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Sugar issues</strong>
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<p></p>Since the first doctor noticed, hundreds of years ago, that the urine of a diabetic patient tasted sweet,
it has been common to call the condition the sugar disease, or sugar diabetes, and since nothing was known about
physiological chemistry, it was commonly believed that eating too much sugar had to be the cause, since the
ability of the body to convert the protein in tissues into sugar wasn"t discovered until 1848, by Claude Bernard
(who realized that diabetics lost more sugar than they took in). Even though patients continued to pass sugar in
their urine until they died, despite the elimination of sugar from their diet, medical policy required that they
be restrained to keep them from eating sugar. That prescientific medical belief, that eating sugar causes
diabetes, is still held by a very large number, probably the majority, of physicians. Originally, diabetes was
understood to be a wasting disease, but as it became common for doctors to measure glucose, obese people were
often found to have hyperglycemia, so the name diabetes has been extended to them, as type 2 diabetes. High
blood sugar is often seen along with high blood pressure and obesity in Cushing's syndrome, with excess
cortisol, and these features are also used to define the newer metabolic syndrome. Following the old reasoning
about the sugar disease, the newer kind of obese diabetes is commonly blamed on eating too much sugar. Obesity,
especially a fat waist, and all its associated health problems, are said by some doctors to be the result of
eating too much sugar, especially fructose. (Starch is the only common carbohydrate that contains no fructose.)
Obesity is associated not only with diabetes or insulin resistance, but also with atheroslcerosis and heart
disease, high blood pressure, generalized inflammation, arthritis, depression, risk of dementia, and cancer.
There is general agreement about the problems commonly associated with obesity, but not about the causes or the
way to prevent or cure obesity and the associated conditions. In an earlier newsletter, I wrote about P. A.
Piorry in Paris, in 1864, and Dr. William Budd in England, in 1867, who treated diabetes by adding a large
amount of ordinary sugar, sucrose, to the patient's diet. Glucose was known to be the sugar appearing in the
diabetics' urine, but sucrose consists of half glucose, and half fructose. In 1874, E. Kulz in Germany reported
that diabetics could assimilate fructose better than glucose. In the next decades there were several more
reports on the benefits of feeding fructose, including the reduction of glucose in the urine. With the discovery
of insulin in 1922, fructose therapy was practically forgotten, until the 1950s when new manufacturing
techniques began to make it economical to use. Its use in diabetic diets became so popular that it became
available in health food stores, and was also used in hospitals for intravenous feeding. However, while fructose
was becoming popular, the cholesterol theory of heart disease was being promoted. This was the theory that
eating foods containing saturated fat and cholesterol caused heart disease. (My newsletter, Cholesterol,
longevity, intelligence, and health, discussed the development of that theory.) A Swedish physician and
researcher, Uffe Ravnskov, has reviewed the medical arguments for the theory that lipids in the blood are the
cause of atherosclerosis and heart disease, and shows that there has never been evidence of causality, something
which some people, such as Broda Barnes, understood from the beginning. In the 1950s, an English professor, John
Yudkin, didn't accept the idea that eating saturated fat was the cause of high blood levels of triglycerides and
cholesterol, but he didn"t question the theory that lipids in the blood caused the circulatory disease. He
argued that it was sugar, especially the fructose component of sucrose, rather than dietary fat, that caused the
high blood lipids seen in the affluent countries, and consequently the diseases. He was sure it was a specific
chemical effect of the fructose, because he argued that the nutrients that were removed in refining white flour
and white sugar were insignificant, in the whole diet. Following the publication of Yudkin's books, and
coinciding with increasing promotion of the health benefits of unsaturated vegetable oils, many people were
converted to Yudkin's version of the lipid theory of heart disease, i.e., that the "bad lipids" in the blood are
the result of eating sugar. This has grown into essentially a cult, in which sugar is believed to act like an
intoxicant, forcing people to eat until they become obese, and develop the "metabolic syndrome," and "diabetes,"
and the many problems that derive from that. The publicity campaign against "saturated fat" as an ally of
cholesterol derived its support from the commercial promotion of the polyunsaturated seed oils as food for
humans. Although the early investigators of vitamin E knew that the polyunsaturated oils could cause sterility,
and others later found that their use in commercial animal foods could cause brain degeneration, there were a
