Laboratory rats that eat raw foods will live about three years. Rats that eat enzyme·Iess chow diets will live only two years, a 30% reduction in lifespan.
The Max Planck Institute for Nutritional Research in Germany has found that there is only 50%
bioavailability in animal protein that has been cooked.

Cooking also coagulates the bioactive mineral/protein complexes and therefore disrupts mineral absorption. Cooking foods disrupts RNA and DNA structure, and destroys most of the nutritive value of fats, while creating carcinogenic and mutagenic structures in the fats, which produce free radicals.

Foods may be up to 200 times more immuno-reactive after cooking.

From 1932 to 1942, Dr. Francis Marion Pottenger, Jr. conducted an experiment to determine the effects of heat—processed food on cats. The experiment included 900 cats over four generations. “Cats fed on cooked meat and milk develop “all kinds” of allergies, and hypothyroidism. When fed raw
foods, the cats’ symptoms go away”. “We have shown that allergic manifestations and dental
disturbances comparable to those seen in human beings result from changes in food preparation. . .
We find animals that receive raw meat show consistent facial development and normal dentition. . .
We also find the converse to be true. Those kittens that receive cooked meat instead of raw develop
all types of malformations of the face, jaws and teeth. . . (When) cats put on the cooked meat diet and
are allowed to become pregnant, their kittens’ skulls show marked variations from the normal . . . Once
such deficiencies are produced and maintained by a faulty diet, they become progressively worse
through the second and third generations. . .The cats fed cooked food may produce a premature or full
term litter of stillborn kittens. One cat proves unable to deliver her kittens even after 72 hours of labor.
lf a mother cat is kept on cooked food for more than two years, she usually dies during delivery.
Delivery complications such as these have not been found in cats placed on raw food.
“Deficient cats exhibit progressive allergic symptoms from generation to generation. They show most
of the common respiratory, gastrointestinal and constitutional problems as well as various skin
disorders. . . Hypothyroidism is prevalent and contributes to marked disturbances in the osseous
development of some deficient cats and to apparent disturbances in their reproductive efficiency.
“The elements in raw food which activate and support growth and development in the young appear
easily altered and destroyed by heat processing and oxidation. . . All tissue enzymes are heat labile
and so destroyed. Vitamin C and some members of the B complex are injured by the process of
cooking and minerals are made less soluble by altering their physiochemical state.”
All four generations of the raw meat and raw milk groups remained healthy throughout their normal
lifespan. The first generation of all three cooked food groups developed diseases and illnesses near the
end of their lives. The second generation of all three cooked food groups developed diseases and
illnesses in the middle of their lives. The third generation of all three cooked food groups developed
diseases and illnesses in the beginning of their lives and many died before six months of age. There
was no fourth generation in any of the three cooked food groups. Either the third generation parents
were sterile or the fourth generation cats died before birth! All four generations of the raw food groups
were healthy throughout their normal lifespan.
These problems have been attributed to lack of taurine. However, Malocclusion was prominent among
the defects and disorders Pottenger saw in cooked—food fed cats. The problem has not gone away,
with the simple addition of taurine to cooked dog and cat food …. A MEDLINE search for “malocclusion
cats” brings up a dozen and a half papers on the subject . . .and 133 papers on the condition in dogs.
Dr. Pottenger even tested the value of cat excreta as fertilizer. He found that plants would not grow in
the presence of waste from cooked—food cats and cooked milk cats.
***Dest1·uctio11 of Vitamins***
Vitamin C is highly sensitive to air, water, and temperature. About 25% of the vitamin C in vegetables
can be lost simply by blanching. Cooking of vegetables and fruits for longer periods of time (10-20
minutes) can result in a loss of over one half the total vitamin C content. When fruits and vegetables are
canned and then reheated, only 1/3 of the original vitamin C content may be left.
Vitamin B1 is highly unstable, and easily damaged by heat, degree of acidity (called pH), and by other
chemical substances. Sulfites and nitrites can inactivate vitamin B1. Heating of processed grain
components can result in the loss of more than half of the grains Bl content.
Vitamin B5 – Pantothenic acid is relatively unstable in food, and significant amounts of this vitamin
can be lost through cooking, freezing, and commercial processing.
