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Study Probes Obesity Link to Fibromyalgia
ScienceDaily (Jan. 1, 2011) — Afflicting up to 5 percent of the U.S. population, mostly women, fibromyalgia is characterized by widespread pain and range of function problems. A new study in The Journal of Pain reports there is close association between obesity and disability in fibromyalgia patients.—The purpose of the study, conducted by University of Utah researchers, was to evaluate the relationship between fibromyalgia and obesity. They hypothesized that obesity significantly adds to the disease and disability burden of the condition. Two hundred fifteen fibromyalgia patients were evaluated in the study and given several physical tests to measure strength, flexibility, range of motion, and strength. Heart rates and sleep quality also were assessed.—The authors reported that consistent with previous studies, obesity is common among those with fibromyalgia. Half the study sample was obese and an additional thirty percent were overweight. Also consistent with previous findings, obese patients in this study showed increased pain sensitivity, which was more pronounced in lower body areas. The obese patients also had impaired flexibility in the lower body and reduced strength.–The study concluded that obesity is a common comorbidity of fibromyalgia that may compromise clinical outcomes. The adverse impact of obesity is evidenced by hyperalgesia, disability, impaired quality of life and sleep problems. The authors also noted that recent evidence suggests weight loss improves fibromyalgia symptoms, perhaps resulting from patients adopting healthier lifestyles and taking more positive attitudes toward symptom management, and overall quality of life. Story Source–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Pain Society.–Journal Reference:–Akiko Okifuji, Gary W. Donaldson, Lynn Barck, Perry G. Fine. Relationship Between Fibromyalgia and Obesity in Pain, Function, Mood, and Sleep. The Journal of Pain, 2010; 11 (12): 1329 DOI: 10.1016/j.jpain.2010.03.006
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Tablet Splitting Is a Highly Inaccurate and Potentially Dangerous Practice
ScienceDaily (Jan. 7, 2011) — Medical experts have issued a warning about the common practice of tablet splitting, after a study found that nearly a third of the split fragments deviated from recommended dosages by 15 per cent or more.–Their study, published in the January issue of the Journal of Advanced Nursing, points out that the practice could have serious clinical consequences for tablets that have a narrow margin between therapeutic and toxic doses.–And they are calling on manufacturers to produce greater dose options and liquid alternatives to make the practice unnecessary.–Researchers from the Faculty of Pharmaceutical Sciences at Ghent University, Belgium, asked five volunteers to split eight different-sized tablets using three techniques commonly used in nursing homes.–They found that 31 per cent of the tablet fragments deviated from their theoretical weight by more than 15 per cent and that 14 per cent deviated by more than 25 per cent. Even the most accurate method produced error margins of 21 per cent and eight per cent respectively. “Tablet-splitting is widespread in all healthcare sectors and a primary care study in Germany found that just under a quarter of all drugs were split” says study lead Dr Charlotte Verrue.–“It is done for a number of reasons: to increase dose flexibility, to make tablets easier to swallow and to save money for both patients and healthcare providers. However, the split tablets are often unequal sizes and a substantial amount of the tablet can be lost during splitting.”—The five researchers comprised a pharmacy student, researcher and professor, an administrative worker and a laboratory technician, ranging from 21 to 55 years of age. With the exception of the technician, none of the other study participants had tablet-splitting experience. The authors believe this replicated nursing home conditions where splitting is not always performed by professional nurses.–Between them they split tablets into 3,600 separate quarters or halves using a splitting device, scissors and a kitchen knife. The eight different tablets were different shapes and sizes, three were unscored, three had one score line and the others had two.—The drugs were prescribed for a range of health conditions, including Parkinson’s, congestive heart failure, thrombosis and arthritis.—After splitting, each fragment was weighed to see how much they deviated from the theoretical weight.
Key results included:
Using a splitting device was the most accurate method. It still produced a 15 to 25 per cent error margin in 13 per cent of cases, but this was lower than the 22 per cent for scissors and the 17 per cent for the knife.
The splitting device produced a deviation of more than 25 per cent in eight per cent of cases, compared with 19 per cent for the scissors and 17 per cent for the knife.
Some drugs were much easier to split accurately than others. The easiest to split produced an overall error margin (15 per cent deviation or more) of two percent and the most difficult tablets produced an error margin of 19 per cent.
“Tablet splitting is daily practice in nursing homes” says Dr Verrue. “However, not all formulations are suitable for splitting and, even when they are, large dose deviations or weight losses can occur. This could have serious clinical consequences for drugs where there is a small difference between therapeutic and toxic doses.—“Based on our results, we recommend use of a splitting device when splitting cannot be avoided, for example when the prescribed dose is not commercially available or where there is no alternative formulation, such as a liquid.–“Staff who are responsible for splitting tablets should receive training to enable them to split as accurately as possible. They should also be made aware of the possible clinical consequences of dose deviations.–“We would also like to see manufacturers introduce a wider range of tablet doses or liquid formulations so that tablet splitting becomes increasingly unnecessary.”Story Source-The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Wiley – Blackwell, via AlphaGalileo.–Journal Reference–Charlotte Verrue, Els Mehuys, Koen Boussery, Jean-Paul Remon, Mirko Petrovic. Tablet-splitting: a common yet not so innocent practice. Journal of Advanced Nursing, 2011; 67 (1): 26 DOI: 10.1111/j.1365-2648.2010.05477.x
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Scientist Shows Link Between Diet and Onset of Mental Illness