few biologists (mostly associated with George Burr) who believed that this type of fatty acid is an essential
nutrient. George and Mildred Burr had created what they claimed to be a disease in rats caused by the absence of
linoleic or linolenic acid in their food. Although well known researchers had previously published evidence that
animals on a fat free diet were healthy--even healthier than on a normal diet--Burr and his wife published their
contradictory claim without bothering to discuss the conflicting evidence. I haven't seen any instance in which
Burr or his followers ever mentioned the conflicting evidence. Although other biologists didn't accept Burr's
claims, and several researchers subsequently published contrary results, he later became famous when the seed
oil industry wanted scientific-seeming reasons for selling their product as an "essential" food. The fact that
eating the polyunsaturated fats could cause the blood cholesterol level to decrease slightly was advertised as a
health benefit. Later, when human trials showed that more people on the "heart healthy" diet died of heart
disease and cancer, more conventional means of advertising were used instead of human tests. Burr's experimental
diet consisted of purified casein (milk protein) and purified sucrose, supplemented with a vitamin concentrate
and some minerals. Several of the B vitamins weren't known at the time, and the mineral mixture lacked zinc,
copper, manganese, molybdenum, and selenium. More of the essential nutrients were unknown in his time than in
Yudkin's, so his failure to consider the possibility of other nutritional deficiencies affecting health is more
understandable. In 1933, Burr observed that his fat-deficient rats consumed oxygen at an extremely high rate,
and even then, the thought didn't occur to him that other nutritional deficiencies might have been involved in
the condition he described. Ordinarily, the need for vitamins and minerals corresponds to the rate at which
calories are being burned, the metabolic rate. Burr recalled that the rats on the fat free diet drank more
water, and he reasoned that the absence of linoleic or linolenic acid in their skin was allowing water vapor to
escape at a high rate. He didn't explain why the saturated fats the rats were synthesizing from sugar didn't
serve at least as well as a "vapor barrier"; they are more effective at water-proofing than unsaturated fats,
because of their greater hydrophobicity. The condensed and cross-linked keratin protein in skin cells is the
main reason for the skin's relatively low permeability. When an animal is burning calories at a higher rate, its
sweat glands are more actively maintaining a normal body temperature, cooling by evaporation; the amount of
water evaporated is an approximate measure of metabolic rate, and of thyroid function. In 1936, a man in Burr's
lab, William Brown, agreed to eat a similar diet for six months, to see whether the "essential fatty acid
deficiency" affected humans as it did rats. The diet was very similar to the rats', with a large part of the
daily 2500 calories being provided at hourly intervals during the day by sugar syrup (flavored with citric acid
and anise oil), protein from 4 quarts of special fat-free skimmed milk, a quart of which was made into cottage
cheese, the juice of half an orange, and a "biscuit" made with potato starch, baking powder, mineral oil, and
salt, with iron, viosterol (vitamin D), and carotene supplemented. Brown had suffered from weekly migraine
headaches since childhood, and his blood pressure was a little high when he began the diet. After six weeks on
the diet, his migraines stopped, and never returned. His plasma inorganic phosphorus declined slightly during
the experiment (3.43 mg./100 cc. of plasma and 2.64 on the diet, and after six months on a normal diet 4.2
mg.%), and his total serum proteins increased from 6.98 gm.% to 8.06 gm.% on the experimental diet. His
leucocyte count was lower on the high sugar diet, but he didn't experience colds or other sickness. On a normal
diet, his systolic blood pressure varied from 140 to 150 mm. of mercury, the diastolic, 95 to 100. After a few
months on the sugar and milk diet, his blood pressure had lowered to about 130 over 85 to 88. Several months
after he returned to a normal diet, his blood pressure rose to the previous level. On a normal diet, his weight
was 152 pounds, and his metabolic rate was from 9% to 12% below normal, but after six months on the diet it had
increased to 2% below normal. After three months on the sugar and milk diet, his weight leveled off at 138
pounds. After being on the diet, when he ate 2000 calories of sugar and milk within two hours, his respiratory
quotient would exceed 1.0, but on his normal diet his maximum respiratory quotient following those foods was
less than 1.0. The effect of diabetes is to keep the respiratory quotient low, since a respiratory quotient of
one corresponds to the oxidation of pure carbohydrate, and extreme diabetics oxidize fat in preference to
carbohydrate, and may have a quotient just a little above 0.7. The results of Brown's and Burr's experiments
could be interpreted to mean that the polyunsaturated fats not only lower the metabolic rate, but especially
interfere with the metabolism of sugars. In other words, they suggest that the normal diet is diabetogenic.
