My Hypothesis About Sudden Unexplained Weight Gain in Cancer
All that we know started with an observation(question) of something around us. Over time the way to take an observation and develop that observation into an accepted fact or thing, has evolved into the Scientific Method. A Hypothesis is not fact. It is a beginning to encourage a search for an answer.
According to the scientific method the first step is the question. Is there is a protective mechanism within the body to gain weight as a means to help the body fight off cancer as manifested by sudden unexplained weight gain?
Next step in the scientific method that directs the study is the hypothesis: Sudden unexplained weight gain can be a sign of developing cancer.
What I would like to accomplish here is to have BC and cancer patients identify their stories that are directly related to the hypothesis. Please, do not include stories that are not related to sudden unexplained weight gain in less than two years before cancer was found. Two years is an arbitrary time, but it is necessary to chose a time frame.
My hope is researcher(s) will be interested enough to research the hypothesis.
(Areas of future studies that are related to the hypothesis, but are not of interest now for this topic. If the body does have a protective mechanism of gaining weight, does the unexplained weight loss in cancer mean that protective mechanism failed? Can that protective mechanism be reversed once it has failed?)
As and off shoot of my interest in looking at weight. I got into the study of the microbiome and Polycyclic Aromatic Hydrocarbons. Studied them while waiting for people to post about the hypothesis.
Comments
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Another topic in this forum has piqued my interest that lead me to writing this topic. The following is what I posted there.
They're were two studies in that topic. I include them here for your review, as my response directly quoted the study and analysis of that study.
The study : http://oncology.jamanetwork.com/article.aspx?articleid=2319235
The analysis of that study: http://www.medpagetoday.com/Endocrinology/Obesity/52103
"I'm going to attempt to raise a different perspective on weight.
The BMI's at baseline were identified. The gain over the study period was identified i.e > 5%. The loss over the period of the study i.e. >5% was identified.
What was not identified in either the study or the analysis was what the overweight and obesity history was in time relationship prior to the inclusion in the study or time prior to the development to cancer. It was identified as linear meaning that it was a direct line. But I'm suggesting that the length of time to cancer is important to the weight gain. Why is this important? I have now had two primary cancers. With each one I had a stable weight. Both BMI's were in the overweight range. Then there was a sudden weight gain that did not correspond to change in diet or activity. It was a frustrating time before each one b/c I couldn't explain what was happening. With the second cancer I was suspicious b/c of what happened with the first cancer.
The first cancer was BC. The second primary cancer was Thyroid. Weight gain can be commonly associated with thyroid dysfunction. The weight gain started in Nov/Dec 2012 and rapidly moved up. TSH was normal. Docs denied there could be a thyroid problem. May 2013, a goiter was found during yearly CT. I said "SEE". Follow-up TSH and thyroid bx didn't identify any abnormality. Jan 2014, I said we need some basic blood work. I requested autoantibodies test along with the TSH, T3, and T4.
The auto antibodies test: Thyroglobulin was 52(normal range 0-30) and antibodies were normal. Indicative of cancer. (long story very shortened). Thyroid came out. Thyroglobulin drawn day after thyroid removal was 109. Pathology was negative. From the day of receiving the results of the original autoantibodies value, I insisted I had cancer. With the pathology report being negative and my belief I had cancer, my surgeon went behind the scene and insisted that a second opinion be obtained on the pathology. Quest labs found cancer in both lobes. The original pathologist admitted after doing a relook at original bx done in July 2013 and slides from thyroidectomy in Feb 2014 that cancer was present in both samples.
What was common to the two cancers was a sudden unexplained weight gain prior to each cancer diagnosis. Needless to say if they're is another sudden unexplained weight gain I'll be even more pushy than I was after the last one.
We know cancers can be present for a long period in the body before they are manifested. In reference to the study and analysis, does my observation of a sudden weight change have any signaling of cancer developing to point that it can be diagnosed by imaging or labs? For this question to be answered, they're would need to be another study done to look at that specifically. I doubt they could do a relook by meta-analysis at this study b/c it doesn't appear that was included in the specific data inclusion at the beginning of the study.
