Wednesday, February 8, 2012
The Inadvertent and Continuous Exposure of Fetuses to Environmentally Active Chemicals
There is a third type of exposure that needs to be addressed: the inadvertent and continuous exposure of fetuses to environmentally active chemicals, such as dioxins and BPA.
The U.S. EPA has established the safe daily intake of BPA to be 50 μg/kg body weight/d based on the assumption that the main source of exposure is oral through food ingestion. However, recent publications suggest that food is not the only relevant source of exposure and that the half-life of BPA in humans is longer than expected (6). Numerous publications addressing fetal exposures to BPA have used parenteral administration. This practice was based on one hand on the fact that the fetus is exposed to BPA through the internal milieu of the mother, and on the other hand that parenteral administration via an osmotic minipump allows for a precise and constant level of exposure. Using this route of administration, exposure of a pregnant mouse dam to 25 and 250 ng BPA/kg body weight/d (namely, 2000 and 200 times lower than the safe dose) for 14 d beginning on d 8 gestation has been shown to impact certain aspects of development in their female offspring. When examined on gestational d 18, fetuses of mothers exposed to the higher dose of BPA exhibited altered growth parameters of the mammary gland anlagen. Changes in the appearance of the mammary epithelium were observed, such as decreased cell size and delayed lumen formation, as well as increased ductal area. In the stroma, BPA exposure promoted advanced maturation of the fat pad and altered localization of fibrous collagen (128). Because maturation of the fat pad is the driving event for ductal growth and branching, it is likely that the increased ductal area in BPA-exposed animals is due to the accelerated formation of their fat pads. By postnatal d 10, in the offspring born to mothers exposed to either dose of BPA, the percentage of proliferating epithelial cells was significantly decreased relative to those not exposed. At 30 d of age, the area and number of terminal end buds relative to the gland ductal area increased, whereas cell death in these structures decreased in BPA-exposed offspring compared with controls. It is likely that the reduced cell death in the terminal end buds of BPA-exposed females may be the cause of the observed ductal growth delay because cell death is essential for both the hollowing and the outward growth of the subtending duct. Collectively, these effects observed at puberty may be attributed to an increased sensitivity to estradiol that has been observed in the BPA-exposed animals (145). Because of the new epidemiological data cited above and the effects found in the low-dose animal studies using parenteral exposure, the EPA recommendations need to be reevaluated.
In animals exposed perinatally to BPA, there was also a significant increase of ductal epithelial cells that were positive for progesterone receptor at puberty. These positive cells were localized in clusters, suggesting future branching points. Indeed, lateral branching was significantly enhanced at 4 months of age in offspring born to mothers exposed to 25 ng BPA/kg body weight/d (145). These results are compatible with the notion that increased sensitivity to estrogens drives the induction of progesterone receptors in epithelial cells, leading to an increase in lateral branching. By 6 months of age, perinatally exposed virgin mice exhibit mammary glands that resemble those of a pregnant mouse, as reflected by a significant increase in the percentage of ducts, terminal ends, terminal ducts, and alveolar buds (146). Additionally, intraductal hyperplasias, which are considered preneoplastic lesions, were observed starting at 3 months of age (147).
To explore the links between prenatal BPA exposure and mammary gland neoplasia, a rat model was chosen because it closely resembles the human disease regarding estrogen dependency and histopathology. BPA was administered to pregnant dams at doses of 2.5, 25, 250, and 1000 μg/kg body weight/d. Fetal exposure to BPA, from gestational d 9 to postnatal d 1, resulted in the development of carcinomas in situ in the mammary glands of 33% of the rats exposed to 250 μg/kg body weight/d, whereas none of the unexposed animals developed neoplasias (148). These cancers were only observed after the animals had reached young adult age. Fetal exposure to BPA significantly increased the number of precancerous lesions (intraductal proliferation) by three to four times, an effect also observed in puberty and during adult life. The lesions observed in the BPA-exposed animals were highly proliferative and contained abundant ER-positive cells, suggesting that the proliferative activity in these lesions may be estrogen mediated. Comparable preneoplastic lesions were found in a study using a different rat strain (149). Additionally, this study found stromal alterations such as desmoplasia and mast cell invasion; these features are often observed during neoplastic development. Moreover, when challenged with a subcarcinogenic dose of nitrosomethylurea, only the BPA-exposed animals developed palpable tumors (carcinomas). The period of vulnerability of the mammary gland to BPA does not cease at the neonatal stage. BPA exposure during lactation followed to exposure to the carcinogen DMBA resulted in mammary tumor multiplicity and reduced tumor latency compared with control animals (exposed solely to DMBA) (150). These results indicate that perinatal exposure to environmentally relevant doses of BPA results in persistent alterations in mammary gland morphogenesis, development of precancerous lesions, and carcinoma in situ. Moreover, the altered growth parameters noted in the developing mammary gland on embryonic d 18 suggest that the fetal gland is a direct target of BPA, and that these alterations cause the mammary gland phenotypes observed in perinatally exposed mice at puberty and adulthood.
