Categories:

Estriol, DES, etc

by Ray Peat, PhD

A review of the use of estrogens reported in J.A.M.A. (only up to 1987) found nearly 200 different “indications for its use. (Palmlund, 1996.) Using the conservative language of that journal, such use could be said to constitute wildly irresponsible “empirical” medical practice. More appropriate language could be used.

Pollution of the environment and food supply by estrogenic chemicals is getting increased attention. Early in the study of estrogens, it was noticed that soot, containing polycyclic aromatic hydrocarbons, was both estrogenic and carcinogenic. Since then, it has been found that phenolics and chlorinated hydrocarbons are significantly estrogenic, and that many estrogenic herbicides, pesticides, and industrial by-products persist in the environment, causing infertility, deformed reproductive organs, tumors, and other biological defects, including immunodeficiency. In the Columbia River, a recent study found that about 25% of the otters and muskrats were anatomically deformed.

Estrogenic pollution kills birds, panthers, alligators, old men, young women, fish, seals, babies, and ecosystems. Some of these chemicals are sprayed on forests by the US Department of Agriculture, where they enter lakes, underwater aquifers, rivers, and oceans. Private businesses spray them on farms and orchards, or put them into the air as smoke or vapors, or dump them directly into rivers. Homeowners put them on their lawns and gardens.

Natural estrogens, from human urine, enter the rivers from sewage. Many tons of synthetic and pharmaceutical estrogens, administered to menopausal women in quantities much larger than their bodies ever produced metabolically, are being added to the rivers.

In the same way that weak estrogens in the environment may become hundreds of times more estrogenic by synergistic interactions (J.A. McLachlan, et al., Science, June 7, 1996), combinations of natural, medical, dietary, and environmental estrogens are almost certain to have unexpected results. The concept of a “protective estrogen” is very similar to the idea of “protective mutagens” or “protective carcinogens,” though in the case of estrogens their promoters don’t even know what the normal natural functions of estrogen are.

In November, 1995, an international conference was held to study the problem of “Environmental endocrine-disrupting chemicals,” and to devise strategies for increasing public awareness of the seriousness of the problem. Their “Statement from the work session” says “New evidence is especially worrisome because it underscores the exquisite sensitivity of the developing nervous system to chemical perturbations that result in functional abnormalities.” “This work session was convened because of the growing concern that failure to confront the problem could have major economic and societal implications.” “We are certain of the following: Endocrine-disrupting chemicals can undermine neurological and behavioral development and subsequent potential of individuals….” “Because the endocrine system is sensitive to perturbation, it is a likely target for disturbance.” “Man-made endocrine-disrupting chemicals range across all continents and oceans. They are found in native populations from the Arctic to the tropics, and, because of their persistence in the body, can be passed from generation to generation.” “…many endocrine-disrupting contaminants, even if less potent than the natural products, are present in living tissue at concentrations millions of times higher than the natural hormones.” “The developing brain exhibits specific and often narrow windows during which exposure to endocrine disrupters can produce permanent changes in its structure and function.”

In spite of this increased exposure to estrogens, there is a new wave of advertising of esteogenic substances, based on the idea that weak estrogens will provide protection against strong estrogens. The environmental background of estrogenic pollution already provides a continuous estrogenic exposure. In the 1940s, Alexander Lipshuts demonstrated that a continuous, weak estrogenic stimulus was immensely effective in producing, first fibromas, then cancer, in one organ after another, and the effect was not limited to the reproductive system. How is it possible that the idea of “protection from a weak estrogen seems convincing to so many? Isn’t this the same process that we saw when the nuclear industry promoted Luckey’s doctrine of “radiation hormesis,” literally the claim that “a little radiation is positively good for us”?

DES (diethyl stilbestrol) is one of the most notorious estrogens, because studies in humans revealed that its use during pregnancy not only caused cancer, miscarriages, blood clots, etc., in the women who used it, but also caused cancer, infertility, and deformities in their children, and even in their grandchildren. (But those transgenerational effects are not unique to it.)

Besides the absurd use of DES to prevent miscarriages, around 1950 it was also used to treat vulvovaginitis in little girls, for menstrual irregularity at puberty, to treat sterility, dysfunctional bleeding, endometriosis, amenorrhea, oligomenorrhea, dysmenorrhea, migraine headaches, nausea and vomiting, and painful breast engorgement or severe bleeding after childbirth.

DES is a “weak” estrogen, in the sense that it doesn’t compete with natural estrogens for the “estrogen receptors.” (Estriol binds more strongly to receptors than DES does: “Cytosolic and nuclear estrogen receptors in the genital tract of the rhesus monkey,” J. Steroid Bioch. 8(2), 151-155, 1977.) Pills formerly contained from 5 to 250 mg. of DES. The 1984 PDR lists doses for hypogonadism and ovarian failure as 0.2 to 0.5 mg. daily. In general, dosage of estrogens decreased by a factor of 100 after the 1960s.

An aggressively stupid editorial by Alvin H. Follingstad, from the Jan. 2, 1978, issue of JAMA, pages 29-30, “Estriol, the forgotten estrogen?” is being circulated to promote the use of estriol, or the phytoestrogens. It argues that women who secrete larger amounts of estriol are resistant to cancer.

By some tests, estriol is a “weak estrogen,” by others it is a powerful estrogen.

When estriol was placed in the uterus of a rabbit only 1.25 mcg. was sufficient to prevent implantation and destroy the blastocyst. (Dmowski, et al., 1977.) Since the effect was local, the body weight of the animal doesn’t make much difference, when thinking about the probable effect of a similar local concentration of the hormone on human tissues. The anti-progestational activity of estriol and estradiol are approximately the same. (Tamotsu and Pincus, 1958.)

When 5 mg. of estriol was given to women intravaginally, this very large dose suppressed LH within 2 hours, and suppressed FSH in 5 hours. Given orally, 8 mg. had similar effects on LH and FSH after 30 days, and also had an estrogenic effect on the vaginal epithelium…These quick systemic effects of a “weak estrogen” are essentially those of a strong estrogen, except for the size of the dose. (Schiff, et al., 1978.)

When administered subcutaneously, estriol induced abortions and stillbirths (Velardo, et al.)

Another indication of the strength of an estrogen is its ability to cause the uterus to enlarge. Estriol is slightly weaker, in terms of milligrams required to cause a certain rate of uterine enlargement, than estradiol. (Clark, et al., 1979.) But isn’t the important question whether or not the weak estrogen imitates all of the effects of estradiol, including carcinogenesis and blood clotting, in addition to any special harmful effects it might have?

When added to long-term culture of human breast cancer cells, estriol stimulated their growth, and overcame the antiestrogenic effects of tamoxifen, even at concentrations hundreds of times lower than that of tamoxifen. “The data do not support an antiestrogenic role for estriol in human breast cancer.” (Lippman, et al., 1977.)

Studies of the urinary output of estriol/estradiol in women with or without breast cancer do not reliably show the claimed association between low estriol/estradiol and cancer, and the stimulating effect of estriol on the growth of cancer cells suggests that any alteration of the estrogen ratio is likely to be a consequence of the disease, rather than a cause. The conversion of estradiol to other estrogens occurs mainly in the liver, in the non-pregnant woman, as does the further metabolism of the estrogens into glucuronides and sulfates. The hormonal conditions leading to and associated with breast cancer all affect the liver and its metabolic systems. The hydroxylating enzymes are also affected by toxins. Hypothyroidism (low T3), low progesterone, pregnenolone, DHEA, etiocholanolone, and high prolactin, growth hormone, and cortisol are associated with the chronic high estrogen and breast cancer physiologies, and modify the liver’s regulatory ability

The decreased output of hormones when the fetal-placental system is dying is a natural consequence, since the placenta produces hormones, and during pregnancy converts estradiol to estriol. Since estradiol in excess kills the fetus, its conversion by the placenta to estriol is in accord with the evidence showing that estriol is the more quickly excreted form. (G. S. Rao, 1973.) The conversion of 16-hydroxy androstenedione and 16-hydroxyDHEA into estriol by the placenta (Vega Ramos, 1973) would also cause fetal exhaustion or-death to result in lower estriol production. But a recent observation that a surge of estriol production precedes the onset of labor, and that its premature occurrence can identify women at risk of premature delivery (McGregor, et al., 1995) suggests that the estriol surge might reflect the mother’s increased production of adrenal androgens during stress. (This would be analogous to the situation in the polycystic ovary syndrome, in which excessive estradiol drives the adrenals to produce androgens.)

Estetrol, which has one more hydroxyl group than estriol, is a “more sensitive and reliable indicator of fetal morbidity than estriol during toxemic pregnancies,” because it starts to decrease earlier, or decreases more, than estriol. (Kundu, et al., 1978.) This seems to make it even clearer that the decline of estriol is a consequence, not a cause, of fetal sickness or death.

A 1994 publication (B. Zumoff, “Hormonal profiles in women with breast cancer, Obstet. GynecoL Clin. Nor-th Am. (U.S.)21(4), 751-772) reported that there are four hormonal features in women with breast cancer: diminished androgen production, luteal inadequacy, increased 16-hydroxylation of estradiol, and increased prolactin. The 16 hydroxylation converts estradiol into estriol.

A new technique for radiographically locating a hormone-dependent breast cancer is based on the fact that estriol-sulfate is a major metabolite of estradiol. The technique showed the tumor to have about a six times higher concentration of estriol sulfate than liver or muscle. (N. Shimura, et al., “Specific of hormone-dependent mammary carcinoma in nude mice with [(131)I]-anti-estriol 3-sulfate antibody,” Nucl. Med. Biol. (England) 22(5), 547-553, 1995.)

Another association of elevated conversion of estradiol to estrone with disease was found to occur in men who had a myocardial infarction, compared to controls who hadn’t. (W. S. Bauld, et al., 1957.)

The estrogens in clover have been known for several decades to have a contraceptive action in sheep, and other phytoestrogens are known to cause deformities in the genitals, feminization of men, and anatomical changes in the brain as well as functional masculinization of the female brain. (Register, et al., 1995; Levy, et al, 1995; Clarkson, et al., 1995; Gavaler, et al., 1995.) The effects of the phytoestrogens are very complex, because they modify the sensitivity of cells to natural estrogens, and also modify the metabolism of estrogens, with the result that the effects on a given tissue can be either proestrogenic and anti-estrogenic. For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.)

Why do plants make phytoestrogens? There is some information indicating that these compounds evolved to regulate the plants’ interactions with other organisms — to attract bacteria, or to repel insects, for example, rather than just as pigment forming materials. (Baker, 1995.) The fact that some of them bind to our “estrogen receptors” is probably misleading, because of their many other effects, including inhibiting enzyme functions involved in the regulation of steroids and prostaglandins. Their biochemistry in animals is much more complicated than that of natural estrogens, which is itself so complicated that we can only guess what the consequences might be when we change the concentration and the ratio of substances in that complex system.

These “natural” effects in sheep were forerunners of the observed estrogenic effects in wild animals, caused by pollutants. Twenty-five years ago I reviewed many of the issues of estrogen’s toxicity, and the ubiquity of estrogenic substances, and since then have regularly spoken about it, but I haven’t concentrated much attention on the phytoestrogens, because we can usually just choose foods that are relatively free of them. They are so often associated with other food toxins-antithyroid factors, inhibitors of digestive enzymes, immunosuppressants, etc. — that the avoidance of certain foods is desirable. Recently an advocate of soybeans said “if they inhibit the thyroid, why isn’t there an epidemic of hypothyroidism in Asia?” I happened to hear this right sfter seeing newspaper articles about China’s problem with 100,000,000 cretins; yes, Asia has endemic hypothyroidism, and beans are widely associated with hypothyroidism.

When I first heard about clover-induced miscarriages in sheep, I began reading about the subject, because it was relevant to the work I was doing at that time on reproductive aging. Sheep which are adapted to living at high altitude, where all animals have reduced fertility, have an adaptive type of hemoglobin, with a greater affinity for oxygen. Fetal hemoglobin, in animals at sea-level, has a great affinity for oxygen, making it possible for the fetus to get enough oxygen, despite its insulation from the mother’s direct blood supply. The high-altitude-tolerant sheep have hemoglobin which is able to deliver aufficient oxygen to the uterus to meet the needs of the embryo/fetus, even during relative oxygen deprivation. These sheep are able to sustain pregnancy while grazing on clover. It seemed evident that estrogen and high altitude had something in common, namely, oxygen deprivation, and it also seemed evident that these sheep provided the explanation for estrogen’s abortifacient effects.

Estrogen’s effects, ranging from shock to cancer, all seem to relate to an interference with the use of oxygen. Different estrogens have different affinities for various tissues, and a given substance is likely to have effects other than estrogenicity, and the presence of other. substances will modify the way a tissue responds, but the stressful shift away from oxidative production of energy is the factor that all estrogens have in common. Otherwise, how could suffocation and x-irradiation have estrogenic effects?

Pharmaceutical misrepresentations regarding the estrogens rank, in terms of human consequences, with the radiation damage from fall-out from bomb tests and reactor-leaks, with industrial pollution, with degradation of the food supply-with genocide, in fact.

Advertising gets a bad name when it can’t be distinguished from mass murder. At a certain point, we can’t afford to waste our time making subtle distinctions between ignorance and malevolence. If we begin pointing out the lethal consequences of “stupid” or quasi-stupid commercial/governmental policies, the offenders will have the burden of proving that their actions are the result of irresponsible ignorance, rather than criminal duplicity. From the tobacco senators to the chemical/pharmaceutical/food/energy industries and their agents in the governmental agencies, those who do great harm must be held responsible.

The idea of corporate welfare, in which public funds are given in massive subsidies to rich corporations, is now generally recognized. Next, we have to increase our consciousness of corporate responsibility, and that ordinary criminal law, especially RICO, can be directly applied to corporations. It remains to be seen whether a government can be made to stop giving public funds to corporations, and instead, to begin enforcing the law against them — and against those in the agencies who participated in their crimes.