During the six months of the experiment, the unsaturation of Brown's serum lipids decreased. The authors
reported that "There was no essential change in the serum cholesterol as a result of the change in diet."
However, in November and December, two months before the experiment began, it had been 252 mg.% in two
measurements. At the beginning of the test, it was 298, two weeks later, 228, and four months later, 206 mg%.
The total quantity of lipids in his blood didn't seem to change much, since the triglycerides increased as the
cholesterol decreased. By the time of Brown's experiment, other researchers had demonstrated that the
cholesterol level was increased in hypothyroidism, and decreased as thyroid function, and oxygen consumption,
increased. If Burr's team had been reading the medical literature, they would have understood the relation
between Brown's increased metabolic rate and decreased cholesterol level. But they did record the facts, which
is valuable. The authors wrote that "The most interesting subjective effect of the 'fat-free' regimen was the
definite disappearance of a feeling of fatigue at the end of the day's work." A lowered metabolic rate and
energy production is a common feature of aging and most degenerative diseases. From the beginning of an animal's
life, sugars are the primary source of energy, and with maturation and aging there is a shift toward replacing
sugar oxidation with fat oxidation. Old people are able to metabolize fat at the same rate as younger people,
but their overall metabolic rate is lower, because they are unable to oxidize sugar at the same high rate as
young people. Fat people have a similar selectively reduced ability to oxidize sugar. Stress and starvation lead
to a relative reliance on the fats stored in the tissues, and the mobilization of these as circulating free
fatty acids contributes to a slowing of metabolism and a shift away from the use of glucose for energy. This is
adaptive in the short term, since relatively little glucose is stored in the tissues (as glycogen), and the
proteins making up the body would be rapidly consumed for energy, if it were not for the reduced energy demands
resulting from the effects of the free fatty acids. One of the points at which fatty acids suppress the use of
glucose is at the point at which it is converted into fructose, in the process of glycolysis. When fructose is
available, it can by-pass this barrier to the use of glucose, and continue to provide pyruvic acid for
continuing oxidative metabolism, and if the mitochondria themselves aren't providing sufficient energy, it can
leave the cell as lactate, allowing continuing glycolytic energy production. In the brain, this can sustain life
in an emergency. Many people lately have been told, as part of a campaign to explain the high incidence of fatty
liver degeneration in the US, supposedly resulting from eating too much sugar, that fructose can be metabolized
only by the liver. The liver does have the highest capacity for metabolizing fructose, but the other organs do
metabolize it. If fructose can by-pass the fatty acids' inhibition of glucose metabolism, to be oxidized when
glucose can't, and if the metabolism of diabetes involves the oxidation of fatty acids instead of glucose, then
we would expect there to be less than the normal amount of fructose in the serum of diabetics, although their
defining trait is the presence of an increased amount of glucose. According to Osuagwu and Madumere (2008), that
is the case. If a fructose deficiency exists in diabetes, then it is appropriate to supplement it in the diet.