Don
Dioxins
Depending on the context (time of exposure, organ, presence or absence of estrogens) dioxins have either estrogenic or antiestrogenic effects. Despite cross-talk between the aryl hydrocarbon and ERs (139), the mechanisms underlying these opposite effects have yet to be elucidated. Rats exposed prenatally (gestational d 15) to TCDD and challenged with the chemical carcinogen DMBA at 50 d of age showed increased tumor incidence, increased number of tumors per animal, and shorter latency period than rats exposed prenatally to vehicle and to DMBA at 50 d of age. These TCDD-exposed animals had increased numbers of terminal end buds at puberty (140). Because these structures are believed to be the site where mammary cancer arises, these results were interpreted as evidence that TCDD increased the propensity to cancer by altering mammary gland morphogenesis. Interestingly, Fenton (31) showed that prenatal exposure to TCDD results in impaired development of terminal end buds that remain in the gland for prolonged periods, whereas in the normal animals terminal end buds are transient structures that regress when ductal development is completed.
BPA, a ubiquitous xenoestrogen
The ubiquitous use of BPA provides great potential for exposure of both the developing fetus, indirectly through maternal exposure, and the neonate, directly through ingestion of tinned food, infant formula, or maternal milk (11). Indeed, BPA has been measured in maternal and fetal plasma and placental tissue at birth in humans (141). A recently published study conducted by the Centers for Disease Control, the first using a reference human population, showed that 92.6% of over 2500 Americans had BPA in their urine (142). Measured urine concentrations were significantly higher in children and adolescents compared with adults. BPA has also been measured in the milk of lactating mothers. These data indicate that the developing human fetus and neonate are readily exposed to this chemical.
In rodents, BPA has been shown to readily cross the placenta (143, 144) and bind α-fetoprotein (the estrogen-binding protein that prevents maternal estrogen from entering the circulation of the fetus) with negligible affinity relative to estradiol; this results in enhanced bioavailability during neonatal development. BPA is present in the mouse fetus and amniotic fluid during maternal exposure in higher concentrations than that of maternal blood. The U.S. EPA has established the safe daily intake of BPA to be 50 μg/kg body weight/d based on the assumption that the main source of exposure is oral through food ingestion. However, recent publications suggest that food is not the only relevant source of exposure and that the half-life of BPA in humans is longer than expected (6). Numerous publications addressing fetal exposures to BPA have used parenteral administration. This practice was based on one hand on the fact that the fetus is exposed to BPA through the internal milieu of the mother, and on the other hand that parenteral administration via an osmotic minipump allows for a precise and constant level of exposure. Using this route of administration, exposure of a pregnant mouse dam to 25 and 250 ng BPA/kg body weight/d (namely, 2000 and 200 times lower than the safe dose) for 14 d beginning on d 8 gestation has been shown to impact certain aspects of development in their female offspring. When examined on gestational d 18, fetuses of mothers exposed to the higher dose of BPA exhibited altered growth parameters of the mammary gland anlagen. Changes in the appearance of the mammary epithelium were observed, such as decreased cell size and delayed lumen formation, as well as increased ductal area. In the stroma, BPA exposure promoted advanced maturation of the fat pad and altered localization of fibrous collagen (128). Because maturation of the fat pad is the driving event for ductal growth and branching, it is likely that the increased ductal area in BPA-exposed animals is due to the accelerated formation of their fat pads. By postnatal d 10, in the offspring born to mothers exposed to either dose of BPA, the percentage of proliferating epithelial cells was significantly decreased relative to those not exposed. At 30 d of age, the area and number of terminal end buds relative to the gland ductal area increased, whereas cell death in these structures decreased in BPA-exposed offspring compared with controls. It is likely that the reduced cell death in the terminal end buds of BPA-exposed females may be the cause of the observed ductal growth delay because cell death is essential for both the hollowing and the outward growth of the subtending duct. Collectively, these effects observed at puberty may be attributed to an increased sensitivity to estradiol that has been observed in the BPA-exposed animals (145). Because of the new epidemiological data cited above and the effects found in the low-dose animal studies using parenteral exposure, the EPA recommendations need to be reevaluated.
