My Hypothesis About Sudden Unexplained Weight Gain in Cancer
Comments
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I would imagine that this sudden weight gain pre-dx phenomenon, if it is to help the body “fight off cancer," would be before a diagnosis of mets ab initio. (i.e., if one were Stage IV at initial dx). Body mass doesn't “fight off cancer;" a higher BMI might provide a hedge against cachexia, to delay the process as long as possible. Cachexia is not a factor in early-stage cancer. Central obesity can even be a risk factor for ER+ cancers.
My hypothesis is that this phenomenon (the one that is this thread’s subject) is a coincidence.
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Hi, Chi, many good points, as usual friend
What's incredibly weird is this thread is wonky right now. It disappeared and reappeared. The Mods are working on "what's up". I came back to get a particular post and the topic box was there , but none of the posts
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https://www.youtube.com/watch?v=oNm5sE9GAFc&feature=push-u&attr_tag=JoTV8iwNuu-qFy8x-6
Gut Microbiome video, The fella's voice is irritating, but the info is good.
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Howdy! I've just finished a marathon reading of this thread and a good majority of the links. Wow - a lot to consume! Thanks to sas-schatzi and others who have contributed here.
Some random thoughts in no particular order...
I gained a fast 10 lbs in the 5 months prior to my BC diagnosis. However, since my weight has fluctuated wildly my entire adult life, I doubt that means anything significant in my case (though it might for those who have much more stable weights and suddenly gain.) So, I don't think my experience counts in gathering any data.I found the discussion and articles about microbiome fascinating and had a few take-aways for me personally. One, I need to find a better probiotic with more strains than the kind I am taking now with only one! Makes sense that the more strains, the better - right? (From what I have read, more different strains seem to be recommended.) Secondly, I need to eat more whole grains, fruits, vegetables and less meats, dairy and processed foods. Should be a no-brainer, but there seems to be a lot of compelling evidence not only in increasing good microbiome. but also should help with my ongoing battle with chronic constipation. I should have been doing this all along. Duh! I have been on a high protein diet (medically necessary) and have been getting that primarily from meat and dairy with little room for much else. I need to make an effort to eat more plant based proteins. Seems both the better diet and probiotics should help with controlling my weight as well - I particularly was interested in one of the articles that discussed the relationship of microbiomes to hunger.
On a different tangent - I had gastric bypass 2.5 years ago. Before my surgery, I had a BMI of 50! It is currently 28. That's a LOT of estrogen being released from my fat cells in a short amount of time (the first 1.5 years) - do you think there is any correlation between rapid weight loss and a Dx of BC? Of course, it could be that I had BC before but was undiagnosed because mammograms are much harder to read when that large. And being obese makes one at a higher risk of BC - I don't know if that is simply because of the higher amount of estrogen stored or what, but I imagine it must play at least some part. BTW - I was 100% ER+.
Another thing my bypass certainly affected was my gut flora. You can't decrease the size of a stomach dramatically (to the size of a walnut initially) and bypass 18 inches of small intestines without changing a LOT of the natural balances. For example - about 7 years ago, I had my gallbladder out and I was one of the rare folks who ended up with chronic bile salt diarrhea. (I had chronic constipation my entire life before that.) This was godawful - I couldn't leave my house before noon each day because it would hit each morning and not stop for hours even with medication to control it. This stopped completely immediately with my bypass! In fact, I went from chronic diarrhea to chronic constipation literally overnight. That had to have done a number on the natural balance in my entire digestive system!! What all else that affected, who knows? But it had to have had some systemic effects to have that drastic of a change.
Looking forward to reading more! -
Hi Ready, So much to digest(pun). Regarding weight. I wish some researcher would pick up the hypothesis and do a retrospective study and then prospective study.
