From thyriodinfo.com.....Mary Shomon: Why do women with treated hypothyroidism
frequently still have inappropriately high levels of cholesterol and
high triglycerides, and what can they do to help lower these levels?
Dr. Ray Peat: Often it's because they were given thyroxine, instead of
the active thyroid hormone, but hypertriglyceridemia can be caused by a
variety of things that interact with hypothyroidism. Estrogen treatment
is a common cause of high triglycerides, and deficiencies of magnesium,
copper, and protein can contribute to that abnormality. Toxins,
including some drugs and herbs, can irritate or stimulate the liver to produce too
much triglyceride. T3, triiodothyronine, is the active thyroid hormone, and
it is produced (mainly in the liver) from thyroxine, and the female liver
is less efficient than the male liver in producing it, as is the female
thyroid gland. The thyroid gland, which normally produces some T3, will
decrease its production in the presence of increased thyroxine.
Therefore,
thyroxine often acts as a "thyroid anti-hormone," especially in women.
When
thyroxine was tested in healthy young male medical students, it seemed
to
function "just like the thyroid hormone," but in people who are
seriously
hypothyroid, it can suppress their oxidative metabolism even more. It's
a
very common, but very serious, mistake to call thyroxine "the thyroid
hormone."
High cholesterol is more closely connected to hypothyroidism than
hypertriglyceridemia is. Increased T3 will immediately increase the
conversion of cholesterol to progesterone and bile acids. When people
have
abnormally low cholesterol, I think it's important to increase their
cholesterol before taking thyroid, since their steroid-forming tissues
won't be able to respond properly to thyroid without adequate
cholesterol.
Mary Shomon: You feel that progesterone can have anti-stress
effects, without harming the adrenal glands. Is progesterone
therapy something you feel is useful to many or most hypothyroid
patients? How can a patient know if she needs progesterone? Do
you recommend blood tests? And if so, at what point in a woman's
cycle?
Dr. Ray Peat: Estrogen blocks the release of hormone from the thyroid
gland, and progesterone facilitates the release. Estrogen excess or
progesterone deficiency tends to cause enlargement of the thyroid gland,
in
association with a hypothyroid state. Estrogen can activate the adrenals
to
produce cortisol, leading to various harmful effects, including brain
aging
and bone loss. Progesterone stimulates the adrenals and the ovaries to
produce more progesterone, but since progesterone protects against the
catabolic effects of cortisol, its effects are the opposite of
estrogen's.
Progesterone has antiinflammatory and protective effects, similar to
cortisol, but it doesn't have the harmful effects. In hypothyroidism,
there
is a tendency to have too much estrogen and cortisol, and too little
progesterone.
The blood tests can be useful to demonstrate to physicians what the
problem
is, but I don't think they are necessary. There is evidence that having
50
or 100 times as much progesterone as estrogen is desirable, but I don't
advocate "progesterone replacement therapy" in the way it's often
understood. Progesterone can instantly activate the thyroid and the
ovaries, so it shouldn't be necessary to keep using it month after
month. If progesterone is used consistently, it can postpone menopause
for many years.
Cholesterol is converted to pregnenolone and progesterone by the
ovaries,
the adrenals, and the brain, if there is enough thyroid hormone and
vitamin
A, and if there are no interfering factors, such as too much carotene or
unsaturated fatty acids.
Progesterone deficiency is an indicator that something is wrong, and
using
a supplement of progesterone without investigating the nature of the
problem isn't a good approach. The normal time to use a progesterone
supplement is during the "latter half" of the cycle, the two weeks from
ovulation until menstruation. If it is being used to treat epilepsy,
cancer, emphysema, migraine or arthritis, or something else so serious
that
menstrual regularity isn't a concern, then it can be used at any time.
If
progesterone is used consistently, it can postpone menopause for many
years.
Mary Shomon: What supplements do you feel are essential for
most people with hypothyroidism?
Dr. Ray Peat: Because the quality of commercial nutritional supplements is
dangerously low, the only supplement I generally advocate is vitamin E,
and
that should be used sparingly. Occasionally, I will suggest limited use
of
other supplements, but it is far safer in general to use real foods, and
to
exclude foods which are poor in nutrients. Magnesium is typically
deficient
in hypothyroidism, and the safest way to get it is by using orange juice
and meats, and by using epsom salts baths; magnesium carbonate can be
helpful, if the person doesn't experience side effects such as headaches
or
hemorrhoids.
Mary Shomon: Do you feel that there are any special
considerations, issues, or treatments for men with hypothyroidism?