In animals exposed perinatally to BPA, there was also a significant increase of ductal epithelial cells that were positive for progesterone receptor at puberty. These positive cells were localized in clusters, suggesting future branching points. Indeed, lateral branching was significantly enhanced at 4 months of age in offspring born to mothers exposed to 25 ng BPA/kg body weight/d (145). These results are compatible with the notion that increased sensitivity to estrogens drives the induction of progesterone receptors in epithelial cells, leading to an increase in lateral branching. By 6 months of age, perinatally exposed virgin mice exhibit mammary glands that resemble those of a pregnant mouse, as reflected by a significant increase in the percentage of ducts, terminal ends, terminal ducts, and alveolar buds (146). Additionally, intraductal hyperplasias, which are considered preneoplastic lesions, were observed starting at 3 months of age (147).
To explore the links between prenatal BPA exposure and mammary gland neoplasia, a rat model was chosen because it closely resembles the human disease regarding estrogen dependency and histopathology. BPA was administered to pregnant dams at doses of 2.5, 25, 250, and 1000 μg/kg body weight/d. Fetal exposure to BPA, from gestational d 9 to postnatal d 1, resulted in the development of carcinomas in situ in the mammary glands of 33% of the rats exposed to 250 μg/kg body weight/d, whereas none of the unexposed animals developed neoplasias (148). These cancers were only observed after the animals had reached young adult age. Fetal exposure to BPA significantly increased the number of precancerous lesions (intraductal proliferation) by three to four times, an effect also observed in puberty and during adult life. The lesions observed in the BPA-exposed animals were highly proliferative and contained abundant ER-positive cells, suggesting that the proliferative activity in these lesions may be estrogen mediated. Comparable preneoplastic lesions were found in a study using a different rat strain (149). Additionally, this study found stromal alterations such as desmoplasia and mast cell invasion; these features are often observed during neoplastic development. Moreover, when challenged with a subcarcinogenic dose of nitrosomethylurea, only the BPA-exposed animals developed palpable tumors (carcinomas). The period of vulnerability of the mammary gland to BPA does not cease at the neonatal stage. BPA exposure during lactation followed to exposure to the carcinogen DMBA resulted in mammary tumor multiplicity and reduced tumor latency compared with control animals (exposed solely to DMBA) (150). These results indicate that perinatal exposure to environmentally relevant doses of BPA results in persistent alterations in mammary gland morphogenesis, development of precancerous lesions, and carcinoma in situ. Moreover, the altered growth parameters noted in the developing mammary gland on embryonic d 18 suggest that the fetal gland is a direct target of BPA, and that these alterations cause the mammary gland phenotypes observed in perinatally exposed mice at puberty and adulthood.
In summary, exposure to estrogens throughout a woman’s life, including the period of intrauterine development, is a risk factor for the development of breast cancer. The increased incidence of breast cancer noted during the last 50 yr may have been caused, in part, by exposure of women to estrogen-mimicking chemicals that have been released into the environment from industrial and commercial sources. Epidemiological studies suggest that exposure to xenoestrogens such as DES during fetal development, to DDT around puberty, and to a mixture of xenoestrogens around menopause increases this risk. Animal studies show that exposure in utero to the xenoestrogen BPA increases this risk. Moreover, these animal studies suggest that estrogens act as morphogens and that excessive perinatal exposure results in structural and functional alterations that are further exacerbated by exposure to ovarian steroids at puberty and beyond. These altered structures include preneoplastic lesions, such as intraductal hyperplasias, and carcinomas in situ. Additionally, these mammary glands are more vulnerable than their normal counterparts to carcinogenic stimuli. Exposures to other endocrine disruptors that are not estrogenic, such as dioxins, were reported to increase breast cancer incidence in humans and to alter mammary gland development in animal models. Collectively, these data support the notion that endocrine disruptors alter mammary gland morphogenesis and that the resulting dysgenic gland becomes more prone to neoplastic development.
Source: http://edrv.endojournals.org/content/30/4/293.fullDon
Endocrine Disruptors - What are they?
The group of molecules identified as endocrine disruptors is highly heterogeneous and includes synthetic chemicals used as industrial solvents/lubricants and their byproducts [polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), dioxins], plastics [bisphenol A (BPA)], plasticizers (phthalates), pesticides [methoxychlor, chlorpyrifos, dichlorodiphenyltrichloroethane (DDT)], fungicides (vinclozolin), and pharmaceutical agents [diethylstilbestrol (DES)].