In the U.S., the death penalty is sometimes reserved for “aggravated homicide.” If those who kill hundreds of thousands for the sake of billions of dollars in profits are not committing aggravated homicide, then it must be that no law written in the English language can be objectively interpreted, and the legal system is an Alice in Wonderland convenience for the corporate state.

The American Acupuncturist.

http://www.encognitive.com/node/12884

Posted in General.

Tagged with , , , , , , , , , , , , , , , .

Comments Off on Estriol, DES, etc

By Team FPS – October 15, 2011

Carbon Monoxide: Cancer Hormone?

by Ray Peat, PhD

When I started graduate school in biology at the University of Oregon, cell “membrane” research was a thriving business, almost as lucrative as genetics. Years earlier, I had been intrigued by Linus Pauling’s suggestion that anesthetics might act by “structuring” the water in nerve cells, and in trying to understand the physiology of hearing, I had concluded that the “unit discharge” (all-or nothing) idea of nervous transmission left almost everything unexplained. As a result, I concentrated on the organized internal complexity of structure in cells, and found no reason to believe that cells were bags of randomly acting enzymes enclosed in an “amazing membrane” which contained an array of pumps that regulated the composition of the enclosed fluid. When people produced pictures of”membrane pores,” I thought they should also have to explain why pores of the same size appear when distilled water is frozen and photographed by the same techniques. If a red blood cell, when etched awa y microscopically looks like a sponge, how can a hypothetical membrane on the surface be all-important? Why did it take so long for electron microscopists to produce images of the membrane, when their microscopes were producing fine images, and why did it take several decades for them to decide how thick these membranes should be? Reading the history of the theory of the “plasma membrane,” I decided that it was almost perfectly irrelevant to biology, because dead cells, as in hair, can demonstrate the same ionic gradients that were the reason for believing in the regulatory membrane.

Many people think of the membrane inside an egg shell when they hear people talk about the “cell membrane,” but the standard lipid bilayer membrane to which so much importance is given should evoke an image of the iridescent sheen that can be seen on puddles when a trace of oil spreads over the surface. This spreading of oil over a mass of water is precisely the physical model that lies behind the membrane theory. But the proteins making up the cell have a great affinity for fats – the cell is far from being the watery mass that the theory says needs to be separated from its environment by an oily film.

When electron microscopes became available, people expected to see the cell membranes they believed in. But in the first pictures, no membranes were visible. After many trials, methods were found to create the appearance of a membrane on cells, but for more than 20 years microscopists were arguing over the thickness of the membrane. The images showed membranes that were as thin as 20 Angstrom units, or as thick as 300 Angstroms. After 30 years, their thickness was decided to be between 60 and 100 Angstrom units. Osmium, which is the standard material used for producing images of cell membranes, was already in medical use for creating “false membranes” on burned or ulcerated tissue. How do you suppose this material came to be used to reveal the membranes which theory required, but ordinary techniques didn’t show?

I believe fats are important in carcinogenesis, but not because of any theoretical membrane function. They have regulatory functions, and I think it is important to avoid associating the idea of “regulation” with the misleading idea of “membranes.”

Around the same time, I read the history of genetic thinking, and found that Weissmanism, which formed the basic orientation for contemporary thinking in genetics, was ludicrously mistaken. The technical definition of the “gene” has quietly changed over the last couple of generations, but the term has kept its mystique, which leads people to feel that they have explained something when they can identify “its gene.” The mystique carries so much weight, that it is customary to accept conclusions regarding “genetic causation” without ordinary statistical support.

At the time I began studying biology at the University, the brain was explained in terms of genes and membranes, with emphasis on membranes, and cancer was explained by genes and membranes, and the dominant thought was that a genetic defect caused a membrane defect, which caused the abnormal behavior of cancer cells. To an outsider, the idea sounded as defective then as it does now, but rhetoric is very important in science, and it was rhetorically persuasive to most scientists.

I have been hearing people say “we don’t know what causes cancer, but we are certain it’s genetic.” John Gofman, in his new book,( 1) argues that 75% of breast cancer is caused by exposure to radiation, and expresses annoyance that so many people seem to forget that radiation is well established as an important cause of the disease. He quotes a statement from a fund-raising appeal: “What’s worse, even the best doctors have no idea what causes breast cancer or how to cure it.” (The 75% figure might sound high at first, until you realize that the incidence of breast cancer in the U.S. has doubled since 1970.)

Samuel Epstein says that the National Cancer Institute and American Cancer Society are indifferent to or ignorant of cancer prevention.( 2) He cites exposure “to chemical and radioactive carcinogens (notably large scale emissions and discharges from civilian nuclear reactors)” as known causes of breast cancer, and mentions “the cancer establishment’s exploitation of women as scientific guinea pigs as evidenced by: their deliberate exposure of some 300,000 women without warning to high dose mammography in the 1970s; their failure to recognize the carcinogenic hazards of current `low dose’ mammography….” Epstein also mentions that “exogenous estrogens synergize the carcinogenic effects of irradiation…”

So, we could reverse the popular claim of the cancer establishment, and say that most of the causes of breast cancer are now known.

Since the 1950s, when Gofman worked for the government and was himself a “radiation apologist,” I have followed his work, and have admired his ability to free himself from mistaken views, even when doing so was costly to his career. He now holds the establishment view regarding the nature of cancer: He says it “is now considered to be a genetic disease. It is thought that a tumor develops in stages from a single cell, as the cell and some of its descendants accumulate a set of several `genetic lesions.'”

I am strongly inclined to doubt this part of the establishment view, too. I have mentioned some of the evidence against it in a previous newsletter For many years, histologists studying carcinogenesis in animals have seen diffuse changes in cells throughout the area which has been irradiated or chemically treated, where the cancer will appear. The uniformity of the precancerous tissue shows either that the “genetic lesion” isn’t random, or that it is already invasive, though not yet cancerous. If we want to emphasize the “genes,” we will say that certain genes are very susceptible to mutations, and that, once a mass of precancerous mutated cells exist, it is likely that other mutations will occur in those cells, “promoting” them from a precancerous to a cancerous state. But the outstanding feature of genetic mutations, which geneticists have insisted upon, is that they are different from physiological changes in being random. The very idea of “promotion,” which is now an accept ed part of the doctrine, violates the traditional idea of what a mutation is. This issue has been coming up repeatedly in connection with the ideas of the cancer gene, the cancer virus, or the viral cancer gene: The gene (or virus) “is activated by the carcinogens or radiation,” which amounts to saying that something – e.g., radiation or chemicals or hormones – causes cancer, leaving the cancer gene unable to explain anything.

In fact, the well-accepted tumor “promoters,” estrogen( 3) and unsaturated fatty acids, turn out experimentally to be fundamental carcinogens, as well as promoters. Phorbol esters, famous as experimental tumor promoters, activate a particular cellular system, which is also activated by unsaturated fatty acids, and by various hormones. Unsaturated fatty acids are now clearly identified as a “target” of ultraviolet radiation damage in skin cells, and increasingly they are seen to be involved in toxic injury and stress injury. Radiation absorbed anywhere in a cell can start a peroxidation chain reaction, causing widespread damage, which can include the inactivation of important enzymes, including those known as “membrane pumps. “( 4) These same chain reactions might also cause breaks in the DNA chain, producing mutations, but that is a separate question. If the antioxidant defenses and the energy reserves of the cell are depleted, permanent damage is very likely. People who see the c ell as being “essentially its genes” have denied that low-level radiation causes cancer, because they think about direct interactions between rays and genes. Even though most of the evidence has been deliberately suppressed and “lost” by the U.S. government, it is now very clear that low doses of radiation are carcinogenic.

The reason people want to say that cancer is “genetic” is simply that cancer cells have a stable identity which is propagated as they multiply. They, unlike the cells they derive from, are immortal, in the sense that they go on dividing, and don’t mature into anything. They are said to be “dedifferentiated” cells, that are more like the cells of an embryo than like the cells of the tissue where they grow.

If cancer cells could mature into cells like those they came from, they would just be like any cell in the tissue-repair process. The cells we know as cancer are somehow stabilized in a relatively undifferentiated state, they inherit that state from the cells that precede them. It is reasonable to consider that genes might have something to do with being stuck in a condition of undifferentiated growth.

But there are many situations in which established, undifferentiated cancer cells have differentiated in the laboratory, under special conditions. This proves that, in those cases, the cancer was not a genetically caused thing, since the conditions didn’t undo any mutation. For example, leukemia cells have differentiated after they were treated with DMSO or dimethyl formamide, for cold storage. Melanoma cells have reverted to a more differentiated type under the influence of the ophylline and testosterone. In one very interesting experiment, cells from a malignant tumor were combined with the cells of an embryo, and the mixed cells grew into a mature animal which was a mosaic, showing inheritance from four parents – that is, the cancer cells were just as good as healthy embryonic cells, and just needed the right environment to mature.

So, to me it seems that the real question is, “what can cause the stabilization of cells in the undifferentiated state, yet allow for certain conditions occasionally to restore the mature state?”

Some of the earliest cancer research demonstrated that tumor cells can be transplanted successfully into certain hosts, and not into others. This led many people to think about the various factors that might make some individuals resistant to cancer, and others susceptible. The immune system and hormones were found to be complexly involved in susceptibility. It occurred to some people that the cancer itself might produce a special hormone, that affected the host organism in a way that tended to allow the tumor to keep growing.

When extracts of cancers were injected into healthy animals, some of them became sick, and were inclined to develop cancer. Several lines of investigation led to the belief that pyrroles and porphyrins, related to heme (the iron-binding pigment in hemoglobin and various oxidative enzymes), might be a “cancer hormone,” but the idea lacked charm, and didn’t catch on.

I made extracts from aged uterine tissue, thinking it might contain estrogen, and found that when I injected it into a hamster, it seemed to cause secretion of porphyrin from the animal’s eye. This led me to get interested in the hormonal significance of the porphyrin pigment, and it was known to be related to estrogen excess and cancer susceptibility.( 5, 6)

Two of cancer’s most mysterious features are its respiratory defect, identified by Otto Warburg, in which it converts glucose to lactic acid even in the presence of oxygen, and its resistance to lipid peroxidation. Lipid peroxidation is intimately involved in the control of cell division and aging, and in susceptibility of cells to elimination by the immune system, so cancer’s antioxidative capacity seems to be closely related to its “immortal” nature. Iron (either free or bound to heine) is known to catalyze lipid peroxidation, but its presence in cancer cells simply supports their growth, rather than causing peroxidation.

Warburg discovered that light desorbs carbon monoxide and cyanide from respiratory pigments. In trying to understand light’s effects on respiration, it occurred to me that it might be desorbing those, or other toxins that bind to and inhibit the respiratory enzymes. Cancer cells lack the ability to detoxify cyanide, so it has seemed possible that cyanide might contribute to the respiratory defect of cancer; bowel bacteria can produce small amounts.

But carbon monoxide is always being produced in the body, by the enzyme heme oxygenase, which is involved in the breakdown of hemoglobin. Carbon monoxide, by binding to heme-iron, inhibits lipid peroxidation,( 7) as well as inhibiting the respiratory pigments in the mitochondria.

Warburg observed that depriving growing cells of oxygen was sufficient to cause some of them to turn into cancer cells.

Anything which causes oxygen deprivation stimulates the formation of heme.(8)

If the breakdown of heme occurs in cancer cells, that is, if heme oxygenase can be demonstrated in them, then the conditions exist for a stable, heritable but non-genetic state which, as a result of the carbon monoxide which is produced in heme metabolism, combines a respiratory defect with resistance to lipid peroxidation. Heme oxygenase is induced by a variety of stresses, especially oxidative stress,( 9, 10) and is known to exist in at least some cancers.”( 11) I think it will turn out to be a universal feature of cancer.

Heme could function as a systemic toxin, if produced in cancer cells in abundance, since it would be metabolized in the liver, with production there of abnormally large amounts of carbon monoxide. Liver abnormalities have long been recognized as an important feature of cancer.

And carbon monoxide, produced by a large tumor, would certainly be a systemic toxin. It could also account for the “regional cancerization” which has been reported to occur in the area immediately around a tumor, in which normal cells seem to be modified by the cancer as if by an inductive agent. These observations have always been discounted by the genetic dogmatists.

The relation between estrogen and porphyrin (which can be seen in some types of porphyria), and their association with cancer susceptibility, probably is a consequence of estrogen’s interference with blood oxygenation, which would tend to cause exaggerated production of heine in various tissues. A sensitive instrument is now available, which can measure carbon monoxide in the breath; this could become an important diagnostic instrument.

Besides using light to desorb toxins from the heme group, there are probably various ways to directly inhibit the formation of heme. For example, ethyl alcohol inhibits heine formation( 12) (the “hemeless” ring sideroblast is often considered to be a sign of alcoholism). Alcohol is superior in many ways to morphine for pain control in cancer patients, and if carbon monoxide produced by heme breakdown turns out to be a factor in cancer’s persistence, alcohol might become an important factor in the prevention or treatment of cancer. It would be necessary to use a highly purified form of vodka, free of estrogen and other carcinogens. Except for bowel and liver cancer, the alcohol should be taken transdermally or intravenously. Anti-inflammatory and antihistamine agents, magnesium, progesterone, pregnenolone and other substances could be used to support oxidative metabolism.

The material used in heme synthesis is diverted from energy production. Useless heme production would contribute to cancer’s energy-depleting effect on the organism.

Although carbon monoxide production by cancer cells will seem merely an incidental feature to the genetic dogmatists, I think it offers the opportunity for a unifying perspective on cancer, explaining both its systemic effects (immune suppression, wasting, and adrenal activation, for example) and its cellular features, including the respiratory defect, dedifferentiation, resistance to killing by lipid peroxidation, and – in some ways the most important feature – its stability, which has led so many people to call it a “genetic disease.” Metabolic stress does cause chromosomal damage and mutations, but without the intrinsic resistance to lipid peroxidation, these defects would lead to the cells’ death.

References

(1.) John W. Gofman, Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of this Disease, CNR-Committee for Nuclear Responsibility, PO Box 421993, San Francisco, CA 94124,1994.