Interesting?
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This is a portion of the second post from the other thread. It was following through on looking at the study and study analysis.
"With a study like this the enrollee's have to answer sooooo many questions. Researchers then do meta-analysis study by developing a core group of questions. Those questions then are plugged into the computer to search the parameters of keywords that answer the specific search. This study specifically address BMI, Weight gain > %5, Weight loss >5%, and BC. The researcher in this case defined the...... "Objective To investigate in this secondary analysis( ancillary study) the associations of overweight and obesity with risk of postmenopausal invasive breast cancer after extended follow-up in the Women’s Health Initiative (WHI) clinical trials."
The researcher et all had a theory. She and the cohort sought material to support their theory. They think they have proven their point. The analysis quoted this from the study: "Women with normal BMIs who gained more than 5% of their body weight during follow up increased their breast cancer risk relative to women with stable weight (HR 1.36; 95% CI 1.11-1.65). The investigators speculated that weight-gain induced increases in breast adipocytes, and exposure to cytokines and estrogens might explain this finding".(emphasis mine)
"The investigators speculated". Speculation doesn't make it true.They identified that women with normal body weight that gained > 5% during the follow-up had an increased risk.
My theory: Is there is a protective mechanism within the body to gain weight as a means to help the body fight off cancer".
If the Women's Health Initiative included a time line from weight gain to diagnosis of BC, and that time line could be defined within a statistically significant range, then that would be a beginning to a new area of study.
They're was a study so many years ago, I wouldn't even begin to know how to find it. But this is what I remember of it, people that had a 25-30 lb higher weight than the weight charts (of the time since revised-higher) had a better ability to fight off illness than those in the normal weight range(of the time). The reason I remember this is b/c I thought to myself --Good, I'm right there.
Conversely, If the body does have a protective mechanism of gaining weight, does that explain the weight loss in cancer when that protective mechanism fails. Weight loss of unknown origin has it's own ICDM-9 code. The reason is when weight loss is unexplained, it is associated with certain diseases. I'll state the most common. Diabetes, thyroid, and cancer. Those are the three biggy rule outs when a doc is presented with a patient that presents with unexplained weight loss.
So, to combine the two thoughts as specific to cancer.
According to the scientific method the first step is the question. Is there is a protective mechanism within the body to gain weight as a means to help the body fight off cancer? If the body does have a protective mechanism of gaining weight, does the weight loss in cancer mean that protective mechanism failed? Can that protective mechanism be reversed once it has failed?
Hypothesis(next step in the scientific method that directs the study): The body has a protective mechanism to gain weight when internal mechanisms identify cancer. That protective mechanism can fail. Once it fails, it can be reversed.
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This is how I have come to write this topic. I know others have had a similar experience. If you have had a sudden unexplained weight gain, please, post. Thanks sassy
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Sas--as I always give my doctor crap about, BMI is not always a good indicator of fitness. My BMI is greater than 25 but my body fat is only 22%. My sister has a low BMI but a high body fat percentage. I didn't start gaining weight until after I developed a benign prolactinoma around 9 years ago and my BMI was borderline overweight with 16% body fat!
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marley thanks for posting. question did you notice any weight gain before the prolactinoma or bc?
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No weight gain until right around the time of the prolactinoma. It was a combination of my body thinking I was breast feeding and developing plantar fasciitis--weight packs on really quickly when one is eating 3500 calories because of exercise then stops exercising but continues to eat at the same rate. I gained 30 lbs in a matter of months. Since BC, I'm up about 3 lbs
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Thanks marley that is very specific information
sassy
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I started to gain weight in the 2yr span leading up to my dx. My normal weight was 61 kgs as an adult in my 30s. Then my weight jumped to 64 and then it started creeping up, for no apparent reason. By the time I started chemo I clocked in at 70. as soon as the cancer started shrinking, so did I. It was weird and the docs insisted it had nothing to do with the cancer, but I always wondered
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Momine, Thanks for posting. I gained 23lbs with BC and then it melted away. When the scale started up 4 years after BC, my response was WTH. You saw the story above. The first time I didn't mention it. The second time I asked each doc. I knew it hadn't been studied. Too many docs will say no in a situation like this versus it hasn't been studied. They're is a world of difference between the two.