For me it happened twice. Right before BC and then right before thyroid cancer. Likely the TC was present before BC and then something changed when it took off??? Weight gain pre BC was around 23 lbs(?forget now exactly) , followed by a 50 lb weight loss -23 post mastectomy and 30lbs with the help of Savella or undx'd Hashimoto's??.
Then two things occurred which muddies relationships or trying to fix a causal relationship. I gained 50 ibs over about 4 months. I stopped Savella and the thyroid developed a goiter. Goiter dx'd in yearly ct exam after weight gain. Doc's ignored my concerns over the weight gain. Told to watch calories. UGH
It did help that I was suspicious re: the rapid weight gain with the thyroid b/c of BC weight gain. with the goiter once it was identified a bx was done---totally negative path report. Serial US's. Jan of '14, I asked for basic bloodwork. Free T3&T4. and autoantibodies. A thyroglobulin (TG) &TG antibodies. TG was 53 (33 top normal). TGab--negative. The TG and TGab are usually used to dx Hashimoto's But can be used in different ways as markers for TC. My doc immediately agreed to do a thyroidectomy. Pathology--negative. TG had moved to 109(Maybe 102).
I was released by the doc, but insisted I had cancer. The specimen was sent out to Quest lab for a second opinion. Path report TC diffusely through out both (edit) Lobes. Plus, Hashi's identified. First pathologist admitted he could see both in the bx 9 months earlier and at "ectomy". He should retire..
Anywhooses, had I not been so suspicious of the weight scenario, I may have not been so emphatic re: having TC. The specimen would have never been looked at again.
MICROBIOME: Lactobacillus colonizes the last two thirds of the small intestine. The Bifidius and others colonize the large intestine aka colon. That's why you need to move to the balanced probiotic.
I did reach a conclusion that the paleo diet was the go to diet. But I didn't want to give up my wine and do hard cider(UGH). I didn't dig into the mediterrenean diet. Previously, I had done the Macrobiotic diet for my dad. Basically, veggies and low animal protein & high protein vegetable. Animal protein is the culprit in all these diets. Already forget the elements of Paleo, but I think that statement is correct.
The section here where I talked about the dysbiosis that allowed endotoxins to cross into the bloodstream is an important read. It was the link on Insulin resistance.
Have fun.
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Hi Sas, so just a week ago I saw a thyroid specialist for two nodules that formed after radiation. He said the nodules weren't big enough to qualify for biopsy and he didn't do any blood work. "Probably. Not cancer". Although one nodule was covered with calcification so they really couldn't determine if it lit up or not. I sent a note to my PCP about what he said as there was nothing in the visit summary except to go for another US in Jan 2018. My PCP never answered my query about why no thyroid panel. But a doctor filling in for her said that the TSH test was the most sensitive and other tests weren't needed. I don't agree and now I see your post above. The specialist did say it was my autoimmune system that was attacking my thyroid. Any suggestions? Wait until Jan? Or?
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Hi Mari, All tests should be done at the same time It's a snapshot of how all are working at that moment in time. The reason I say this is my most recent studies were done. Of course, the order got screwed up. Two studies weren't done and one came back abnormal. The doc then 3 weeks later wanted to do just the two missed studies. I kept talking until she sweetly said would it make me happy to have the test repeated.
It came back normal. Well that's highly weird. Highly weird. Shouldn't be bouncing around, if I'm compliant with the med b/c my thyroid is gone. But had I not insisted on a redo we wouldn't know that. I would have had an increase in medicine that may or may not be needed. Thyroid meds are not benign drugs. Too much can be like a wrecking ball on the heart and bones.
Still diverging for a moment till I answer your question. TSH measurement is a lab test that was first developed around 1975. It did become the "gold standard" for thyroid testing. To the detriment of all patients. Yes a detriment. For a hundred years before that doctors treated thyroid patients by symptoms. Then with the TSH the docs believed the thyroid to be normal, if the TSH was in normal range. That normal range was arbitrarily established by clinicians. The range was too wide and only recently made more narrow, and lowered. For decades thyroid patients have had to suffer b/c of bad science.