Besides being one of the forms of sugar involved in ordinary energy production, interchangeable with glucose,
fructose has some special functions, that aren't as well performed by glucose. It is the main sugar involved in
reproduction, in the seminal fluid and intrauterine fluid, and in the developing fetus. After these crucial
stages of life are past, glucose becomes the primary molecular source of energy, except when the system is under
stress. It has been suggested (Jauniaux, et al., 2005) that the predominance of fructose rather than glucose in
the embryo's environment helps to maintain ATP and the oxidative state (cellular redox potential) during
development in the low-oxygen environment. The placenta turns glucose from the mother's blood into fructose, and
the fructose in the mother's blood can pass through into the fetus, and although glucose can move back from the
fetus into the mother's blood, fructose is unable to move in that direction, so a high concentration is
maintained in the fluids around the fetus. The control of the redox potential is sometimes called the "redox
signalling system," since it coherently affects all processes and conditions in the cell, including pH and
hydrophobicity. For example, when a cell prepares to divide, the balance shifts strongly away from the oxidative
condition, with increases in the ratios of NADH to NAD+, of GSH to GSSG, and of lactate to pyruvate. These same
shifts occur during most kinds of stress. In natural stress, decreased availability of oxygen or nutrients is
often the key problem, and many poisons can produce similar interference with energy production, for example
cyanide or carbon monoxide, which block the use of oxygen, or ethanol, which inhibits the oxidation of sugars,
fats, and amino acids (Shelmet, et al., 1988). When oxygen isn't constantly removing electrons from cells (being
chemically reduced by them) those electrons will react elsewhere, creating free radicals (including activated
oxygen) and reduced iron, that will create inappropriate chemical reactions (Niknahad, et al., 1995;
MacAllister, et al., 2011). Stresses and poisons of many different types, interfering with the normal flow of
electrons to oxygen, produce large amounts of free radicals, which can spread structural and chemical damage,
involving all systems of the cell. Ethyl alcohol is a common potentially toxic substance that can have this
effect, causing oxidative damage by allowing an excess of electrons to accumulate in the cell, shifting the
cells' balance away from the stable oxidized state. Fructose has been known for many years to accelerate the
oxidation of ethanol (by about 80%). Oxygen consumption in the presence of ethanol is increased by fructose more
than by glucose (Thieden and Lundquist, 1967). Besides removing the alcohol from the body more quickly, it
prevents the oxidative damage, by maintaining or restoring the cell's redox balance, the relatively oxidized
state of the NADH/NAD+, lactate/pyruvate, and GSH/GSSH systems. Although glucose has this stabilizing,
pro-oxidative function in many situations, this is a general feature of fructose, sometimes allowing it to have
the opposite effect of glucose on the cell's redox state. It seems to be largely this generalized shift of the
cell's redox state towards oxidation that is behind the ability of a small amount of fructose to catalyze the
more rapid oxidation of a large amount of glucose. Besides protecting against the reductive stresses, fructose
can also protect against the oxidative stress of increased hydrogen peroxide (Spasojevic, et al., 2009). Its
metabolite, fructose 1,6-bisphosphate, is even more effective as an antioxidant. Keeping the metabolic rate high
has many benefits, including the rapid renewal of cells and their components, such as cholesterol and other
lipids, and proteins, which are always susceptible to damage from oxidants, but the high metabolic rate also
tends to keep the redox system in the proper balance, reducing the rate of oxidative damage. Endotoxin absorbed
from the intestine is one of the ubiquitous stresses that tends to cause free radical damage. Fructose, probably
more than glucose, is protective against damage from endotoxin. Many stressors cause capillary leakage, allowing
albumin and other blood components to enter extracellular spaces or to be lost in the urine, and this is a
feature of diabetes, obesity, and a variety of inflammatory and degenerative diseases including Alzheimer's
disease (Szekanecz and Koch, 2008; Ujiie, et al., 2003). Although the mechanism isn't understood, fructose
supports capillary integrity; fructose feeding for 4 and 8 weeks caused a 56% and 51% reduction in capillary
leakage, respectively (Chakir, et al., 1998; Plante, et al., 2003). The ability of the mitochondria to oxidize
pyruvic acid and glucose is characteristically lost to some degree in cancer. When this oxidation fails, the
disturbed redox balance of the cell will usually lead to the cell's death, but if it can survive, this balance
favors growth and cell division, rather than differentiated function. This was Otto Warburg's discovery, that
was rejected by official medicine for 75 years. Cancer researchers have become interested in this enzyme system
that controls the oxidation of pyruvic acid (and thus sugar) by the mitochondria, since these enzymes are
crucially defective in cancer cells (and also in diabetes). The chemical DCA, dichloroacetate, is effective
against a variety of cancers, and it acts by reactivating the enzymes that oxidize pyruvic acid. Thyroid
hormone, insulin, and fructose also activate these enzymes. These are the enzymes that are inactivated by
excessive exposure to fatty acids, and that are involved in the progressive replacement of sugar oxidation by
fat oxidation, during stress and aging, and in degenerative diseases; for example, a process that inactivates
the energy-producing pyruvate dehydrogenase in Alzheimer's disease has been identified (Ishiguro, 1998).