(2.) Samuel S. Epstein, The Cancer Establishment Ignores Avoidable Causes of Breast Cancer, Health Resources Management (M/C 922), School of Public Health West, The University of Illinois at Chicago, Box 6998, Chicago, IL 60680,1994.

(3.) Han, X.L., and J.G. Liehr, 8-Hydroxylation of guanine bases in kidney and liver DNA of hamsters treated with estradiol: Role of free radicals in estrogen-induced carcinogenesis, Cancer Res. 54(21), 5515-5517, 1994

(4.) Hitschke, et al., Inactivation of the Na,K ATPase by radiation-induced free radicals-evidence for a radical-chain mechanism, FEBS Lett 353(3), 297-300,1994.

(5.) Figge, H.J., The relationship of pyrrol compounds to carcinogenesis, Res. Conf. on Cancer, pp. 117-128, 1944.

(6.) Strong, L.C., Sex differences in pigment content of Harderian glands of mice, Proc. Soc. Exp. Biol Med 50, 123, 1942.

(7.) Dodge, J.T. et al., Peroxidative hemolysis of red blood cells from patients with abetalipoproteinemia (acanthocytosis), J. Clin. Invest. 46, 357-368, 1967.

(8.) Falk, J.E., et al., Effect of oxygen tension on haem and porphyrin biosynthesis, Nature 184, 1217, 1959.

(9.) Paschen, W., et al., Hemeoxygenase expression after reversible ischemia of rat brain, Neurosci. Lett. 180(1), 5-8, 1994

(10.) Tyrrell, R.M., and S. Basumodak, Transient enhancement of heme oxygenase I mRNA accumulation: A marker of oxidative stress to eukaryotic cells, Oxygen Radicals in Biolog. 234, 224-235, 1994.

(11.) Takeda, K., et al., Identification of a cisacting element that is responsible for cadmium mediated induction of the human heme oxygenase gene, J. Biol. Chem. 269(36), 22858-22867, 1994.

(12.) Ali, M.A.M. and M.C. Brain, Ethanol inhibition of hemoglobin synthesis: in vitro evidence for a heme correctable defect in normal subjects and in alcoholics, Br. J. Haematol. 28, 311-316,1974.

Townsend Letter for Doctors & Patients.

http://www.encognitive.com/node/13878

Posted in General.

Tagged with , , , , , , , , , , , , , , .

Comments Off on Carbon Monoxide: Cancer Hormone?

By Team FPS – October 15, 2011

Ray Peat on PubMed

Bartos DC, Duchatelet S, Burgess DE, Klug D, Denjoy I, Peat R, Lupoglazoff JM, Fressart V, Berthet M, Ackerman MJ, January CT, Guicheney P, Delisle BP.
Heart Rhythm. 2011 Jan;8(1):48-55. Epub 2010 Sep 17.

Little DG, McDonald M, Sharpe IT, Peat R, Williams P, McEvoy T.
J Orthop Res. 2005 Jul;23(4):862-8. Epub 2005 Feb 25.

Baker NL, Mörgelin M, Peat R, Goemans N, North KN, Bateman JF, Lamandé SR.
Hum Mol Genet. 2005 Jan 15;14(2):279-93. Epub 2004 Nov 24.

Oral absorption of progesterone.
Peat R.
J Natl Med Assoc. 1986 Mar;78(3):182, 185. No abstract available.

Estrogen stimulated pathway changes and cold-inactivated enzymes.
Peat R, Soderwall AL.
Physiol Chem Phys. 1972;4(3):295-300. No abstract available.

http://www.ncbi.nlm.nih.gov/pubmed?term=%22Peat%20R%22[Author]

Posted in General.

Tagged with , , , , , , .

Comments Off on Ray Peat on PubMed

By Team FPS – October 15, 2011

A Physiological Approach to Ovarian Cancer

by Ray Peat, PhD

Several years ago, George Crile, of the Cleveland Clinic, observed that his clinic had removed only 11 thyroids that year, and that they had done more than 5000 thyroidectomies annually in the 1920s. The reason for the change was that they found that there was rarely any reason to remove the gland; even thyroid cancers of most types could be controlled safely by using a thyroid supplement, to reduce the growth-stimulating action of the pituitary hormone.

Since many physicians still believe that destruction of the thyroid gland, by radiation or surgery, is an appropriate treatment for thyroid disease, it isn’t surprising that there is so little attention given to the possibility of physiologically controlling the more aggressive ovarian cancers. The recent report that ovarian cancer is more common among women who have taken gonadotrophins, to promote fertility, will probably bring increasing attention to the physiology of ovarian tumors.

Around menopause, the pituitary gonadotrophins increase. Menopausal estrogen treatment shouldn’t be called “estrogen replacement therapy,” because the amount given is typically about 15 times higher than occurs in younger women. The reason for the use of such high doses is that the dose is increased until the pituitary gonadotrophins are suppressed. The reason for the menopausal increase in pituitary hormones is that the nerve cells which regulate their secretion have been killed or desensitized by their past exposure to estrogen; it is their reduced sensitivity that requires the very large doses of estrogen to suppress secretion of the gonadotrophic hormones.

Clonidine (normally used for high blood pressure) can be used as a skin patch, to control menopausal flushing; progesterone and DHEA prevent osteoporosis. After those issues have been taken care of, the question of pituitary hyperfunction should be considered, in relation to preventing ovarian cancer. (Combinations of safe substances including progesterone and naloxone can probably be worked out empirically.) A variety of other possibilities exist, including Gonadotrophin Inhibiting Substance, and antagonists to the specific gonadotrophin release hormones. Normalizing the menopausal gonadotrophins would have far-reaching effects, possibly improving the immune response.( 1)

For years, it has been known that nuns have a high incidence of ovarian, breast, and endometrial cancer. Women who have children, or who take oral contraceptives that might suppress ovulation, are believed to have a lower incidence of ovarian cancer because of reduced exposure to the gonadotrophins. (Though cancers of liver, breast, and other organs are reported to be more frequent among pill users; prolactinomas seemed to become epidemic after the pill was introduced.)

Normal factors in the physiological control of the ovaries include an interaction between the thyroid and the gonadotrophins; the combination of hypothyroidism and stimulation by gonadotrophins can cause ovarian cysts to develop. Small amounts of estrogen can increase both FSH and LH, and large amounts of progesterone decrease both FSH and LH.( 2)

If ovaries are removed from their normal location, and transplanted into the spleen, so that their secretions go directly to the liver where they are inactivated, they produce tumors because they are subject to “hypersecretion of gonadotrophic hormones.”( 3) Other experiments support the idea that ovarian tumors develop from excess pituitary stimulation. For example, removal of one ovary was essential to produce a tumor in the other ovary even after it had been irradiated.(4) Similarly, no tumors developed in irradiated ovaries transplanted into other mice, irradiated or not, as long as they had their own ovaries, which kept the pituitary functioning normally.(5)

Progesterone and estrogen “receptors” can be demonstrated in some ovarian tumors, and by analogy with breast and uterine tissue, in which progesterone generally retards cell division and estrogen stimulates it, hormones have been investigated as possible therapies for ovarian cancer. Although in vitro studies show that there might be a direct action on the tumor cells,(6) the reports of positive responses in patients treated with progesterone or synthetic progestins(7) are more interesting, since the most logical approach involves normalization of the pituitary gonadotrophins.

If it is true that a “deficiency” of the so-called “essential” fatty acids suppresses gonadotrophin secretion,(8) then a diet lacking those estrogen-promoting(9) substances should be both protective and therapeutic for ovarian cancer (assuming that the results seen with progestin therapy are produced by gonadotrophin inhibition.) If our purpose is to delay the menopausal rise of the gonadotrophins, then it is interesting that lipid peroxidation of polyunsaturated fatty acids (which increases with age) can be intimately involved in loss of progesterone forming ability by human steroidogenic tissues.(10) That is, aging decreases the ability of certain brain cells to inhibit the pituitary gonadotrophins, and it also tends to decrease the steroidogenic tissues’ ability to produce the regulatory steroids.

After menopause, estrogen is produced less by the ovary than by other tissues, including fat cells. Breast cancer cells can produce their own estrogen. This means that estrogen is one of the “cancer hormones” which, secreted by the tumor, promotes the growth of the tumor and also has a systemic pro-cancer action. Ovarian tumors, too, can cause great systemic hormonal imbalances, which should be investigated routinely in a physiological approach to the disease. After menopause, estrogen is largely produced by conversion of “androgenic” steroids from the adrenal glands. It would be desirable to be able to inhibit the conversion of the adrenal steroid precursor to estrogen. Newton, et al.(11) showed that progesterone inhibits the conversion of the precursor to estrogen, and P.K. Siiteri showed a similar effect for thyroid hormone.

A diet low in polyunsaturated fats facilitates thyroid hormone secretion, transport, and tissue response to it, and would minimize the stress-related or age-related inhibition of progesterone formation by lipid peroxidation. Vitamin E and vitamin A also protect against lipid peroxidation, and vitamin A is specifically involved in progesterone synthesis. Vitamin A also has a variety of anti-estrogen functions,(12) that are often considered to be relevant to protection against cancer.(13)

All of these dietary and hormonal approaches to normalizing the pituitary gonadotrophins and controlling ovarian cell division are things which also tend to optimize the immune response. A slight deficiency of iron is probably protective against cancer, since there are several ways that iron can promote cancer, apart from its role in damage to the immune system and the steroidogenic system by lipid peroxidation.(14)

Correspondence:

Ray Peat, Ph.D.

Ray Peat’s Newsletter

1585 Moss

Eugene, OR 97403

References
(1.) E.W. Adcock, Maternal lymphocytes: suppression by human chorionic gonadotrophin, Science 184, 913-914, 1974.

(2.) C. Martin, Endocrine Physiology, Williams and Wilkins, Baltimore, 1976.

(3.) M.H.Li and W.U. Gardner, Experimental studies on the pathogenesis and histogenesis of ovarian tumors in mice, Cancer Research 7, 549-4566, 1949.

W.U. Gardner, Hormonal imbalance in tumorigenesis, Cancer Research 8, 397-411, 1948.

M.H. Li and W.U. Gardner, Further studies on the pathogenesis of ovarian tumors in mice, Cancer Research 9, 35-41, 1949.

(4.) L. Lick, A. Kirschbaum and H. Mixer, Mechanism of induction of ovarian tumors by x-rays, cancer Research 9, 35-41, 1949.

(5.) H.S. Kaplan, Influence of ovarian function on incidence of radiation-induced ovarian tumors in mice, J. Natl. Cancer Inst. 11, 125-132, 1950.

(6.) M. Gronroos, et al., Steroid receptors and response of ovarian cancer to hormones in vitro, Br. J. Ob. Syn. 91, 472-478, 1984.

(7.) A. Berqvist, et al. A study of estrogen and progesterone cytosol receptor concentration in benign and malignant ovarian tumors and a review of malignant ovarian tumors treated with medroxyprogesterone acetate, Acta Obstet. Gynecol. Scand.. (Supple. 101), 75-81, 1981.

C.J. Jolles, et al. Estrogen and progesterone therapy in advanced ovarian cancer, preliminary report, Gyn. Onc. 16, 352-359, 1983.

H.W.C. Ward, Progestogen therapy for ovarian carcinoma, J. Ob. Gyn., 555-559, 1972.

(8.) S.S. Smith, et al. Essential fatty acid deficiency delays the onset of puberty in the female rats, Endocrinology 125, 1650-1659, 1989.

(9.) K. Obinata, et al. The effects of essential fatty acid deficiency on hepatic bile salt sulphotransferase in rats, J. Steroid Biochem. Molec. Biol. 42(6), 625-627, 1992.

(10.) J. Klimek, The influence of NADPH-dependent lipid peroxidation on the progesterone biosynthesis in human placental mitochondria, J. Steroid Biochem. Molec. Biol. 42(7), 729736, 1992.

(11.) C.J. Newton, et al. Aromatase activity and concentrations of cortisol, progesterone and testosterone in breast and abdominal adipose tissue, J. Steroid Biochem. 24(5), 1033-1035, 1986.

(12.) W.I. Bo, Relation of vitamin A deficiency and estrogen to induction of keratinizing metaplasia, Amer. J. Clin. Nutr. 516, 666, 1954. Also, Proc. Soc. Exp. Biol. Med. 76, 1951.

(13.) M. Koga and R.L. Sutherland, Retinoic acid acts synergistically with 1,25-Dihydroxyvitamin D, or antioestrogen to inhibit T-47-D human breast cancer cell proliferation, J. Steroid Biochem. Molec. Biol. 39(4A), 455-460, 1991.

T.E. Rohan, et al. Breast, Cancer Research 50, 3176-81, 1990.

M.I. Dawson and W.H. Okamura, Chemistry and Biology of Synthetic Retinoids, CRC Press, Boca Raton, 1990.

(14.) R.J. Bergeron, et al. Influence of iron on in vivo proliferation and lethality of L1210 cells, J. Nutrition 115( 3), 369-374, 1985.

E.E. Letendre, Importance of iron in the pathogenesis of infection and neoplasm, Trends in Biochem. Sci., April, 1985, 166-168.

Townsend Letter for Doctors & Patients.

http://www.encognitive.com/node/3675

Posted in General.

Tagged with , , , , , , , , , , , .

Comments Off on A Physiological Approach to Ovarian Cancer

By Team FPS – October 15, 2011

The Myth of Iodine Deficiency: An Interview with Dr. Ray Peat

Is iodine supplementation safe and, if not, is there a safe amount of supplemental iodine?

Dr. Peat: “A dosage of 150 mcg (micrograms, not milligrams, e.g., ug not mg) is a safe amount of iodine. There are excellent references describing the effect of a moderate iodine excess (even below a milligram per day) on the thyroid. An iodine deficiency can cause hypothyroidism (rare now), but so can an excess. Iodine deficiency is an unusual cause of hypothyroidism, except in a few places, like the mountains of Mexico and China, and the Andes.

“Most goiters now are from estrogen-like effects, but they used to be from iodine deficiency. Chronic excess iodine tends to cause thyroiditis, regardless of the gland’s size. The amounts used by Abraham and Flechas are much larger than this — very toxic doses, enough to cause severe thyroid problems.”