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In following the breadcrumb trail of obesity and how it relates to breast cancer, I've been studying Microbiota. From Wiki the definition of microbiota is "the ecological community of commensal, symbiotic and pathogenic microorganisms that literally share our body space". The science has explored some specific areas and is proceeding to expand into other areas as discoveries are made. A connection has been established between microbiota and obesity, but it is only beginning with much research to be done.
This link is to Wiki. Wiki has gathered the central ideas related to microbiota. Studying this will give us a basic framework to understand the definitions, and focus of the projects related to the microbiome.
https://en.wikipedia.org/wiki/Microbiota
This link is to a study of the "Obesity and the Human Microbiome". Studying this will give us the basic understanding of the connection between obesity and the bodies microbiome
http://www.medscape.com/viewarticle/714569
This link is to a study of the " Emerging Roles of Microbiota". The study discusses the relationship of microbiota and specific diseases and cancers.
http://carcin.oxfordjournals.org/content/35/2/249.full#T1
I have not found any articles yet directly related to any microbiota research related to breast cancer. We are all aware of continued publications linking breast cancer to obesity. I can make the following statement :If obesity has been shown to be related to microbiota and obesity is a risk factor in the development of BC, then hypothetically they're is a relationship between microbiota and BC until a definitive study that either proves or disproves a relationship.
Okay now done, this should stir things up
sassy
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How did I make the connection between microbiome, obesity, and BC? The chance recreational reading of an article related to the microbiome research of a venuzalan indigenous people. The people have been poked, prodded, and sampled. Their bacteria has been analysed from skin, all orifices, and their poop. Since I hadn't studied microbiome it was worth a look. Low and behold, it was 'no shit' moment. The subject dovetails into the BC and obesity controversy
For anyone interested in the indigenous tribe ..........
the study http://advances.sciencemag.org/content/1/3/e1500183
Article on the study http://www.techtimes.com/articles/47066/20150419/gut-bacteria-amazonian-tribe-reveals-new-information-human-microbiome.htm
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kayb. I was into the dashboard to send you a Pm to come visit here and got sidetracked. Thank you so much for bringing that article. I haven't got into it yet....b/c your comment about the bacteria being present in stage 1 and then in decreasing amounts as the stage increased. Is very interesting...........I'll read and get back to you. This is beginning study for me, so it'll take awhile to get a solid handle.
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kayb the link was broke, but I found the article
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083744
Abstract
Breast cancer affects one in eight women in their lifetime. Though diet, age and genetic predisposition are established risk factors, the majority of breast cancers have unknown etiology. The human microbiota refers to the collection of microbes inhabiting the human body. Imbalance in microbial communities, or microbial dysbiosis, has been implicated in various human diseases including obesity, diabetes, and colon cancer. Therefore, we investigated the potential role of microbiota in breast cancer by next-generation sequencing using breast tumor tissue and paired normal adjacent tissue from the same patient. In a qualitative survey of the breast microbiota DNA, we found that the bacterium Methylobacterium radiotolerans is relatively enriched in tumor tissue, while the bacterium Sphingomonas yanoikuyae is relatively enriched in paired normal tissue. The relative abundances of these two bacterial species were inversely correlated in paired normal breast tissue but not in tumor tissue, indicating that dysbiosis is associated with breast cancer. Furthermore, the total bacterial DNA load was reduced in tumor versus paired normal and healthy breast tissue as determined by quantitative PCR. Interestingly, bacterial DNA load correlated inversely with advanced disease, a finding that could have broad implications in diagnosis and staging of breast cancer. Lastly, we observed lower basal levels of antibacterial response gene expression in tumor versus healthy breast tissue. Taken together, these data indicate that microbial DNA is present in the breast and that bacteria or their components may influence the local immune microenvironment. Our findings suggest a previously unrecognized link between dysbiosis and breast cancer which has potential diagnostic and therapeutic implications.