ScienceDaily (Dec. 13, 2010) — Changes in diet have been linked to a reduction of abnormal behaviors in mentally ill people or animals, but a Purdue University study shows that diet might also trigger the onset of mental illness in the first place.–Joseph Garner, an associate professor of animal sciences, fed mice a diet high in sugar and tryptophan that was expected to reduce abnormal hair-pulling. Instead, mice that were already ill worsened their hair-pulling behaviors or started a new self-injurious scratching behavior, and the seemingly healthy mice developed the same abnormal behaviors.–“This strain of mouse is predisposed to being either a scratcher or a hair-puller. Giving them this diet brought out those predispositions,” said Garner, whose results were published in the December issue of the journal Nutritional Neuroscience. “They’re like genetically at-risk people.”–Garner studies trichotillomania, an impulse-control disorder in which people pull out their hair. The disorder, which disproportionately occurs in women, is thought to affect between 2 percent and 4 percent of the population. Mice that barber, or pull their hair out, have been shown to have low levels of serotonin activity in the brain. That neurotransmitter is known to affect mood and impulses. Garner hypothesized that increasing serotonin activity in the brain might cure or reduce barbering and possibly trichotillomania.–Serotonin is manufactured in the brain from the amino acid tryptophan, which is consumed in diets. The problem is that tryptophan often doesn’t make it across the barrier between blood and the brain because other amino acids can get through more easily and essentially block the door for tryptophan. Garner modified a mouse diet to increase simple carbohydrates, or sugars, and tryptophan. The sugars trigger a release of insulin, which causes muscles to absorb those other amino acids and gives tryptophan a chance to make it to the brain.–Using eight times as much sugar and four times as much tryptophan, Garner observed a doubling of serotonin activity in the brain. But the mice that barbered did not get better.—“We put them on this diet, and it made them much, much worse,” Garner said.–A second experiment divided the mice into three groups: those that were seemingly normal, others that had some hair loss due to barbering and a group that had severe hair loss. All the mice soon got worse, with conditions escalating over time.–“Three-quarters of the mice that were ostensibly healthy developed one of the behaviors after 12 weeks on the new diet,” Garner said.–Some of the mice developed ulcerated dermatitis, a fatal skin condition thought to be caused by an unidentified pathogen or allergen. Garner saw that the only mice that contracted the condition were the scratchers.—“What if ulcerated dermatitis, like skin-picking, another common behavioral disorder, is not really a skin disease at all?” Garner said. “We now have evidence that it may be a behavioral disorder instead.” When taken off the new diet, the negative behaviors stopped developing in the mice. When control mice were switched to the new diet, they started scratching and barbering.—Garner’s study raises questions of how diet might be affecting other behavioral or mental illnesses such as autism, Tourette syndrome, trichotillomania and skin-picking. He said that before now, a link between diet and the onset of mental disorders hadn’t been shown.–“What if the increase of simple sugars in the American diet is contributing to the increase of these diseases?” Garner said. “Because we fed the mice more tryptophan than in the typical human diet, this experiment doesn’t show that, but it certainly makes it a possibility.”—Garner next wants to refine the experiments to better imitate human dietary habits, including the amount of tryptophan people consume. Internal Purdue funding paid for his work. Story Source–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Purdue University, via EurekAlert!, a service of AAAS. Journal Reference–Brett D. Dufour, Olayiwola Adeola, Heng-Wei Cheng, Shawn S. Donkin, Jon D. Klein, Edmond A. Pajor, Joseph P. Garner. Nutritional up-regulation of serotonin paradoxically induces compulsive behavior. Nutritional Neuroscience, 2010; 13 (6): 256 DOI: 10.1179/147683010X12611460764688
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HRT=Misery
Potential ‘Safe Period’ For Hormone Replacement Use Identified
ScienceDaily (Feb. 8, 2009) — A new study makes important new findings on the role of hormone use on the risk of breast cancer, confirming that the use of estrogen plus progesterone increases the risk of both ductal and lobular breast cancer far more than estrogen-only; suggesting a two-year “safe” period for the use of estrogen and progesterone; and finding that the increased risk for ductal cancers observed in long-term past users of hormone replacement therapy drops off substantially two years after hormone use is stopped.–Previous studies have shown that hormone replacement therapy after menopause increases the risk of breast cancer and that use of a regimen that includes both estrogen and progesterone is more detrimental for the breast than the use of estrogen alone. But more data from large prospective studies are needed to fully characterize the impact of exogenous hormones (Exogenousor exogeneous) refers to an action or object coming from outside a system. It is the opposite of endogenous, something generated from within the system ) on breast cancer incidence by type of hormone preparation and histology of the cancer.—To investigate the association in more detail, American Cancer Society epidemiologists led by Eugenia E. Calle, PhD, did a prospective study of 68,369 postmenopausal women who were cancer-free at baseline in 1992. They examined the use of estrogen-only and estrogen and progesterone in current and former users of varying duration, and the subsequent risk of developing invasive ductal and lobular carcinoma of the breast. They also looked at whether the risk for each type of breast cancer and each type of hormone regimen varied by body mass index (BMI), stage of disease at diagnosis, and estrogen receptor (ER) and progesterone receptor (PR) status. For the present study, the follow-up period ended on June 30, 2005.—They confirmed the findings from previous work that estrogen and progesterone increases the risk of both ductal and lobular breast cancer far more estrogen alone. They also found the risk associated with use of estrogen and progesterone increases significantly and substantially within three years of beginning hormone use. The data showed no increased risk for women who used estrogen and progesterone for less than two years, potentially identifying a “safe” period for estrogen and progesterone use.—The study also found no increased risk of breast cancer in women who had stopped using estrogen and progesterone two or more years ago, suggesting a window of two to three years for the risks of estrogen and progesterone both to become apparent after initial use and to diminish after cessation. Few estimates of risk within two to three years of initiation and cessation are available, so these findings need replication in other large studies. The study found the use of estrogen and progesterone was associated with a doubling of risk of lobular cancer after three years of use, and a doubling of risk of ductal cancer with 10 years of use. Estrogen-only use was not associated with increased risk of ductal cancer, even after 20 years of use, but was associated with a 50 percent increase in risk of lobular cancer after 10 years of use.—Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Cancer Society, via EurekAlert!, a service of AAAS. — Journal Reference: –Eugenia E. Calle et al. —Postmenopausal hormone use and breast cancer associations differ by hormone regimen and histologic subtype. Cancer, Published Online: January 20, 2008 DOI: 10.1002/cncr.24101
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Long-Term Estrogen Therapy Linked To Breast Cancer Risk
