Use fiber-rich, vegetable-based diet for fibroid treatment

Use fiber-rich, vegetable-based diet for fibroid treatment

by Sarka-Jonae Miller

Up to 77 percent of women have fibroids, according to "What Your Doctor May Not Tell You About Fibroids." Many women have them and never know, but they can cause symptoms that significantly lower your quality of life. Eating the right foods helps to shrink fibroids by lowering estrogen levels naturally.

Fibroids

Fibroids are small, noncancerous growths on the uterus. In some cases, they can cause pain, excessive bleeding and even infertility. A surgical procedure to remove the uterus called a hysterectomy is a guaranteed way to get rid of fibroids. Although the cause of fibroids is unknown, fibroid growth is linked to estrogen, according to Medline Plus. Drugs can block or suppress estrogen in order to treat fibroids. Gonadotropin releasing hormone medication can shrink fibroids by 30 to 90 percent by causing the ovaries to stop making estrogen, according to "The New York Times." Fibroids often shrink when women go through menopause, which is a time when they make less estrogen. Eating foods that reduce estrogen levels may therefore also shrink fibroids.

Fiber

The most important thing you can do to combat fibroids with your diet is to eat a high-fiber diet of vegetable-based foods. Aim for at least 20 to 30 grams of fiber daily, according to the authors of "What Your Doctor May Not Tell You About Premenopause." Apples, whole grains, oatmeal, nuts and seeds are all good sources of fiber. Eating a high-fiber diet helps significantly decrease your circulating estrogen levels. Too much estrogen causes your uterus to grow excessively, which sometimes causes fibroids. Less estrogen because of diet may cause your fibroids to shrink as your estrogen levels lower, just as fibroids shrink during menopause or when taking estrogen-lowering medications.

Phytoestrogens

Eating a vegetable-based diet is important because plant foods contain substances called phytoestrogens, or plant estrogens. These substances bind themselves to the same cell receptors as estrogen. This blocks estrogen's ability to affect your cells. Without the excess estrogen causing your uterus to grow, it can shrink along with your fibroids. Foods with high amounts of phytoestrogens include soy products, nuts, seeds and ground flaxseeds. Dr. Michael T. Murray, author of more than 30 books and a member of the Board of Regents of Bastyr University in Washington, recommends eating one to two tablespoons of ground flaxseeds every day.

Foods to avoid

Avoiding certain foods may also help lower estrogen levels. Dr. Murray suggests avoiding sugar, caffeine and saturated fat. The authors of "What Your Doctor May Not Tell You About Premenopause" also suggest that women with fibroids cut back on coffee, dairy products and non-organic meats to avoid contact with hormone drugs and pesticides.

Sources for this article include:

Fibroid101.com: Get Rid of Your Uterine Fibroid
http://www.fibroid101.com/hanley.htm

DoctorMurray.com: Uterine Fibroids
http://www.doctormurray.com/health-conditions/uterine-fibroids/

PowerSurge: What Your Doctor May Not Tell You About Fibroids
http://www.power-surge.com/educate/fibroids_broder.htm

"Fibroids: The Complete Guide to Taking Charge of Your Physical, Emotional and Sexual Well-Being" by Johanna Skilling and Eileen Hoffman; 2006

The New York Times Health Guide: Uterine Fibroids
http://www.power-surge.com/educate/fibroids_broder.htm

Medline Plus: Uterine Fibroids
http://www.nlm.nih.gov/medlineplus/ency/article/000914.htm

Medline Plus: Menopause
http://www.nlm.nih.gov/medlineplus/ency/article/000894.htm

"What Your Doctors May Not Tell You About Premenopause;" John R. Lee, Jesse Hanley and Virginia Hopkins; Hachette Digital, Inc; 1999

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Can vitamin D halt growth of triple-negative breast cancer? (Article by Natural News)

Can vitamin D halt growth of triple-negative breast cancer?

by David Gutierrez, staff writer

Vitamin D supplementation may be able to slow or even halt the progression of the most dangerous variety of breast cancer, according to a study conducted by researchers from Saint Louis University and IRBLleida, Spain, and published in The Journal of Cell Biology. In addition, the researcher’s isolated biomarkers that could help physicians identify women that could benefit from vitamin D treatment.

The researchers came to this discovery by identifying, for the first time, one of the molecular pathways that leads to the variety of breast cancer known as triple-negative. This cancer is more likely to affect younger women, and is most resistant to treatment.

