My Hypothesis About Sudden Unexplained Weight Gain in Cancer
Comments
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Quoting you " Did you consider that maybe the weight gain is NOT a defense mechanism but the first sign that actually cancer itself caused that because it's trying to make the body produce more "food" for it and able to sustain it for a longer time, instead of the body running out of steam and due to feeding the cancer, it starts losing weight and being depleted thus going into the great beyond and the cancer going there with it?"
Yes
from the topic box " (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?)". Plus the hypothesis itself " " hypothesis: Sudden unexplained weight gain can be a sign of developing cancer." Day we are saying the same thing. Verbiage isn't identical, but it's so close it's splitting hairs.
What I object to is the promulgation that has occurred over the last couple of years(particularly bombarded this year) with BC is the "Maintain a Healthy Lifestyles". First thing on the list is maintain a healthy weight. If a person is seen as overweight the assumption(public) b/c of the healthy lifestyles promulgation is the person can be perceived as being at fault i.e they caused their cancer b/c they were overweight. But if overeating is not part of a persons modus operandi what other factors are at play. One example( they're others) in the study that the evidence supports is the overuse of antibiotics alters the gut microbiome. Endotoxins develop b/c of this alteration affecting the gut wall and make it permeable to endotoxins to cross into the vascular system. Those endotoxins aren't pathogenic enough to cause overt disease, but are pathogenic enough to cause disease in the long run. A thief in the night.
Think about circulating endotoxins constantly wearing on the immune system. An analogy is sleep. The body can only go so long without sleep, before systems start malfunctioning. Lack of proper sleep alters immune system functioning. Apply that concept to the immune system on alert for a protracted period due to circulating sub-pathogenic endotoxins, it is not going to react the same way an unstressed immune system will.
A major importance in the mouse studies was that they were able to show an alteration of anatomy of cells in the liver by these endotoxins. This affected the physiology(work). Those cells were directly related to glucose metabolism and insulin resistance. You alter those two things weight gain will occur. Plus, other malfunctions i.e. type 2 diabetes.
Back to the chicken and the egg. You believe it's a malfunction of the immune system. I don't disagree. I think where we disagree is the origin of the immune dysfunction. What I think is a major step forward is the identification that factors other than what we put in our mouths as food has an impact on not just weight, but are whole well being, and the function or dysfunction of the being. Think about how the body is divided into compartments. The Gi tract takes in all sorts of things. It digests. It absorbs. It keeps out what shouldn't be absorbed. That is a healthy gut. Change that healthy "china wall" and the hordes cross into the protected space.
I read that you believe it's a failure of the immune system. Something stressed to cause failure. Nothing like long term chronic anything will eventually lead to overload.
The way polcyclic aromatic hydrocarbons got into tissues can occur in one of three way.1.absorbed through the skin, 2.absorbed through the GI tract. 3. absorbed through the pulmonary membranes(alveoli). Then circulated through the body by the vascular system to distant places. Once lodged in tissue time allows them to do their dirty work. Did the immune system identify them? Did the immune system work for years against their dirty work? Did the immune system fail to recognize? Can the immune system work against this chemical? Is the immune system so overwhelmed at a certain point it starts to fail?
What is known they're PAH's identified in tissues. They're particular cancers caused by PAH's. How the cancer cascade occurs is under study and has been for decades. The oncogene. That word at one time was revolutionary. In the early days, the thought was once we identify an oncogene we could just eliminate it. Uh-huh. ..........
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Just a couple quick thoughts. Why is there less cancer in rural India than in the cities? Pollution, change in diet? Why is there half the rate of BC in Polish women with BRCA mutations than in North American women with BRCA mutations. Diet or exercise or pollution? Really hard to tease out. Why do Japanese women have so much lower rates of cancer until they move to Hawaii or the U.S? Diet or environment?
There's a lot of focus on carb vs. fat these days (just read "The Big Fat Surprise" by Nina Teicholz), but what about fiber? Obviously sugar is evil, and simple carbs close behind, but complex carbs are a whole nother story.