Is the Iodine Test Kit (from Dr. Abraham) valid and does it reveal thyroid deficiency?

“Guy Abraham and some of his followers claim that an iodine deficiency can be shown by the quick disappearance of a spot of iodine painted on the skin. The skin test of iodine deficiency is completely unscientific. Iodine is converted to colorless iodide by reductants, including vitamin C, glutathione, and thiosulphate. “G. Abraham’s Iodine Test Kit contains iodine overdose pills. The test is completely irrational. It implies that the body should be saturated with iodine.”

Is there a rational way to determine iodine deficiency or excess?

“It’s easy to recognize a chronic iodine deficiency, because it causes the thyroid gland to enlarge. Goiters can be caused in various ways, for example by being exposed to various goitrogens, including excess iodine, or by excessive estrogen and deficient progesterone, as well as by an iodine deficiency. “However, a chronic excess of iodine is harder to recognize, because it can produce a variety of degenerative changes. Measurement of the average daily iodine intake or excretion in the urine would be needed to confirm an excess. High iodine intake can suppress TSH, and since high TSH is pro-inflammatory, the iodine can have some protective anti-inflammatory actions, but in the long run, the thyroid suppression becomes a problem.”

Note: I have a list of references on iodine toxicity that are too lengthy for this newsletter. If you are interested in these references, please email me at lita@litalee.com, and I will send them to you.

Reference

To Your Health – July 2008 by Lita Lee

==============

Also:

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.

Source

Posted in General.

Tagged with , , , , , , , , .

rev="post-3085" 1 comment

By Team FPS – October 12, 2011

The Omnivore’s Solution

Posted on August 17, 2011 by DODIE3905

ARE YOU AN OMNIVORE?
Of course you are. An omnivore is a creature that eats ‘all’ (or ‘omni’) of the foods available. Carnivores eat meat, which means they have to live near prey animals to survive. Herbivores eat vegetable matter, which means they usually wander and migrate to take advantage of rainfall and its ability to grow plants. Simply put, herbivores use symbiotic bacteria for digestion of food, while carnivores use enzymes (from internal production and from eaten meat) for digestion. You use both enzymes and bacteria, and thereby have a wider choice of foods to eat because you can digest them. A lion is a carnivore. A steer is an herbivore. Pigs and chickens are omnivores like you. Just look into basic biology to find all the “-vores” on earth, but more important remember you are an omnivore. Your digestive system is designed for that. There is no science that is credible that denies this. The growing human population on earth is proof enough of the strength of this evolutionary fact. An omnivore is part of who you are.

HOW DID YOU GET HERE?
You have evolved to your present omnivore state as a species over at least 7 MILLION years. You started farming about 10 THOUSAND years ago, which is a blink of an eye in comparison. So, you are an omnivorous hunter and gatherer, not really a farmer. The industrial era is even shorter than the agrarian era. Technology as you know it is very new to you. Virtually all our DNA was in place BEFORE the agrarian age. Farming and food processing with technology are therefore only a very recent set of experiments. You probably are wondering how these experiments are doing.

IS MODERN FOOD OUR BEST BET FOR THE FUTURE?
Michael Pollan is a Professor at Berkeley and a famous author on modern food production. He has pointed out a lot about how these experiments are coming along. His conclusion (in books like ‘The Omnivore’s Dilemma’ and ‘The Botany of Desire’, etc.) is that we are not doing very well in producing food lately. Some of his findings are positively horrifying in fact. We have been doing these intensive food modifications over the last 100 years, and there are very ominous growth rates of chronic diseases that seem to accompany these modifications. We do very well reducing the cost of food, while disease care costs are climbing exponentially. Certainly diabetes Type 2 and obesity can be related to food, at least. Perhaps heart disease and cancer as well.

The latest World Health Organization forecast for chronic diseases in 2030 indicates no slowdown of chronic disease. Infectious diseases are forecast to be reduced, but WHO expects no progress on the chronic diseases. Killers such as heart and vascular deterioration, stroke, diabetes, cancer and arthritis and other such chronic problems are projected to grow. All the billions of dollars spent in research so far seems to be yielding nothing on which we can depend in the way of progress.

The longest ever recorded life span for human beings approaches 140 years among the Hunza people in the Himalayas. The modern world does not enjoy this kind of life span. Why? Food supply between the two locations is very different, but the medical care in the modern world is thought to be far superior! It would appear that medical care has little to do with a long healthy life for our species. Food is much more potent in extending healthy life span if you consider these facts. Beyond that, the life expectancy (predicted life span) for citizens of the US was reduced by one month for the first time ever in October of 2010. Is our food supply actually getting less healthy for us? Organ replacement is becoming more common and this may help, but eradication of chronic deadly disease is forecast to continue to elude us. Even if the lifespan numbers are approximate, this is a remarkable state of affairs. Something seems gravely wrong, doesn’t it? Could your food be wrong for you? It appears it may be.

Unfortunately all we know about these chronic diseases is that they are occurring, and seem to be reaching epidemic proportions. We do not know enough about their root causes to have cures or preventive methods for them. We do know, for small pox, tuberculosis, malaria and polio for example, enough to deal with their bacterial causes and remedies. But no one knows the real causes of chronic heart disease, cancer, diabetes and obesity. We may know proximate causes, the last things that preceded their onset, but not the whole chain of causation back to where we can count on prevention advice. Worse yet, we seem to be looking for drugs that will cure them, based on statistical observations of groups of people. This gives you statistical chances, or ‘odds’ as they say at the race track. You can only bet on this work, not count on it. Statistical analysis is a useful shortcut to the unshakeable truth, but the margin of error is very wide. Laboratory demonstrations helped us find real cures for most infectious diseases because the microbes involved became visible as microscopes, laboratory techniques and equipment improved. We have not improved our methods for biochemical demonstrations enough to conquer human chronic diseases as they develop within the human body however. It also takes a lot of time and resource to do this work.

If you knew the whole story of a disease, rather than just the nearest cause and its chances of happening to you, better decisions as to what action to take would be obvious to you. The whole story is what Louis Pasteur uncovered for rabies vaccinations, and what Dr. Fleming did for penicillin. You can deal with infectious diseases because science was applied. This is the success part of modern science. It was the ‘miracle drug’ era that had hard evidence that looked just like miraculous cures for infectious disease, and in fact was.

What we seem to do now with chronic diseases is rush to market with drugs that have a chance of working. No one sells sure cures to you. Most drugs come with a piece of paper called the ‘package insert’. One of its main purposes is to explain what the chances of the drug working are, and what the side effects might be. This seems to be a kind of apology to you for not having finished the full scientific research necessary to prevention or cure.

The reason for this shortcut process lies in the trail of money of course. That is what steers us to do what we do. The cost of doing the full science in research is too expensive for the drug makers, and not enough independent pure research money is available to solve this problem. In free economies, the first step in becoming a true scientist seems to be to take a vow of poverty.

So you are left with really big questions about the role of food in our chronic disease increases. Is our food supply experimentation actually helping you or hurting you? Michael Pollan calls this the ‘omnivore’s dilemma’. Is your food cheaper at the expense of life span and disease care costs later in life? Since you have to live now, and will not get definitive sure cure information from anywhere, you might as well take on the problem directly yourself. Make your own decisions about what to eat. Your body will probably give you better information than anyone else can supply you. If it is a bet and not a sure thing, why not make the best bet you can by yourself by learning as much as you can and taking charge? At least it will be your best intelligent bet.

ARE YOU STILL EATING AS AN OMNIVORE?
A close look at our food today would say we are not eating like omnivores now, even though we have always done so for millions of years previously. We do not hunt as we used to. We gather, but only what is presented to us in stores. We don’t know where our food actually comes from any more.

In the last 70 years or so, three examples of massive change in our diet in the modern world have been so great they are hard to ignore. First, our meat animals have been switched over to a largely grain based diet instead of grass. As a result steers mature in 17 months, about half what they used to, but the meat contains a different mix of nutrients. Pigs don’t dig up food from the ground any more, they are fed corn and other waste mixtures. Chickens don’t peck the ground now, we actually cut off their beaks so they can’t fight each other in the cages we keep them in. We feed them grain and other products. They, like pigs, are another omnivore no longer eating as an omnivore. They grow fast but the meat has changed for the worse. Are we eating the animal protein we always have? Not now.

Second, fat consumption has gone up in the modern world, and almost all of it is polyunsaturated fat from grain and vegetable sources, not saturated fats from animals. These fats are consumed today at a rate four times the rate of 70 years ago, when vegetable oils were used in paint and varnish primarily. They are cheaper, but certainly not traditional.
Third, we get our sugar from grain now in the form of mostly maltose. This sugar has replaced fruit sugar, or sucrose, because it is cheaper. But the new sugar has twice the glycemic index, or impact on our blood sugar balance, as the old. It is cheap, but not what we are used to eating to fuel our bodies with energy.

Changing these foods back to where they were would make a difference no doubt. But what would your best strategy be overall? You need to think changes through to avoid increasing your risk. You need a thought out strategy.

WHAT STRATEGIC TOOLS DO YOU HAVE?

1. You are free. The good side of this is that you have the right to take full responsibility for your own health without interference. No government, doctor or richer person can force you to eat what you choose to avoid.

2. You have the internet. Look for some answers there. Watch out because some of the answers on the internet are grossly misleading. Don’t think for a minute that it is just Wikipedia that is the problem because anyone can modify the information in it. Most available medical research can be misleading also. Just ask Dr. Ioannidis (he works in Greece at the moment). He was published in the Journal of the American Medical Association several years ago. He studies all the research done in medicine worldwide to estimate its accuracy. He found an error rate of 80% in the medical studies that were published for us all to read which were done without statistical care. This is the largest group of studies. Of the next largest group, those done with certain statistical improvements, 25-40% still contained grossly wrong conclusions. Even the very large ‘golden’ studies (rare) had wrong conclusions 10% of the time. Doctors in general agree with this, and realize it in the daily frustration of dealing with individual patients. (See The Atlantic magazine for November, 2010.) You haven’t heard much about this because our institutions are very concerned about maintaining medical credibility in the public. They want to protect medical procedure acceptance for those procedures which do in fact work. Dr. Ioannidis disagrees. He thinks you are smart enough to handle the truth. He is never embarrassed by truth. So what good is the internet? It is an excellent tool with which you can learn to recognize good science from bad or unfinished science. Don’t forget to search for helpers like Dr. Ioannidis, too.

3. Your own body will tell you when it is happy if you listen. After our decades of consultation with thousands of people on two continents, we are astounded at how rarely people will believe the signals their own unique bodies send them every day. They defer in a very docile way to doctors, magazine articles and the advertising on our public media. Please realize that you do not really have a choice for better information than from your own body. Good doctors will look first at your body for clues. They do not prejudge diagnosis before you arrive. You can do the same thing. You live with your body much more than the Doctor does. There is no better source of information about your health than your body. Listen to it, its information is available nowhere else.

4. Natural food experiments are hardly ever fatal. Students eat goldfish, aborigines eat meal worms, and a human baby will try to eat anything. They all survive. Try natural foods courageously. Try natural foods to see what your body does with them. Learn by doing, and believe what your body says about what you are doing. You are an omnivore, test the limits of it, remembering not to do this with foods made or modified by man.

5. There is a bit of true science around to count on. Most of it is hard to find, but it is useful.

6. You have never had more food available in the western world than now. I think you will agree you have too much. Getting food is not our problem, but choosing the right food is, along with getting it to everybody on the planet.

WHAT IS THE OMNIVORE’S SOLUTION?
So you do have some strategic tools. If you have courage to act on your own, you can implement a strategy for yourself. What makes sense?

First, let’s not expect answers to everything. You are in a world of uncertain truth about nutrition so you need humility and courage to succeed. There will never be an end to your discovery, or your need for more truth. Just ask any true scientist. Let’s get over that and push on regardless, on your own. Be skeptical, but forge ahead and learn true from false as best you can.

Your courage will not be tested very hard in the beginning. That will happen when and if you ever get seriously ill. You might lose confidence in our own ability to deal with disease. With courage, you will have prepared to recognize true answers from false ones without faith in somebody else’s proclamations. Stick to them in what you do now, and in what help you may ask for in the future.

Next is to accept that our evolved bodies are well equipped to survive. The best source of health and healing for the human body is the body itself. Respect your body as the best servant to your health, happiness and longevity. Your body uses your DNA as a resource for survival, just as it uses food that is available if it can. You are not doomed by your DNA at birth, you are enabled by it. Become an ally of your own body in what you eat. Eat to release your body’s full potential.

What follows then is that you should eat to arm your body to serve your health, happiness and longevity. How do you do this?

Choosing food is the problem element of your strategy, and you need to know which nutrients are in which foods, and as you experiment with foods, let your body tell you which foods in which combination seem best. You can adjust as body signals change and as time goes on. A daily food diary helps.

Choosing food is actually pretty simple. You need protein, fats and carbohydrates. Carbon, Hydrogen and Oxygen are the chemical bases for your food, and fall neatly into those three categories. The only major exception is nitrogen, which is the sign of protein in food. You can add minerals, vitamins, and enhancing substances later if you first get protein, fats and carbohydrates right. They are the main event, and longer term you can address trace elements you need. Let’s worry about calcium, potassium, phosphorus, iron, magnesium, etc. later.

THE KEY TO THE OMNIVORE’S SUCCESS
The hard questions are which proteins, which fats, and which carbohydrates are best for you? Foods vary widely in their content of types of nutrients. You have to find the right ones. Fortunately, you have some pretty big clues for that. If you start with the 7 million years of our evolution that scientific study of our evolution (paleoanthropology) has made so clear, especially over the last 30 years, some good answers start to emerge. Test them in your own body to see what fits you uniquely. All this is from the true sciences of biology and paleoanthropology, not from statistical studies of various groups of human beings.