Dr. Ray Peat: Thyroid supplements can be useful for prostate hypertrophy
and some cases of impotence and infertility. Occasionally, a man who
can't
put on a normal amount of weight finds that a thyroid supplement allows
normal weight gain. Leg cramps, insomnia and depression are often the
result of hypothyroidism. Heart failure, gynecomastia, liver disease,
baldness and dozens of other problems can result from hypothyroidism.
Mary Shomon: Many people describe how they are clinically
hypothyroid, with elevated TSH levels, but have extremely high
pulse rates. Do you have any thoughts as to what might be going
on in that situation?
Dr. Ray Peat: In hypothyroidism, thyrotropin-release hormone (TRH) is
usually increased, increasing release of TSH. TRH itself can cause
tachycardia, "palpitations," high blood pressure, stasis of the
intestine,
increase of pressure in the eye, and hyperventilation with alkalosis. It
can increase the release of norepinephrine, but in itself it acts very
much
like adrenalin. TRH stimulates prolactin release, and this can interfere
with progesterone synthesis, which in itself affects heart function.
I consider even the lowest TSH within the "normal range" to be
consistent
with hypothyroidism; in good health, very little TSH is needed. When the
thyroid function is low, the body often compensates by over-producing
adrenalin. The daily production of adrenalin is sometimes 30 or 40 times
higher than normal in hypothyroidism. The adrenalin tends to sustain
blood
sugar in spite of the metabolic inefficiency of hypothyroidism, and it
can
help to maintain core body temperature by causing vasoconstriction in
the
skin, but it also disturbs the sleep and accelerates the heart. During
the
night, cycles of rising adrenalin can cause nightmares, wakefulness,
worry,
and a pounding heart. Occasionally, a person who has chronically had a
heart rate of 150 beats per minute or higher, will have a much lower
heart
rate after using a thyroid supplement for a few days. If your
temperature
or heart rate is lower after breakfast than before, it's likely that
they
were raised as a result of the nocturnal increase of adrenalin and
cortisol
caused by hypothyroidism.
Mary Shomon: You have written that for some people, there is a
problem converting T4 to T3, but that diet can help. You
recommend a piece of fruit or juice or milk between meals, plus
adequate protein, can help the liver produce the hormone. Can you
explain a bit more about this idea and how it works?
Dr. Ray Peat: The amount of glucose in liver cells regulates the enzyme
that converts T4 to T3. This means that hypoglycemia or diabetes (in
which
glucose doesn't enter cells efficiently) will cause hypothyroidism, when
T4
can't be converted into T3. When a person is fasting, at first the
liver's
glycogen stores will provide glucose to maintain T3 production. When the
glycogen is depleted, the body resorts to the dissolution of tissue to
provide energy. The mobilized fatty acids interfere with the use of
glucose, and certain amino acids suppress the thyroid gland. Eating
carbohydrate (especially fruits) can allow the liver to resume its production of T3.
Mary Shomon: You have recommended if supplemental T3 is used,
a thyroid patients "nibble on a 10-15 mg Cytomel tablet throughout
the day." Can you explain why? Would compounded time-released
T3 as available in some compounding pharmacies do the same?
Dr. Ray Peat: Most hypothyroid people can successfully use a supplement
that contains four parts of thyroxine for each part of T3, but some
people
need a larger proportion of T3 for best functioning. The body normally
produces several micrograms of T3 every hour, but if a large amount of
supplementary thyroid is taken in a short time, the liver quickly
inactivates some of the excess T3. Taking a few micrograms per hour
provides what the body can use, and doesn't suppress either the liver's
or
the thyroid's production of the hormone.
I have only rarely talked to
anyone who had good results with the so-called time-release T3, and I
have
seen analyses of some samples in which there was little or no T3
present.
It is hard to compound T3 properly, and the conditions of each person's
digestive system can determine whether the T3 is released all at once,
or
not at all. I don't think there is a valid scientific basis for calling
anything "time-release T3."
I have been told that the company which now owns the Armour name and
manufactures "Armour thyroid USP" has added a polymer to the formula, and
I
think this would account for the stories I have heard about its apparent
inactivity. Some people have found that the tablets passed through their
intestine undigested, so I think it's advisable to crush or powder the
tablets.
Mary Shomon: You feel that excessive aerobic exercise can be a
cause of hypothyroidism. Can you explain this further? How much
is too much?