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Fallleaves - The carbs vs fat vs fiber - I am in total agreement with that. Not sure if I read it on this thread or another, one of the sisters here on BC said that she tried to lose weight using LCHF/Atkins but every time she stopped she put it back on and some. With my weight loss (also using LCHF diet), I took it very gradually - at 50+y.o. you can't count on your skin to tighten back up right away when you lose weight and I didn't want to have folds of skin hanging all over the place. In one year I lost 54 lbs, went from 191 lbs to 137 lbs. But it was pretty much in leaps and bounds. I'd lose 10-15 lbs in 2-3 months then go more or less on a "maintenance" phase for a 2-3 weeks time span - in which I increased the carbs, decreased the fat some but definitely pumped up protein and fiber and used some herbal teas. It worked like a charm each time. Of course, the fact that I DO have a degree in alternative medicine helped tremendously on this journey.
Also, what made me really happy is seeing in the last few months more doctors and nutritionists coming up and saying that BMI is less important than waist-to-hip ratio is.
And THAT, sas-schatzi would follow the train of thought right down your alley. Because what needs to be taken into consideration is that fat can be seen also as the "backpack" of the body. Actually not that, more like a combination between a backpack and a trash can. Most of us know by now that once you're in menopause, the ovaries stop producing estrogen and that task is taken over by the adrenal glands. And any surplus estrogen is deposited in the fat. But it's not only that, most toxins that the "filtration system" of our bodies can't get rid of will be deposited in the fat as well. So obviously "gut fat", the fat that is insidiously depositing in-between and around the internal organs of the abdominal cavity will be the most prone to be the storage place for these toxins.
Talking immune system, on the other hand, is a little bit more peculiar. Most of the immune system diseases known to the medical world actually come from genetic mutation. Take Graves, for example (as I am suffering from it I did a lot of research on that). You can carry the gene your whole life and never manifest the disease. Or you can carry the gene for 4.5 decades and then bam! something triggers it - like was my case. Sometimes the trigger is obvious - stress, eating disorders, smoking, etc - and sometimes it's out of the blue sky and the doctors and scientists are left scratching their heads in puzzlement
I wonder for how long the adenovirus-36 has been along. The virus that in the last decade was discovered to actually cause obesity. And how it could have influenced the whole cascade that leads to cancer thriving. Because, the focus is not on how the cancer appears in the first place - at any given time, everybody has some cancerous cells going around in their body but the self-defense mechanism of the body does not allow it to thrive. The focus is not so much on what triggers the failure of the self-defense mechanism. The focus is to first figure out if the self-defense mechanism DOES nullify the cancer stem cells or just the daughter cells, and if so, to attempt to replicate it. Otherwise, this whole line of research would be useless, because the treatments now in place do exactly that - kill the daughter cells but don't touch the cancer stem cells.
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I forgot to add another thing. Lately there have been discussions and studies done concerning the effect a ketogenic diet has on tumors - essentially starving them. Think about it: cancer cells have high levels of insulin receptors and are avid for sugar. That is essentially the mechanism the PET scan is based on. Normal cells can switch from glucose to ketones if the need arises, while cancer cells cannot.
http://www.medscape.com/viewarticle/749855
http://www.canceractive.com/cancer-active-page-link.aspx?n=3117
The ketogenic diet is also known to be one of the most effective in terms of weight loss - it's just people not being able to stick to it or go into a well-managed maintenance phase who fail, as it's a way of life more than a diet. People nowadays are conditioned to eat sugar. We all know it's more addictive than heroin.
There is also a recognized effect that ketogenic diet has on the microbiota, practically reversing the bacterial percentages that favor obesity.
http://caloriesproper.com/impact-of-a-low-carbohydrate-high-fat-diet-on-gut-microbiota/
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Afternoon Ladies
Spent the day rereading from the beginning. Regretfully, didn't make notes as I was going along. But the sense of it was that we are all on the same path. The articles and studies are all supportive of each other.I did learn the name of the mouse line that is used in all the studies http://irp.nih.gov/catalyst/v19i4/germ-free-mice
That lead to the Human Microbiome project through NIH https://commonfund.nih.gov/hmp/overview
brain dead again
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Ok let me throw in one more thing to make sure your head hurts.