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Okay kayb. this is so cool.
From abstract :"Taken together, these data indicate that microbial DNA is present in the breast and that bacteria or their components may influence the local immune microenvironment. Our findings suggest a previously unrecognized link between dysbiosis and breast cancer which has potential diagnostic and therapeutic implications."
My statement (from my post before kayb's post): " I can make the following statement :If obesity has been shown to be related to microbiota and obesity is a risk factor in the development of BC, then hypothetically they're is a relationship between microbiota and BC until a definitive study that either proves or disproves a relationship."
kayb, shucks, I done good on hypothesizing. The science is already started to make a link. The next step is doing a study re. microbiota & weight & BC. Started thinking parameters of the study. But getting close to brain dead. Entirely pleased with how this is progressing. Long way in a short time.
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Kayb from the discussion section of the Plos page of the article. Bolding & Italics is my emphasis.
"The dramatic reduction in bacterial load found in breast tumor compared to healthy breast tissue warrants further study to determine if bacterial load could be an additional indicator of diagnosis or staging of breast cancer. In addition, the inverse correlation between bacterial load and tumor stage implies that bacterial load might be used in conjunction with current methods to monitor the progression of breast cancer and to facilitate staging of the disease. Furthermore, it is tempting to speculate that a decrease in bacterial load in a healthy individual may be a signal of heightened breast cancer risk. Based on our studies, further investigation into the role of microbes in breast cancer would be of interest."
" In our study, the association of S. yanoikuyae with normal breast tissue and the dramatic reduction in its abundance in corresponding tumor tissue suggests that this organism may have probiotic functions in the breast. Interestingly, S. yanoikuyae express glycosphingolipid ligands, which are potent activators of invariant NKT (iNKT) cells [31]. iNKTs are important mediators of cancer immunosurveillance [36] and have been reported to have an integral role in controlling breast cancer metastasis [37]. Further studies are aimed at investigating the potential role of S. yanoikuyae in breast cancer development and progression."
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My comment: WOW! Not only in diagnosing, staging, or monitoring progression...........Why not study S.yanoikuyae as a treatment if not a curative? That's a leap of course, but it sure is a fun one
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This was in the results section of the breast study on the Plos page:
"Interestingly, there was a strong inverse correlation between the abundance of S. yanoikuyae and M. radiotolerans in paired normal tissue (Figure 1e top panel, p = 0.0003) which was not found in the corresponding tumor tissue (Figure 1e bottom panel). These data suggest that in paired normal tissue, S. yanoikuyae and M. radiotolerans may occupy similar niches and thus counterbalance each other in abundance. Meanwhile in tumor tissue, the quantity of S. yanoikuyae becomes significantly lower as the quantity of M. radiotolerans remains constant."
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MY Comment: I like S.yanoikuyae.
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From Wiki
Sphingomonas yanoikuyae
Sphingomonas yanoikuyae Scientific classification Kingdom: Bacteria Phylum: Proteobacteria Class: Alpha Proteobacteria Order: Sphingomonadales Family: Sphingomonadaceae Genus: Sphingomonas Binomial name Sphingomonas yanoikuyaeYabuuchi et al. 1990 Sphingomonas yanoikuyae is a species of bacteria.[1] Its type strain is JCM 7371 (= GIFU 9882). It is notable for degrading a variety of aromatic compounds including biphenyl, naphthalene, phenanthrene, toluene, m-, and p-xylene.[2][3] S. yanoikuyae was discovered by Brian Goodman on the southern coast of Papua New Guinea.
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From Wiki: link is to the genus description for Sphingomonas. S. yanoikuyae. is a sphingomonas.
https://en.wikipedia.org/wiki/Sphingomonas .
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Brainstorming: Why is this bacteria in my boob? Why is it depleted when BC becomes present? Why does it decrease as the BC gets worse?
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From Wiki. This is the description from Wiki. It will be used as a reference as we learn about the impact on the Microbiome of external things that can upset the human microbiome environment.