Vitamin B6 -When food is heated, the acidity of the food often determines how much B6 is lost or
retained. In general, the more acidic the food, the poorer the B6 retention. Also, in the context of the
home kitchen, the freezing of foods high in B6 can result in the loss of approximately l/3 to 1/2 of the
total B6 content.
Folate contained in animal products (like liver) appears to be relatively stable to cooking, unlike folate
in plant products which can lose up to 40% of their folate content Hom cooking.
Vitamin E also gets damaged by high heat cooking. F or example, heating olive oil at 340″F will lead
to a slow destruction of the vitamin E, with almost half lost at three hours, and almost all of it gone by
six hours.

Loss of the Wulzen Factor
The Wulzen factor is a hormone-like substance that ensures that calcium in the body is put into the
bones rather than the joints and other tissues. Called the “anti—stiffness” factor, this compound is
present in raw sugar cane juice, raw leafy greens, various raw nuts etc. and raw animal fat (from the
raw grass they eat). Researcher Rosalind Wulzen discovered that this substance protects humans and
animals from calcification of the joints, and degenerative arthritis. It also protects against hardening of
the arteries, cataracts and calcification ofthe pineal gland. Calves fed pasteurized milk or skim milk
develop joint stiffness and do not thrive. Their symptoms are reversed when raw butterfat is added to
the diet. Pasteurization destroys the Wulzen factor.
Loss of Taurine
Taurine is very sensitive to heat, and 50-75% of its natural value is destroyed by cooking. Cats camrot
_ make taurine, so it is essential for them. Taurine is distributed throughout the body with high
concentration in certain tissues including heart wall muscles, in the retina of the eye, and brain. The
exact function of taurine in these tissues remains elusive, but it is well known that taurine deficiency in
cats can lead to blindness and heart failure due to enlargement of the heart (dilated cardiomyopathy).
With taurine replacement this condition is usually fully, or at least partially reversible.
Taurine, a conditionally essential amino acid
Taurine is a unique animal amino acid found in virtually all animal protein, eggs, milk (esp. goat milk)
and meat, fish, and insects. It is generally absent or present in traces in plant foods, (except algae).
Cooking destroys up to 2/3 of the taurine in food. This makes raw goat milk a superior source. (Goat
milk contains 20 times more taurine than cow milk.)
Evidence shows that the longest—living populations all have one thing in common: high dietary intake
of taurine. Researchers have dubbed taurine, “T he nutritional factor for the longevity ofthe
Japanese. ”
Taurine promotes cardiovascular health, insulin sensitivity, electrolyte balance, hearing ftmction, and
immune modulation. In animal research, taurine protected against heart failure, reducing mortality by
nearbz 80%.
Taurine is important for vision, the brain and nervous system, the heart, and is a conjugator of bile
acids, which helps increase cholesterol elimination in the bile, helps with fat absorption and elimination
of toxins, and helps prevent gall stones. It is also a detoxifier. lt seems that taurine and zinc, both found
in animal foods, provide protection from excess vitamin A ——a vitamin found full in form only in animal
foods. We see a synergism here. Zinc deficiency leads to increased excretion of taurine.
Taurine can be made in the body from cysteine and methionine. It is considered to be a non—essential
amino acid however in certain circumstances, it is actually considered essential. In htunan beings,
the ability to synthesize taurine is apparently limited. Animals that are more herbivorous (e. g., the rat)
synthesize taurine with three times greater efficiency than human beings do.
Disease states——including liver, kidney, or heart failure, diabetes, and cancer—can all cause a
deficiency in taurine. And aging bodies often cannot internally produce an optimal amount of taurine.
Laidlaw et al. studied the taurine levels of a group of vegans compared to a control group.
The results indicated that the plasma taurine concentrations in the vegans were significantly reduced to
78% of control values. Urinary taurine was reduced in the vegans to only 29% of control values…
These fmdings suggest there may be a nutritional need for taurine and that plasma levels and urinary ‘
excretion fall with chronically low taurine intakes. Possibly the diet of the vegans was low in metabolic
substrates or in cofactors for taurine synthesis…
The current study suggests that the rate of taurine synthesis is inadequate to maintain normal plasma
taurine concentrations in the presence of chronically low taurine intakes.
Low taurine levels have been found in patients with anxiety, depression, hypertension, hypothyroidism,
gout, infertility, obesity, kidney failure and autism, among other conditions.