Scientists have known for some time that a malfunction of a tumor-suppressing gene known as BRCA1 can lead to the development of breast cancer. This gene is part of the cellular defense system by which the body ensures that any damaged DNA is not passed on to new cells, using mechanisms such as screening DNA for errors and sending cells carrying damaged DNA into hibernation or even programmed cell death. This is an important cancer-preventive role, because an accumulation of DNA damage can lead a cell to the out-of-control replication associated with cancerous tumors.

BRCA1 plays a role in screening DNA and repairing double-strand breaks, a particularly dangerous form of damage. It also plays a role in verifying that DNA has been replicated and transferred properly to new cells. When BRCA1 fails, it may lead to the development of breast cancer, and often the particular variety that is negative for receptors of two hormones and a protein: estrogen, progesterone and HER2. Because such tumors are not dependent on these external factors for growth, they are harder to "starve" and kill.

The vitamin D link

Yet not all BRCA1-mutated cells turn into breast tumors. In a recent study, researchers determined that in the presence of another DNA repair factor known as 53BP1, BRCA1-deficient cells can still survive and reproduce in health. As 53BP1 levels decrease, the development of triple-negative tumors becomes more likely.

In the new study, the researchers found that the loss of BRCA1 begins a chain of events in which a protein-degrading chemical is produced that starts to break down 53BP1.

"It's a new pathway that explains how breast cancer cells lose 53BP1," lead researcher Susana Gonzalo said.

Significantly, prior research has shown that in the presence of vitamin D, this chemical is less effective at degrading 53BP1. In the new study, they found that when BRCA1-deficient tumor cells were exposed to vitamin D, 53BP1 levels rose and proliferation slowed.

This is a particularly important discovery because triple-negative breast cancers tend to be resistant to many of the most advanced cancer drugs, while the therapy that they are more likely to respond to - chemotherapy - carries potentially severe side effects.

The researchers now believe that even in people who have already developed a drug-resistant, triple-negative cancer, vitamin D supplementation may actually render the tumors sensitive to drugs.

Sources:

http://www.sciencedaily.com/releases/2013/01/130122142911.htm
http://phys.org

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All content posted on this site is commentary or opinion and is protected under Free Speech. Truth Publishing LLC takes sole responsibility for all content. Truth Publishing sells no hard products and earns no money from the recommendation of products. NaturalNews.com is presented for educational and commentary purposes only and should not be construed as professional advice from any licensed practitioner. Truth Publishing assumes no responsibility for the use or misuse of this material. For the full terms of usage of this material, visit www.NaturalNews.com/terms.shtml

Bacterial and fungal microflora in surgically removed lung cancer samples

Panagiotis Apostolou¹, Aggeliki Tsantsaridou², Ioannis Papasotiriou¹, Maria Toloudi¹,Marina Chatziioannou¹ and Gregory Giamouzis^3*

• *Corresponding author: Gregory Giamouzis ggiamou@emory.edu

Author Affiliations

¹Research Genetic Cancer Centre Ltd (R.G.C.C. Ltd), Filotas, Florina, Greece

²Department of Cardiovascular and Thoracic Surgery, Larissa University Hospital, Larissa, Greece

³Cardiology Department, Larissa University Hospital, Larissa, Greece

For all author emails, please log on.

Journal of Cardiothoracic Surgery 2011, 6:137  doi:10.1186/1749-8090-6-137

The electronic version of this article is the complete one and can be found online at:http://www.cardiothoracicsurgery.org/content/6/1/137

Received:	8 August 2011
Accepted:	14 October 2011
Published:	14 October 2011

© 2011 Apostolou et al; licensee BioMed Central Ltd. 

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

Clinical and experimental data suggest an association between the presence of bacterial and/or fungal infection and the development of different types of cancer, independently of chemotherapy-induced leukopenia. This has also been postulated for the development of lung cancer, however the prevalence and the exact species of the bacteria and fungi implicated, have not yet been described.

Aim

To determine the presence of bacterial and fungal microflora in surgically extracted samples of patients with lung cancer.

Materials and methods

In this single-center prospective, observational study, tissue samples were surgically extracted from 32 consecutive patients with lung cancer, and reverse-transcription polymerase chain reaction (RT-PCR) was used to identify the presence of bacteria and fungi strains.

Results

The analysis of the electrophoresis data pointed out diversity between the samples and the strains that were identified. Mycoplasma strains were identified in all samples. Strains that appeared more often were Staphylococcus epidermidis, Streptococcus mitis and Bacillus strains, followed in descending frequency by Chlamydia, Candida, Listeria, and Haemophilus influenza. In individual patients Legionella pneumophila and Candida tropicalis were detected.