Importance of aromatic compounds[edit]
Aromatic compounds play key roles in the biochemistry of all living things. The four aromatic amino acids histidine, phenylalanine, tryptophan, and tyrosine each serve as one of the 20 basic building-blocks of proteins. Further, all 5 nucleotides (adenine, thymine, cytosine, guanine, and uracil) that make up the sequence of the genetic code in DNA and RNA are aromatic purines or pyrimidines. The molecule heme contains an aromatic system with 22 π electrons. Chlorophyll also has a similar aromatic system.
Aromatic compounds are important in industry. Key aromatic hydrocarbons of commercial interest are benzene, toluene, ortho-xylene and para-xylene. About 35 million tonnes are produced worldwide every year. They are extracted from complex mixtures obtained by the refining of oil or by distillation of coal tar, and are used to produce a range of important chemicals and polymers, including styrene, phenol, aniline, polyester and nylon.
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kayb not that it contributes to cancer development. My perception is that it modulates control i.e. present in normal tissue>>decrease in early staged cancer>>>decrease further as the stage increases. As if it's being used up or something is causing it to die.How it's used in industry is bioremediation/biodegradation of industrial waste of aromatic hydrocarbons :Polycyclic aromatic hydrocarbons(PAH)>>>petroleum spills>>>>converts PAH's to CO2 and H20. Biodegrades plastics
http://link.springer.com/article/10.1038%2Fsj.jim.2900475#page-1
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From Wiki:
"Sphingomonas is a rod-shaped bacterium (0.3-0.8 * 1.0-2.7µm) that has yellow or white color. Sphingomonas completely lacks lipopolysaccharides (LPS) that can carry endotoxins, which makes the bacterium almost unique among Gram-negative bacteria. Instead, it has a cell membrane that consists of proteins, phospholipids, and respiratory quinones and an outer membrane that contains glycosphingolipids (GSLs) (Balkwill et al). The GSLs occupy a position similar to that of LPS in other Gram-negative bacteria and appear to have many of the same functions, such as a barrier to batericidal substances. Also, because the carbohydrate part of a GSL is shorter than that of LPS, the cell surface of Sphingomonas is more hydrophobic than that of other Gram-negative bacteria. This is the probable reason for the bacterium's ability to degrade hydrophobic polycyclic aromatic hydrocarbons and its susceptibility to hydrophobic antibiotics. "(emphasis mine)
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For those that haven't used google to do extensive searches. What happens the longer the search goes on the google gremlins are working. They will continue to work. If I return to the same topic and keywords tomorrow or next week more hits will come up. This following link is to an immensely readable article, that encompasses allot said here today. It would have been nice to have it pop early, but that is fine now. There is a statement at the end in reference to bacteria that "Perhaps the most important revelation is the discovery of a possible new means to prevent breast cancer altogether". Cool.http://www.popsci.com/blog-network/under-microscope/link-between-breasts-cancer-and-germs
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Kayb I agree with the red herring thought that it was found in new Guinea. Please, bring that study re: spinach here for completeness, I would like to follow-up on that. The only reference I found in nature was with the mulberry tree. Your thought that it can't survive a tumor environment is an important one.
These questions below are unknowns at this point, but would be important to have answers too. No particular order, I'm just brainstorming.
1. What is in the tumor that causes the decrease in the S. yanoikuyae presence in the tissue?
2. If S.yanky's function is to degrade PAH's, what is S. yanoikuyae degrading in the breast tissue?
3. In degrading the "substances" in the tissue, how is S. yanoikuyae affected?
4. Can S. yanoikuyae be reintroduce to the tissues once depleted?
5. Where in the body is S. yanoikuyae found?
6. When is S. yanoikuyae introduced into the body?
7. What is the impact of oral supplementation of S. yanoikuyae on the human microbiome?
8. When they're no PAH's available in the environment what does S. yanoikuyae survive on?
"YOOOHOoooooo, researchers come and get it"
Today --maybe---I will follow a PAH breadcrumb that I read yesterday. It will lead to allot more questions.