Now to your question. TSH, FreeT3, FreeT4, Thyroglobulin, Thyroglobulin Antibodies. Minimum.
The whole body works like a fine running car when that car is at the top of it's performance. When the pistons, carberator, brakes, lines are malfunctioning the car won't work right.
There are other Thyroid function tests and there is discussion on their value depending on where you read.
I wish I had done a thread in 2014 on what I learned when I was learning it. I have forgotten so much. The memory used to be a steel trap. Now it's a sieve.
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Don't you just love the words "Probably , not cancer". We all know people that are dead because of those words. It's part of why I study so much. Real fast after becoming a nurse, I knew docs were fallible. That pushed me into studying harder than when I was in school and I studied hard in school. I had to study so hard to know whether what the doc was saying or ordering was correct. I saved a lot of lives and prevented a lot of errors b/c of this approach. I was , also, able to surround myself with excellent docs, b/c I knew whether or not they knew their stuff.
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Mari, get the labs done and insist on a ultrasound guided bx of two node on opposite lobes. Ask for an independent major lab to do a second opinion on the pathology. My first bx and then the thyroidectomy were done at a community hospital. The pathologist had about 30years experience, but missed my cancer twice I happened to read that hospitals end of year statistics for 2013. They had only 4 Thyroid cancer patients in 2013. Per Medicare standards that ratio would not define that hospital as meeting the minimum standards for pathology competency. This could have been just a really lacking pathologist as he also misdiagnosed a friend with melanoma TWICE. She was met'ds by the time she got a proper dx. But it was a lesson.
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Thank you Sas! So did you have thyroid surgery then and what else - radiation? And what medicines are you taking for your thyroid.
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I had the thyroid out, The proper pathology dx, then Radioactive Iodine 131 which is a one time pill. (23,000$). Now on thyroid replacement hormone. Levothyroxine 175 mcg.
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Ok, I see above you asked for the thyroid removed and then they found the cancer in the pathology lab. So it was the TG test that would have determined that you have TC? So if the tests can determine that you have TC - done correctly and read correctly of course, then why is there a need for a biopsy? I have three things going on at once - thyroid nodules, PVD and vitreous clouding, and thirdly deciding whether to continue AI. Any my weight is just stuck. Went up after gabapentin for pain and so hard to get it down.
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The primary use for Thyroglobulin(TG) &Thyroglobulin autoantibodies (TGab) is for the dx of Hashimoto's. For Hashi's they would both be abnormal. If there is a variation on this to dx hashi's, I don't know it.
How TG &TGab applies to Thyroid cancer?
TG abnormal high & TGab normal can be associated with cancer. Classically, the reading will tell you it should not be used as a cancer biomarker unless the dx of cancer is established. Hence, the bx to confirm or negate the dx of cancer. Otherwise, abnormalities would be dx'd as hashimoto's.
TG normal and TGab abnormal can be associated with TC, but not sure how, this combo was told to me at Moffitt NCCN in Tampa. I asked why as I hadn't seen that in my reading. We got diverted and I forgot about it.
Once the dx of TC is made then these two become the biomarkers for return of TC. Mine are run a couple of times a year. IF I can get the orders done right.
Can't tell you how many times all the orders have been screwed up. Just as an FYI, from here on out, I will check all orders that are put in the computer.
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Mari, Shouldn't PVD Peripheral vascular disease contraindicate taking AI's? That would take a bit of a search. But generally, PVD definition pulled from the net. PVD is the umbrella name of the condition. I'll place the definition I pulled and then put any additional thoughts after it.