Taurine is the most abundant amino acid in the body. Taurine deficiency may become symptomatic in
virtually any organ system, since taurine’s mzgor metabolic role is regulation of the electrical charge on
cell membranes, a role synergistic with magnesium. Heart muscle and the retina contain the highest
concentration of taurine.
Taurine plays an important role in the function of the adrenal, pituitary and thyroid glands. Taurine
drastically counteracts or down-regulates the body‘s stress reaction, helping stabilize carbohydrate
metabolism, insulin levels and epinephrine levels and muscle tension.
Taurine is antimociceptive — it assists in reducing pain, as well as assisting in regulation of serotonin,
prolactin, growth hormone, immune function and cholesterol metabolism. It inhibits both serotonin
and histamine.
Taurine decreased the inflammatory response in rat gastrointestinal cells. ln a model of gastric mucosal damage,
taurine decreased histamine release in acid—perfused stomachs of rats. Taurine also significantly reduced the
release of histamine from intestinal epithelial cells in response to laural sulfate. ln both systems, taurine acted as
a cytoprotectant. Part of the cytoprotective effect of taurine may result from its ability to decrease the release of
Taurine has a powerful effect on the heart and blood vessels and studies show that people with high
levels have lower rates of coronary heart disease. Taurine is the most abundant amino acid found in the
heart cells. It increases the regularity and strength of the heartbeat, regulates blood pressure, and lowers
cholesterol levels. Also, it reduces arterial thickening and stiffness, which is a factor in atherosclerosis.
Taurine supplementation has been used in the treatment of a wide variety of conditions, including:
cardiovascular diseases, epilepsy and other seizure disorders, macular degeneration, Alzheimer’s
disease, hepatic disorders, and cystic fibrosis. Taurine has also been used for migraines, insomnia,
agitation, restlessness, irritability, obsessions and depression.Epidemiological evidence suggests that
groups of people with longest life spans consume higher amounts of taurine.
A study released in November 2012 made the bold statement that taurine is one of the most essential
substances in the body. The authors wrote: “Considering its broad distribution, its many eytoprotective
attributes, and its functional signyieanee in cell development, nutrition, and survival taurine is
undoubtedly one ofthe most essential substances in the body ”
Taurine has a calming or stabilizing effect on the brain. lt is the second most abundant amino acid
in the CNS (central nervous system), but is also found ubiquitously in all mammalian tissues. Because
of its widespread presence and high physiological concentration, taurine exerts a variety of effects
throughout the body. For example, the effectiveness of taurine on diabetes mellitus alone include
reducing insulin resistance and complications such as retinopathy, nephropathy, neuropathy,

atherosclerosis and cardiomyopathy, and other anti-diabetic effects independent of hypoglycemia, as
reported in various animal models. Moreover, taurine is a potent inhibitor of protein glycation and
formation of AGEs that are responsible for many of the complications of diabetes as well as
contributing importantly to other age-associated diseases.
Taurine has important effects on brain function. One would expect that due to taurine’s potent
protective effects against excitotoxicity, for example, a variety of sleep dysfunctions stemming from
excitotoxicity would be beneficially affected by taurine. There was a substantial amount of data on the
neuroprotective effects of taurine in cell-damaging conditions (such as ischemia and hypoxia as well as
excitotoxicity) in the developing and aging hippocampus. Under ischemic conditions, there is a
massive release of taurine in the brain, which might be to deliver taurine to brain tissues as a defense
against excitotoxicity. There are also data on the protective effects of taurine on cognitive function.
Taurine May Be N europrotective Against Sleep Apnea — The brain release of taurine under ischemic
conditions could be of considerable importance in individuals with sleep apnea, which transiently
i reduces tissue oxygen availability; excito-toxicity is induced during sleep apnea by glutamate in
hippocampal neurons.
Taurine is a neur0—modulator, anti—oxidant, calcium ion regulator, and osmoregulator. The taurine
content of the striatum is decreased in old rats with learning deficits, but the decline was less severe in
old rats that were not impaired in a spatial memory task. Excretion of taurine via the urine appears to be
decreased with aging, reflecting, as the authors of some papers have put it, a condition of taurine
deficiency with advanced aging.