It is difficult to predict whether a compound may or may not exert endocrine-disrupting actions. Nevertheless, in very broad terms, EDCs such as dioxins, PCBs, PBBs, and pesticides often contain halogen group substitutions by chlorine and bromine. They often have a phenolic moiety that is thought to mimic natural steroid hormones and enable EDCs to interact with steroid hormone receptors as analogs or antagonists. Even heavy metals and metalloids may have estrogenic activity, suggesting that these compounds are EDCs as well as more generalized toxicants. Several classes of EDCs act as antiandrogens and as thyroid hormone receptor agonists or antagonists, and more recently, androgenic EDCs have been identified.
Exposure occurs through drinking contaminated water, breathing contaminated air, ingesting food, or contacting contaminated soil.
Source: http://edrv.endojournals.org/content/30/4/293.full
Natural chemicals found in human and animal food (e.g., phytoestrogens, including genistein and coumestrol) can also act as endocrine disruptors. These substances, whereas generally thought to have relatively low binding affinity to ERs, are widely consumed and are components of infant formula (1, 2). A recent study reported that urinary concentrations of the phytoestrogens genistein and daidzein were about 500-fold higher in infants fed soy formula compared with those fed cow’s milk formula (3). Therefore, the potential for endocrine disruption by phytoestrogens needs to be considered.
It is difficult to predict whether a compound may or may not exert endocrine-disrupting actions. Nevertheless, in very broad terms, EDCs such as dioxins, PCBs, PBBs, and pesticides often contain halogen group substitutions by chlorine and bromine. They often have a phenolic moiety that is thought to mimic natural steroid hormones and enable EDCs to interact with steroid hormone receptors as analogs or antagonists. Even heavy metals and metalloids may have estrogenic activity, suggesting that these compounds are EDCs as well as more generalized toxicants. Several classes of EDCs act as antiandrogens and as thyroid hormone receptor agonists or antagonists, and more recently, androgenic EDCs have been identified.
Exposure occurs through drinking contaminated water, breathing contaminated air, ingesting food, or contacting contaminated soil.
Source: http://edrv.endojournals.org/content/30/4/293.full
Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement
If this doesn't one thinking about what's going in their body or the need to do a purification program yearly read again!
Review: Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement (2009)
Abstract
There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use. We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.
Outline of what is covered in the position statement:
I. General Introduction to Endocrine Disruption
Don
Review: Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement (2009)
Abstract
There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use. We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.
Outline of what is covered in the position statement:
I. General Introduction to Endocrine Disruption
- A. Important issues in endocrine disruption
- B. The role of endocrinologists in discerning effects of EDCs
- A. Clinical aspects of endocrine disruption in humans
- B. Clinical dimorphism of EDCs on male and female reproduction
- C. Experimental and clinical evidence of EDCs and potential mechanisms
- A. Introduction to female reproductive development and function
- B. Polycystic ovarian syndrome (PCOS)
- C. Premature ovarian failure, decreased ovarian reserve, aneuploidy, and granulosa steroidogenesis
- D. Reproductive tract anomalies
- E. Uterine leiomyomas
- F. Endometriosis
- A. Windows of vulnerability to carcinogenic agents and “natural” risk factors
- B. Theories of carcinogenesis
- C. Susceptibility of the breast during puberty and adulthood
- D. Susceptibility of the mammary gland during the perinatal period
- E. Perinatal exposure to environmentally relevant levels of endocrine disruptors
- A. Introduction to male reproductive health
- B. Male reproductive function and development
- C. Semen quality: temporal trends and EDC exposure
- D. Male urogenital tract malformations
- E. Testicular germ cell cancer
- F. Conclusions
- A. Introduction to prostate cancer
- B. Evidence and mechanisms for EDC effects on the prostate
- A. Endocrine disruption of reproductive neuroendocrine systems
- B. Hypothalamic-pituitary-adrenal (HPA) effects of EDCs
- C. Thyroid, metabolism, and growth
- D. Hormonal targets of neuroendocrine disruption
- A. Introduction to thyroid systems
- B. Environmental chemicals impacting thyroid function
- C. Environmental chemicals impacting thyroid hormone transport, metabolism, and clearance
- D. Environmental chemicals impacting the thyroid hormone receptor
- A. Introduction to EDCs and the obesity epidemic
- B. Environmental estrogens and obesity
- C. Peroxisome proliferator-activated receptor (PPAR) γ and organotins
- D. Phytoestrogens
- E. Endocrine disruptors, diabetes, and glucose homeostasis
- F. Endocrine disruptors and cardiovascular systems
- G. Estrogenic EDCs and cardioprotection
- H. Advanced glycation end-products (AGEs)
- I. Conclusions
Don
Sunday, January 29, 2012
Commercial vs Whole Food Vitamin
Multivitamins
There has never been a single study, out of all that have been done, that shows the American public comes remotely close to consuming the minimum requirements for vitamins and minerals in their daily diet. Disease prevention and health enhancement in the United States appear to be possible only through supplementation.