Dr. Ray Peat: I'm not sure who introduced the term "aerobic" to describe
the state of anaerobic metabolism that develops during stressful
exercise,
but it has had many harmful repercussions. In experiments, T3 production
is
stopped very quickly by even "sub-aerobic" exercise, probably becaue of
the
combination of a decrease of blood glucose and an increase in free fatty
acids. In a healthy person, rest will tend to restore the normal level
of
T3, but there is evidence that even very good athletes remain in a
hypothyroid state even at rest. A chronic increase of lactic acid and
cortisol indicates that something is wrong. The "slender muscles" of
endurance runners are signs of a catabolic state, that has been
demonstrated even in the heart muscle. A slow heart beat very strongly
suggests hypothyroidism. Hypothyroid people, who are likely to produce
lactic acid even at rest, are especially susceptible to the harmful
effects
of "aerobic" exercise. The good effect some people feel from exercise is
probably the result of raising the body temperature; a warm bath will do
the same for people with low body temperature.
Mary Shomon: You feel that chronic protein deficiency is a
common cause of hypothyroidism. How much protein should
people get (as much as 70-100 grams a day?) and what types of
protein, in order to prevent hypothyroidism?
Dr. Ray Peat: The World Health Organization standard was revised upward by
researchers at MIT, and recently the MIT standard has been revised
upward
again by military researchers; this is described in a publication of the
National Academy of Sciences (National Academy Press, The Role of
Protein and Amino Acids in Sustaining and Enhancing Performance,
1999). When too
little protein, or the wrong kind of protein, is eaten, there is a
stress
reaction, with thyroid suppression. Many of the people who don't respond
to
a thyroid supplement are simply not eating enough good protein. I have
talked to many supposedly well educated people who are getting only 15
or
20 grams of protein per day. To survive on that amount, their metabolic
rate becomes extremely low. The quality of most vegetable protein
(especially beans and nuts) is so low that it hardly functions as
protein.
Muscle meats (including the muscles of poultry and fish) contain large
amounts of the amino acids that suppress the thyroid, and shouldn't be
the
only source of protein. It's a good idea to have a quart of milk (about
32 grams of protein) every day, besides a variety of other high quality
proteins, including cheeses, eggs, shellfish, and potatoes. The protein
of potatoes is extremely high quality, and the quantity, in terms of a
percentage, is similar to that of milk.
Mary Shomon: You talk about darkness and shorter days of winter
as a stress. It's known that more thyroid hormone is needed by
some patients during colder weather. Are there other things you
recommend patients do to "winterproof" their metabolism?
Dr. Ray Peat: Very bright incandescent lights are helpful, because light
acts on, and restores, the same mitochondrial enzymes that are governed
by
the thyroid hormone. In squirrels, hibernation is brought on by the
accumulation of unsaturated fats in the tissues, suppressing respiration
and stimulating increased serotonin production. In humans, winter
sickness
is intensified by those same antithyroid substances, so it's important
to
limit consumption of unsaturated fats and tryptophan (which is the
source
of serotonin). When a person is using a thyroid supplement, it's common
to
need four times as much in December as in July.
Mary Shomon: You have reported that pregnenolone can be helpful
for Graves' patients with exophthalmus. Can you explain further?
Dr. Ray Peat: Graves' disease and exophthalmos can occur with
hypothyroidism or euthyroidism, as well as with hyperthyroidism.
Pregnenolone regulates brain chemistry in a way that prevents excessive
production of ACTH and cortisol, and it helps to stabilize mitochondrial
metabolism. It apparently acts directly on a variety of tissues to
reduce
their retention of water. In the last several years, all of the people I
have seen who had been diagnosed as "hyperthyroid" have actually been
hypothyroid, and benefitted from increasing their thyroid function; some
of
these people had also been told that they had Graves' disease.
Mary Shomon: You are a proponent of coconut oil for thyroid
patients. Can you explain why?
Dr. Ray Peat: An important function of coconut oil is that it supports
mitochondrial respiration, increasing energy production that has been
blocked by the unsaturated fatty acids. Since the polyunsaturated fatty
acids inhibit thyroid function at many levels, coconut oil can promote
thyroid function simply by reducing those toxic effects. It allows
normal
mitochondrial oxidative metabolism, without producing the toxic lipid
peroxidation that is promoted by unsaturated fats.
Mary Shomon: Do you have any thoughts for thyroid patients who
are trying to do everything right, and yet still can't lose any weight?