ScienceDaily (May 9, 2006) — Long-term estrogen therapy may be related to a higher risk of breast cancer among postmenopausal women who have had a hysterectomy, according to an article in the May 8 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. —Previous studies have linked the use of hormone therapy to breast cancer among postmenopausal women, but have primarily focused on the hormone combination of estrogen plus progestin, according to background information in the article. Recently released results from the Women’s Health Initiative (WHI), a large clinical trial of hormone therapy, found no significant link between estrogen therapy and breast cancer in women who took the hormone for seven years. —Wendy Y. Chen, M.D., M.P.H., Brigham and Women’s Hospital and Dana Farber Cancer Institute, Boston, and colleagues evaluated women who were part of the Nurses’ Health Study, a group of female nurses that have been followed since 1976. In 1980, 11,508 women from the study were postmenopausal and had had a hysterectomy. Every two years the researchers enrolled all the additional women who become postmenopausal and had a hysterectomy, so 28,835 women were included by the end of the study in 2002. Women were asked by questionnaire every two years if they used hormones and whether they had developed breast cancer. For women who developed breast cancer, the researchers obtained permission to review the women’s medical records, which they used to record the hormone receptor information. Tumors were classified as positive or negative for estrogen receptor or progesterone receptor based on how they responded to specific hormonal therapies. —Throughout the study period, 934 invasive breast cancers developed, 226 among women who had never used hormones and 708 among women who were using estrogen at the time. The longer a woman used estrogen, the higher her risk of breast cancer. Those who had been taking estrogen for fewer than 10 years did not appear to have a higher risk than those who had never taken hormones, but those who had been taking estrogen for more than 20 years had a significantly increased risk. The association was strongest for cancers that were estrogen receptor positive and progesterone receptor positive. The results were similar when the researchers evaluated only women who were older than age 60; only women who had begun estrogen therapy after reaching age 50; and only women who were at least age 50 and had undergone a hysterectomy, even if they had not gone through menopause. —“In conclusion, we found that estrogen therapy was associated with an increased risk of breast cancer with longer-term use,” the authors write. “Although current use of estrogen therapy for less than 10 years was not associated with a statistically significant increase in breast cancer risk, the WHI has shown an increased risk of stroke and deep-vein thrombosis in the same time period. Women who take estrogen therapy for prevention or treatment of osteoporosis typically require longer-term treatment and should thus explore other options, given the increased risk of breast cancer with longer-term use.”—(Arch Intern Med. 2006; 166: 1027-1032. Available pre-embargo to media at http://www.jamamedia.org.) –Editor’s Note: This study was supported by a grant from the National Institutes of Health, Bethesda, Md. —Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals, via EurekAlert!, a service of AAAS —
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Estrogen Therapy May Be Associated With Kidney Stones in Postmenopausal Women
ScienceDaily (Oct. 12, 2010) — Use of estrogen therapy is associated with an increased risk of developing kidney stones in postmenopausal women, according to a report in the October 11 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.– “Nephrolithiasis [kidney stones] is a common condition that affects 5 percent to 7 percent of postmenopausal women in the United States,” according to background information in the article. “Because the process of kidney stone formation is influenced by a variety of lifestyle and other health-related factors, the true impact of estrogen therapy on the risk of kidney stone formation is difficult to infer from observational studies.” — Using data from the national Women’s Health Initiative study, Naim M. Maalouf, M.D., of the University of Texas Southwestern Medical Center, Dallas, examined data from two trials: 10,739 postmenopausal women with hysterectomy who received either an estrogen-only treatment or matching placebo and 16,608 postmenopausal women without hysterectomy who received either an estrogen plus progestin treatment or matching placebo. Data were collected for an average of 7.1 years in the estrogen-only trial and 5.6 years for the estrogen plus progestin trial. — A total of 335 cases of kidney stones were reported in the active treatment groups, while 284 cases occurred in the placebo groups. The beginning demographic characteristics and risk factors for kidney stones were similar in the two groups, and the authors found that estrogen therapy was associated with a significant increase in risk of kidney stones. The corresponding annualized incidence rate per 10,000 women per year was 39 in the treatment group and 34 in the placebo group. Development of kidney stones was five times more common in women with a history of kidney stones at the beginning of the study, but was not significantly altered by estrogen therapy. In this trial, estrogen therapy increased the risk of development of kidney stones irrespective of age, ethnicity, body mass index, prior hormone therapy use or use of coffee or thiazide diuretics.The authors conclude that their results “indicate that estrogen therapy increases the risk of nephrolithiasis in healthy postmenopausal women. The mechanisms underlying this higher propensity remain to be determined. In view of the sizable prevalence of nephrolithiasis in this segment of the population, these findings need to be considered in the decision-making process regarding postmenopausal n use.”—Story Source:–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.–Journal Reference: N. M. Maalouf, A. H. Sato, B. J. Welch, B. V. Howard, B. B. Cochrane, K. Sakhaee, J. A. Robbins. Postmenopausal Hormone Use and the Risk of Nephrolithiasis: Results From the Women’s Health Initiative Hormone Therapy Trials. Archives of Internal Medicine, 2010; 170 (18): 1678 DOI: 10.1001/archinternmed.2010.342
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Show of the Week January 17 2011
Garlic– Recipe for Garlic and Uses- Garlic & Lecithin Recipe
Dietary zinc and prostate cancer survival in a Swedish cohort1
Digested green tea compounds show dementia and cancer benefits
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Garlic
English _ Garlic.
Ayurvedic _ Lashuna, Rasona,
Yavaneshta, Ugragandha, Mahaushadh,
Arishta.
Unani _ Seer, Lahsun.
Siddha/Tamil _ Ullippoondu, Vellaippondu.
Action _ Antibiotic, bacteriostatic, fungicide, anthelmintic, antithrombic, hypotensive, hypoglycaemic, hypocholesterolaemic. Also used for upper respiratory tract infections and catarrhal conditions.
Key application _ As a supportive to dietary measures for elevated levels
of lipids in blood; as a preventive measure for age-dependent vascular
changes. (German Commission E, ESCOP, WHO, The British Herbal
Pharmacopoeia.) Also as an antimicrobial. (The British Herbal
Pharmacopoeia). Garlic has been shown to be effective in respiratory
infections and catarrhal conditions. (The British Herbal Compendium.)