Can we mix into this also the direct obesity effect that the raise in Firmicutes in the microbiota has. This has been directly observed in several studies on the "starvation" effect that a ketogenic diet has on various cancer cells. ketogenic diet = low Firmicutes high Bacteriodetes=lean humans. Regular carb diet = high Firmicutes low Bacteriodetes=obese humans. Fecal transplant from obese people (with the related high percentage of Firmicutes) caused obesity in the subjects who received the transplant. It is a well known fact that 80% of the good functioning of the immune system starts in the gut. And that the immune system can be easily disrupted by the wrong nutrition. The wrong nutrition/diet being actually the norm for most Westerners. Just google the mechanism through which IBD appears.
So I'd say the weight gain that preceded the cancer diagnostic was somehow caused by a change in the microbiota, causing carbs and protein craving and obesity; thus the cancer making sure it will receive the required glucose so it can thrive (known fact that while normal cells easily convert to ketosis if the diet is changed, cancer cells do not - they might turn to extracting required glucose through protein metabolism).
Question is how?
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Not enough data to surmise anything on the weight change. Remember the hypothesis on weight change is a separate discussion from the microbiome. However weight is part of the microbiome discussion.
Well, you can surmise all you want LOL, Surmising makes the world go round. Yay for surmising.
The study on Insulin resistance a couple pages back has the technical data related to the mice or at least has pulled from the same study on bacteroides and firmicetc. Those mice have been busy. I think I only saw two studies posted that were the same when I did the reread yesterday. Your fresh on the two bugs. Would you mind taking a look at that study and see if they are the same one or different ones. Puleese
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Just an observation, of course, perhaps not even causational: I had been taking GTF chromium and gymnema silvestre to help with carb metabolism once I went on maintenance from my LCHF (not strictly ketogenic) diet, as well as forskolin. I had begun to regain, but slowly--even with small “cheats” during European vacations. However, with my bc diagnosis I dropped all supplements except my multivite, probiotic, fiber, Vit. D & B12, biotin, melatonin and calcium--and I have been craving carbs ever since (and, alas, giving in). My weight gain settled out to w/in 1.5 lbs. +/- per week, but it’s an uphill battle to stay on the good side of the big two-oh-oh. I wonder if giving up the forskolin, chromium, gymnema, krill oil and ALA has had an effect on not just my metabolism but also my appetite.
A strict ketogenic diet--hard enough to follow in the real-world unless one never dines out and must cook for others of normal weight--is even tougher to do these days in light of the latest findings on the carcinogenic properties of processed and red meats, which had been my mainstays during the initial ketogenic phase of my LC diet.
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Seachain, forget that request. Had a thought. IF I remember, I'm going to call NIH. It would seem that they would develop a multiplan study when they get into using the mice. This may not make since, LOL it does though to me.
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Does to me too, Sas.
ChiSandy, it's not hard at all. I found that I spend on strict LCHF about half the money that I spend on regular carb,, even lower than normal but still carb. For the simple reason that on lchf I am never hungry, I actually have to force myself to eat to reach my RDI.
I did not take any supplements except my regular melatonin, Vit D3, calcium and hair & skin formula with biotin, collagen, hyaluronic acid and the joints formula with glucosamine, msm and all that stuff. It's not hard at all to prepare my foods, I usually reserve Saturday mornings to prepare all I need for a week. Essentially two types of meat (as in preparation not different meats), several containers of chopped stuff to make a salad in a few minutes, several types of desserts, some low carb bread or muffins or waffles. I eat very rarely pork, never beef, mostly chicken and white fish. And of course, eggs. The rest is essentially "foundation" vegetables, some cheese and of course whipped cream. I found that if I follow the "12-15 g of netcarbs from foundation vegetables" and 65% fat 20% protein 15% carbs rules, I am fine. I never crave carbs. Well, almost never. I might indulge in a pomegranate now and then.
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Seachain, you jogged my memory when you said cancer cells have a lot of insulin receptors. They also have a lot of leptin receptors---and obese people frequently become leptin resistant (leptin usually tells you when to stop eating), so maybe it's several things at work.
Here are a few studies:
http://www.ncbi.nlm.nih.gov/pubmed/26009703
http://www.ncbi.nlm.nih.gov/pubmed/21056997
http://erc.endocrinology-journals.org/content/18/4...
http://www.ncbi.nlm.nih.gov/pubmed/24025407
(Just a little more to see how much it takes to crack Sassy's brain!)