Studies due indicate levels of malnutrition. Doctors have reported to me from the University of California Medical Center their disbelief at finding scurvy (Vitamin-C deficiency disease) in their patients. Meanwhile, agricultural departments, such as at the University of Texas, are finding the nutritional levels of food are lower than ever historically, with a steady significant decline from the early 1900s up to the present.
Better Health Through Better Nutrition
The most recent in-depth study on multiple nutrients recognizes how difficult it is to generalize. (See Block G, Jensen CD, Nordus EP, Dalvi TB, Wong LG, McManus JF and Hudes ML, "Usage Patterns, Health and Nutritional Status of Long-term Multiple Dietary Supplement Users," a cross-sectional study that was published in the October 24, 2007 issue of Nutritional Journal.) The study nevertheless could make some statistical statements based upon the 278 long-term users of multiple dietary supplements, 176 users of a single multivitamin/multimineral supplement, and 602 nonusers of supplements whom the scientists studied.
At least half of the subjects in the multiple dietary-supplements group consumed a multivitamin/mineral, B-complex, Vitamin C, carotenoids, Vitamin E, calcium with Vitamin D, omega-3 fatty acids, flavonoids, lecithin, alfalfa, Coenzyme Q10 with resveratrol, glucosamine, and an herbal immune supplement.
The majority of women in this group also consumed gamma linolenic acid and a probiotic supplement. The majority of men additionally consumed zinc, garlic, saw palmetto, and a protein supplement.
Overall, the study showed that the use of multiple dietary supplements led to better health. As the researchers themselves said, individuals who consume a number of nutritional supplements were found to have better biomarkers of health than those who do not consume any supplements or who only consumed a multivitamin/mineral.
Among other benefits, multiple-supplement users also had lower levels of C-reactive protein and triglycerides and higher levels of HDL (the so-called "good") cholesterol. Other findings in the multiple supplements group included lower risks of elevated blood pressure, diabetes (73% less compared to nonusers), and coronary heart disease (52% less compared to nonusers). Subjects consuming multiple dietary supplements also reported having "good or excellent" health status 74 percent more often than non-supplement users.
Other corollary findings included the discovery of various nutrient deficiencies in both the non-supplement users and the multivitamin/mineral users, especially with low levels of Vitamin C. Far from being a danger to health as the mass media would have us believe, using multiple nutritional supplements confers various health benefits that merit further study, not blind condemnation.
Source: http://vitaminsinamerica.com/2009/03/
Selecting a Multivitamin
Additives and Quality
Often overlooked by consumers who see generic vitamin names on multivitamin labels and rarely look beyond, additives and quality are nevertheless of paramount importance. And it is here where the two types of multivitamins have important differences.
Just consider one of the top-selling multiples in the marketplace, which happens to be a drug-store multiple supplement for seniors. It is highly endorsed by both MDs and pharmacists. First, let's look at its excipients (the extra chemicals needed to make the tablet, complete the filling of the capsule, or added for some other unknowable reason):
Polyethylene Glycol, Polyvinyl Alcohol, Pregelatinized Corn Starch, Sodium Benzoate, Sucrose, Talc, Maltodextrin, Calcium Stearate, Sodium Aluminosilicate, Sunflower Oil, Colloidal Silicon Dioxide, Corn Starch, Crospovidone, FD&C Blue No. 2 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, Gelatin, Hydrogenated Palm Oil, Hypromellose, and Modified Food Starch.
Let's now look at a health-food based multivitamin and see the difference.
Catalyn by Standard Process
Proprietary Blend: 766 mg
Defatted wheat (germ), carrot (root), calcium lactate, nutritional yeast, bovine adrenal, bovine liver, magnesium citrate, bovine spleen, ovine spleen, bovine kidney, dried pea (vine) juice, dried alfalfa (whole plant) juice, mushroom, oat flour, soybean lecithin, and rice (bran).
Other Ingredients:
Honey, glycerin, arabic gum, ascorbic acid, calcium stearate, cholecalciferol, pyridoxine hydrochloride, starch, sucrose (beets), vitamin A palmitate, cocarboxylase, and riboflavin.
What Makes Catalyn Unique
Product Attributes: Whole food multivitamin.The nutrients in Catalyn are processed to remain intact, complete nutritional compounds. Contains important vitamins, minerals, enzymes, and trace minerals in combination with their naturally occurring synergistic cofactors. Combines vital nutrients from a wide variety of plant sources to introduce a unique diversity of complete vitamin and mineral complexes (Phytonutrients).