Taurine and Sleep Regulation- Taurine has been reported to interact with neurotransmitter receptors
involved in sleep regulation, including GABA—A, GABA-B, and glycine. In many instances taurine
p exerted its cytoprotective effects against excitotoxic and/or energy depriving insults in vitro by a
mechanism involving interaction with GABA-A receptors. This is consistent with the fact that
j activation of GABA—A receptors counteracts the activation of NMDA receptors and generation of nitric
oxide.” As of the time of the publication of this paper, however, the interaction of endogenous taurine
[ with GABA-A receptors in vivo remained tmcertain. The authors thus note, “by far the strongest
5 evidence speaks in favor of glycine receptors being the major and most specific target of endogenous
taurine.” However, they also noted that, “exogenous taurine has in many instances turned out to have
profotmd neuroprotective effects, many of which can be ascribed to interaction with GABA-A
Taurine Protection Against the Neurotoxicity of Beta Amyloid and Glutamate Receptor Agonists
in Alzheimer’s Disease – Accumulation of beta amyloid is a well-known factor in Alzheimer’s disease
which has been linked to other neurodegenerative disorders as well via over—activation of glutamatergic
neurotransmission and excitotoxicity. Researchers have reported that taurine protected chick retinal
neurons in culture against the neurotoxicity of amyloid beta and glutamate receptor agonists. Taurine
might also provide protection against other neurodegenerative diseases such as Huntington’s disease,
Lou Gehrig’s disease, and Parkinson’s disease, as well as acute insults leading to massive brain cell
death as a result of excitotoxicity such as hypoglycemia, neurologic trauma, stroke, and epilepsy. The
authors claim that their study showed for the first time that taurine prevents the neurotoxicity of beta
amyloid and that that protection is related to the activation of GABA—A receptors. As they also report,
other GABA—A agonists, including melatonin, carbamazepine, phenyloin, and valproic acid have also
been shown to attenuate the neurotoxic effects of beta amyloid, the latter three by stabilization of
intracellular calcium levels.Taurine as a Scavenger of Reactive Carbonyl Species and Inhibitor of Protein Glycation and
AGE Products — Taurine is one of a few important endogenous low molecular weight chemicals
(including, in addition to taurine, carnosine, histamine, and pyridoxamine), that provide protection
against reactive carbonyl species and AGEs. Researchers found that taurine prevented in vitro glycation
and the accmnulation of AGEs and, in in vivo studies with rats, the contents of glucose, glycated
protein, glycosylated haemoglobin and fructosamine were significantly lowered by tamine treatment in
high fructose diet-fed rats.
Taurine Improves Learning and Memory Retention in Aged Mice — Supplementation with taurine
in aged mice significantly ameliorated the age-dependent decline in memory acquisition and retention.
“These changes include increased levels of the neurotransmitters GABA and glutamate, increased
expression of glutamic acid decarboxylase and the neuropeptide somatostatin and increase in the
number of somatostatin—positive neurons. These specific alterations of the inhibitory system caused by
taurine treatment oppose those naturally occturing in aging, and suggest a protective role of taurine
against the normal aging process? Taurine has been shown to act as an agonist of GABA-A receptors.
As we noted above, GABA-A is involved in sleep.
Cholinergic Dysfunction as a Result of Excitatory Amino Acids May Be Responsible for
Cognitive Decline
Another possible mechanism that may contribute to cognitive dysfunction is the inhibition of choline
acetyltransferase reported to take place as a result of the action of excitatory amino acids in the central
nervous system. Although this paper did not test for the protective effects of taurine against these
deleterious effects of excitatory amino acids, it is reasonable to suppose that taurine, found in high
concentrations in the brain and known to have protective effects against excitotoxicity, would provide
some protection. Choline acetyltransferase is the enzyme responsible for converting choline to
acetylcholine; hence, its activity is critical for normal cholinergic function in the CNS.
Glutamate Receptor—mediated Taurine Release During Oxidative Stress in the Hippocampus
Excitotoxicity as a result of oxidative stress induced by glutamate in the hippocampus was reported in
another paper to cause taurine release. The authors here concluded that: “Taurine eiiiux via VRAC is
critical for volume regulation of hippocampal slices exposed to oxidative stress.”