Dr. Ray Peat: Coconut oil added to the diet can increase the metabolic
rate. Small frequent feedings, each combining some carbohydrate and some
protein, such as fruit and cheese, often help to keep the metabolic rate
higher. Eating raw carrots can prevent the absorption of estrogen from
the
intestine, allowing the liver to more effectively regulate metabolism. If
a
person doesn't lose excess weight on a moderately low calorie diet with
adequate protein, it's clear that the metabolic rate is low. The number
of
calories burned is a good indicator of the metabolic rate. The amount of
water lost by evaporation is another rough indicator: For each liter of
water evaporated, about 1000 calories are burned.
Mary Shomon:You have talked about internal malnutrition as a
problem for many thyroid patients, due to insufficient digestive
juices and poor intestinal movements. Are there ways patients who
are treated for hypothyroidism can help alleviate this problem.
Dr. Ray Peat: The absorption and retention of magnesium, sodium, and
copper, and the synthesis of proteins, are usually poor in
hypothyroidism.
Salt craving is common in hypothyroidism, and eating additional sodium
tends to raise the body temperature, and by decreasing the production of
aldosterone, it helps to minimize the loss of magnesium, which in turn
allows cells to respond better to the thyroid hormone. This is probably
why
a low sodium diet increases adrenalin production, and why eating enough
sodium lowers adrenalin and improves sleep. The lowered adrenalin is
also
likely to improve intestinal motility.
Mary Shomon: You've mentioned eggs, milk and gelatin as good
for the thyroid. Can you explain a bit more about this?
Dr. Ray Peat: Milk contains a small amount of thyroid and progesterone,
but it also contains a good balance of amino acids. For adults, the
amino
acid balance of cheese might be even better, since the whey portion of
milk
contains more tryptophan than the curd, and tryptophan excess is
significantly antagonistic to thyroid function. The muscle meats contain
so
much tryptophan and cysteine (which is both antithyroid and potentially
excitotoxic) that a pure meat diet can cause hypothyroidism. In poor
countries, people have generally eaten all parts of the animal, rather
than
just the muscles--feet, heads, skin, etc. About half of the protein in
an
animal is collagen (gelatin), and collagen is deficient in tryptophan
and
cysteine. This means that, in the whole animal, the amino acid balance
is
similar to the adult's requirements. Research in the amino acid
requirements of adults has been very inadequate, since it has been
largely
directed toward finding methods to produce farm animals with a minimum
of
expense for feed. The meat industry isn't interested in finding a diet
for
keeping chickens, pigs, and cattle healthy into old age. As a result,
adult
rats have provided most of our direct information about the protein
requirements of adults, and since rats keep growing for most of their
life,
their amino acid requirements are unlikely to be the same as ours.
Mary Shomon: Do you think the majority of people with
hypothyroidism get too much or too little iodine? Should people
with hypothyroidism add more iodine, like kelp, seaweeds, etc.?
Dr. Ray Peat: 30 years ago, it was found that people in the US were
getting about ten times more iodine than they needed. In the mountains
of Mexico and in the Andes, and in a few other remote places, iodine
deficiency still exists. Kelp and other sources of excess iodine can
suppress the thyroid, so they definitely shouldn't be used to treat
hypothyroidism.
Mary Shomon: What are your thoughts for Graves'
disease/hyperthyroidism patients? Should they move ahead quickly to get
radioactive iodine treatment, or are there natural things they might be
able to try to temporarily - or even
permanently - get a remission?
Dr. Ray Peat: Occasionally, a person with a goiter will temporarily become
hyperthyroid as the gland releases its colloid stores in a corrective
process. Some people enjoy the period of moderate hyperthyroidism, but
if
they find it uncomfortable or inconvenient, they can usually control it
just by eating plenty of liver, and maybe some cole slaw or raw cabbage
juice. Propranolol will slow a rapid heart. The effects of a thyroid
inhibitor, PTU, propylthiouracil, have been compared to those of
thyroidectomy and radioactive iodine. The results of the chemical
treatment are better for the patient, but not nearly so profitable for
the
physician.
Besides a few people who were experiencing the unloading of a goiter,
and
one man from the mountains of Mexico who became hypermetabolic when he
moved to Japan (probably from the sudden increase of iodine in his diet,
and maybe from a smaller amount of meat in his diet), all of the people
I
have seen in recent decades who were called "hyperthyroid" were not.
None
of the people I have talked to after they had radioiodine treatment were
properly studied to determine the nature of their condition. Radioiodine
is
a foolish medical toy, as far as I can see, and is never a proper
treatment.