The Ayurvedic Pharmacopoeia of India indicates the use of the bulb as
a brain tonic in epilepsy and psychic disorders. Heavy consumption of garlic prior to surgery led to increased clotting time or reduced platelet aggregation (in human case reports). Garlic tablets at a dose of 400 mg twice daily for 12 weeks reduced platelet aggregation 59% compared with placebo in 80 patients (in human clinical study). (Francis Brinker.) Garlic cloves are high in sulphurcontaining amino acids known as alliin (no taste, no smell, no medicinal action). With crushing or chewing alliin comes into contact with the enzyme alliinase. Alliinase, in less than 6 s, transforms alliin into allicin (strongly medicinal), which breaks down into a number of sulphur compounds including ajoene, vinyldithin and diallyl disulfide, and trisulfide. The antibiotic effect is attributed to allicin; hypoglycaemic effect to allicin and allylprophyldisulphide (also to S-allyl Cysteine sulfoxide); anticarcinogenic activity to diallyl monosulfide; platelet aggregation inhibitory effect to diallyl-di- and tri-sulphides. Ajoene inactivated human gastric lipase, which is involved in digestion and absorption of dietary fats. Diallyltetra, penta-, hexa- and heptasulphides are potential antioxidants. AlliumleptophyllumWall. is equated with Vana Lashuna, Jangali Lahsun. Dosage _1 Bulb=3 g
Garlic inhibits the activity of 5-Lipoxygenase.
Lipids–Garlic inhibits the production of Prostaglandin F2 alpha (PGF2 alpha). Garlic inhibits the production of Prostaglandin I2 (PGI2). Garlic suppresses the production of Thromboxane A2 (TXA2).
Minerals–Garlic helps to prevent the cellular damage caused by excessive Arsenic ingestion.
Garlic facilitates the removal of accumulated Cadmium from the body. Garlic facilitates the removal of accumulated Lead from the body. Garlic facilitates the removal of accumulated Mercury from the body.
Nucleic Compounds–Garlic inhibits the incorporation of Thymidine into the Deoxyribonucleic Acid (DNA) of many types of Cancer Cells (and thereby inhibits the ability of Thymidine to function as a growth factor for some types of Cancer Cells
Garlic increases Glutathione Reductase levels.
Garlic activates Nitric Oxide Synthase (NOS).
Hormones—Garlic increases plasma Luteinizing Hormone (LH) levels (due to the Diallyl Disulfide content of Garlic).
Garlic increases Testosterone levels (due to the Diallyl Disulfide content of Garlic increasing Luteinizing Hormone (LH) levels.
Neurotransmitters–Garlic increases plasma Norepinephrine levels
Garlic protects Chromosomes from the damage caused by exposure to Gamma-Rays
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Aged garlic extract delays the appearance of infarct area in a cerebral ischemia model, an effect likely conditioned by the cellular antioxidant systems.
Phytomedicine. 2010 Mar;17(3-4):241-7
Authors: Aguilera P, Chánez-Cárdenas ME, Ortiz-Plata A, León-Aparicio D, Barrera D, Espinoza-Rojo M, Villeda-Hernández J, Sánchez-GarcÃa A, Maldonado PD
Experimental evidence has shown that some garlic-derived products have a protective effect against ischemic brain injury. The present study was designed to investigate the effect of aged garlic extract (AGE), establish the therapeutic window, and determine its protective mechanism in a cerebral ischemia model. Animals were subjected to middle cerebral artery occlusion (MCAO) for 2h and treated with 1.2ml/kg body wt.(i.p.) of AGE 30min before, at the beginning of (0R), or 1h after reperfusion. The 0R treatment significantly reduced the size of the infarct area after 2h of reperfusion. Repeated doses subsequent to the 0R treatment (at 1, 2, or 3h after reperfusion) had no effect on the temporal window of protection. The protective 0R treatment with AGE prevented the increase in nitrotyrosine and the decrease in total superoxide dismutase, glutathione peroxidase, and extracellular superoxide dismutase activities induced by MCAO. These data indicate that AGE delays the effects of ischemia/reperfusion-induced neuronal injury. However, this treatment itself was not associated with a noticeable improvement in the neurological outcome, or with an effect on the inflammatory response. We conclude that the neuroprotective effect of AGE in the 0R treatment might be associated with control of the free-radical burst induced by reperfusion, preservation of antioxidant enzyme activity, and the delay of other pathophysiological processes.–PMID: 19577455 [PubMed – indexed for MEDLINE]
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Recipe for Garlic and Uses—Take 2 bulbs of garlic and add to blender ( peeled) the add 1 ½ cup of vinegar ( any will do ) then blend for 10 minutes and strain Put into glass container—then take 2 bulbs of garlic ( peeled) and add to a oil or fat again blend for about 10 minutes –strain the mix so only the oil comes out add to glass container –then take these specific vitamins –zinc ( use approximately 100mgs ) Selenium ( 1 mg ) B1 ( 600mgs) then add equal parts of the oil and the vinegar mixes of garlic ( do not use the whole amounts approximately 1-2 oz when doing this of each of the mixes ) blend for 5 minutes then pour this into a seperate container –and use ¼ tsp increments
RThis will have sugar regulating effects—chelating effects ( removing- lead cadmium-mercury-arsenic) Anti Cancer Impact- Strength and endurance increase-anti inflammatory effect-reproductive aid-healing factor-Brain functioning improvement—heart health-liver health-pancreatic support-wound healing properties-Protects against alcohol poisoning—anti glycating of cells-Anti Aging-Antioxidant-Anti Microbial-Anti Bacterial-Anti Fungal—Cholesterol regulating
RThe Garlic vinegar can be utilized as well independently as a tonic –healant—in cooking –as a protectant against differing pathogens in foods-again as a digestive aid-cholesterol impacting and as well has all the other attributes associated with vinegar and garlic-use 1 teaspon as neded or 1 X 3 aday
RThe garlic oil can as well be utilized like the vinegar –use it ½ tsp increments
RGarlic & Lecithin Recipe—you will need lecithin( sunflower or egg yolk not soy) 1 table spoon—1 whole bulb of garlic-1/4 cup of garlic vinegar-1/4 cup of garlic oil—then add zinc citrate 300mgs ( open capsule ) 600mgs of B1 ( open capsule) selenium 1 mg ( open either 5 capsules at 200 mcg strength or 10 capsules at 100mg strength ) if you like add cq 10 to this 200 mgs ( again depending on capsule strength open the appropriate amount ) and again you can increase these or decrease as you see fit—add all to blender and blend for 10 minutes at medium to high speed—add garlic oil or garlic vinegar if needed if to thick—when done pour into a glass bottle and use ½ tsp several times a day—the impact will be noticeable on the legs a renewed strength will be noticed—this will again impact the Norepinephrine levels of the brain ( flight or fright—clear thinking—cognitive ability-sex drive) cellular health and increases immune health—liver health—cholesterol regulating anti cancer—anti fungal-anti viral-anti bacterial-anti microbial—general tonic as well—can be used on a spread –in yogurt—on foods –taken straight—use ½ tsp several times a day
RThese can be spread on your eggs –integrated in your cooking oils can be used in soups and have the benefits as well as protective properties-mixed in salads or salad dressings
RThe garlic mix with the combo of supplements and vinegar can be used as a supplement—a tonic—immune restorer—immune supporter and again ¼ tsp 1 X3 a day or as needed
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Dietary zinc and prostate cancer survival in a Swedish cohort1,2,3
1. Mara M Epstein, Julie L Kasperzyk, Ove Andrén, Edward L Giovannucci, Alicja Wolk, Niclas Håkansson, Swen-Olof Andersson,
2. Jan-Erik Johansson, Katja Fall, and Lorelei A Mucci
+ Author Affiliations
1. 1From the Departments of Epidemiology (MME, JLK, ELG, KF, and LAM) and Nutrition (ELG), Harvard School of Public Health, Boston, MA; the Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA (MME, JLK, ELG, and LAM); the Örebro University Hospital, Örebro, Sweden (OA, S-OA, and J-EJ); The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (AW and NH); the Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden (KF); and The Centre for Public Health Services, University of Iceland, Reykjavik, Iceland (KF and LAM).