Niacinamide, by lowering free fatty acids and regulating the redox system, supporting sugar oxidation, is useful
in the whole spectrum of metabolic degenerative diseases. A few times in the last 80 years, people (starting
with Nasonov) have recognized that the hydrophobicity of a cell changes with its degree of excitation, and with
its energy level. Recently, even in non-living physical-chemical systems, hydrophobicity and redox potential
have been seen to vary together and to influence each other. Recent work shows how the oxidation of fatty acids
contributes to the dissolution of mitochondria (Macchioni, et al., 2010). At first glance it might seem odd that
the presence of fatty material could reduce the "fat loving" (lipophilic, equivalent to hydrophobic) property of
a cell, but the fat used as fuel is in the form of fatty acids, which are soap-like, and spontaneously introduce
"wetness" into the relatively water-resistant cell substance. The presence of fatty acids, impairing the last
oxidative stage of respiration, increases the tendency of the mitochondrion to release its cytochrome c into the
cell in a reduced form, leading to the apoptotic death of the cell. The oxidized form of the cytochrome is more
hydrophobic, and stable. Burr didn't understand that it was his rats' high sugar diet, freed of the
anti-oxidative unsaturated fatty acids, that caused their extremely high metabolic rate, but since that time
many experiments have made it clear that it is specifically the fructose component of sucrose that is protective
against the antimetabolic fats. Although Brown, et al., weren't focusing on the biological effects of sugar,
their results are important in the history of sugar research because their work was done before the culture had
been influenced by the development of the lipid theory of heart disease, and the later idea that fructose is
responsible for increasing the blood lipids. In 1963 and 1964, experiments (Carroll, 1964) showed that the
effects of glucose and fructose were radically affected by the type of fat in the diet. Although 0.6% of
calories as polyunsaturated fat prevents the appearance of the Mead acid (which is considered to indicate a
deficiency of essential fats) the "high fructose" diets consistently add 10% or more corn oil or other highly
unsaturated fat to the diet. These large quantities of PUFA aren't necessary to prevent a deficiency, but they
are needed to obscure the beneficial effects of fructose. Many studies have found that sucrose is less fattening
than starch or glucose, that is, that more calories can be consumed without gaining weight. During exercise, the
addition of fructose to glucose increases the oxidation of carbohydrate by about 50% (Jentjens and Jeukendrup,
2005). In another experiment, rats were fed either sucrose or Coca-Cola and Purina chow, and were allowed to eat
as much as they wanted (Bukowiecki, et al, 1983). They consumed 50% more calories without gaining extra weight,
relative to the standard diet. Ruzzin, et al. (2005) observed rats given a 10.5% or 35% sucrose solution, or
water, and observed that the sucrose increased their energy consumption by about 15% without increasing weight
gain. Macor, et al. (1990) found that glucose caused a smaller increase in metabolic rate in obese people than
in normal weight people, but that fructose increased their metabolic rate as much as it did that of the normal
weight people. Tappy, et al. (1993) saw a similar increase in heat production in obese people, relative to the
effect of glucose. Brundin, et al. (1993) compared the effects of glucose and fructose in healthy people, and
saw a greater oxygen consumption with fructose, and also an increase in the temperature of the blood, and a
greater increase in carbon dioxide production. These metabolic effects have led several groups to recommend the
use of fructose for treating shock, the stress of surgery, or infection (e.g., Adolph, et al., 1995). The
commonly recommended alternative to sugar in the diet is starch, but many studies show that it produces all of
the effects that are commonly ascribed to sucrose and fructose, for example hyperglycemia (Villaume, et al.,
1984) and increased weight gain. The addition of fructose to glucose "can markedly reduce hyperglycemia during
intraportal glucose infusion by increasing net hepatic glucose uptake even when insulin secretion is