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Now if they could only crack the code to get leptin to our brains and keep them out of the cancer cells! Perhaps one day they’ll develop a SLRM (selective leptin receptor modulator) analogous to SERMs like tamoxifen & raloxifene for estrogen receptors!
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Sheesh..............................
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Ha-ha! So those are brain cells in my posterior?
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If breast cells can migrate as far as someone's foot sole, why wouldn't brain cells migrate to your behind?
Reminds me of this commercial. I remember at the time I saw it (It was after about 5 of my recon surgeries) I thought "If it could only be that simple.
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I was looking into AI's and ran across this study which has an interesting conclusion about leptin.
https://www.ncbi.nlm.nih.gov/pubmed/26571369 -
That IS an interesting one, 123! Leptin to adiponection ratio...hunh. That's a new one for me.
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Getting back to neutrophils, ran across this interesting mouse study:
"Gut bacteria require neutrophils to promote mammary tumorigenisis"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC449622...
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... and the neutrophils levels plummet during chemo.
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Interesting study on how metformin changes the gut microbiota to produce more short chain fatty acids (like butyric and propionic acids).
http://medicalxpress.com/news/2015-12-intestinal-b...
Also a study showing that metformin increases adiponectin and lowers leptin levels in the blood stream
http://www.ncbi.nlm.nih.gov/pubmed/26473366
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Hi Falls, I saw your post right when you posted. I've been reading for the last two hours. Hope I can remember what I read. The thing I know for certain is tomorrow will be even less.
Very nice insight by the researchers in the first article that drugs may alter microbiota. Would expect that with antimicrobials, antifungals, anti mycobacteriums. This will be a core study. Lot's of other drugs will be looked at for the same activity. Plus covering three different cultures in a wide geographic area is significant b/c it rules out dietary practices as the origin of the differences found. Cool.
The second study at the bottom it says "free PMC Article". Suggest reading it. It reads more like the study than an article about the study. I suggest reading the introduction and the discussion by pass the middle.
What would be nice is if they follow through and see what affect if any the combined application of the criteria in each study means?
There was one sentence that got me off on a tangent 'Thus, metformin, as the longest established oral antidiabetic agent, has been widely used in patients". Longest? I was there when it was first brought on the market, but couldn't remember what year it was. 1995. This link is to a history of Metformin. At the bottom, they're links to the resource articles. I read them all. Easy recreational reading. What science proved about the chemical that came to be eventually identified as Glucophage?Metformin in 1957 has a pretty amazing history. It's a perennial. Used particularly in the Middle Ages, but documented much farther back than that.
http://www.news-medical.net/health/Metformin-History.aspx
What surprises me after reading it's history is that Metformin is not used in the overweight non diabetic. There were two early studies that clearly showed that a nondiabetic experiences only none to mild reduction in glucose while the diabetic(type2) experiences a significant reduction.The study in the PCOS group showed that those with more centrally located adipose tissue had a weight loss where those that didn't have central fat didn't. Sounds to me like a study. Too lazy right now to go and see if that's an existing finding already. I know the weight loss is a known effect of Glucophage, but not if the identification of the central fat loss is known. Maybe someone will pop in a say YEAH that's been known for years LOL.
I'll volunteer for the study. i.e. nondiabetic with central fat
Thought I'd bring these links here. They were at the bottom of the above article and identified as the source for that article.
- http://www.jci.org/articles/view/14178
- http://onlinelibrary.wiley.com/doi/10.1002/pdi.606/pdf
- http://www.rsc.org/images/eic_nov2011_metformin_tcm18-210010.pdf
- http://media.wiley.com/product_data/excerpt/19/04707254/0470725419.pdf
- http://www.ncbi.nlm.nih.gov/pubmed/9742976
- Bailey CJ, Campbell IW, Chan JCN, Davidson JA, Howlett HCS, Ritz P. Metformin - The Gold Standard: A Scientific Handbook. Chichester: Wiley, 2008; 1-36.