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Work in progress
The information on the internet is vast re: Polycyclic Aromatic Hydrocarbons (PAH) and Bacteria/ fungi that "eat" PAH's. Going to attempt to describe why they are important to this discussion." Polycyclic aromatic hydrocarbons (PAHs) are a group of more than 100 different chemicals that are released from burning coal, oil, gasoline, trash, tobacco, wood, or other organic substances such as charcoal-broiled meat". (free internet dictionary). Initially the reading was driving me towards looking at individual PAH's, but I've determined that would make us crazy. People get degrees up to PhD level. What we want to know is how they relate to each other in our body
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This section is a brief overview of PAH's. Don't commit it to memory. The need to know is PAH's exist and they cause harm to the body. It's completely plagiarized from the internet.
PAH's can be incorporated into the body through absorption through the skin, respiration, and ingestion.
PAH's In genetics, a mutagen is a physical or chemical agent that changes the genetic material, usually DNA, of an organism and thus increases the frequency of mutations above the natural background level. As many mutations can cause cancer, mutagens are therefore also likely to be carcinogens. The most significant endpoint of PAH toxicity is cancer.
PAHs generally have a low degree of acute toxicity to humans.
The most significant endpoint of PAH toxicity is cancer.
Increased incidences of lung, skin, and bladder cancers are associated with
occupational exposure to PAHs. Data for other sites is much less persuasive.
It is difficult to ascribe observed health effects in epidemiological
studies to specific PAHs because most exposures are to PAH mixtures.
Animal studies show that certain PAHs affect the hematopoietic, immune,
reproductive, and neurologic systems and cause developmental effects. http://www.atsdr.cdc.gov/csem/csem.asp?csem=13&po=11--------------------------------------------------------------------------------------------------------
This section defines the way bacteria degrade or remediate aromatics and PAH's. It's here only to allow us to get to our endpoint. The need to know info is that bacteria can take in these substances>>metabolise them>>then expel the metabolites that are harmless. It's completely plagiarized from the internet
Protoemics and Metabolomics in Understanding of Bacterial Degradation of PAHs
Proteomics and metabolomics have been recently employed in studies of environmental microbiology and have shown their high impact on the field of biodegradation and bioremediation [158, 159]. Proteomics is an effective technique to identify proteins and their functions involved in the biodegradation of aromatics while metabolomics can be used to profile degradation products of PAHs and primary metabolites in response to PAH exposures. Intent of a brief discussion of proteomics and metabolomics here is to bring attention to these emerging fields rather than offering a comprehensive review and a long list of references.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672333/
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This section identifies a link to research publish in 2011. The research identifies that human tissue has been analyzed for the presence of PAH. The need to know is that tissues have been studied for the presence of PAH's.
Human exposure to PAHs occurs by inhalation, ingestion and topical absorption, and subsequently formed metabolites are either rendered hydrophilic and excreted, or bioactivated and bound to cellular macromolecules. The formation of PAH-DNA adducts (DNA binding products), considered a necessary step in PAH-initiated carcinogenesis, has been widely studied in experimental models and has been documented in human tissues This study include tissue from esophagus, prostate, human placenta, cervix, and vulva. Other studies have cover the oral mucosa, liver, and breast.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155323/
These two studies were referenced in the above study
Breast study evaluating smokers and
http://www.ncbi.nlm.nih.gov/pubmed/12727801
breast study evaluating char cooked meats
http://www.ncbi.nlm.nih.gov/pubmed/14504191
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This section identifies a a study published in 2014 on the "Microbial Dysbiosis Is Associated with Human Breast Cancer". This study was previously identified above. This article lead us on the quest to know more about the microbiome. The need to know is that breast tissue has been studied for the presence of bacteria.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083744
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This study published in 2013, identifies the risk factors for the development of breast cancer. The bolded area is my emphasis. The need to know is that the identified risk factors are the current factors accepted by science and doctors as causative to Breast cancer