Phytonutrients (Phytochemicals):
Phytonutrients are the important nutrients found in plants that are necessary to maintain a healthy body. They may serve as antioxidants; support a healthy immune response; and support cell-to-cell communication. There are many phytonutrients that have been identified, while their possible functions/actions have yet to be discovered. Some of the best known phytochemicals are the carotenoids, like alpha- and beta-carotene and lycopene. At Standard Process, our multivitamins are packed with health-promoting phytonutrients, which ensure maximum efficacy.
Don
There has never been a single study, out of all that have been done, that shows the American public comes remotely close to consuming the minimum requirements for vitamins and minerals in their daily diet. Disease prevention and health enhancement in the United States appear to be possible only through supplementation.
Studies due indicate levels of malnutrition. Doctors have reported to me from the University of California Medical Center their disbelief at finding scurvy (Vitamin-C deficiency disease) in their patients. Meanwhile, agricultural departments, such as at the University of Texas, are finding the nutritional levels of food are lower than ever historically, with a steady significant decline from the early 1900s up to the present.
Better Health Through Better Nutrition
The most recent in-depth study on multiple nutrients recognizes how difficult it is to generalize. (See Block G, Jensen CD, Nordus EP, Dalvi TB, Wong LG, McManus JF and Hudes ML, "Usage Patterns, Health and Nutritional Status of Long-term Multiple Dietary Supplement Users," a cross-sectional study that was published in the October 24, 2007 issue of Nutritional Journal.) The study nevertheless could make some statistical statements based upon the 278 long-term users of multiple dietary supplements, 176 users of a single multivitamin/multimineral supplement, and 602 nonusers of supplements whom the scientists studied.
At least half of the subjects in the multiple dietary-supplements group consumed a multivitamin/mineral, B-complex, Vitamin C, carotenoids, Vitamin E, calcium with Vitamin D, omega-3 fatty acids, flavonoids, lecithin, alfalfa, Coenzyme Q10 with resveratrol, glucosamine, and an herbal immune supplement.
The majority of women in this group also consumed gamma linolenic acid and a probiotic supplement. The majority of men additionally consumed zinc, garlic, saw palmetto, and a protein supplement.
Overall, the study showed that the use of multiple dietary supplements led to better health. As the researchers themselves said, individuals who consume a number of nutritional supplements were found to have better biomarkers of health than those who do not consume any supplements or who only consumed a multivitamin/mineral.
Among other benefits, multiple-supplement users also had lower levels of C-reactive protein and triglycerides and higher levels of HDL (the so-called "good") cholesterol. Other findings in the multiple supplements group included lower risks of elevated blood pressure, diabetes (73% less compared to nonusers), and coronary heart disease (52% less compared to nonusers). Subjects consuming multiple dietary supplements also reported having "good or excellent" health status 74 percent more often than non-supplement users.
Other corollary findings included the discovery of various nutrient deficiencies in both the non-supplement users and the multivitamin/mineral users, especially with low levels of Vitamin C. Far from being a danger to health as the mass media would have us believe, using multiple nutritional supplements confers various health benefits that merit further study, not blind condemnation.
Source: http://vitaminsinamerica.com/2009/03/
Selecting a Multivitamin
Additives and Quality
Often overlooked by consumers who see generic vitamin names on multivitamin labels and rarely look beyond, additives and quality are nevertheless of paramount importance. And it is here where the two types of multivitamins have important differences.
Just consider one of the top-selling multiples in the marketplace, which happens to be a drug-store multiple supplement for seniors. It is highly endorsed by both MDs and pharmacists. First, let's look at its excipients (the extra chemicals needed to make the tablet, complete the filling of the capsule, or added for some other unknowable reason):
Polyethylene Glycol, Polyvinyl Alcohol, Pregelatinized Corn Starch, Sodium Benzoate, Sucrose, Talc, Maltodextrin, Calcium Stearate, Sodium Aluminosilicate, Sunflower Oil, Colloidal Silicon Dioxide, Corn Starch, Crospovidone, FD&C Blue No. 2 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, Gelatin, Hydrogenated Palm Oil, Hypromellose, and Modified Food Starch.
Let's now look at a health-food based multivitamin and see the difference.
Catalyn by Standard Process
Proprietary Blend: 766 mg
Defatted wheat (germ), carrot (root), calcium lactate, nutritional yeast, bovine adrenal, bovine liver, magnesium citrate, bovine spleen, ovine spleen, bovine kidney, dried pea (vine) juice, dried alfalfa (whole plant) juice, mushroom, oat flour, soybean lecithin, and rice (bran).