"Description
Peripheral vascular disease includes a group of diseases in which blood vessels become restricted or blocked. Typically, the patient has peripheral vascular disease from atherosclerosis. Atherosclerosis is a disease in which fatty plaques form in the inside walls of blood vessels. Other processes, such as blood clots, further restrict blood flow in the blood vessels. Both veins and arteries may be affected, but the disease is usually arterial. All the symptoms and consequences of peripheral vascular disease are related to restricted blood flow. Peripheral vascular disease is a progressive disease that can lead to gangrene of the affected area. Peripheral vascular disease may also occur suddenly if an embolism occurs or when a blot clot rapidly develops in a blood vessel already restricted by an atherosclerotic plaque, and the blood flow is quickly cut off."
Do you see why I question whether you should be on an AI?
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Mari, The Vitreous clouding---are you under the care of a Retinologist? I developed wet macular degeneration in Nov. 2016. I have rec'd 5 eye injections since. Oddly, when I had the first eye scan, the technician dropped in conversation that I was the 4th of 8 patients that day that had a history of BC. Eye fluroscien scans can be done for many reasons.
Was it a fluke that 50% of that days patients had BC or is it a problem unidentified? I tried to address it with the doc. He blew me and the question off.
I checked the net and there is very little info on chemo(1) and AI's(0). Initially, I figured this is an area that has been ignored b/c the connection isn't being made. WHY? It's not the retinologists body part or problem. Direct eye cancers are rare. They don't tend to think outside their body part.
A friend recently entered a new trial, and for the first time an opthamologist evaluation was part of the work up.
So, what's your complete history on this?
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I hope it's ok to post this here...
PVD is Posterior Vitreous Detachment in my case, again also have PCO from cataract surgery, and Vitreous clouding.
Breast cancer medications and vision: effects of treatments for early-stage disease.
Author information
Abstract
This review concerns the effects on vision and the eye of medications prescribed at three phases of treatment for women with early-stage breast cancer (BC): (1) adjuvant cytotoxic chemotherapy, (2) adjuvant endocrine therapy, and (3) symptomatic relief. The most common side effects of cytotoxic chemotherapy are epiphora and ocular surface irritation, which can be caused by any of several different regimens. Most notably, the taxane docetaxel can lead to epiphora by inducing canalicular stenosis. The selective-estrogen-receptor-modulator (SERM) tamoxifen, long the gold-standard adjuvant-endocrine-therapy for women with hormone-receptor-positive BC, increases the risk of posterior subcapsular cataract. Tamoxifen also affects the optic nerve head more often than previously thought, apparently by causing subclinical swelling within the first 2 years of use for women older than ~50 years. Tamoxifen retinopathy is rare, but it can cause foveal cystoid spaces that are revealed with spectral-domain optical coherence tomography (OCT) and that may increase the risk for macular holes. Tamoxifen often alters the perceived color of flashed lights detected via short-wavelength-sensitive (SWS) cone response isolated psychophysically; these altered perceptions may reflect a neural-response sluggishness that becomes evident at ~2 years of use. The aromatase inhibitor (AI) anastrozole affects perception similarly, but in an age-dependent manner suggesting that the change of estrogen activity towards lower levels is more important than the low estrogen activity itself. Based on analysis of OCT retinal thickness data, it is likely that anastrozole increases the tractional force between the vitreous and retina. Consequently, AI users, myopic AI users particularly, might be at increased risk for traction-related vision loss. Because bisphosphonates are sometimes prescribed to redress AI-induced bone loss, clinicians should be aware of their potential to cause scleritis and uveitis occasionally. We conclude by suggesting some avenues for future research into the visual and ocular effects of AIs, particularly as relates to assessment of cognitive function.
- PMID:
- 21819259
- PMCID:
- PMC3205820
- DOI:
- 10.3109/02713683.2011.594202
- [Indexed for MEDLINE]
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Publication types, MeSH terms, Substances, Grant support
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Let me correct a misconception about fat cells and estrogen. The fact is that fat itself doesn’t secrete the androgen that aromatase helps convert to estrogen. The fat cells do, not the fat they contain. Fat is fat. It either gets stored or burned. It does nothing on its own. (Biochemically at the molecular level, the fat inside fat cells is not very different from any other animal fat, be it suet or lard—it is a substance, not an organ. The cells that house it are organs). The functional differences between “brown fat” and “white fat” are due to the types of cells that contain it and to a lesser degree their location.