compromised" (Shiota, et al., 2005). "Fructose appears most effective in those normal individuals who have the
poorest glucose tolerance" (Moore, et al., 2000). Lipid peroxidation is involved in the degenerative diseases,
and many publications argue that fructose increases it, despite the fact that it can increase the production of
uric acid, which is a major component of our endogenous antioxidant system (e.g., Waring, et al., 2003). When
rats were fed for 8 weeks on a diet with 18% fructose and 11% saturated fatty acids, the content of
polyunsatured fats in the blood decreased, as they had in the Brown, et al., experiment, and their total
antioxidant status was increased (Girard, et al., 2005). When stroke-prone spontaneously hypertensive rats were
given 60% fructose, superoxide dismutase in their liver was increased, and the authors suggest that this "may
constitute an early protective mechanism" (Brosnan and Carkner, 2008). When people were given a 300 calorie
drink containing glucose, or fructose, or orange juice, those receiving the glucose had a large increase in
oxidative and inflammatory stress (reactive oxygen species, and NF-kappaB binding), and those changes were
absent in those receiving the fructose or orange juice (Ghanim, et al., 2007). One of the observations in Brown,
et al., was that the level of phosphate in the serum decreased during the experimental diet. Several later
studies show that fructose increases the excretion of phosphate in the urine, while decreasing the level in the
serum. However, a common opinion is that it's only the phosphorylation of fructose, increasing the amount in
cells, that causes the decrease in the serum; that could account for the momentary drop in serum phosphate
during a fructose load, but--since there is only so much phosphate that can be bound to intracellular
fructose--it can't account for the chronic depression of the serum phosphate on a continuing diet of fructose or
sucrose. There are many reasons to think that a slight reduction of serum phosphate would be beneficial. It has
been suggested that eating fruit is protective against prostate cancer, by lowering serum phosphate (Kapur,
2000). The aging suppressing gene discovered in 1997, named after the Greek life-promoting goddess Klotho,
suppresses the reabsorption of phosphate by the kidney (which is also a function of the parathyroid hormone),
and inhibits the formation of the activated form of vitamin D, opposing the effect of the parathyroid hormone.
In the absence of the gene, serum phosphate is high, and the animal ages and dies prematurely. In humans, in
recent years a very close association has been has been documented between increased phosphate levels, within
the normal range, and increased risk of cardiovascular disease. Serum phosphate is increased in people with
osteoporosis (Gallagher, et al., 1980), and various treatments that lower serum phosphate improve bone
mineralization, with the retention of calcium phosphate (Ma and Fu, 2010; Batista, et al., 2010; Kelly, et al.,
1967; Parfitt, 1965; Kim, et al., 2003). At high altitude, or when taking a carbonic anhydrase inhibitor, there
is more carbon dioxide in the blood, and the serum phosphate is lower; sucrose and fructose increase the
respiratory quotient and carbon dioxide production, and this is probably a factor in lowering the serum
phosphate. Fructose affects the body's ability to retain other nutrients, including magnesium, copper, calcium,
and other minerals. Comparing diets with 20% of the calories from fructose or from cornstarch, Holbrook, et al.
(1989) concluded "The results indicate that dietary fructose enhances mineral balance." Ordinarily, things (such
as thyroid and vitamin D) which improve the retention of magnesium and other nutrients are considered good, but
the fructose mythology allows researchers to conclude, after finding an increased magnesium balance, with either
4% or 20% of energy from fructose (compared to cornstarch, bread, and rice), "that dietary fructose adversely
affects macromineral homeostasis in humans." (Milne and Nielsen, 2000). Another study compared the effects of a
diet with plain water, or water containing 13% glucose, or sucrose, or fructose, or high fructose corn syrup on
the properties of rats' bones: Bone mineral density and mineral content, and bone strength, and mineral balance.