Conclusions

A diversity of pathogens could be identified in surgically extracted tissue samples of patients with lung cancer, with mycoplasma strains being present in all samples. These results point to an etiologic role for chronic infection in lung carcinogenesis. Confirmation of these observations and additional studies are needed to further characterize the etiologic role of inflammation in lung carcinogenesis.

Keywords: 

lung cancer; bacteria; fungi; reverse-transcription polymerase chain reaction

Introduction

Lung cancer is the most common cancer worldwide, with 1.35 million incident cases annually, and consists one of the leading causes of mortality worldwide [1]. In addition to cigarette smoking, the major lung cancer risk factor [1], recent studies underscore an etiologic role for chronic pulmonary infection in lung carcinogenesis, acting either independently or as a cofactor to tobacco smoke in increasing lung cancer risk [2-5]. Experimental and clinical data correlate cancer development with the presence of certain pathogens, independently of chemotherapy-induced leucopenia [6-8]. Indeed, mycoplasma is one of the most often observed pathogen in lung carcinomas [9], and it has been postulated that mycoplasma-infected cells have a higher ability to metastasize in vivo than non-mycoplasma-infected cells [10]. Very similarly, the bacterium Chlamydia pneumoniae, a common cause of community-acquired pneumonia, has been implicated in lung carcinogenesis[11-16]. Staphylococcus strains likewise have been observed in many cases of patients with lung cancer [6,7,17-19]. Other studies have demonstrated the presence of colonies in respiratory tract in patients with cancer [19]; Haemophilus influenza [6,7,19-21] and Candida albicans [7,20-22] have been found in patients with lower respiratory tract malignancies. Legionella pneymophila has been diagnosed in patients with cancer [23], as well as strains of Bacillus [7], Listeria [24], and Streptococcus [6,7,17,19,25].

Importantly, previous retrospective and prospective studies have relied on serologic characterization of chronic bacterial and fungal infections [14]. To the best of our knowledge, the prevalence of bacterial and/or fungal infection in surgically extracted samples of patients with lung cancer has not been previously reported. The aim of the present study, therefore, was to determine the presence of bacterial and fungal microflora in surgically removed tissue samples of patients with lung cancer, by using PCR methods and special primers.

Materials and methods

In this single-center prospective, observational study, tissue samples were surgically removed from 32 consecutive patients with lung cancer. The samples were maintained in RPMI culture medium (Sigma, R0883, Germany). The tissue was dissociated and 2 ml Trypsin - 0,25% EDTA (Invitrogen, 25200-072, California) was added in order to detach the cells. The trypsin has been inactivated by using FBS (Invitrogen, 10106-169, California) and cells were centrifuged at 1,200 rpm for 10 min. Then cells were incubated in 25 cm² flasks (Orange Scientific, 5520200, Belgium) at 37°C, in a 5% CO2 atmosphere, until well developed. RNA was extracted using TRIZOL (Invitrogen, 15596-026, California) and was used as a template to generate cDNA using the First strand cDNA synthesis kit (Fermentas, K1612, Canada). The First strand cDNA was used as a template for the Gradient-PCR reaction, which was performed using GoTaq Flexi polymerase (Promega, M8305, USA). Primers have been designed with Gene Expression 1.1 software. The PCR conditions were set as follows: initial denaturation at 95°C for 10 min to activate the polymerase, 35 cycles of denaturation at 94°C for 45 sec, followed by annealing at 52-58°C for 45 sec and an extension step at 72°C for 60 sec. A final extension step was performed at 72°C for 10 min. The PCR products were then separated on 1.5% agarose gel (Merck, 1012360500, USA) stained with GelGreen (Gentaur, 41005, Belgium), and finally observed under UV-light. A 100-bp ladder (Promega, G2101, USA) was used as marker.

This study was in compliance with the Helsinki Declaration. All participants gave informed consent and the study was approved by the institutional board review.

Results

Table 1 shows the primer pairs that were used in PCR to identify the specific pathogen strains. Table 2 presents the frequency of different species and strains in the samples that were examined. The analysis of the electrophoresis data pointed out diversity between the samples and the strains that were identified in them. Mycoplasma strains were identified in all samples (Figure 1demonstrates electrophoresis results for Mycoplasma strains). Strains that appeared more often were Staphylococcus epidermidis, Streptococcus mitis and Bacillus strains, followed in descending frequency by Chlamydia, Candida, Listeria, and Haemophilus influenza. In individual patients Legionella pneumophila and Candida tropicalis were detected.

Table 1. Primer pairs that have been used in PCR

Table 2. Prevalence by different species and strains

Figure 1. Electrophoresis results for Mycoplasma strains.