You are an omnivore hunter, so what do you hunt? The answer is furry, herbivorous, warm blooded animals. They are prey for humans. They live in our environment, and at about our body temperature too. Carnivores prey on them with you, but you do it differently. You do not have fur, claws, fangs, or blinding running speed over the ground as carnivores do. You are a naked ape, who can trot or run for long distances instead, and you kill from afar, not ‘up close and personal’. You have a big toe on the front of your foot for running; our predecessor primates have one on the side for climbing. Your teeth include grinding molars for eating more than meat, while your fangs and incisors are very small. Naked as you are you can chase wounded game over long distances and they succumb to heat first because they have fur and you don’t. You can wound them, run after them, and collect them for food. Your shoulders contain modified rotator cuff structure so you can throw things; many more things than baseballs. You can pick up a rock and throw it accurately to kill or wound a rabbit, and best of all you have a huge brain that allows you to figure out how to shorten the distance between you and prey and how to enhance your killing tools. There is no conceptual difference between early man throwing a rock at a rabbit, and a farmer hunting with a rifle. The same human brain is the key to both. Weapons have always been improved by humans since the spear. Your style is still to kill from afar. You clearly evolved around furry herbivorous animals, be they rabbits in the desert, or mammoths in the polar regions, or steers slaughtered and dressed by people today delivering food to your door.

What did you do with hunted animals? You ate them. You ate all parts of them. Organ meat, muscle meat, milk, boiled bones for gelatin and marrow, and the saturated fat that is part of them. No oils, just saturated fats. Your brain allowed you to figure out how to eat animals with the help of knives, cooking, boiling water and so forth to make up for our tooth structure, freeing that anatomy to enable chewing of fruits, tubers and vegetables. You discovered that saturated animal fat is a preservative since it doesn’t rot as fast as above ground plants which don’t contain saturated fat. Prey animals convert those plants into saturated fats for you. You used it to mix with other foods for storage. Native Americans call that mixture of fat with meat, berries, nuts, etc. pemmican, the original fast food for humans. You could carry it in your belt pouch and munch on it while traveling for days and never stop at McDonalds. Without the saturated fat, it would rot. Eating the saturated fat also gives you an alternate source of energy since our bodies can do that conversion.

What about gathering? You clearly gathered lots of food. Fruits and berries had to be first on the list, they are favored by you and the other primates on earth even today, and you brought those with you out of the trees as you evolved. Eskimos know all about berries, and, they can freeze them to store them. Further south you evolved on honey too. It stores well for the bees and for you even at higher temperatures. Fruit and honey is where you got the glucose intake to support your huge brain, which runs on glucose. You got glucose from fruit/honey sugar or sucrose. (Sucrose is glucose plus fructose.)

Some vegetables are fruits and some are leaves. Above ground versions of those are easy to gather but seasonal and dependent on rainfall. They had to be eaten seasonally since they rotted very fast after picking. You eventually figured out how to use ice in the summer and canning for storage of foods, but not until very late in your evolutionary history.

Below ground vegetables and tubers, on the other hand, were stored by nature not you, and you could gather them during dry seasons if you remembered where they were growing in the wet seasons. Potato, taro root (poi), turnips, jicama, carrots, beets, rutabagas, and the like had to be very important to you. When the seasonal fruits were not in season, you could dig up underground vegetables and survive. There are some true science experiments in hand today that indicate that you use the same armaments in your digestive systems that below ground vegetables use in defense against fungi, microbes and wrong bacteria in the soil. These storable vegetables had to be important to you, and supplemented your hunting. Archeology shows that early tribes of humans buried stocks of corn below ground as a storage strategy that preceded ice and was an alternate to drying. The root cellar was our first impulse, borrowing from nature. The naturalist Colin Turnbull studied rain forest native tribes and desert native tribes. These storage strategies became obvious to him. He also discovered that above ground, bad tasting leaves and the soil itself, eaten with water, were last resort emergency foods for the desert tribes when droughts went on too long. Rain forests didn’t induce this kind of extreme but food storage was needed everywhere.
A big brain is a metabolically expensive organ to have, but it enables the kind of reliable food storage technology necessary to sustain it, no matter what the climate. You can figure out how to gather and store foods that work for you.

Gathering also had to lead to eating shellfish, and eventually to the other tricky brain teaser, fishing, and you were back to hunting again, even under water.

Furry herbivorous animals, shellfish, underground vegetables and fruits in season have to be the best foods for you. Grains, nuts, seeds and leafy aboveground vegetables are back up foods, or supply condiments for your meals. Note that even today, in places famous for vegetable diets, meat is present in the food supply. This is the universal history of man. India, for example, is importing dramatically more meat as food, adding it to the very many vegetable diets traditional there. This is a matter of choice as the economy grows in India, and the affordability of foods allows access to more animal protein. The sacred cows are not being slaughtered, as far as we know, but India is acting like a nation of omnivores, not some other species. Hindu and Muslim traditional specific food prohibitions will remain, but meat will be eaten when people have the capability to gather it, if not hunt it.

What nutrients comprise this factual truth about human history and evolution? Knowing a little of the chemistry of the body helps validate the diet advice we have so far.

Here is the gist of it what we need:

Proteins: We use protein amino acids as the basic building and repair material of our tissues. 22 protein amino acids from herbivorous animals if you include muscle meat, organs and bones/tissues. Only 14 or so dominate the muscle meat, so that is not enough for you.

Fats: A ‘cocktail’ of fats, primarily animal fats, primarily saturated fat, smaller amounts of unsaturated fats such as those in modern vegetable oils. You can make the polyunsaturated fats you need from food, notably Omega 9. We use all fats as part of our tissue repair work, and as a reserve fuel that can be stored for longer stamina. Some trace nutrients also require fat to dissolve easily in the body.

Carbohydrate: First fruit sugar/honey (sucrose), followed by complex carbs from underground vegetables including other glucose compounds, and topped off by seasonal availability of above ground vegetables. (perhaps 1 to 3 servings per day?) Sucrose is the prime source of our energy for all purposes the body has for it. Glucose is what actually is used, and without it, you die quickly. Sucrose is the best form of it, since the fructose in it controls the reaction of our body to glucose, keeping the effect of it positive, not negative. Just plain glucose, as in many other sugars, can imbalance your body.

There were no drugs for most of your evolutionary life, except for ones found in nature and tested on enough individuals to become part of oral folklore over generations. Shamans and medicine men did experiments, not statistical studies of groups of people. You learned to prevent disease through food and experience. If it worked on your body, you used it. Survival meant not relying on statistics or betting on odds. Lately you have forgotten this major part of our evolutionary history.

You will notice that today’s public fear of animal protein is not supported by this evolutionary reality. Neither is fear of saturated fat. Nor is fear of sucrose (fruit sugar) as our primary source of glucose. These fears have been stimulated in the efforts to cheapen our food supply by artificially extracting nutrients from grain and hydrocarbon commodities like petroleum. Producers of the new less expensive substances would have you believe that they are better than those from natural food, or at least more profitable, and also ignore the complex interaction of all the nutrients in the food as they interact in our bodies. Study of these interactions is hard to do, and expensive, and rarely done at all.

Natural salt and fructose (the other constituent of sucrose that regulates the human impact of the glucose in sucrose) are next on the list for demonization, if you pay attention to current publicity. Both are current targets for artificial replacements. You will see ‘nutra-salt’ products replacing natural salt as did nutra-sweets for sugar, and you will see drugs for controlling blood sugar levels rather than just eating appropriate fruits for the fructose in them. These new products will probably be petroleum derivatives just like the long line of drugs and food additives before them or they will come from grain sources. Fears will be stimulated in the public about salt and fructose to drive the market to high volumes for these new products, with very shaky scientific information, but very effective marketing methods.

You will also realize that your strategy for good human food to arm your body is to eat in ways opposite to current ambient opinion. This serves further to focus the obvious. We all need more true science on food selection and its impact on human biochemistry. We cannot
continue to spend billions of dollars on studies of groups of people yielding only statistical information that leads to usually false conclusions and new drugs and food additives.
You need science to focus on foods you evolved on, to make them affordable without convenient replacement from cheap commodities and unfinished science.

How about growing your own food using your own knowledge to do so? Can’t that be part of your personal strategy? Michael Pollan did it, why not you? You might even try to feed your own chickens as the omnivores they are, instead of the vegetarians the food industry has declared them to be. You can find out how they do, what a good egg is, and how chicken really tastes. Your body will tell you
that, so let it.

If you don’t live in the country, perhaps seeking out friends who do would help you. Go to the local Farmers Market and for fun follow some of them home to see how they grow the food you get from them.

Let’s summarize the simple strategy:

• Take personal control of your own nutrition, really. Don’t abdicate that responsibility.
• Teach yourself to discern true science from unfinished science. If you need help for that, find it.
• Study food and its impact on your own body actively using your body as the laboratory.
• Realize that your diet will be like no one else’s, so don’t assume someone out there has the answer.
• Start separating your food supply from all those modern sources based on unfinished science.
• Gather what works for you and eat it.
• Your scorecard will be filled out by your own body’s reaction to that food, and no other approval is needed.
• Don’t be daunted by unanswered questions. That they continue to arrive is proof of progress.
• Don’t be afraid to act in directions that seem the reverse of current popular thinking. You are a predator, not a conforming herd animal.

If you feel that vegetables are ‘clean food’ and the only food to eat, it may be difficult to embrace the idea that we evolved hunting and eating prey animals. Not many of us kill animals any more. Some of us think that killing other animals is somehow immoral and unnatural.

Perhaps it will help to recognize that the natural cycles of the earth value every part of the cycle. Vegetables are dependent on animals in many ways, and vice versa. One does not exist without the other. Plants deplete the soil, and manure restores it. To choose one part of the natural life cycle of our planet over the others is a violent denial of the order of things. It is immoral for us to be so arrogant. Killing animals is part of the natural order of things and should be respected. As the Sioux hunter said, ‘This honored buffalo died for us today. Give thanks for his blessed gift to us, and honor him as he honored us.’ Of course native Americans didn’t own land either, they regarded it as on loan from their descendants. Nothing is more immoral than to defile the earth’s processes by owning them for our own selfish purposes and not preserving them for our children and grandchildren in the ways they were designed to work.

There is much for the modern world to learn from the ‘third world’. We can be corrupted by the power of the brain that we developed for natural use as we survive and flourish.

Strategy is simple to write down, but hard to do, right? You will need to summon all your courage to do this. Start slowly. How can you really harm yourself by trying natural good foods in combinations? Start now.

http://www.thenutritionwhisperer.com/blog1/?p=72

Posted in General.

Tagged with , , , , , , , , , , , , , , , , , , .

Comments Off on The Omnivore’s Solution

By Team FPS – October 8, 2011

Popping The Food Bubble

Posted on April 27, 2011 by DODIE3905

Before the Bubble

Humans have spent the vast portion of their time on earth as hunter-gatherers, not as farmers and especially not as industrialists. That’s why it is important to learn about our food legacy of hunting and gathering prior to the complete transformation our food supply over the last 100 years. We may have overrun our natural evolutionary speed of adaptation to food.

We now base our agrarian and industrial food strategy on corn, wheat and soybeans. These are the capital intensive crops that power lower food costs for us, and attract massive government subsidies each year. We feed these subsidized cheap crops to ourselves, our pets, our food animals, and are now seeking ways to fuel our cars with them. Capital intensive crops benefit greatly from money and economy of scale; costs go down. This strategy, however, has been accompanied by dramatic increase in chronic diseases like heart disease, vascular disease, cancer and diabetes.

We can either wait for more study of this, or to evolve over time and catch up with the massive change in food, or we can modify what we eat now to align our natural body mechanics and our hunter-gatherer past with today’s realities. Action now makes common sense.

If we rely on evolving to suit our new foods, there will be a lot of death and shortened lives as a result. That’s why the better choice is to see if we can “hunt and gather” good food now, in our present situation, from the huge variety of food available at the neighborhood supermarket.

Popping the Food Bubble will help you go “afield” to hunt and gather food that works for you. The foods you choose to eat can be the most powerful healing and health strategy you can adopt. That is, if you know what you are eating and why you should eat it.

The Food Bubble

To thrive in today’s world, we must realize that we are entering a period in human history that will eventually be called the Food Bubble.

We’ve recently experienced several “Bubbles”: the Housing Bubble, the Dot.Com Bubble, the various Wall Street Trading Bubbles. Each Bubble is a lesson in greed and profit followed by human suffering, sometimes widespread and drastic. Clever individuals make fortunes by getting out early, while the general public pays dearly for years after.

The Housing Bubble, which is perhaps still bursting now, created havoc from greed in the mortgage market at the hands of industry and government. Unfortunately, we are now counting on the same industry and government that produced the Bubble to work together to fix it.

We have also had a Tobacco Bubble in which a few tobacco companies made a lot of money marketing tobacco while denying the myriad health problems their product inflicted. Although tobacco companies were prosecuted, smoking was initially and continually made socially acceptable by industry and government efforts. Industry advertised smoking as sexy, and government delayed recognition of tobacco’s health threats for decades. Tobacco was finally directly linked to disease, but the Tobacco Bubble had a directly lethal aspect for years before then and will remain for years.

What does the future hold? Many signs show we are now building pressure toward a Food Bubble. It hasn’t happened yet, but the signs are everywhere. It started slowly at the beginning of the last century with the introduction of corn flake cereal in 1909 and Crisco in 1911, grain-based foods aimed at mass markets. Technology was at work again, this time by cheapening our food supply. Our government is busy aiding and abetting this for political reasons, not health concerns.

One hundred years on, we are now well into the pre-crash suffering phase of the Food Bubble. In the 1970s and 80s, cheap, plentiful, processed and manufactured food took over U.S. markets and those of many other countries. This cheap food began being marketed as modern, convenient, safe and tasty, and was aided by massive subsidies from rich governments.

This new model was based on cheap and readily available grains consumed as never before in human evolution. But as with the Housing and Tobacco Bubbles, some people get rich while others suffer. Food companies and chemical companies profit enormously from a greedy rush for the cheapest food in the world. Fortunes are made in the food industry by lowering price and increasing volume sold. At the same time, heart disease, obesity, diabetes, cancer and various mental disorders grow unabated at an alarming pace. So, like the food industry, the disease-treatment industry (AKA health care) is booming as health deteriorates from eating cheaper, less-healthy food. And yes, Wall Street is in on the act by financing these initiatives to cheapen food.