· ↵2 Supported by the National Institutes of Health research training grant R25CA098566 (to MME).
· ↵3 Address reprint requests and correspondence to MM Epstein, Channing Laboratory, Brigham and Women’s Hospital, 181 Longwood Avenue, 3rd Floor, Boston, MA 02115. E-mail: [email protected].
Abstract
Background: Zinc is involved in many essential cellular functions, including DNA repair and immune system maintenance. Although experimental evidence supports a role for zinc in prostate carcinogenesis, epidemiologic data are inconsistent; no data on cancer-specific survival have been reported. –Objective: Our objective was to determine whether dietary zinc assessed near the time of prostate cancer diagnosis is associated with improved disease-specific survival. –Design: This population-based cohort consists of 525 men aged <80 y from Örebro County, Sweden, with a diagnosis of prostate cancer made between 1989 and 1994. Study participants completed self-administered food-frequency questionnaires, and zinc intake was derived from nutrient databases. Cox proportional hazards regression was used to estimate multivariate hazard ratios (HRs) and 95% CIs for time to death from prostate cancer as well as death from all causes through February 2009 by quartile (Q) of dietary zinc intake. Models were also stratified by disease stage at diagnosis (localized or advanced). –Results: With a median follow-up of 6.4 y, 218 (42%) men died of prostate cancer and 257 (49%) died of other causes. High dietary zinc intake was associated with a reduced risk of prostate cancer–specific mortality (HRQ4 vs Q1: 0.64; 95% CI: 0.44, 0.94; P for trend = 0.05) in the study population. The association was stronger in men with localized tumors (HR: 0.24; 95% CI: 0.09, 0.66; P for trend = 0.005). Zinc intake was not associated with mortality from other causes. -Conclusion: These results suggest that high dietary intake of zinc is associated with lower prostate cancer–specific mortality after diagnosis, particularly in men with localized disease
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Digested green tea compounds show dementia and cancer benefits
Digested polyphenol compounds from green tea could protect the brain against developing Alzheimer’s and other forms of dementia,
The in vitro study, published in Phytomedicine, confirmed that post-digestion, extracts of the phytochemical rich drink shows protective effects for dementia, and could play an important role in protecting the body against cancer. –The researchers investigated whether the protective properties of green tea – which have previously been shown to be present in the undigested, freshly brewed form of the drink – were still ‘active’ once the drink had been digested. –Lead researcher Dr Ed Okello from Newcastle University, U.K.said that just because a consumed food is generally accepted to contain health-boosting properties; it should not be assumed that such compounds will ever be absorbed in the body. –“What was really exciting about this study was that we found when green tea is digested by enzymes in the gut, the resulting chemicals are actually more effective against key triggers of Alzheimer’s development than the undigested form of the tea,” explained Okello –“In addition to this, we also found the digested compounds had anti-cancer properties, significantly slowing down the growth of the tumour cells which we were using in our experiments,” added Okello.
Dementia
Alzheimer’s disease – the most common form of dementia – is a progressive and irreversible neurodegenerative disorder associated with cognitive dysfunction. The authors noted that “mounting evidence” suggests that beta-amyloid peptides in conjunction with free radical species (such as hydrogen peroxide) in the brain play a significant role in the development and pathogenesis of Alzheimer’s. Many previous studies, have suggested that both black and green teas possess protective properties, which have been mainly attributed to their polyphenol content. —Green tea is high in flavan-3-ols, which are believed to be efficient scavengers of highly reactive free radical species, and have been shown to exhibit anti-carcinogenic; hypocholesterolaemic and neuroprotective properties . –Okello said that although research has identified certain compounds as beneficial for health, and in many cases has identified foods with high concentrations of such compounds, he explained that “what happens during the digestion process is crucial to whether these foods are actually doing us any good.” “Flavan-3-ols have been reported to possess properties beneficial to health, [but] they are known to undergo significant metabolism and conjugation in the gastrointestinal tract,” said the researchers. –“It is unknown how such metabolism and conjugation may influence the putative properties of these polyphenols, hence the focus of our study on a digested green tea extract,” they explained.