And the sad fact is that unless they are surgically removed (cut or sucked out) or frozen to death, we can never lose fat cells. We can only decrease their size by diet and exercise burning the fat inside them. So why do our MOs tell us as soon as we’re diagnosed to maintain our weight and not gain any more?
Because there are two types of obesity: hypertrophic and hyperplastic.* (“Trophic” refers to a cell's behavior, and “plastic” to its creation. “Hyper” of course means “too much”). Hypertrophic obesity happens when your fat cells store increased amounts of fat, filling and stretching. Men and women are both susceptible to it. It is what we think of when we think of “gaining weight.” But here’s the sad and unfair fact: women are also vulnerable to hyperplastic obesity. Yup, when our fat cells get too full, they signal our body to make more fat cells! This does not happen in men, unless they have too much unopposed estrogen in their bodies (and is how they can become ultra-morbidly obese). Here’s the vicious cycle: fat cells make an androgen converted to estrogen. And unless (as in non-morbidly-obese and otherwise normally-hormonally-balanced men whose adrenals aren’t out of whack) there is enough androgen (usually gonad-secreted testosterone in men) unopposed by estrogen, estrogen itself helps transmit the fat cells' signal of fullness to the brain to make more fat cells.
Therefore, no matter how much weight we lose, i.e., how much fat we burn and how much we empty our existing fat cells, that will not reduce the amount of estrogen being produced and therefore not reduce the risk of getting an initial ER+ tumor or its recurrence. However, if we fail to maintain our weight and gain fat instead, at some point that weight gain will be due to making new fat cells in response to our existing fat cells’ signals of fullness. And the more fat cells we have (again, irrespective of the amount of fat in them), the more estrogen we will produce, the harder aromatase inhibitors will have to work to prevent that (and the less effective the drug will be), and the more “fuel” there is for ER+ tumor cells to divide and proliferate.
*For example, the term describing that something that has grown too big without having generated any new cells is “hypertrophy.” When that hypertrophy is the result not of distension, edema, or vascularization but rather of new cells being created, it’s referred to as “hyperplasia.” e.g., swollen gums are called hypertrophic gingiva; an oil gland that has begun to grow due to new oil gland cells proliferating is a sebacious hyperplasia.
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Oh, and as to why myopic AI users are more vulnerable to traction-related (uveal or retinal detachment) vision loss? Myopia, or “nearsightedness," is caused by images being focused too far forward of the retina—and this in turn is caused by an elongated eyeball. The longer the eyeball, the more myopic one is.* The longer the eyeball, the more traction (“pulling force") is exerted on its structures, and therefore the greater the risk that something's gotta give. As estrogen declines, those structures lose their elasticity, and eventually could tear.
*True "farsightedness," or hyperopia, however, is--like myopia--age-independent; the image hasn't fully focused when it reaches the retina because the eyeball is too short. But our decreasing need for reading correction as we age? That's presbyopia—"presby-" referring to age-related. It can happen whether the eyeball is too long, too short, or just right—and it is caused by the tiny muscles that let a natural lens focus on near objects stiffening with age, so it's harder to focus on near images. When a natural lens is replaced by a plastic one via cataract surgery, it's already in focus; and if that lens has been chosen to correct near rather than far vision, reading glasses are less necessary. But most people choose to have the lens correct distance vision; and sometimes the lenses that correct astigmatism (“toric”) are so expensive that insurance—including Medicare—won’t cover them. So if you’re very astigmatic, drugstore reading glasses don’t cut it. That’s why not everyone gets to give up their glasses after cataract surgery. (That was the explanation my ophthalmologist gave at my pre-cataract-surgery orientation consult).