Taurine Provides Potent Retina Protection — Adequate levels of taurine can help prevent age—related
vision loss; while a deficiency can lead to troubling vision problems. While taurine is fotmd in very
high concentrations in the retina, it declines significantly with age. Additionally, the taurine fotmd in
the retina fights oxidative stress, especially in diabetes, and helps restore deficient levels of nerve
growth factor, required for maintaining retinal health. When taurine levels are deficient, a variety of
vision problems can occur including retinal ganglion cell degeneration, and in children, retinal
dysfunction; taurine supplementation has been shown to ameliorate diabetic retinopathy. Evidence is
strong that taurine is vital in maintaining optimal retinal ftmction.
Taurine deficient cats can develop central retinal degeneration resulting in blindness.
Solution for Seizures – While there are many types and many causes of epilepsy (seizures), a
disruption in the function of excitable brain tissue underlies all of them. One of taurine’s major roles is
the regulation of such excitable tissues. Animal studies reveal that taurine depletion makes seizures
more likely, while supplementation with taurine is capable of preventing seizures induced by a numberdrugs and chemical toxins. Taurine appears to work by increasing the levels of glutamic acid
decarboxylase (GAD), the enzyme responsible for the production of the neurotransmitter GABA, as
well as by binding to so-called GABA receptors in brain cells, calming them and reducing their
likelihood of participating in the random, uncoordinated electrical tiring that produces an epileptic
Parkinson’s Disease
A few days ago it has been reported that the cause for Parkinson has been found — DOPAL.
I surfed a bit in the net and found two other interesting articles: Taurine reduces DOPAL.
And Parkinson’s Patients have a lower taurine concentration in brain tluid than healthy people.
Is a low taurine level indirect responsible for Parkinson’s?
Taurine content of foods
1c. goat milk 100 (same a human milk)
1oz. Chicken liver 30 (cooked, raw’?)
1oz. Fish (cooked, raw?) 30
l 1 oz. Chicken / Beef 10 raw, 2 cooked
1c. cow milk 5
Average taurine intake is estimated to be about 60mg.per day (with a range of 40 to 400 mg). The average in
Japan is about 225 mg. per day, which is considered high intake.
1,800 calories of goat milk (same as human) would provide at least 750 mg per day. Of course babies probably
require quite a bit more than adults. —M
Successful clinical studies have used daily doses of 1,500 -3,000 mg.
Taurine has a wide margin of safety, being well tolerated at 2 grams/day or even (for most patients) up to 12
grams/day as an adjunct therapy for liver disease.
We studied the role of diminished sympathetic nervous system (SNS) activity and endogenous opiate activation
in the hypotensive action of taurine, a sulfur amino acid, in deoxycorticosterone acetate (DOCA)—salt
hypertensive rats. Supplementation of taurine could prevent the development of DOCA—salt hypertension in rats,
but failed to change blood pressure in vehicle-treated control rats. Cardiac NE turnover, which was determined
from the rate of decline of tissue NE concentration after the administration of aIpha—methyl-p—tyrosine, was
markedly accelerated in DOCA—salt rats, but 1% taurine supplement restored it to normal. Moreover, naloxone (2
mg/kg), the specific opiate antagonist, increased blood pressure in taurine-treated DOCA—salt rats, restoring it to
levels similar to those in the DOCA-salt rats. ln contrast, taurine did not decrease cardiac NE turnover in the
control rats, nor did naloxone increase blood pressure in the taurine-treated control rats. Moreover,
supplementation of taurine increased both beta—end0rphin-like immunoreactive material and taurine contents in
the hypothalamus of DOCA-salt rats, whereas it did not increase beta·endorphin in that of control rats despite
increased taurine contents. Thus, taurine not only normalized the increased cardiac SNS activity but also elicited
an opiate-mediated vasodepressor response only in DOCA—salt rats. lt is suggested, therefore, that endogenous
opiate activation, which is intimately related to SNS suppression, may contribute to the anti-hypertensive effect
of taurine in sodium chloride hypertension.

*Loss of Glutathi0ne***
Glutathione precursors, which raise the glutathione status in the body, are present in raw milk, raw egg
white, and raw meat. They are destroyed by heat. ‘
Glutathione plays four major roles within the body:
• Safe storage of the highly vulnerable and potentially toxic amino acid cysteine.
• Protection against oxidative stress.
· Detoxification.
• Cellular communication and regulation of protein function.