Digested extract
Green tea extract – from brewed Temple of Heaven, Gunpowder China tea, purchased by the researchers from a local store – was subjected to a simulated gastrointestinal digestion and a ‘colon-available’ extract (CAGTE) was prepared and assessed for its potential protective effects against the damaging effects of hydrogen peroxide and beta-amyloid on neuronal cells in the brain – which are believed to play a role in the development of dementia. –The CAGTE, which represents green tea phytochemicals potentially available after upper gastrointestinal digestion, was found to be depleted in flavan-3-ols when compared to the pre-digested green tea extract; yet was still found to protect cells in a brain neurone model from both hydrogen peroxide and beta-amyloid toxicity. –“At high concentrations, CAGTE exhibited direct anti-proliferative effects, in line with the reputed anti-cancer properties of green tea polyphenols,” wrote the authors. –“The CAGTE, which effectively lacked flavan-3-ols, had a protective effect on beta-amyloid induced toxicity in vitro at 0.03–0.125 μg/ml … This figure is much lower than the 20 μg/ml reported for effective protection in whole green tea extracts,” said the researchers.
Next step
He said that the next step in the research is to investigate whether the beneficial compounds found in the digestion model are produced during digestion in human volunteers that consume green tea polyphenols – for which the team has already secured funding from the Biotechnology and Biological Sciences Research Council (BBSRC).
Source: Phytomedicine–Published online ahead of print, doi: 10.1016/j.phymed.2010.11.004 –“In vitro protective effects of colon-available extract of Camellia sinensis (tea) against hydrogen peroxide and beta-amyloid (Aβ(1–42)) induced cytotoxicity in differentiated PC12 cells” –Authors: E.J. Okello, G.J. McDougall, S. Kumar, C.J. Seal
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Show of the Week Jan 21- 2011
Calorie Restricted Diet Prevents Pancreatic Inflammation And Cancer
How Calorie-Restricted Diets Fight Obesity and Extend Life Span
Fueling the Body on Fat Critical Tuning Dial for Controlling Energy Found
Key Enzyme In Fat Absorption Discovered
How Progesterone & Estrogen Increases Breast Cancer Risk
BRCA1 Gene Found To Inhibit Two Sex Hormones, Not Just One
Anti Estrogenic Antidote
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Calorie Restricted Diet Prevents Pancreatic Inflammation And Cancer
ScienceDaily (Apr. 17, 2008) — Prevention of weight gain with a restricted calorie diet sharply reduced the development of pancreatic lesions that lead to cancer in preclinical research reported April 15 by researchers from The University of Texas at Austin and The University of Texas M. D. Anderson Cancer Center at the American Association for Cancer Research annual meeting.—The research sheds light on the connection between obesity, calorie intake and pancreatic cancer by comparing a calorie restricted diet, an overweight diet and an obesity-inducing diet in a strain of mice that spontaneously develops pancreatic lesions that lead to cancer.—“Obesity is a known risk factor for pancreatic cancer, but the mechanism underlying that relationship is unknown,” said senior author Stephen D. Hursting, Ph.D., professor in M. D. Anderson’s Department of Carcinogenesis and Chair of the Division of Nutritional Sciences at the University of Texas. “Our findings indicate that calorie restriction hinders development of pancreatic cancer, which could have implications for prevention and treatment of pancreatic tumors caused by chronic inflammation and obesity.”–The group’s analysis points to a connection between calorie intake and a protein called Insulin-like Growth Factor (IGF) -1, with obesity increasing and calorie restriction decreasing levels of IGF-1. IGF-1 is an important growth factor known to stimulate the growth of many types of cancer cells. Inflammatory signaling proteins also were found to be reduced in the blood of the calorie-restricted mice.—“Mice on the heavier diets had significantly more lesions and larger lesions than those on the restricted calorie diet,” said first author Laura Lashinger, Ph.D., a post-doctoral fellow in Hursting’s laboratory. The strain of mice, developed by Susan Fischer, professor in M. D. Anderson’s Department of Carcinogenesis, spontaneously develops lesions associated with pancreatitis – inflammation of the pancreas. These lesions develop into pancreatic cancer and virtually all of these mice die within six to eight months.-The researchers fed the calorie restricted group a diet that was 30 percent lower in calories than that consumed by the overweight group and 50 percent lower than the obese group. Only 7.5 percent of mice on the calorie-restricted diet developed pancreatic lesions at the end of the experiment, and these lesions were so small that none exhibited symptoms of illness. For mice on the overweight diet, 45 percent developed lesions, as did 57.5 percent of those on the obesity-inducing diet. Lesions were also much larger in the overweight and obese mice than the calorie restricted mice.—While calorie restriction has been shown to have an anti-cancer effect in multiple species and for a variety of tumor types, its impact had not been well-studied in a model of pancreatic cancer. Pancreatic cancer is the fourth leading cause of cancer death and remains mostly intractable to existing treatments.–The decline in blood levels of inflammatory proteins in the calorie restricted mice makes sense, Lashinger notes, because fat tissue is a major source of inflammatory factors such as cytokines.–[U1]The research was funded by grants from the National Institute of Health and the University of Texas, and is a collaboration between M. D. Anderson’s Department of Carcinogenesis, based at the The Virginia Harris Cockrell Cancer Research Center at M. D. Anderson’s Science Park – Research Division in Smithville, Texas, and the University of Texas at Austin Department of Nutritional Sciences.–Co-authors with Lashinger, Hursting and Fischer are Lauren Malone, Elizabeth Daniels, Nicole Smith, and Susan Perkins of the UT Department of Nutritional Sciences and Amy Pavone of M. D. Anderson’s Department of Carcinogenesis.–Story Source–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Texas M. D. Anderson Cancer Center
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How Calorie-Restricted Diets Fight Obesity and Extend Life Span