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I was willing to pay the extra for better lenses - multifocal I think they were called, but was told by my opthamalogist I couldn't have them due to Fuch's disease. Also have astigmatsm in myright eye. Very very helpful information. Thank you.
Sonobello freezes fat cells
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So it came to me earlier today that the stereotype is people with cancer lose weight? At least I thought it was. My MO always asks if I've had unintentional weight loss? No. And I wish. Still wondering if Sonobello will be the cure : ))
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Hi Marijen- You have Fuch's corneal dystrophy? I was diagnosed with that three years ago. I am still in the beginning stages. Are you seeing a cornea specialist for it? I belong to the group fuch's friends, which is a group that recently moved to iogroup. They always stress there that you need to be followed by a cornea specialist, and preferably by someone who has seen lots of Fuchs. The best Fuch's specialists are in Indianapolis, Baltimore, and Portland. I live in the Chicago area, and many people in the support group here, have had cornea transplants done by Dr. Price in Indianapolis. We are finally getting a Fuch's specialist here in August who was trained by Dr, Terry in Portland, and who has been practicing in Boston since then. He is moving to the University of Chicago, and everybody in Chicago is ecstatic, because that means they will not have to go to Indianapolis to have the surgery done. Everybody in Boston loved him, and are sorry to see him go. If you go to the Fuchs friends site, there is a list of recommended doctors to go to. It is a wonderful support group. Even if you are just going to have cataract surgery, you want to go to a cornea specialist who knows about Fuch's.
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ChiSandy - thanks for the explanation about fat cells and estrogen. I see now how it is a fallacy that just losing weight increased my estrogen - it was rather the other way around - GAINING it was the problem. I suppose that is why obesity is a risk factor for breast cancer - we produce more fat cells to produce more estrogen, not just have more fat. Before my gastric bypass, I had a BMI of 50, so that certainly put me past the threshold of "full fat cells" to the creation of probably a whole lot of new ones. (I had been over 200 lbs 3 times previously and had lost weight only to gain it back quickly, so it was highly probable that I had already increased the number of my fat cells years before as well.)
This is interesting to me because my PS said he needs to take a small amount of fat from my belly to fill in areas on my breasts, so will do liposuction. I had joked that he could take ALL the fat from my belly and he told me he actually could do that and a tummy tuck at the same time if I was interested since insurance will pay for most of the surgery anyway (anesthesia, hospital charges, etc.) I'll only have to pay a small difference. I jumped at the chance since I have a flap of loose skin in my lower belly and still have a lot of fat in my mid belly I just can't get rid of no matter how much weight I lose. He would remove most of that. So - if what you are saying is true - actually removing it will give me a much higher chance of keeping that weight off. Which makes me even more sold on the idea, not just from the weight standpoint but also estrogen too now. -
Here's a wild thought..... what if the decrease in estrogen from menopause and AI treatment causes sugar cravings?
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And I hope it's ok to post this here...
Send to
J Clin Oncol. 2017 Jun 27:JCO2016720326. doi: 10.1200/JCO.2016.72.0326. [Epub ahead of print]
Low-Fat Dietary Pattern and Breast Cancer Mortality in the Women's Health Initiative Randomized Controlled Trial.
Chlebowski RT1, Aragaki AK1, Anderson GL1, Thomson CA1, Manson JE1, Simon MS1, Howard BV1, Rohan TE1, Snetselar L1, Lane D1, Barrington W1, Vitolins MZ1, Womack C1, Qi L1, Hou L1, Thomas F1, Prentice RL1.