Massive food advertising today praises supermarket and fast foods, but also includes the demonizing of historically excellent and healthy human foods, such as animal protein, fruit sugar, saturated animal fats and even salt. Private interests exploit the government to assure the medical credibility of false information about food. Again, a classic Bubble strategy is at work.

It’s a matter of time until the public rises up against this offence, forces government to abandon its denial, and the Food Bubble comes crashing down by force, as all Bubbles have before it.

Are You a “Food Bubble” Yourself?

How are you going to sidestep the negative impacts of the Food Bubble? Are you already suffering its effects?

The supreme irony of the Food Bubble is that not only are sales and profit rates inflating, but your own body may be inflating as well. One trip to France will convince you that today’s U.S. citizens are showing signs of being inflatable. Obesity is the hallmark of U.S. tourists, when compared to, say, French or Japanese touring crowds. Alarmingly young American children show that this trend is not explainable by the usual excuses like stress, age, disease or genetics.

Some of the biggest Bubble makers are visible even now: McDonald’s and Monsanto. McDonald’s hasn’t even noticed the current monstrous recession. Monsanto’s stock chart looks suspiciously like a Bubble already. They make fertilizer for grains, insecticides for grain crops, and genetically modified and patented soybeans.

Clever folks are already benefiting from upswings in demand for cheaper food. An uninformed public is getting fatter and sicker. The news media rarely if ever reports on the food industry’s greed. You have to find this information yourself.

What’s the Big Deal?

Aren’t we much better off now? Stop into any McDonald’s or supermarket and you can buy a vast variety of food mostly ready to eat. And aren’t we healthier too? We’ve cut way back on cholesterol and saturated fats. We eat less meat, eggs and drink less milk. Everybody we know has eaten this way for years. With all these great advances, just look at us.

Yes, look at us:

• We comprise the fattest nation in the world.
• The U.S. incidence of obesity and diabetes is climbing so fast that our children are predicted to live a shorter lifespan than we do.
• Infertility is at an all-time high.
• The top three complaints to doctors are fatigue, depression, or unexplainable anxiety.
• We have three times the heart disease of the Philippines or Costa Rica, two countries that don’t share our market structure for food. They also consume much more animal protein, saturated fat (e.g., coconut oil), salt and fruit sugar than we do. Unlike Americans, they have not been taught that these are “bad” foods.

What About Science?

Independent scientists, those scientists who do not work for industry or the government, are almost impossible to find. Gilbert Ling, PhD, and Raymond Peat, PhD, for example, have brought some sanity to finding true nutritional research. They aren’t rich, but they are still with us. No credible scientist has ever said that corn, soy and wheat can replace good old-fashioned food. Ray Peat has written about this for over 35 years. We don’t hear his voice, though. We are so used to listening to talking heads on TV that we do not bring a critical ear to what we hear every day. Remember that American media is a mouthpiece for industry (where the money is), not for you.

That’s sad because the more traditionally correct science is enlightening: It shows that we have dramatically lowered our metabolism as a nation by eating mostly corn, soy and wheat. Put simply, we are no longer burning our food efficiently. For many people, this equates to weight gain, but for many others it also means fatigue, emotional ups and downs, poor memory, attention deficit disorder, constipation, bloating, water retention, insomnia and much more. Without the financial backing to research these findings, and as long as huge industrial/governmental resources are distributed to ignore facts in service to profit, most of us will only wake up when the Food Bubble finally bursts. This will be too late.

What Should We Do?

We can’t turn the clock back to before the Food Bubble. We can, however, use today’s tools to do better. We would like to invite you to try this as a serious effort for yourself in three ways:

1. Learn about effective nutrition from high-quality, high-integrity science, not from science funded by companies manipulating the Food Bubble. Quality science does not produce the answer first, then the science to back it up. The sequence is the opposite: Do the science; then discover the answer. This makes it very hard for large companies to fund science because reliable profit planning cannot be done when no one knows where the answers may be found in the end. Will any of the effort pay off? That can’t be known until the effort is expended to find out. This fits science, but not business. Fortunately, some of us have spent years of effort piecing together high-quality, classic science with practical daily eating. Consider the Popping the Food Bubble your initiation into effective nutrition based on sound science and the human legacy. Make it your business to manage your own health.

2. Start assessing your own situation more carefully. Take charge of your own health care, and let our disease treatment industry do their work only if you should ever fail or give up. Don’t expect people who make money off your sickness to help you avoid getting sick. Your health is up to you, your body is the most powerful healer you have, and it takes your diligent efforts to allow your body to work to your advantage. Feed your body good food to take care of your health. Silver bullets only worked for the Lone Ranger.

3. Add the Internet to your arsenal of learning tools. Modern life allows you to hunt and gather information that is invaluable, but perhaps not very well funded, and therefore not on television and radio or in the newspaper. It may just be on the Internet. Speaking of hunting and gathering, we can carefully hunt and gather food from the Internet as well: Small local farms often have websites. With Popping the Food Bubble, you’ll learn how to support and buy from people who grow and sell food directly through the Internet and your local farmer’s market, not from large companies who can afford to bring you food from heaven knows where.

Turn your body loose from history and today’s restraints of the Food Bubble. Start by adopting the principles from Popping the Food Bubble as part of your nutritional life. Learn to identify true human food. It will be your guide to better food, abundant food, affordable food, and food that will sustain your body for the long and productive life you deserve.

http://www.thenutritionwhisperer.com/blog1/?p=24

Posted in General.

Tagged with , , , , , , , , , , , , , , , .

rev="post-3056" 2 comments

By Team FPS – October 8, 2011

Dear Doctor Why Do You Insist on Synthroid Instead of Armour? — A Patient’s Letter

Thanks to Shirley Grose, a thyroid patient, for sharing with us the following powerful letter she wrote to her doctor, after he insisted on prescribing Synthroid (a brand name synthetic levothyroxine sodium/T4 thyroid hormone replacement drug) instead of the Armour Thyroid (a brand name naturally derived T4/T3 drug) she’d been taking. (See “A Quick Look at Thyroid Hormone Replacement” for more about these different drugs.) Shirley’s letter is strong and clearly asks many excellent questions many people want answered. She’s generously agreed to allow her letter to be posted for other thyroid patients to read or modify for their use, in the hopes that it might help empower her fellow thyroid sufferers who are having the same problems with their doctors. (Note: Shirley’s doctor never responded…)

Dear Doctor ______________:

I would like for you to clarify several points which came up during our recent discussion. You said Armour Natural Thyroid, my thyroid replacement preference, was impure, not predictably the same strength and old fashioned. I am concerned about this information because I have uncovered some research which indicates flaws in this reasoning.

Would you clarify your statements on Armour Natural Thyroid product? If you feel those statements were valid, can you provide documentation to confirm your opinion that Armour Thyroid is an inferior product to Synthroid? Is Synthroid really a “new ” product or was it “grandfathered-in” around 1930? I would like to know, why, when I changed to Armour Natural Thyroid, you didn’t consider the definite improvement in my health important? I would like to know why you felt I was unqualified to say how my own body felt? Why would you insist upon prescribing a drug that I have tried and does not work well with my body?

Why do you prescribe one drug for all patients? According to Dr. Stephen E. Langer’s book Solved, The Riddle of Illness, “It is possible, because of the liver’s role in the T-4 and T-3 conversion, to have an over-or under-conversion as a result of liver function.” For some patients, Armour Thyroid, because it contains both T-3 and T-4, may provide the extra energy they need to stay employed, continue relationships, or feel good. Synthroid does not contain both, Synthroid has to convert to T3 from T4. Furthermore, author Dr. Ray Peat states, “Unfortunately, our physicians often fail to understand or explain the benefits of natural (marketed under the name ‘Armour’) over synthetic thyroid medication.” Though the formula has changed somewhat in recent years, Dr. Peat calls the natural {thyroid} “the most generally effective,” since “many people whose thyroids are suppressed by stress cannot respond to synthetic thyroxine, T4.” Finally, is it possible that those impurities or unknowns you mentioned might possibly be as yet undiscovered substances which assist thyroid function, a substance or substances which cannot possibly exist in a synthetic product?

Your first statement during my consultation as a new patient was that the Armour Natural Thyroid should be discarded, it was full of impurities, it was of inconsistent strength and it “went out in the 70s.” Synthroid was the drug of choice. Armour was clearly inferior. I explained that I felt better on the Armour Thyroid. You ordered me to throw the Armour Natural Thyroid away and take the Synthroid dosage you prescribed. You said that a TSH test would not be valid if taken while on Armour Natural Thyroid. Can you document this last statement? I understand the TSH is considered one objective measurement for thyroid supplementation; however, I question the inference that a patient’s subjective opinion is unimportant. You seem to disregard how your patients feel. Have there been any major published studies indicating which product the health consumer preferred? Customers have apparently had no choice in thyroid medication in most instances. Therefore, sales volume is not indicative of customer preference. Also, does the Synthroid company fund or in any way contribute to organizations which you belong or to the university, itself? If so, does this influence your decision to singularly prescribe Synthroid?

At the end of my appointment, when you began to write my prescription for Synthroid, I indicated that would not be necessary. You asked, “Why?” I said I was continuing with the Armour Thyroid at the dosage my family physician had prescribed. Your response was, “You don’t need to return do you?” I said, “No, I don’t.” You further explained you did not use the Armour Natural Thyroid, and you would not treat me if I continued taking it.

Do you refuse to treat thyroid cancer patients who refuse to take Synthroid? Should I develop thyroid cancer at some point in the future, would you refuse treatment to me on the basis that I chose not to take Synthroid? Can you legally refuse to treat a patient who has thyroid cancer because the patient takes Armour Natural Thyroid? Why should I or any patient be intimidated into taking what they feel is an inferior product. Why should I or any patient suffer a lesser quality of life because of physician bias for a particular brand name?

I called Forest Pharmaceuticals, Inc. the manufacturer’s of Armour Natural Thyroid, and spoke to Neal Sailer, the Product Manager, Thyroid Products. He is sending a packet of documentation supporting the consistency of Armour Natural Thyroid.

He took exception that Armour Natural Thyroid is of “unpredictable variability.” He explained that desiccated Thyroid powder is a U.S.P. product which means potency content is consistent and he added that the active drug product is constantly assayed during the entire manufacturing process, the FDA insists on this for all products. In addition, Mr. Sailer explained that samples from every batch are retained and periodically assayed for potency. I understand that the limit for T3 and T4 for U.S.P. Thyroid powder is 90% to 110% and natural thyroid is a more stable product than the synthetics. Mr. Sailer would like to know how you came to a determination of Armour being an “impure” or sub-potent drug substance, and would like to see your data. Are you suggesting that Armour Natural Thyroid be recalled?

Additionally, Mr. Sailer informed me of a study recently published in the Journal of the American Medical Association (JAMA), entitled Bioequivalence of Generic and Brand-name Levothyroxine Products in the Treatment of Hypothyroidism, by Betty J. Dong, PharmD; et. al. Are you familiar with the study? Why are you prescribing a product that is 50% more expensive than Levoxyl and Levothroid? Are you assured of the potency of Synthroid? I also understand that Synthroid was reformulated in 1982 because the potency of Synthroid was not near its stated content. In fact, in a letter from Dr. Betty Dong, to the editor of The Journal of Clinical Pharmacy, Dr. Dong assayed several 200 mg tablets of levothyroxine from several brands and generic and found Levothroid had 99% of it s stated potency content and Synthroid had only 78%. I understand that it was this information that prompted the reformulation of Synthroid. I also understand that patients were not informed of this change in formulation, which was clearly dangerous. Which now leads me back to the U.S.P. standard and something else I have learned about Synthroid.

Mr. Sailer informed me that Synthroid is failing the original U.S.P. standard for dissolution for levothyroxine preparations. It is also my understanding that they requested and were given a separate standard for dissolution by the U.S.P. which Mr. Sailer said was most unusual. If this separate dissolution standard for Synthroid is successfully challenged, Synthroid may have to once again reformulate. Will you or the public be informed if this happens? I understand also that there are several class action lawsuits pending against the makers of Synthroid probably initiated as a result of the several articles that appeared in the Wall Street Journal and news stories that were carried on NBC Nightly News. After all of the above, why did you insist on prescribing Synthroid? Could _________ University provide me with any information regarding support from the makers of Synthroid, whether it is Knoll or Boots or Flint?

I would sincerely appreciate an answer with documentation, in writing about the statements you have made about Synthroid and Armour Thyroid. I feel these are important questions, not only for me, but for the future physicians _______________ University educates. These future doctors, including the student who took my thyroid history, have not been given complete information which would allow them and their patients to make educated decisions about their health and their lives.

Sincerely,

Shirley E. Grose

http://thyroid.about.com/cs/thyroiddrugs/l/blletter.htm

Posted in General.

Tagged with , , , , , , , , , , , , .

rev="post-3058" 1 comment

By Team FPS – October 5, 2011

Light is Right

Also see:
10 Tips for Better Sleep Quality
Using Sunlight to Sustain Life
Red Light Improves Mental Function
Light as Medicine? Researchers explain how
Red Light and Near-Infrared Radiation: Powerful Healing Tools You’ve Never Heard of
PUFA, Aging, Cytochrome Oxidase, and Cardiolipin
Blue Light, Cytochrome Oxidase, and Eye Injury
Get a “Chicken Light” and Amp Up Your Energy!
The Therapeutic Effects of Red and Near-Infrared Light (2015)
The Benefits of Near Infrared Light
Blue light has a dark side
Tuning the mitochondrial rotary motor with light

-Consult a medical professional regarding all things related to your health.

“When I moved from Mexico, first to Montana and then to Oregon in 1966, I became very conscious of how light affects the hormones and the health. (For example, in Montana I experienced an interesting springtime shedding of body hair.) Many people who came to cloudy Eugene to study, and who often lived in cheap basement apartments, would develop chronic health problems within a few months. Women who had been healthy when they arrived would often develop premenstrual syndrome or arthritis or colitis during their first winter in Eugene.