Introduction:Breast cancer is the most common cancer worldwide, and the second leading cause of cancer death.1 One in nine women in the UK and USA will develop the disease in their lifetimes.1 It is more common in the Western countries than in Africa, South America or Asia, and several aetiological factors have been implicated in its pathogenesis.2These causative factors include age, genetics, family history, diet, alcohol, obesity, lifestyle, physical inactivity, as well as endocrine factors (both endogenous and exogenous).3 Triple negative breast cancer (TNBC) has recently been identified in certain sub-groups of patients, and has a higher recurrence rate, faster growth and poorer prognosis.4 Other associated factors for breast cancer are mammographic density5 and previous benign disease.6 However, it is still not very clear which of the factors has any predominant role (s) over others, in the pathogenesis of breast cancer.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3948957/
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Conclusion is my analysis: This search has rocked my world a bit, but it doesn't surprise me. The accepted risk factors have been promulgated for years. We all have been made aware of them time after time. Much of the time we have been made to feel that we are the cause of our cancer. How many studies have we read that support the party line by looking at the same factors without identifying anything new. Well that's all changed. For anyone following all the breadcrumbs from the beginning we have identified our bodies are subject to and incorporate PAH's from the air we breathe, the food we eat, and products applied to our skin. That the PAH's have been identified by well applied science to exist in our tissue's. Further, we have one study that identifies S. yanoikuyae as being part of the microbiome of the breast without explanation as to why. S. yanoikuyae is part of a group of bacteria/fungi called proteomics and metabolomics. These bacteria/fungi are used in industry to biodegrade and bioremediate PAH presence, but at least one of these has been found as a resident bacteria in our breast. No study to date on tissues(unless I've missed it) has identified PAH"s, proteomics and metabolomics bacteria /fungi within the same tissues.
I believe the research needs to identify all proteomics and metabolomics in study of human tissue. That concurrent analysis of the presence of PAH's be done in these same tissues. I think in the end what we will find that we have developed a symbiotic relationship with bacteria and fungi that protects us from PAH's. A couple of questions have come to mind. Is there and end point that the symbiotic bacteria are overwhelmed and can no longer prevent disease? If this be true than we can develop strategies for the use of proteomics and metabolomics in the treatment of cancer? Why not the prevention of cancer?
In looking at the bacteria and fungi that are used for different chemicals for either remediation or degradation, what struck me was the number of bacteria familiar to me from culture reports. These bacteria were seen as harmful to the body treated with antibiotics. What if their presence in a wound was a signal of not infection, but something else. What that something else could be, I don't know. But someone with great knowledge than me could possible surmise. Or maybe as this gels, other thoughts will come forward.
I'm ending here for the moment. The gist of my thoughts are documented here. I will revisit it a thoughts occur.
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No significant weight gain for me 2 years prior to dx; however, I can't seem to pin point the 5lbs gain after TE placement (since January). For me 5lbs is significant because I am small frame. For sure it is not the implants because they are small. I did not have chemo because small microinvasion and am not onTamoxifen. I notice that I have been shedding a lot of hair. Seeing my MO tomorrow for quarterly check up and will ask for thyroid fxn tests to make sure thyroid is behaving.
Edit to add: no changes in diet or activity.
I have history of IBS. Got it in 2010 after I came back from Nepal. Stomach has not been the same since. Very interesting studies on dysbiosis
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I had a sudden weight gain starting about 6-8 months before my Stage IV diagnosis. It's what eventually sent me to the doctor, along with chest pain. (Pleural mets).
When my weight gain first appeared, I began exercising to combat it. I climbed stairs 6 days a week in my apt building. At first I could do 20 flights with no problem. Then I began to feel out of breath, and had to rest after 15 flights, then 10 flights. I couldn't increase my exercise, even after 3 months. So I suspected something terrible. And my weight continued to climb. On my wedding day, a few weeks before I was diagnosed, I barely squeezed into a size 12 street dress. (I add this because it wasn't a wedding dress, which runs small.) My usual size was 8-10, and my normal weight fluctuated between 135-150 lbs. I weighed 168 when I was diagnosed. Within 6 months of treatment I had dropped down to 127 (probably within 3 months, but I wasn't checking my weight often).