Other Ingredients:
Honey, glycerin, arabic gum, ascorbic acid, calcium stearate, cholecalciferol, pyridoxine hydrochloride, starch, sucrose (beets), vitamin A palmitate, cocarboxylase, and riboflavin.
What Makes Catalyn Unique
Product Attributes: Whole food multivitamin.The nutrients in Catalyn are processed to remain intact, complete nutritional compounds. Contains important vitamins, minerals, enzymes, and trace minerals in combination with their naturally occurring synergistic cofactors. Combines vital nutrients from a wide variety of plant sources to introduce a unique diversity of complete vitamin and mineral complexes (Phytonutrients).
Phytonutrients (Phytochemicals):
Phytonutrients are the important nutrients found in plants that are necessary to maintain a healthy body. They may serve as antioxidants; support a healthy immune response; and support cell-to-cell communication. There are many phytonutrients that have been identified, while their possible functions/actions have yet to be discovered. Some of the best known phytochemicals are the carotenoids, like alpha- and beta-carotene and lycopene. At Standard Process, our multivitamins are packed with health-promoting phytonutrients, which ensure maximum efficacy.
Don
Tuesday, October 4, 2011
Buckwheat protein shows potential for cholesterol reduction
Proteins from tartary buckwheat and common buckwheat helped reduce cholesterol levels in rats on a high cholesterol diet by at least 25 per cent, report Japanese researchers.
If the results can be reproduced in humans, the proteins may offer an alternative for functional food formulators and dietary supplements to tap into the burgeoning cholesterol reduction market, currently dominated by phytosterols and stanols.
The research, published in the Journal of Food Science, reports that supplementation of a high cholesterol diet with protein from common buckwheat (Fagopyrum esculentum Moench) and tartary buckwheat (Fagopyrum tataricum Gaertn) reduced serum cholesterol levels in rats by 32 and 25 per cent, respectively.
In a second experiment, the researchers looked at the effect of the proteins to reduce the formation of gallstones (lithogenesis), measured by the lithogenic index.
Supplementation with common (BWP) and tartary buckwheat (TBP) led to reductions of the lithogenic index of 62 and 43 per cent, respectively. "Taken together, these results suggest a potential source of TBP as a functional food ingredient as well as BWP," wrote the authors. High cholesterol levels, hypercholesterolaemia, have a long association with many diseases, particularly cardiovascular disease (CVD), the cause of almost 50 per cent of deaths in Europe, and reported to cost the EU economy an estimated €169bn ($202bn) per year. Analysis of the chemical composition of TBP was found to be 45.8 per cent protein, 7.8 per cent lipids, and 2.7 per cent dietary fibre, while BWP was composed of 65.8 per cent protein, 22.0 per cent lipids, and 7.0 per cent dietary fibre. TBP was also found to contain more rutin and quercetin than BWP, with 5.3 and 4.4 mg of rutin per 100 grams, respectively, and 1710 and 5.4 mg of quercetin per 100 grams, respectively.
Standard Process has a source of Buckwheat! Cyruta (Cholesterol Metabolism) #3250 90T Each tablet supplies 250 mg Buckwheat Leaf Juice and Seed and 85 mg Inositol.
Ingredients: Honey, bovine adrenal cytosol extract, ascorbic acid, oat flour, and calcium stearate. Cholesterol metabolism and reduction.
Dose: 1 Tab/meal increasing weekly to a maximum dose of 3 Tab/Meal.
NOTE: A-F Betafood should be used with Cyruta to help remove fats through the biliary system. (Take with full glass of water)
Commentary: Buckwheat is an anti-scurvy staple that goes back to ancient Mesopotamia. It was the staple of the American pioneer. It has been largely forgotten in the modern diet and with it the strong vitamin P group of anti-capillary fragility factors from the vitamin C complex. Cyruta and Cyruta-Plus are both made from the green buckwheat plant. This is very high in the naturally occurring P factors for the person with pink toothbrush (bleeding gums) or who bruises easily. Cyruta is made from the seeds as well as the leaves of the plant. This contains inositol and the calcium and cholesterol metabolizing factors, as well as the naturally occurring P factors.