***Loss of the protective aniino acids, Proline and Glycine***
The availabilities of lysine, proline, aspartic acid, glutamic acid, threonine, alanine, glycine and serine
were particularly affected. Severe heating at aW 0.97 did not seem to favour the Maillard reaction, but
the availabilities of cystine, tyrosine and arginine were decreased, probably as a result of structural
modifications of the protein upon heating. Heating whey protein concentrates in the presence of lactose
not only affected lysine, but also impaired enzymic liberation of other amino acids, according to the
severity of heat treatments and a.
***CO-ENZYME Q10***
Coenzyme Q10 is a powerful protector of the heart and blood vessels. CoQ10 is found primarily in red
meats, especially organ meats like liver and heart. Coenzyme Q10 is heat-sensitive, and is destroyed
progressively as meat is cooked. A well-done steak will have dramatically less CoQ10 than a rare steak.
To obtain maximal CoQ10 benefit, meat should be eaten as rare as is tolerable to the diner.
The functions of coenzyme Q10 range from energy-production to anti-oxidant activity. Coenzyme Q10
acts as an anti-oxidant itself; and is also necessary for the proper anti-oxidant function of vitamin E.
CoQ10 is an essential component of the mitochondria, where it is involved in the production of ATP,
the body’s fundamental unit of energy, from fats and carbohydrates, and appears to regulate the pH of ‘
cellular compartments called “lysosomes” where digestion of various materials takes place.
Coenzyme Q10 has been shown in studies to improve congestive heart failure, and animal experiments
have shown it to reduce damage to the heart done by heart attacks and open—heart surgery. Evidence
also shows that it may be a powerful treatment for lowering high blood pressure.
Dr. Al Sears has found that patients who come to his center with heart disease, or various risk factors
for heart disease, such as diabetes, high blood pressure, or low HDL, tend to be deficient in coenzyme
Q10. He fnds that supplementing with CoQ10 makes a dramatic difference in helping these patients to
recover their energy and cardiovascular health.
Coenzyme Q10 is found in the highest amotmts in red meat. Beef heart and liver are believed to be the
richest sources of CoQ10. Beef has almost twice as much coenzyme Q10 as chicken. Some fish have
levels approaching the level of beef muscle meat. There are much higher levels of CoQ10 in the organ
meats of beef.
Organ meats of grass—fed ruminants have up to 10 times more coenzyme Q10 than the organ meats of
grain-fed animals.
Enzymes help us digest our food. Enzymes are proteins though, and they have
a very specific 3—dimensional structure in space. Once they are heated much
above 118 degrees, this structure can change, and the enzymes are are no longer
able to provide the function for which they were designed. Digestion of cooked
food demands much more energy than the digestion of raw food. In general, raw
food is so much more easily digested that it passes through the digestive tract in
1/2 to 1/3 of the time it takes for cooked food.
H€i€1’0CyCliC 31I1ill€S (HCAs) and polycyclic aromatic hydrocarbons (PAHs) are chemicals
formed when muscle meat, is cooked using high-temperature methods, such as pan frying or grilling
directly over an open flame. ln laboratory experiments, HCAs and PAHs have been found to be
mutagenic—that is, they cause changes in DNA that may increase the risk of cancer.
HCAs are formed when amino acids, sugars, and creatine (a substance found in muscle) react at high
temperatures. PAHs are formed when fat and juices Hom meat grilled directly over an open fire drip
onto the fire, causing flames. These flames contain PAHs that then adhere to the surface of the meat.
PAHs can also be formed during other food preparation processes, such as smoking of meats.
HCAs are not found in significant amounts in foods other than meat cooked at high temperatures. PAHs
can be found in other charred foods, as well as in cigarette smoke and car exhaust fumes.
The formation of HCAs and PAHs varies by meat type, cooking method, and “doneness” level.
Whatever the type of meat, however, meats cooked at high temperatures, especially above 300°P (as in
grilling or pan frying), or that are cooked for a long time tend to form more HCAs. For example, well
done, grilled, or barbecued chicken and steak all have high concentrations of HCAs. Cooking methods
that expose meat to smoke or charring contribute to PAH formation.
HCAs and PAHs become capable of damaging DNA only after they are metabolized by specific
enzymes in the body, a process called “bio—activation.” The activity of these enzymes, which can differ
among people, may be relevant to cancer risks associated with exposure to these compounds.



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