Discussion

Lung cancer is the most common cancer worldwide and is a leading causes of mortality worldwide[1]. Many recent studies have underscored the etiologic role of chronic pulmonary infection in lung carcinogenesis, concluding that inflammation increases the risk for incident lung cancer [2-5]. Numerous studies on lung cancer have pointed out the appearance of Mycoplasma strains in patients and suggest association of infection with tumorigenesis; it has been postulated that mycoplasma-infected cells have a higher ability to metastasize in vivo than non-mycoplasma-infected cells [10]. Candida species have been isolated from patients with lower respiratory tract infection [7,20-22]. Haemophilus influenza [6,7,19-21], Staphylococcus epidermidis [6,7,17-19], Streptococcus species [6,7,17,19,25], Legionella pneymophila [23], as well as strains of Bacillus[7], Listeria [24] and Streptococcus [6,7,17,19,25] have been also identified in patients with different pulmonary diseases. Very similarly, the bacterium Chlamydia pneumoniae, a common cause of community-acquired pneumonia, has been implicated in lung carcinogenesis [11-16]. A recent meta-analysis by Zhan et al. [16] of 12 studies involving 2595 lung cancer cases and 2585 controls from four prospective studies and eight retrospective studies, was conducted to analyze the association between C. pneumoniae infection and risk of lung cancer. Overall, people exposed to C. pneumoniae infection had an odds ratio (OR) of 1.48 (95% confidence interval (CI), 1.32-1.67) for lung cancer risk, relative to those not exposed. Of interest, a higher titre was an even better risk prognosticator (OR for IgA ≥64 cutoff group, 2.35; 95% CI, 1.88-2.93; OR for IgA ≥16 cutoff group, 1.22; 95% CI, 1.06-1.41).

These data strongly support the idea that lung cancer is a biofilm associated chronic infection. Biofilms are microorganism populations organized in a form of colonies using self-produced extracellular matrix that works as infrastructure material. The vast majority of the micro-"colonists" establish biofilms on any inert or diseased biological surface. They adhere to each other, divide, cooperate, and, progressively, their bio-mass grows, matures and finally disperses. It resembles malignant behavior (tumors composed by cancer cells and by stroma cells-monocytes, lymphocytes, microvessels, can metastasize). Therefore, many researchers imply that lung malignancies are communities of diverse pathogens resistant to antibiotics.

One of the major limitations in most of the previous studies was the use of serologic characterization to identify chronic bacterial or fungal infections [14]. This has resulted in conflicting results and great variability in relative risk estimations among seropositive individuals[14,15,26-29]. This wide variability could also reflect the retrospective nature of most of the studies, the small sample sizes, or inadequate adjustment for confounding factors [14]. New techniques, such as PCR-RFLPs, Matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) and microcolony methods allow examination and analysis of microbial communities [30,31]. Analyzing the constituents of microbial biofilms responsible for lung disease may help us discover novel strategies to control malignancies.

To the best of our knowledge, the prevalence of bacterial and/or fungal infection in surgically extracted samples of patients with lung cancer has not been previously reported. Therefore, the main purpose of the present study was to determine the presence of bacterial and fungal microflora in surgically removed tissue samples of patients with lung cancer, by using PCR methods and special primers. In this study, specific primers were designed in order to amplify as many different strains of microorganisms. Pairs of primers that were designed were capable of amplifying Treponema, Neisseria, Legionella, Borrelia, Listeria, Helicobacter, Staphylococcys, Haemophilus, Bacillus, Leptospira, Streptococcus, Mycoplasma, Candida and Brachyspira species. It is worth noting that Mycoplasma species were observed in all samples. Staphylococcus epidermidis and Streptococcus mitis were almost seen in one quarter of patients. Neither Treponema strains nor Leptospira, Helicobacter, and Staphylococcus aureus strains were observed in this study.

Conclusion

A diversity of pathogens could be identified in surgically extracted tissue samples of patients with lung cancer, with mycoplasma strains being present in all samples. These results point to an etiologic role for chronic infection in lung carcinogenesis. Confirmation of these observations and additional studies are needed to further characterize the etiologic role of inflammation in lung carcinogenesis, thus making it possible to apply new therapeutic modalities.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

PA carried out the molecular studies and drafted the manuscript. AT participated in the design of the study and collected all tissue samples. IP participated in the design of the study and coordination. MT carried out the molecular studies and drafted the manuscript. MC carried out the molecular studies and drafted the manuscript. GG performed the statistical analysis and drafted the manuscript.

All authors read and approved the final manuscript.

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