Author information
Abstract
Purpose Earlier Women's Health Initiative Dietary Modification trial findings suggested that a low-fat eating pattern may reduce breast cancers with greater mortality. Therefore, as a primary outcome-related analysis from a randomized prevention trial, we examined the long-term influence of this intervention on deaths as a result of and after breast cancer during 8.5 years (median) of dietary intervention and cumulatively for all breast cancers diagnosed during 16.1 years (median) of follow-up. Patients and Methods The trial randomly assigned 48,835 postmenopausal women with normal mammograms and without prior breast cancer from 1993 to 1998 at 40 US clinical centers to a dietary intervention with goals of a reduction of fat intake to 20% of energy and an increased intake of fruits, vegetables, and grains (40%; n = 19,541) or to a usual diet comparison (60%; n = 29,294). Results In the dietary group, fat intake and body weight decreased (all P < .001). During the 8.5-year dietary intervention, with 1,764 incident breast cancers, fewer deaths occurred as a result of breast cancer in the dietary group, which was not statistically significant (27 deaths [0.016% per year] v 61 deaths [0.024% per year]; hazard ratio [HR], 0.67; 95% CI, 0.43 to 1.06; P = .08). During the same period, deaths after breast cancer (n = 134) were significantly reduced (40 deaths [0.025% per year] v 94 deaths [0.038% per year]; HR, 0.65; 95% CI, 0.45 to 0.94; P = .02) by the dietary intervention. During the 16.1-year follow-up, with 3,030 incident breast cancers, deaths after breast cancer also were significantly reduced (234 deaths [0.085% per year] v 443 deaths [0.11% per year]; HR, 0.82; 95% CI, 0.70 to 0.96; P = .01) in the dietary group. Conclusion Compared with a usual diet comparison group, a low-fat dietary pattern led to a lower incidence of deaths after breast cancer.
- PMID:
- 28654363
- DOI:
- 10.1200/JCO.2016.72.0326
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sorry, FOLKS , from my last post I took a thinking break. Haven't seriously looked at any of the posts, just wanted you to know I was being lazy. But will get back to this................................
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Mari, Ah-Hah PVD Periperherl vascular disease is the more common thought for a nurse as it's a pretty common disease. The older term for your condition used to be retinal detachment. I suppose they changed the term b/c it is more descriptive of the process. That happens a lot over time with conditions. The joke with this type of thing is "What are we calling it this year(decade)" i.e. x-ray>>>>radiology>>>>diagnostic imaging,
What's Fuch's disease? What's Sonobello? Ah-hah, her is Peaches with a fuch's definition
Nice abstract/study, I will try to bring this to my retinologists attention. What's your treatment plan for the eye(s)?
Chi Sandy, I enjoyed your description of fat. Useful info, but the discussion of how whether the there is a connection between Rapid weight gain and cancer in a time period before cancer is manifested. I, also, enjoyed your description of the "opia's. I think I'd choose near vision as I read constantly. Which did you choose?
Of course, then we diverged multiple times.
Peaches thanks for your addition on Fuch's disease. Is there any association of the disease with cancer treatments? Definitely need to be careful writing Fuch's.
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Sas, my treatment is return in a month for DFE - Dilated Fundus exam. Not sure if he did that last week, but I was blurried eyed for hours afterwards.
Sas, please in all your wisdom, tell me what to do about sugar cravings!! Donuts are getting the best of me. And you can't say fruit because I eat too much already...
Thanks!
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Sas-schatzi I'm not going to comment at this time other than to say I find your question fascinating. I spent hours yesterday reading all of the links you've given since the beginning. Oh I'veadded your thread to my favorites
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Mari, If you ascribe to the Microbiome research. Then your biome is off. It's really the gut bacteria signaling that they want more sugar. What was that movie Pretty in Pink? The plant eater said "Feed Me"
Their is a study here, I will try to find it.. I , also, suggest the following search terms. If you find any evidenced based research please, add it
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Mari, top of page 3, Aug 6th, 2015, 1015 am. " http://care.diabetesjournals.org/content/33/10/2277.full
Mechanisms linking gut microbiota to obesity, IR, and type 2 diabetes"
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