The largest differences were between animals drinking the glucose and the fructose solutions. The rats getting
the glucose had reduced phosphorus in their bones, and more calcium in their urine, than the rats that got
fructose. "The results suggested that glucose rather than fructose exerted more deleterious effects on mineral
balance and bone" (Tsanzi, et al., 2008). An older experiment compared two groups with an otherwise well
balanced diet, lacking vitamin D, containing either 68% starch or 68% sucrose. A third group got the starch
diet, but with added vitamin D. The rats on the vitamin D deficient starch diet had very low levels of calcium
in their blood, and the calcium content of their bones was low, exactly what is expected with the vitamin D
deficiency. However, the rats on the sucrose diet, also vitamin D deficient, had normal levels of calcium in
their blood. The sucrose, unlike the starch, maintained claim homeostasis. A radioactive calcium tracer showed
normal uptake by the bone, and also apparently normal bone development, although their bones were lighter than
those receiving vitamin D. People have told me that when they looked for articles on fructose in PubMed they
couldn't find anything except articles about its bad effects. There are two reasons for that. PubMed, like the
earlier Index Medicus, represents the material in the National Library of Medicine, and is a medical, rather
than a scientific, database, and there is a large amount of important research that it ignores. And because of
the authoritarian and conformist nature of the medical profession, when a researcher observes something that is
contrary to majority opinion, the title of the publication is unlikely to focus on that. In too many articles in
medical journals, the title and conclusions positively misrepresent the data reported in the article. When the
idea of "glycemic index" was being popularized by dietitians, it was already known that starch, consisting of
chains of glucose molecules, had a much higher index than fructose and sucrose. The more rapid appearance of
glucose in the blood stimulates more insulin, and insulin stimulates fat synthesis, when there is more glucose
than can be oxidized immediately. If starch or glucose is eaten at the same time as polyunsaturated fats, which
inhibit its oxidation, it will produce more fat. Many animal experiments show this, even when they are intending
to show the dangers of fructose and sucrose. For example (Thresher, et al., 2000), rats were fed diets with 68%
carbohydrate, 12% fat (corn oil), and 20% protein. In one group the carbohydrate was starch (cornstarch and
maltodextrin, with a glucose equivalence of 10%), and in other groups it was either 68% sucrose, or 34% fructose
and 34% glucose, or 34% fructose and 34% starch. (An interesting oddity, fasting triglycerides were highest in
the fructose+starch group.) The weight of their fat pads (epididymal, retroperitoneal, and mesenteric) was
greatest in the fructose+starch group, and least in the sucrose group. The starch group's fat was intermediate
in weight between those of the sucrose and the fructose+glucose groups. At the beginning of the experimental
diet, the average weight of the animals was 213.1 grams. After five weeks, the animals in the fructose+glucose
group gained 164 grams, those in the sucrose group gained 177 grams, and those in the starch group gained 199.2
grams. The animals ate as much of the diet as they wanted, and those in the sucrose group ate the least. The
purpose of their study was to see whether fructose causes "glucose intolerance" and "insulin resistance." Since
insulin stimulates appetite (Chance, et al, 1986; Dulloo and Girardier, 1989; Czech, 1988; DiBattista, 1983;
Sonoda, 1983; Godbole and York, 1978), and fat synthesis, the reduced food consumption and reduced weight gain
show that fructose was protecting against these potentially harmful effects of insulin. Much of the current
concern about the dangers of fructose is focussed on the cornstarch-derived high fructose corn syrup, HFCS. Many
studies assume that its composition is nearly all fructose and glucose. However, Wahjudi, et al. (2010) analyzed
samples of it before and after hydrolyzing it in acid, to break down other carbohydrates present in it. They
found that the carbohydrate content was several times higher than the listed values. "The underestimation of
carbohydrate content in beverages may be a contributing factor in the development of obesity in children," and
it's especially interesting that so much of it is present in the form of starch-like materials. Many people are