Friday, November 29, 2013
Corn Muffins made with Masa Harina
From arkofwellness.com...Corn Muffins made with Masa Harina:
Corn is not something that I normally recommend. Corn is a starch, it does not digested easily, and it is has PUFA.Ray Peat mentions that “Starch grains, or other hard particles, can be found in the blood, urine, and other fluids after they have been ingested” (not a good thing!).
However, there is version of corn that I do recommend: masa harina.
Indigenous to the Americas, masa harina is a traditional food that has been eaten for a very long time (possibly even since 10,000 BC). Masa harina is a type of yellow, corn-meal flour. To make this flour, the corn is first removed from the cob and dried. The corn is then soaked in a lime or wood ash-lye water. The solution softens the corn and loosens the hulls from the kernels. This lengthy process is called nixtamalized. The word “nixtamalized” comes from Nauhatl, the language spoken by the Aztecs in central Mexico at the time of the Spanish conquest. After soaking for a while the Nixtamal is ground and made into masa.
The nixamalized process improves the nutritional profile of the corn. It balances the amino acids – so there is actually more available (and usable protein). 28 grams of masa harina actually has 3 grams of protein. The lime also reacts with the corn so that the nutrient niacin can be assimilated by the digestive tract. The nixtamalized process changes the corn’s physical and chemical properties – it even adds calcium to the flour from the lime solution used. Soaking the corn in lime water also saponifies the fat (removes the PUFA!).
Ray Peat lived (and taught) in Mexico for quite some time which is why (I believe) he has a giant sumbrero on his website. While Dr. Peat was in Mexico he ate foods prepared with traditional masa harina. He did some experiments with the traditional masa and reported that his students showed that the starch particles from nixtamalized corn, unlike those from untreated corn, do not pass whole into the blood stream. He proved that the nixtamalized corn was very different from untreated corn. He writes: “In 1979 some of my students in Mexico wanted a project to do in the lab. Since several traditional foods are made with corn that has been boiled in alkali, I thought it would be valuable to see whether this treatment reduced the ability of the starch grains to be persorbed. For breakfast one day, they ate only atole, tamales, and tortillas, all made from the alkali treated corn. None of the students could find any starch grains after centrifuging their blood and urine. That led me to substitute those foods whenever possible for other starches.” Masa Harina is a healthy food!
Here is a great recipe that my friend Clint Mongan gave me, with a couple of slight changes. This is an easy recipe even for those of us that aren’t great bakers- like me. I like it served with a nice poached egg and honey butter!
ingredients:
makes 12 muffins
1 cup masa harina
1/4 cup powdered milk
3/4 cup Non-GMO fructose ( preferably powdered)
1/8 teaspoon baking soda
1 Tablespoon baking powder
1/2 teaspoon salt
a pinch of nutmeg
Two (organic and pastured) eggs plus one egg yolk
1 1/2 cups milk
1/2 cup of honey
1/3 cup of melted coconut oil
1 Tablespoon of melted butter
directions:
Mix dry ingredients and wet ingredients separately, then combine. Pour batter into unbleached muffin liners (or muffin molds that are well coated with coconut oil) and bake at 375 degrees for approximately 15-20 minutes or until golden brown. Serve with lots of honey butter.
- Estrogen blocks the release of hormone from the thyroid gland, and progesterone facilitates the release. Estrogen excess or progesterone deficiency tends to cause enlargement of the thyroid gland, in association with a hypothyroid state.
- Instead of taking dietary supplements, it is far safer in general to use real foods, and to exclude foods which are poor in nutrients. For example, magnesium is typically deficient in hypothyroidism, and the safest way to get it is by using orange juice and meats, and by using epsom salts baths.
- Men should be aware that leg cramps, insomnia and depression are often the result of hypothyroidism. Heart failure, gynecomastia, liver disease, baldness and dozens of other problems can result from hypothyroidism.
- He considers even the lowest TSH within the "normal range" to be consistent with hypothyroidism; in good health, very little TSH is needed.
- When too little protein, or the wrong kind of protein, is eaten, there is a stress reaction, with thyroid suppression. Many of the people who don't respond to a thyroid supplement are simply not eating enough good protein.
- When a person is using a thyroid supplement, it's common to need four times as much in December as in July. Another thing from Ray Peat.
Tuesday, November 26, 2013
My Problems
I am a milk/wheat free boy and when my mom found ray peat he told me to take d&a(medicine) and i was healthy, and then i got very sick and i am doing bad.Please give me ideas
I copyed this from Raypeat.com..... 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.
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