GMO grains. Certified
Organic has been outsourced to companies most of whom do sham
inspections.
[5]
High sugar fruits with high glycemic index compared to most other fruits.
[6] In
2015 “Sugar added” is to
be listed (maybe) under sugar in food labels.
For current labels, how much has been added depends on ingredients,
vegetables have natural low levels of sugar, fruits higher. There are 56
different sweeteners used in processed foods.
If in doubt, look at the list of
ingredients for sweeteners. Ingredients
are listed in order of percentage by weight.
[7]
Fruit juices having most of the fiber removed produce a serum glucose increase
comparable to like amount of soda.
[8]
Polyunsaturated fats undergo in the body unhealthful rancidification, and they
are high in omega-6 fatty acids which block the healthful conversion of omega-3
fatty acids. Like trans-fats they
cause CVD.
US regulations are just a pseudo fix—see fats.
[9]
Vinegar reduces insulin resistance and increase satiation.
[10] These oils are lowest in polyunsaturated fats,
including omega 6 fatty acids And because they are from trees they are free of
GMOs.
[11] Given the broken food-inspection process, they
pose a major risk factor, which has been grossly under reported in our
corporate media. A 2008 study in France
showed that their rate of food poisoning was 1/4th the US rate
[12] Avoid because of high insulin index, and they
have a GMO gene that causes corn to produces a pesticide—same for other crops
such as canola, soya bean and others. Testing
and review is a regulatory façade: and
the companies do tobacco science to “prove” the changes in the crops are
beneficial, and the FDA is business friendly. There is very little true science
on GMOs.
[13]
Soybean has estrogen-testosterone mimic, for which there is evidence that the
detrimentally interfere with their functions.
|