claiming that fructose consumption has increased greatly in the last 30 or 40 years, and that this is
responsible for the epidemic of obesity and diabetes. According to the USDA Economic Research Service, the 2007
calorie consumption as flour and cereal products increased 3% from 1970, while added sugar calories decreased
1%. Calories from meats, eggs, and nuts decreased 4%, from dairy foods decreased 3%, and calories from added
fats increased 7%. The percentage of calories from fruits and vegetables stayed the same. The average person
consumed 603 calories per day more in 2007 than in 1970. If changes in the national diet are responsible for the
increase of obesity, diabetes, and the diseases associated with them, then it would seem that the increased
consumption of fat and starch is responsible, and that would be consistent with the known effects of starches
and polyunsaturated fats. In monkeys living in the wild, when their diet is mainly fruit, their cortisol is low,
and it rises when they eat a diet with less sugar (Behie, et al., 2010). Sucrose consumption lowers ACTH, the
main pituitary stress hormone (Klement, et al., 2009; Ulrich-Lai, et al., 2007), and stress promotes increased
sugar and fat consumption (Pecoraro, et al., 2004). If animals' adrenal glands are removed, so that they lack
the adrenal steroids, they choose to consume more sucrose (Laugero, et al., 2001). Stress seems to be perceived
as a need for sugar. In the absence of sucrose, satisfying this need with starch and fat is more likely to lead
to obesity. The glucocorticoid hormones inhibit the metabolism of sugar. Sugar is essential for brain
development and maintenance. The effects of environmental stimulation and deprivation-stress can be detected in
the thickness of the brain cortex in as little as 4 days in growing rats (Diamond, et al., 1976). These effects
can persist through a lifetime, and are even passed on transgenerationally. Experimental evidence shows that
polyunsaturated (omega-3) fats retard fetal brain development, and that sugar promotes it. These facts argue
against some of the currently popular ideas of the evolution of the human brain based on ancestral diets of fish
or meat, which only matters as far as those anthropological theories are used to argue against fruits and other
sugars in the present diet. Honey has been used therapeutically for thousands of years, and recently there has
been some research documenting a variety of uses, including treatment of ulcers and colitis, and other
inflammatory conditions. Obesity increases mediators of inflammation, including the C-reactive protein (CRP) and
homocysteine. Honey, which contains free fructose and free glucose, lowers CRP and homocysteine, as well as
triglycerides, glucose, and cholesterol, while it increased insulin more than sucrose did (Al-Waili, 2004).
Hypoglycemia intensifies inflammatory reactions, and insulin can reduce inflammation if sugar is available.
Obesity, like diabetes, seems to involve a cellular energy deficiency, resulting from the inability to
metabolize sugar. Sucrose (and sometimes honey) is increasingly being used to reduce pain in newborns, for minor
things such as injections (Guala, et al., 2001; Okan, et al., 2007; Anand, et al., 2005; Schoen and Fischell,
1991). It's also effective in adults. It acts by influencing a variety of nerve systems, and also reduces
stress. Insulin is probably involved in sugar analgesia, as it is in inflammation, since it promotes entry of
endorphins into the brain (Witt, et al., 2000). An extracellular phosphorylated fructose metabolite,
diphosphoglycerate, has an essential regulatory effect in the blood; another fructose metabolite, fructose
diphosphate, can reduce mast cell histamine release and protect against oxidative and hypoxic injury and
endotoxic shock, and it reduces the expression of the inflammation mediators TNF-alpha, IL-6, nitric oxide
synthase, and the activation of NF-kappaB, among other protective effects, and its therapeutic value is known,
but its relation to dietary sugars hasn't been investigated. A daily diet that includes two quarts of milk and a
quart of orange juice provides enough fructose and other sugars for general resistance to stress, but larger
amounts of fruit juice, honey, or other sugars can protect against increased stress, and can reverse some of the
established degenerative conditions. Refined granulated sugar is extremely pure, but it lacks all of the
essential nutrients, so it should be considered as a temporary therapeutic material, or as an occasional
substitute when good fruit isn't available, or when available honey is allergenic. <h3>
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