The absence of bright light would create a progesterone deficiency, and would leave estrogen and prolactin unopposed. Beginning in 1966, I started calling the syndrome “winter sickness,” but over the next few years, because of the prominence of the premenstrual syndrome and fertility problems in these seasonally exacerbated disorders, I began calling it the pathology of estrogen dominance. In the endocrinology classes I taught at the National College of Naturopathic Medicine, I emphasized the importance of light, and suggested that medicine could be reorganized around these estrogen-related processes” -Ray Peat, PhD

“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.” -Ray Peat, PhD

==========================

Changes in the seasons have significant effects on our body function. Why do I feel depressed, have worse PMS, and poor energy during the winter? Why am I more prone to sickness when it’s cold and overcast outside? Seasonal changes, poor sleep quality, graveyard shifts, and hectic work schedules can take a toll on the body.

Exposure to darkness has a major effect on our health. Light has a multitude of positive effects on our hormonal systems and the way we feel. Avoidance of the sun is recommended to “avoid” cancers of the skin. Such recommendation and modern habits create a society that is experiencing symptoms of light deficiency. This blog explores the topic.

Light It Up
It’s no coincidence that places like Texas, California, and Florida have large populations. Most people want to live in areas with a warmer climate as opposed to the frozen tundra of the likes of Green Bay, WI or Regina, Saskatchewan. Generally, humans enjoy the energizing warmth of the sun, the light it provides, and how it makes us feel. Light exposure and warmer temperatures support metabolism, mood, and optimal body temperature maintenance. Because of improved cellular energy production, our capacity to handle stress improves in relation to our exposure to light.

In comparison, the cumulative effects of darkness over an extended period of time reduces our ability to handle stress. Darkness is a stress because it impairs energy production and is associated with a rise in a variety of inflammatory substances some of which compensate for decreased energy production.

Red light from sunlight (and bright incandescent light) helps cells produce energy, synthesize protective steroid hormones, and reduce the stress hormones that result from darkness and low energy production. Since light exposure improves the metabolic rate and darkness does the opposite, we’d expect that low metabolism and stress related symptoms would surface more during the winter than during the summer months in some people.

Summer v. Winter
During the summer, days are longer and temperatures are higher than during the winter. The summer weather encourages people to do more activities outdoors. The immune system is strongest in the summer as a result. In all aspects, the opposite can be said regarding the winter months.

During the winter, the body is more prone to symptoms of low resting metabolism like seasonal depression (seasonal affective disorder), weight gain, PMS, anxiety, food cravings, fatigue, poor sleep quality, and colds/flus which come about due to lowered temperatures and less light exposure associated with winter. Flu season just happens to occur during the winter when the metabolism slows and immunity is weakest. Endotoxin (lipopolysaccharides), defensive toxins made by gut bacteria, enter the bloodstream during stress (darkness), aging, and malnutrition and can be blamed on symptoms associated with colds and flus. The medical use of antibiotics lowers endotoxin (and estrogen) and the symptoms associated with these issues.

Adrenal stress hormones like adrenaline and cortisol rise during darkness. These stress chemicals suppress metabolism, lower immunity, decrease blood flow to the intestines, and contribute to storage of belly and back fat. Lowered vitamin D production may also play a role in increased susceptibility to infection during winter and prolonged darkness. Vitamin D is obtained in the diet from animal foods and formed endogenously from cholesterol in the skin when exposed to sunlight.

Light deprivation induces a progesterone deficiency allowing cortisol, aldosterone, estrogen, and prolactin to act unopposed creating PMS symptoms, other women’s issues, fatigue, mood change, and weight gain. The darkness causes chronic rises in melatonin and adrenaline as well. Consistently high melatonin has been shown to inhibit progesterone production and lower thyroid hormone output. Melatonin and adrenaline’s liberation of stored PUFA during darkness further poison energy production. This situation mimics that of chronic stress and its metabolic suppression and body temperature lowering effects. The resulting low progesterone, low thyroid, and high inflammatory mediator state doesn’t allow us to resist stresses creating the groundwork for health issues.

The symptoms and markers (high TSH) of thyroid deficiency do seem to appear more so during the dark winter than summer. Populations of the northwest and northeast United States likely experience these season related metabolism changes more so than individuals living in Arizona or Southern California.

Modern Life Mimics Winter
Due to concerns about skin cancer, many are told to avoid sun exposure. Changes in the diet particularly the change toward more consumption of polyunsaturated fatty acids, (which are found in restaurant foods, processed/boxed foods, and “health” foods like grains, beans, nuts, seed, fatty fish, above ground vegetables, seed oils, fish oils, nut butters, and vegetable oils) are to blame for the increase incidence of skin cancer. Some populations develop melanomas on parts of the body (bottoms of feet) where the skin isn’t exposed to the sun. The use of some sunscreens predictably increase likelihood of skin cancers.

Our ancestors likely had more sun exposure than we do as well as far less exposure to anti-metabolic food stuffs. Modern life has manipulated the summer v. winter scene that I have discussed here as even during the summer months people aren’t getting light exposure.

The typical nine to five worker often suffers from light deficiency as the day often entails getting up early, rushing out of the house to make it to work, sitting in a car on the commute, then sitting inside all day at work under fluorescent lighting, traveling home, and then heating up a prepared meal and watching TV.

Children these days aren’t immune to this same scenario as they are more likely to play Xbox 360 or be on the internet after school than ride bikes and play outside. Whether it’s winter or summer really doesn’t matter because people aren’t outside anyway, and it’s important to note that indoor fluorescent lighting (rich in blue light) unfortunately has the same effects as darkness on the cellular energy production.

Sleep – Friend or Foe?
“For many years, it has been known that the death rate increases during the winter months and also increases at night (winter or summer). Most deaths occur just before dawn when the body is in its least efficient state.” -Ray Peat, PhD

For many, night time is a very stressful time. The symptoms associated with a cold, flu, or infection are often noticeably worse at night than during the day. Immune function at night (and throughout winter) suffers as the metabolic rate falls and stress substances rise to compensate. Without ample energy, the body cannot fight the presenting infection properly and symptoms emerge more forcefully.

People with low metabolic rates (i.e. seniors) often pass away in their sleep because of how stressful it is irregardless of the season. Grave yard shift workers who I have worked with often have a terrible time with weight management and are very low energy despite the attempt to “catch up on sleep” during the day. Those with inflammatory conditions like rheumatoid arthritis often awaken with the worst pain they experience the entire day, and the pain centers where the tissue temperature is the lowest – in the hands and feet. This doesn’t happen by coincidence.

Blood sugar falls during sleep especially if the person cannot store glycogen; carbon dioxide production suffers; circulation is poor; and body temperature falls. Stress mediators are produced (like cortisol, adrenaline, aldosterone, serotonin, melatonin) in the attempt to maintain the metabolism, blood sugar, and circulation just as they are during the waking hours. This results in poor sleep quality, inflammation, and in extreme cases death. In essence, sleep is not peaceful especially when the metabolic rate is poor.

Protection from Darkness
Our best protection against the stress of darkness is youthful sleep. Healthy children can seemingly sleep through a nuclear bomb because they have a high metabolic rate and optimal body temperature that keeps the aforementioned inflammatory mediators down & CO2 up allowing the body to fully relax and avoid the stress of darkness.

A very high metabolic rate allows us to shutdown, sleep deeply, and awaken refreshed. This degree of sleep quality and energy production is possible throughout life if a thyroid supportive diet and lifestyle is utilized. Much of what people are being told to eat and supplement with unfortunately does not have this goal in mind.

“Many health food stores are now selling melatonin, to induce sleep and “prevent cancer.” They have taken some information out of context, and don’t realize how dangerous melatonin is. It makes the brain sluggish, causes the sex organs to shrink, and damages immunity by shrinking the thymus gland. It is the hormone of darkness and winter, and is produced in the pineal gland by any stress which increases adrenalin. Adequate sun light suppresses the formation of melatonin.” -Ray Peat, PhD

Melatonin is an anti-metabolic, inflammatory mediator, and body temperature lowering substance that rises in response to darkness. People often supplement with melatonin to improve sleep quality not knowing of the real effects of such a strategy.

Protective Diet and Lifestyle
If darkness is as a stressor, and melatonin’s rise along with other inflammatory markers occurs during the night which serve to suppress mitochondrial energy production, this modifies melatonin’s status as the “sleep hormone” into another part of a nocturnal inflammatory cascade.

Bright light therapy for seasonal affective disorder, the bipolar, and the depressed decreases melatonin and improves thyroid function lowering symptoms associated with each respective dysfunction. This type of therapy would be beneficial for anyone with a “light deficiency.” The reduction in trytophan rich foods (egg whites, muscle and organ meats, whey protein, some fruits), particularly later in the day, in favor of more gelatin rich proteins reduces the nocturnal formation of serotonin and melatonin resulting in better sleep quality and duration. This dietary strategy mimics the effect created by the bright light therapy.

Balanced blood sugar is key to good sleep as is the ability to store glycogen. The brain, liver, and muscle are the primary sites where sugar is stored as glycogen. A healthy person has upward of eight hours of stored glycogen available which is ideal for use when sleeping when blood sugar drops. The ability to store glycogen depends on the health of the metabolism. Fructose from ripe fruits encourages glycogen storage. The chronic stress and hypoglycemia that results from a low metabolism often leaves a person with depleted glycogen stores and less than optimal sleep quality and duration.

Milk/sugar/salt consumed before bed helps to improve sleep quality in many people from my experience. It does so by improving circulation, lowering aldosterone/cortisol/adrenaline, and helping balance blood sugar. If you awaken frequently during the night, this combination can help put you back to sleep as will a ripe fruit or glass of fruit juice. The anti-stress and thyroid-promoting effects of these recommendations improve sleep quality.

Here is a word from Ray Peat, PhD on what a metabolism-protective diet entails.

“This would emphasize high protein, low unsaturated fats, low iron, and high antioxidant consumption, with a moderate or low starch consumption. In practice, this means that a major part of the diet should be milk, cheese, eggs, shellfish, fruits and coconut oil, with vitamin E and salt as the safest supplements. It should be remembered that amino acids, especially in eggs, stimulate insulin secretion, and that this can cause hypoglycemia, which in turn causes cortisol secretion. Eating fruit (or other carbohydrate), coconut oil, and salt at the same meal will decrease this effect of the protein. Magnesium carbonate and epsom salts can also be useful and safe supplements, except when the synthetic material causes an allergic bowel reaction.” -Ray Peat, PhD

Anything that lowers the metabolic rate will affect sleep quality. A workout late in the day often disrupts sleep. Exercise suppresses metabolism, affects blood sugar, increases blood viscosity making clots more common, and raises stress hormones in a similar way that darkness does.

“Since the blood becomes more concentrated, viscous, and clottable during the night (especially during long winter nights), the risk of a heart attack or stroke would probably be reduced by drinking orange juice before getting out of bed (and at bed-time), to dilute the blood and decrease adrenaline and the free fatty acids, which contribute to the increased tendency to form clots in the morning.” -Ray Peat, PhD

Serotonin, PUFA, estrogen, lack of light exposure, chronic stress, and endotoxin are main players in lowering the metabolic rate because of the stress they create. The health of the liver is important in destroying endotoxin, PUFA, and estrogen and in maintenance of the metabolism. The liver requires protein, b-vitamins, thyroid, and sugar to function well. Regular elimination takes stress off of the liver and lowers serotonin, estrogen, and endotoxin.

Digestible foods should pervade the diet and be combined in a way that balances blood sugar – meals should should contain a carbohydrate source and a protein source. Protein intake from animal sources should be a minimum of 70g of protein daily. Carbohydrate intake should often be 1.5 to 2 time higher than protein intake to energize the body and blunt the stress response and the inflammatory, anti-mitochondria mediators that accompany it.

Consider avoidance of fluorescent lights and overnight shifts when possible and increase sun exposure or supplement with incandescent light during the winter or during times when sun exposure isn’t possible due to work or other commitments. Short bouts of summer sun or bright light supplementation (5 to 20 minutes) several times daily are beneficial to health, reduce the stress reaction associated with darkness, and limit chances of skin damage. Sunburn should be avoided.

Consult a medical professional regarding all things related to your health. FPS coaches a 12 to 16 week nutrition course based solely on the methodology of Ray Peat, PhD. Please click here for more information.

Resources
Barnes BO, Ratzenhofer M, Gisi R. The role of natural consequences in the changing death patterns. J Am Geriatr Soc. 1974 Apr;22(4):176-9.

“Aging Eyes, Infant Eyes, and Excitable Tissues” by Ray Peat, PhD

“Bleeding, clotting, cancer” by Ray Peat, PhD

“Regenerative Energy” by Ray Peat, PhD

Peat, R. (1996). Using Sunlight to Sustain Life. Townsend Letter for Doctors & Patients, (155)

“Hypothyroidism: The Unsuspected Illness” by Broda Barnes, MD and Lawrence Galton

“Type 2 Hypothyroidism” by Mark Starr, MD

Am J Psychiatry. 1976 Oct;133(10):1181-6.
Negative effects of melatonin on depression.
Carman JS, Post RM, Buswell R, Goodwin FK.

Eur J Endocrinol. 1995 Dec;133(6):691-5.
Melatonin enhances cortisol levels in aged but not young women.
Cagnacci A, Soldani R, Yen SS.

J Affect Disord. 2004 Apr;79(1-3):253-7.
Decreasing TSH levels in patients with Seasonal Affective Disorder (SAD) responding to 1 week of bright light therapy.
Martiny K, Simonsen C, Lunde M, Clemmensen L, Bech P.

J Affect Disord. 1999 Dec;56(2-3):195-9.
Free thyroxine and thyroid-stimulating hormone levels in patients with seasonal affective disorder and matched controls.
Sher L, Rosenthal NE, Wehr TA.