Fruits and vegetables are a key part of calorie-restricted diets, which may increase longevity.–ScienceDaily (Dec. 29, 2009) — Scientists searching for the secrets of how calorie-restricted diets increase longevity are reporting discovery of proteins in the fat cells of human volunteers that change as pounds drop off. The proteins could become markers for monitoring or boosting the effectiveness of calorie-restricted diets — the only scientifically proven way of extending life span in animals.–Their study appears online in ACS’ Journal of Proteome Research.–Edwin Mariman and colleagues note that scientists have long known that sharply restricting intake of calories while maintaining good nutrition makes animals live longer and stay healthier. Recent studies suggest that people may gain similar benefits. But scientists know little about how these diets work in humans, particularly their effects on cells that store fat.–The new study focused on proteins in abdominal subcutaneous fat cells from a group of overweight people before and after they went on a five-week-long calorie-restricted diet. The volunteers each lost an average of 21 pounds[U2]. Scientists identified changes in the levels of 6 proteins as the volunteers shed pounds, including proteins that tell the body to store fat. These proteins could serve as important markers for improving or tracking the effectiveness of therapies involving calorie-restricted diets, they say.-Story Source-The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Chemical Society, via EurekAlert!, a service of AAAS.-Journal Reference–Bouwman et al. The Physiologic Effects of Caloric Restriction Are Reflected in the <i>in Vivo</i> Adipocyte-Enriched Proteome of Overweight/Obese Subjects. Journal of Proteome Research, 2009; 8 (12): 5532 DOI: 10.1021/pr900606m
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Fueling the Body on Fat Critical Tuning Dial for Controlling Energy Found
ScienceDaily (Jan. 5, 2011) — Researchers have found what appears to be a critical tuning dial for controlling whole body energy, according to a new report in the January issue of Cell Metabolism, a Cell Press publication. When energy levels within cells drop, it sets off a series of events designed to increase the amount of calorie-rich dietary fat that the body will absorb.—This energy reset mechanism is surely critical for survival under natural conditions of scarcity to ensure a steady supply of fuel, the researchers say. Today, many of us who enjoy a Western diet loaded with fat might do better if we could find a way to turn the activity of the so-called AMPK-SRC-2 pathway down.–“Thousands of years ago, this would have been crucial,” said Bert O’Malley of Baylor College of Medicine. “Now it’s trouble because we eat so much fatty food.”[U3]–Earlier studies had shown the enzyme AMPK to be an ancient energy sensor. The enzyme causes cells to consume less energy in the form of ATP and to produce more. AMPK also drives appetite.–The new work shows that AMPK also allows for the optimal absorption of THE MOST ENERGY-RICH FUEL from the diet: fat[U4]. That effect of AMPK depends on its activation of SRC-2, a master control gene whose job is to switch other genes on.—When SRC-2 springs into action, it controls genes that lead to the secretion of bile from the gall bladder into the intestine. “You need bile to emulsify and absorb fat,” O’Malley explained.- Mice lacking SRC-2 fail to absorb fat normally, they report. Those deficiencies can be corrected by restoring bile acids to the gut.[U5]-Together with earlier work, the findings present a “pretty picture” in which SRC-2 is involved in absorbing and storing fat. SRC-2 is also known to play a role in releasing stored glucose from the liver. “It’s all about energy accretion, storage and delivery,” O’Malley says.–This process takes place on a daily basis even when there is already plenty of fat stored in the body. “It’s designed to get in more fat,” he says. “Over evolutionary time, when you didn’t know when the next meal would be, you really couldn’t get enough fat. Now, our next meal is at the corner McDonald’s.”–The discovery reveals a key mechanism linking the cellular energy state with the whole-body energy state and may ultimately have important clinical implications, the researchers say.–“Obesity is all about fat absorption and storage,” O’Malley said. “If you could turn that down, you could have a major effect on a disease that is slowly killing the population.” He says his team is now conducting studies in search of SRC-2 inhibitors that might do exactly that.—Story Source-The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Cell Press, via EurekAlert!, a service of AAAS.–Journal Reference–Atul R. Chopra, Ramakrishna Kommagani, Pradip Saha, Jean-Francois Louet, Christina Salazar, Junghun Song, Jaewook Jeong, Milton Finegold, Benoit Viollet, Franco DeMayo, Lawrence Chan, David D. Moore, Bert W. O’Malley. Cellular Energy Depletion Resets Whole-Body Energy by Promoting Coactivator-Mediated Dietary Fuel Absorption. Cell Metabolism, 2011; 13 (1): 35-43 DOI: 10.1016/j.cmet.2010.12.001
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Key Enzyme In Fat Absorption Discovered
ScienceDaily (Mar. 18, 2009) — Scientists at the Gladstone Institutes of Cardiovascular Disease (GICD) have found that a key enzyme involved in absorbing fat may also be a key to reducing it. The enzyme, acyl CoA: [U6]monoacylglycerol acyltransferase 2 or Mgat2 is found in the intestines and plays an important part in the uptake of dietary fat by catalyzing a critical step in making triglyceride, a kind of fat. –Triglyceride accounts for nearly one-third of the fat eaten by people in developed countries.–Researchers in the laboratory of Robert V. Farese, Jr. MD, found that mice that were genetically modified to lack Mgat2 remain normal on a low-fat diet. However, when fed a high-fat diet that is similar to that eaten by many Americans, the mice do not get fat and do not develop other symptoms of obesity, such as glucose intolerance, hypercholesterolemia, and fatty livers. The mice eat the same number of calories as other mice, and the calories are fully absorbed. –“Because mice that lack this enzyme do not gain weight on a high-fat diet, it is an intriguing target for future interventions to prevent weight gain and the problems associated with that extra weight,” said Dr. Farese.–The mechanism of action, the researchers identified was that the lack of Mgat2 may reduce the uptake of fat in the small intestine and delay its entry into the blood. This process may dissociate fat from carbohydrate absorption and insulin secretion and ultimately lower the amount of fat stored and used. How this happens is not clear. One possibility is that the absorbed fat is partitioned more to tissues where it is burned up.–“Differences in Mgat2 expression may contribute to the propensity of some people to gain weight from diets rich in fat,” said Eric Yen, PhD, lead author of the study. “Our findings suggest that inhibiting this enzyme in the small intestine might be an effective way to treating metabolic diseases that result from excessive fat intake.”–Results of their study were published in the current issue of the journal Nature Medicine.–Story Source–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Gladstone Institutes, via EurekAlert!, a service of AAAS
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How Progesterone & EstrogenIncreases Breast Cancer Risk