Supplementation with common (BWP) and tartary buckwheat (TBP) led to reductions of the lithogenic index of 62 and 43 per cent, respectively. "Taken together, these results suggest a potential source of TBP as a functional food ingredient as well as BWP," wrote the authors. High cholesterol levels, hypercholesterolaemia, have a long association with many diseases, particularly cardiovascular disease (CVD), the cause of almost 50 per cent of deaths in Europe, and reported to cost the EU economy an estimated €169bn ($202bn) per year. Analysis of the chemical composition of TBP was found to be 45.8 per cent protein, 7.8 per cent lipids, and 2.7 per cent dietary fibre, while BWP was composed of 65.8 per cent protein, 22.0 per cent lipids, and 7.0 per cent dietary fibre. TBP was also found to contain more rutin and quercetin than BWP, with 5.3 and 4.4 mg of rutin per 100 grams, respectively, and 1710 and 5.4 mg of quercetin per 100 grams, respectively.
Standard Process has a source of Buckwheat! Cyruta (Cholesterol Metabolism) #3250 90T Each tablet supplies 250 mg Buckwheat Leaf Juice and Seed and 85 mg Inositol.
Ingredients: Honey, bovine adrenal cytosol extract, ascorbic acid, oat flour, and calcium stearate. Cholesterol metabolism and reduction.
Dose: 1 Tab/meal increasing weekly to a maximum dose of 3 Tab/Meal.
NOTE: A-F Betafood should be used with Cyruta to help remove fats through the biliary system. (Take with full glass of water)
Commentary: Buckwheat is an anti-scurvy staple that goes back to ancient Mesopotamia. It was the staple of the American pioneer. It has been largely forgotten in the modern diet and with it the strong vitamin P group of anti-capillary fragility factors from the vitamin C complex. Cyruta and Cyruta-Plus are both made from the green buckwheat plant. This is very high in the naturally occurring P factors for the person with pink toothbrush (bleeding gums) or who bruises easily. Cyruta is made from the seeds as well as the leaves of the plant. This contains inositol and the calcium and cholesterol metabolizing factors, as well as the naturally occurring P factors.
Increase your Energy with these Three Things
Overview
Vitamin B6, zinc and magnesium all interact with each other in carbohydrate, fat and protein metabolism and proper DNA synthesis. Vitamin B6 is a water-soluble vitamin that cannot be stored in your body. Zinc is found mostly in your blood plasma and liver, while magnesium is stored in your bones and muscle.
Vitamin B6, zinc and magnesium all interact with each other in carbohydrate, fat and protein metabolism and proper DNA synthesis. Vitamin B6 is a water-soluble vitamin that cannot be stored in your body. Zinc is found mostly in your blood plasma and liver, while magnesium is stored in your bones and muscle.
Are vitamins and trace elements that support many
enzymatic processes within the body. According to research, the nutrients all
work together to provide synergistic results that would not be found when
taking these nutrients separately.
FUNCTIONS
FUNCTIONS
You body needs vitamin B6 for over 100 enzyme functions
that are involved with metabolism and hormone formation. Vitamin B6 carries out
protein synthesis of hemoglobin formation in your red blood cells, synthesis of
white blood cells and developing neurotransmitters.
Zinc is involved with over 300 enzymatic functions; regulating
protein synthesis and proper growth development. According to the Linus Pauling
Institute at Oregon State University, it is also a component of an antioxidant
called superoxide dismutase, or SOD, which protects cells from free radical
damage. Zinc also plays a role in storing and releasing insulin, moving vitamin
A from the liver and keeping your blood pH in balance. Zinc is depleted during
intense exercise, and deficiencies also tend to arise. In fact, in a study with
160 athletes, 23% of the males and 43% of the females had significantly low
levels of zinc.
Magnesium is one of the more common nutritional
deficiencies among healthy adults, especially women and the elderly.
Deficiencies are also very common among weight trainers, due to increased loss
of these nutrients during workouts.
Besides maintaining bone structures, magnesium works with
potassium in conducting nerve impulses; metabolizing carbohydrates, fats and
proteins; and DNA and RNA synthesis. Magnesium is involve in 300 enzymes. It also regulates blood calcium balance
and helps vitamin D absorb calcium and phosphorous into your bones. Magnesium
ensures our muscle tissues get sufficient amounts of oxygen. When there is a
magnesium deficiency, muscles are depleted of oxygen therefore muscles exhaust
more easily. Magnesium on its own aids strength, endurance, and relaxation and
is necessary to support the metabolism of carbohydrates and proteins.
Dosage
For adult male athletes, scientific studies support
taking 20-30 mg of zinc liver chelate and 450 mg of magnesium lactae daily as well as 50-100 mg of
B6-niacinaminde per day. According to researchers, both female and teenage male
athletes need half that amount daily (10 to 15 mg of zinc and 225 mg of
magnesium) taken in 2 divided dosages. It is recommended to be taken 30 minutes
before a workout and again about 30 minutes prior to bedtime, preferably on an
empty stomach.
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