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Sign me up too, sas-schatzi! Back in 2012, when I was about to be discharged from Northwestern Memorial to rehab after my first knee replacement, my peri-operative doctor paid me a visit. She noted my fasting glucose was higher than usual (I’d always been in the low 90s but following surgery it rose to 120-130), and suggested that I go on Metformin regardless, because she’d read research that it helped not just diabetics and prediabetics but also nondiabetics with central obesity lose weight. I’d resisted because I’d heard that all oral diabetes drugs raise LDL. After 2-1/2 yrs. on a low-carb diet (and ditching atorvastatin after six weeks), my glucose is back down to 92. (It went up immediately after my other knee replacement but fell steadily the further out from surgery I got--I suspect the stress of surgery, pain and rehab can increase it). Now I read that Femara can also raise not just LDL but glucose--I think I’ll raise the issue of whether to take Metformin with my MO when I see her a month and a half into my endocrine therapy. The issue of increased coliform bacteria might be a non-issue, as I take probiotics anyway. Anything that helps me lose or not gain weight (especially fat) once treatment starts will also make it easier for AIs to reduce estrogen, since I wouldn’t have the (mostly adipose) weight gain that would sabotage aromatase inhibition and keep my estrogen too high. My PCP concedes I must take Femara--endocrine therapy is do-or-die for me; but isn’t a big fan of taking too many prescriptions, which is one reason he’s counseling against starting bone-strengthening drugs which have much scarier side effects than either AIs or Metformin.
But isn’t the mechanism by which endocrine therapy causes weight gain due to estrogen-deprivation lowering metabolism? Would increasing metabolism--or at least keeping it steady--cause residual tumor cell proliferation?
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"First, metformin decreases the amount of glucose produced by the liver and reduces the bloodstream level and cellular uptake of insulin. In turn, the reduced insulin stimulation results in reduced activation of insulin receptors on cell membranes, triggering a cascade of intracellular molecular effects, such as the downregulation of the Ras/Raf/MEK/ ERK and PI3K/AKT/mTOR signaling pathways. One or both of these pathways are often activated in many types of cancer cells. In addition, metformin appears to upregulate AMP-activated protein kinase, a key molecule in glucose and insulin regulation and also an inhibitor of mTOR."
http://www.mdanderson.org/publications/oncolog/pre...
Lots of studies at MD Anderson: "On the basis of retrospective and preclinical studies that indicated metformin's potential as an anticancer agent, the drug is now being combined with traditional chemotherapy, radiation therapy, targeted therapy, and other cancer treatments in clinical trials. Metformin is also being studied in a single-agent cancer prevention trial. At the time of this writing, MD Anderson has six open clinical trials involving metformin, with several more under development."
(and 36 total on metformin and "breast cancer" at clinicaltrials.gov)
Here's an interesting study in non-diabetic women with BC who got metformin for 18 days before surgery (comparing biopsy tumor to surgery tumor).
"Decreased tumor expression of the IR (insulin receptors), combined with reduction in PI3K and Ras-MAPK signaling following metformin administration, points to the indirect insulin-dependent effects of metformin as its mechanism of antitumor action in the neoadjuvant setting."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC438149...
And another study that indicates metformin works through the gut: http://www.sciencedaily.com/releases/2015/08/15081...
ChiSandy, interesting question about increasing metabolism and residual cancer cells. Here's a paper I haven't quite digested yet (lol):
http://genesdev.cshlp.org/content/26/9/877.full
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Chi and Falls Yahoo and hootie hoooooooooooooo we are off on another search LOL.
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Just not tonight
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Hmmmm......if Metformin doesn’t raise metabolism but does inhibit tumor growth while preventing weight gain or inducing weight loss, perhaps it ought to be given to endocrine-therapy-receiving patients to prevent the weight gain inherent in that therapy, rather than encouraging patients to try to increase their metabolic rate. Exercise is still needed for bone conservation, and common sense dietary measures would be a good idea to both keep from sabotaging anti-estrogen therapy and allow metformin to better do its job.
And as generic drugs go, it’s not very expensive (until the mfrs. catch on and jack up the prices).
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kayb I have a friend. Define PCORI. Is it the same organization that you got your research grant through?
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kayb,
That's exactly what I was thinking about metabolism---exercise decreases risk of cancer (at least in every study I've seen), even though it ramps up metabolism. It's probably through reduction of inflammation and enhancement of the immune system, as this study indicates. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444650...
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As well as the increased insulin sensitivity that you mentioned, Kayb....
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