Psychoneuroendocrinology
Volume 17, Issues 2-3, May-July 1992, Pages 231-241
Clinical evidence for thyroid dysfunction in patients with seasonal affective disorder
Martin N. Raitiere

Journal of Psychiatric Research
Volume 24, Issue 2, 1990, Pages 129-137
Morning or night-time melatonin is ineffective in seasonal affective disorder
Anna Wirz-Justice Corresponding Author Contact Information, Peter Graw, Kurt Kräuchi, Beatrice Gisin, Josephine Arendt∗, Margaret Aldhous∗, Walter Pöldinger

Med Hypotheses. 2000 Jul;55(1):56-9.
The role of brain thyroid hormones in the mechanisms of seasonal changes in mood and behavior.
Sher L.

Harefuah. 2010 Aug;149(8):529-34, 550, 549.
The use of thyroid hormones in the treatment of depression
Cooper R, Lerer B.

J Clin Psychiatry. 1992 Jan;53(1):16-8.
T3 augmentation of antidepressant treatment in T4-replaced thyroid patients.

Panminerva Med. 2010 Dec;52(4):277-82.
Prevalence of depression in patients affected by subclinical hypothyroidism.
Demartini B, Masu A, Scarone S, Pontiroli AE, Gambini O.

Rev Bras Ginecol Obstet. 2010 Jul;32(7):321-6.
Depression and anxiety symptoms in hypothyroid women.
Andrade Junior NE, Pires ML, Thuler LC.

J Affect Disord. 2011 Jul;132(1-2):200-8. Epub 2011 Mar 23.
Seasonal symptoms in bipolar and primary care patients.
Simonsen H, Shand AJ, Scott NW, Eagles JM.

World J Biol Psychiatry. 2006;7(3):138-51.
Melatonin in mood disorders.
Srinivasan V, Smits M, Spence W, Lowe AD, Kayumov L, Pandi-Perumal SR, Parry B, Cardinali DP.

J Med Screen. 2010;17(3):121-4.
Effect of temperature changes on the occurrence of congenital hypothyroidism.
Aminzadeh M, Chomeili B, Riahi K, Dehdashtian M, Cheraghian B, Valavi E.

Arctic Med Res. 1995;54 Suppl 2:9-15.
Circannual changes in thyroid hormone physiology: the role of cold environmental temperatures.
Reed HL.

Comp Biochem Physiol A Comp Physiol. 1987;87(4):983-8.
Relationship between seasonal energy economy and thyroid activity in farm-raised raccoon dogs.
Korhonen H.

Thyroid. 2007 Sep;17(9):869-74.
Seasonality in the incidence of congenital hypothyroidism in Japan: gender-specific patterns and correlation with temperature.
Gu YH, Kato T, Harada S, Inomata H, Saito T, Aoki K.

Am J Physiol Endocrinol Metab. 2003 Jun;284(6):E1172-6. Epub 2003 Feb 25.
Acute cold exposure, leptin, and somatostatin analog (octreotide) modulate thyroid 5′-deiodinase activity.
Lisboa PC, Oliveira KJ, Cabanelas A, Ortiga-Carvalho TM, Pazos-Moura CC.

Int J Circumpolar Health. 2003 Sep;62(3):255-67.
Effect of the Antarctic environment on hormone levels and mood of Chinese expeditioners.
Xu C, Zhu G, Xue Q, Zhang S, Du G, Xi Y, Palinkas LA.

Int J Circumpolar Health. 1998;57 Suppl 1:383-5.
Seasonal variation of serum TSH and thyroid hormones in males living in subarctic environmental conditions.
Leppäluoto J, Sikkilä K, Hassi J.

J Appl Physiol. 1990 Oct;69(4):1467-72.
Decreased free fraction of thyroid hormones after prolonged Antarctic residence.
Reed HL, Brice D, Shakir KM, Burman KD, D’Alesandro MM, O’Brian JT.

J Clin Endocrinol Metab. 2001 Jan;86(1):110-6.
Impairment in cognitive and exercise performance during prolonged antarctic residence: effect of thyroxine supplementation in the polar triiodothyronine syndrome.
Reed HL, Reedy KR, Palinkas LA, Van Do N, Finney NS, Case HS, LeMar HJ, Wright J, Thomas J.

Comp Biochem Physiol A Mol Integr Physiol. 2007 Aug;147(4):863-7. Epub 2007 Feb 21.
Seasonal and diurnal melatonin production in exercising sled dogs.
Dunlap KL, Reynolds AJ, Tosini G, Kerr WW, Duffy LK.

Horm Metab Res. 2005 Sep;37(9):555-8.
Iodine uptake and loss-can frequent strenuous exercise induce iodine deficiency?
Smyth PP, Duntas LH.

Soc Psychiatry Psychiatr Epidemiol. 1998 May;33(5):211-7.
Seasonal variations in hospital admissions for affective disorders by gender and ethnicity.
Suhail K, Cochrane R.

Biol Psychiatry. 1994 Jan 1;35(1):36-41.
Lack of seasonal variation in abnormal TSH secretion in patients with seasonal affective disorder.
Coiro V, Volpi R, Marchesi C, De Ferri A, d’Amato L, Caffarri G, Davolio M, Rossi E, Caffarra P, Chiodera P.

J Clin Endocrinol Metab. 1990 Sep;71(3):650-5.
Nocturnal serum thyrotropin (TSH) surge and the TSH response to TSH-releasing hormone: dissociated behavior in untreated depressives.
Bartalena L, Placidi GF, Martino E, Falcone M, Pellegrini L, Dell’Osso L, Pacchiarotti A, Pinchera A.

J Psychiatr Res. 1994 Mar-Apr;28(2):135-45.
Mood and behavioral effects of four-week light treatment in winter depressives and controls.
Bauer MS, Kurtz JW, Rubin LB, Marcus JG.

J Affect Disord. 1994 Jan;30(1):47-56.
Effects of morning light treatment on subjective sleepiness and mood in winter depression.
Partonen T.

Arch Gen Psychiatry. 1998 Oct;55(10):883-9.
Bright light treatment of winter depression: a placebo-controlled trial.
Eastman CI, Young MA, Fogg LF, Liu L, Meaden PM.

Arch Gen Psychiatry. 1998 Oct;55(10):890-6.
Morning vs evening light treatment of patients with winter depression.
Lewy AJ, Bauer VK, Cutler NL, Sack RL, Ahmed S, Thomas KH, Blood ML, Jackson JM.

Biol Psychiatry. 1996 Nov 1;40(9):899-907.
Serum concentrations of thyroid hormones in patients with nonseasonal affective disorders during treatment with bright and dim light.
Baumgartner A, Volz HP, Campos-Barros A, Stieglitz RD, Mansmann U, Mackert A.

Biol Psychiatry. 1992 Jan 15;31(2):119-34.
Controlled trial of bright light for nonseasonal major depressive disorders.
Kripke DF, Mullaney DJ, Klauber MR, Risch SC, Gillin JC.

J Affect Disord. 1989 Mar-Jun;16(2-3):121-5.
Phototherapy increases platelet 3H-imipramine binding in patients with winter depression.
Szádóczky E, Falus A, Arató M, Németh A, Teszéri G, Moussong-Kovács E.

J Affect Disord. 1991 Aug;22(4):179-84.
Effect of phototherapy on 3H-imipramine binding sites in patients with SAD, non-SAD and in healthy controls.
Szádóczky E, Falus A, Németh A, Teszéri G, Moussong-Kovács E.

Biull Eksp Biol Med. 1984 Apr;97(4):420-3.
Seasonal structural and functional changes in the rabbit heart.

Posted in General.

Tagged with , , , , , , , , , , , , , , , , , , , , , , , , , , , , .

rev="post-2906" 6 comments

By Team FPS – September 30, 2011

Low Blood Cholesterol Compromises Immune Function

Also see:
High Cholesterol and Metabolism
The Truth about Low Cholesterol
Thyroid Status and Oxidized LDL
Inflammatory TSH
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
Thyroid Status and Cardiovascular Disease
The Cholesterol and Thyroid Connection
High Blood Pressure and Hypothyroidism
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns

by Barry Groves
http://www.second-opinions.co.uk/immunity3.html

There is a substantial amount of evidence that relatively low cholesterol levels in apparently healthy individuals is associated with increased subsequent mortality from cancer. It is also associated with other, non-heart related deaths. A group at the Center for Clinical Pharmacology, University of Pittsburgh, Pennsylvania, tested whether the effectiveness of their immune systems differed in individuals with high and low levels of blood cholesterol.[i] The low cholesterol group’s cholesterol averaged 3.9 mmol/L (151 mg/dL); the high cholesterol group averaged 6.8 mmol/L (261 mg/dL). The immune systems of the men in the low cholesterol group were significantly less effective than those of the high cholesterol group. This finding was not surprising as several studies have shown that cholesterol is necessary for the proper functioning of blood cells — macrophages and lymphocytes — that form part of our immune systems. For this reason low blood cholesterol undoubtedly adversely affects our bodies’ ability to fight infection. This could well be another reason why infectious diseases are becoming more prevalent in our society.

Tuberculosis (TB), a disease thought to have been conquered decades ago, is returning. It has been noticed that low levels of cholesterol are common in patients suffering from TB. TB patients with low cholesterol also have higher death rates, particularly those cases with small (military) nodules. A hospital for respiratory diseases tested whether giving TB patients high-cholesterol meals would be effective in treating their condition.[ii] They split patients into two groups. One had meals containing 800 mg of cholesterol per day; the other had 250 mg of cholesterol per day. The trial was a success. By the second week, the numbers of TB bacteria in sputum was reduced 80% in the high-cholesterol group; it was only reduced by 9% in the low-cholesterol group. High-cholesterol diets now form part of the treatment for TB.

Low cholesterol is also linked to increased susceptibility to infection, including development of postoperative infection,[iii] and it predicts death and adverse outcomes in hospitalised patients.[iv] While some of this could be due to illness causing lower cholesterol, it may also be that low cholesterol contributes to illness; indeed, animal studies suggest lipoproteins may serve to protect against bacterial infection-induced death.[v]

It has been suggested in cases of critical surgical illness that a low cholesterol level is more likely to lead to the development of organ failure and death.

A study of patients undergoing surgery for gastrointestinal diseases at the Universita di L’Aquila in Italy, found that ‘Hypocholesterolemia [low blood cholesterol] seems to represent a significant predictive factor of morbidity and mortality in critically ill patients.'[vi] Of the patients studied, 35.1% contracted a postoperative infection. The highest incidence of postoperative septic complications (72.7%) was encountered in patients withcholesterol levels below 2.73 mmol/L (105 mg/dl). The authors say ‘The results of this study seem to indicate a significant relationship between preoperative hypocholesterolemia and the incidence of septic complications after surgery. Moreover, evaluation of bloodcholesterol levels before major surgery might represent a predictive factor of septic risk in the postoperative period.’

Low cholesterol levels have also been associated clinically with the development of hospital infections. A study conducted at the Department of Surgery, Weill Medical College of Cornell University, New York, set out to verify this. They found that lower levels of total cholesterol, and of LDL and HDL occurred early in the course of critical illness; this led to the development of a hospital infection; and with or without the infection, lower cholesterol was independently associated with a higher death rate.[vii] The authors conclude: ‘Decreased serum cholesterol concentration is an independent predictor of mortality in critically ill surgical patients. Repletion of serum lipids is a feasible therapeutic approach for the management of critical illness.’

Many patients in hospitals have or acquire infections during or after major abdominal surgery. The Department of Surgery at the CatholicUniversity, Rome, Italy, conducted a study to identify factors that influenced mortality in patients who are affected by such infections.[viii] The hospital records of patients who had had a variety of abdominal operations and who had acquired an infection such as peritonitis were reviewed. Checking deaths against a battery of blood measurements, the authors of thestudy found that low cholesterol levels and low protein levels were both ‘strongly and independently associated with the outcome’.

Professor Uffe Ravnskov would not be at all surprised. He found that: ‘There is much evidence that blood lipids play a key role in the immune defence system. Bacterial endotoxin and Staphylococcus aureus a-toxin bind rapidly to and become inactivated by low-density-lipoprotein (LDL).'[ix] (Staphylococcus aureus is what the ‘SA’ in MRSA stands for.) Ravnskov also pointed out that ‘Total cholesterol is inversely associated with mortality caused by respiratory and digestive disease, the aetiologies of which are mostly infectious.Total cholesterol is also inversely associated with the risk of being admitted to hospital because of an infectious disease.’ In other words, if you have low cholesterol, you are more likely to end up in hospital and more likely to contract an infection while there.

References

[i]. Muldoon MF, Marsland A, Flory JD, et al. Immune system differences in men with hypo- or hypercholesterolemia. Clin Immunol Immunopathol 1997; 84: 145-9.

[ii]. Perez-Guzman C, Vargas, MH, Quinonez, F, et al. A Cholesterol-Rich Diet Accelerates Bacteriologic Sterilization in Pulmonary Tuberculosis. Chest 2005; 127: 643-651.

[iii]. Leardi S, Altilia F, Delmonaco S, et al. Blood levels of cholesterol and postoperative septic complications. Ann Ital Chir 2001; 71: 233-237.

[iv]. Crook MA, Velauthar U, Moran L, Griffiths W. Hypocholesterolaemia in a hospital population. Ann Clin Biochem 1999; 36: 613-616.

[v]. Read TE, Harris HW, Grunfeld C, et al. The protective effect of serum lipoproteins against bacterial lipopolysaccharide. Eur Heart J 1993; 14(suppl K): 125-129.

[vi]. Leardi S, Altilia F, Delmonaco S, et al. Op cit.

[vii]. Bonville DA, Parker TS, Levine DM, et al. The relationships of hypocholesterolemia to cytokine concentrations and mortality in critically ill patients with systemic inflammatory response syndrome. Surg Infect (Larchmt). 2004; 5: 39-49.

[viii]. Pacelli F, Doglietto GB, Alfieri S, et al. Prognosis in intra-abdominal infections. Multivariate analysis on 604 patients. Arch Surg 1996; 131: 641-5.

[ix]. Uffe Ravnskov. High Cholesterol May Protect Against Infections and Atherosclerosis. Quart J Med 2003; 96: 927-34.

Posted in General.

Tagged with , , , , , , , , , , , .

Comments Off on Low Blood Cholesterol Compromises Immune Function

By Team FPS – September 22, 2011