ScienceDaily (Jan. 18, 2011) — Researchers have identified how the hormones progesterone and estrogen interact to increase cell growth in normal mammary cells and mammary cancers, a novel finding that may explain why postmenopausal women receiving hormone replacement therapy with estrogen plus progestin are at increased risk of breast cancer.–The discovery that both estrogen and progesterone must be present for the increased production of the protein amphiregulin, which binds to mammary cells and promotes cell growth, could lead to new treatment methods for the disease, said Sandra Haslam, director of Michigan State University’s Breast Cancer and the Environment Research Center and lead researcher on the project.–The study, funded by the Department of Defense’s Breast Cancer Research Program and published in Hormones and Cancer, looked at why progesterone combined with estrogen may contribute to increased breast cancer risk. In the study, researchers used both the native hormone, progesterone, and a synthetic compound, progestin — obtaining the same results.—The finding might help explain earlier results from the groundbreaking Women’s Health Initiative showing the risk of breast cancer is significantly greater for postmenopausal women who received hormone replacement therapy with combined estrogen plus progestin compared to women receiving estrogen alone.–“Also, breast cancers that develop in women receiving estrogen plus progestin are more invasive and deadlier,” Haslam said. “What is the progestin doing to increase the risk of tumor growth?”–Along with co-investigator Anastasia Kariagina, a colleague in the College of Human Medicine and Department of Physiology, Haslam identified the protein amphiregulin and its receptor as one potential culprit.—“Amphiregulin — acting through its receptor, epidermal growth factor receptor — along with progesterone leads to the activation of intracellular pathways that regulate cell growth,” Haslam said. “When activated, this promotes normal cell growth and the growth of tumors.”—The study was performed in rats because breast cancers in rats contain receptors for estrogen and progesterone — similar to the human breast — and tumor growth is hormone-dependent, as are the majority of human breast cancers. The research team also confirmed the same phenomenon in human breast cancer cell cultures.–In addition, the research team found that Iressa, a cancer drug that blocks the epidermal growth factor receptor, effectively stopped the proliferation caused by amphiregulin. While those studies were done only in cell cultures and not on tumors growing in animals, the results are promising, Haslam said.—“The results indicate that the interactions between estrogen, progesterone and epidermal growth factor receptor pathways may be considered relevant targets for the treatment of hormone-dependent breast cancers,” she said. “This may be especially important in premenopausal breast cancer because women produce their own estrogen and progesterone.–“A combined approach of inhibiting both the hormones and the epidermal growth factor receptor may be beneficial for some women in treating hormone-dependent breast cancer.”–Story Source:–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Michigan State University.–Journal Reference-Anastasia Kariagina, Jianwei Xie, Jeffrey R. Leipprandt, Sandra Z. Haslam. Amphiregulin Mediates Estrogen, Progesterone, and EGFR Signaling in the Normal Rat Mammary Gland and in Hormone-Dependent Rat Mammary Cancers. Hormones and Cancer, 2010; 1 (5): 229 DOI: 10.1007/s12672-010-0048-0
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BRCA1 Gene Found To Inhibit Two Sex Hormones, Not Just One
ScienceDaily (Jan. 26, 2006) — It’s been known that the breast cancer susceptibility gene BRCA1 regulates use of estrogen in breast and other cells, but now researchers at Georgetown University Medical Center have discovered that it also controls activity of a second sex steroid hormone, progesterone. —The findings, conducted in cell culture and in mice and reported by the researchers in the January issue of Molecular Endocrinology, could help explain why women who have mutations in their BRCA1 gene are susceptible to a number of different “hormone-dependent” cancers, including those of the breast, endometriun and cervix. —It also has implications for ordinary cancers that arise because a normal BRCA1 gene is under-expressed, said the study’s principal investigator, Eliot Rosen, MD, PhD, professor of oncology, cell biology, and radiation medicine at the Lombardi Comprehensive Cancer Center. —For example, he says that up to 40 percent of breast tumors are deficient in BRCA1, “and it may be that some patients could benefit not only from an anti-estrogen therapy, like tamoxifen, but also from an anti-progesterone agent. —“We don’t know if that is true yet, of course, but it is certainly worth investigating, given our findings,” Rosen said. –The BRCA1 gene and a second gene, BRCA2, were discovered to be breast cancer susceptibility genes in 1994 and 1995, respectively. Women who inherit faulty copies of one of these genes have up to an 80 percent increased risk of developing breast cancer by age 70, and are also more likely to be diagnosed with ovarian cancer. –Rosen and his research team undertook the study to understand why loss of the BRCA1 gene results in cancers in tissues that are dependent on hormones. They focused on the progesterone hormone, in part, because of the observation that women who use hormone replacement therapy that includes both estrogen and progestin (a synthetic form of progesterone) are at greater risk of developing breast cancer than women who use only estrogen replacement. [U7]–The use of progesterone in the breast is tightly regulated and is primarily activated when growth in cells is needed, such as during the female menstrual cycle and to support a pregnancy. A cell’s use of progesterone and other such hormones is controlled by specific receptor proteins, located inside cells, which bind on to the hormone. This process activates the receptor, which then migrates to the cell nucleus to stimulate gene expression. —To find out what role BRCA1 played in progesterone receptor signaling, the Lombardi research team conducted a series of experiments. In one set of cell culture studies in the laboratory, they used breast cancer cells that were responsive to progesterone, and then genetically manipulated them to either over or under-express the BRCA1 gene in order to assess the gene’s effect on progesterone receptor signaling. –They also used mice in which the BRCA1 gene was partially deleted, but only in breast tissue. The animals were treated with estrogen, or progesterone, or both, and response of the mammary gland was compared with that of normal mice. –In this way, the researchers concluded that BRCA1 interacts physically with the progesterone receptor, and stops it from activating other genes. It does this even in the absence of the progesterone hormone, and, thus, acts as a strong check on errant growth. —“But in mice deficient in BRCA1, we found that estrogen plus progesterone has a particularly large effect in stimulating the growth of mammary epithelial cells − an effect much greater than the effects of either hormone used alone,” Rosen said. —The study was funded by grants from the Susan G. Komen Breast Cancer Foundation and the National Cancer Institute. Contributing to the study were Yongxian Ma, MD; Pragati Katiyar, MS; Laudette P. Jones, PhD; Saijun Fan, MD, PhD; Yiyu Zhang, MD; and Priscilla A. Furth, MD. –Story Source-The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Georgetown University Medical Center