I've discussed this weight gain with doctors, since weight LOSS is described as a symptom of cancer. I have urged my doctors to look closer at former breast cancer patients who suddenly gain weight. It took several weeks for my recurrence to be diagnosed. I had to first undergo a mammogram, then an X-RAY, then a scan. Had the doctor ordered a CT scan immediately, I could have started my treatment 3 months earlier.
I hope doctors and researchers pay attention to all this free observations and data you have supplied. :-)
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TarheeM, Thanks for posting, Your story is important. I'm hoping others will post to that had similar observations. I also, hope you will come along as we find breadcrumbs to follow. I've learned so much in the last days. Exciting. There was an old doc that I have quoted often "If you listen to your patients, they will tell you what's wrong". Conversely, (new)" if I listened to my docs, I'd be dead." Sorry, you missed out on earlier treatment. Do you think your experience will change their response when you tell them something's wrong?
Loverly, thanks for posting too. Same as TarheeM. 5 LBs to the doc is nothing. They so missed the boat. BTW I have some suggestions re: dysbiosis
To all, The ultimate goal is to get an ICDM9 code--unexplained weight gain. At that point we will have changed the world.
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Okay friends, if you will go back four posts. Let me know what you think? They're have been few posting, but the numbers are large as to lurkers. Several hundred just in about 3 days. To those lurking, I have felt comforted by your presence. I felt you were just as interested as I was to see where this would lead. I overwhelmed my computer. Twice had to shut it down to let it unclog it's memory. Now I'm going to shut down me for awhile and play.
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kayb thanks, I'm brain dead right now. Thanks for being here. We've had some great times in the past on Hot Flash forum and 2D6. depend on your insight and help. Let me know what you think about the post on PAH, Bacteria and research--5 posts ago? I worked on it for hours this morning. They're lot's of links. You don't necessarily have to read the entire link info.
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In the 2 1/2-3 years prior to my diagnosis, I gained 20 lbs. I'd weighed 135 for most of my adult life (30 odd years) and then all the sudden I weighed 155.
I then lost about 25 lbs over 6 months on a very strict Paleo diet (started diet not to loose weight but to heal gut/manage autoimmune disorder). I was down to 125-128 when diagnosed with BC, but I'd been at 155 for 2 years prior to that and while a strict Paleo diet is not the same as an act of God, it was a pretty radical change for me. Fats from very specific sources only, no gluten, no sugar, no dairy, all make a big difference in gut health.
Perhaps my weight gain three or so years prior to my BC diagnosis was a signal something was amiss.
Interesting discussion.
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Labelle thank you for posting. it's Important. Interesting story. Glad you are enjoying the discussion
Kayb, I think they're should be a rule that a second copy of all studies should be written in common English. Not that we didn't have a clue that all body parts are related to and dependent on each other, the intricacies that are now coming to light are like discovering the universe. Then I took a swim and came in and took my probiotics. I feed my bacteria with Hershey's chocolate(sugar), beer(yeast), and cheese(?). I need to take another shot at the study. May stick with the abstract and conclusion. I actually grasped more on the HAP & protoemics and metabolomics on the first read through. ..........Have you plowed through my post yet? Don't want to sound like Sheldon, but it's groundbreaking.
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Kayb, I posted this on the research forum just before we got into the microbiome. It is another example of gut flora affecting another distant body area. Thought I'd bring it here since we are looking at this as an organism thing---we are the organism LOL. I asked Cp4 if I could bring her post on weight and Vitamin D. I seriously need to play a little. BBL sassy
http://www.theatlantic.com/health/archive/2015/06/gut-bacteria-on-the-brain/395918/
When Gut Bacteria Changes Brain Function
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Thanks Cp4, hope you join us
Data gathering
This link is to a very nice study on weight and Vitamin D. The researchers proved very well that weight loss and Vitamin decreased Cytokines inflammatory markers. The weakness in the study is how did the impact of the exercise influence the reduction of cytokines. The participants exercised 5 days a week. Nonetheless, the percentages are nice. Why I thought this would be of value to the discussion is Vitamin D is big now in looking at cancer and cancer prevention. Which dovetails here.
https://community.breastcancer.org/forum/73/topic/832925?page=1#idx_2
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