As a result, of a bad blood test at the end of September, I reexamined what I was eating and doing and ended up inventing the "ABCDE minus L" diet for fighting CLL which I will try until my next blood test 3 months from now:
A is for Anardana, an Indian medicinal spice made by grinding up pomegranate seeds.
B is for Brambles. Fruits of the bramble family including strawberries, raspberries, blackberries, rose hips, and pomegranates.
C is for the Cole family. These include cabbage, broccoli, Brussels sprouts, cauliflower, broccoli sprouts and sauerkraut.
D is for Drinking lots of water. This is important because I am increasing aerobic exercise in order to build blood volume.
E is for EGCG from green tea. I also drink green tea all day long with some rose hips bags (see Brambles) thrown in.
The other part of the "ABCDE minus L" diet is cutting back on lipids (fats and oils) as CLL cells love lipids the way other cancer cells love sugar.
Here are studies that appear to support this diet:
I'm at the watch and worry stage with my CLL. I'll let you know after my next blood test If it appears to be working for me. I invite others at the same stage to do the same. But check with your oncologist before starting anything new.
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HowardR
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That actually sounds like a healthy diet, I would want more protein added though.
I am on the cpjfg diet for the cooler months. Crawfish pie, jambalaya, filet gumbo. 😎
I’ll wash it down with some db. Diet beer. Gotta cut calories somewhere.
Good luck with your diet Howard. The bramble, cole and water parts of it sound quite healthy to me. I have never put cabbage in my gumbo, usually okra, but I bet cabbage would be good. I’ll try it and report back.
I enjoyed your humor! Of course this isn't everything I eat. I still eat meat (after draining out as much of the fat as possible during the cooking process) and I eat yogurt made with non-fat dry milk every day (with anardana and maple syrup stirred in).
I have actually cut way back on red meat. Its mostly chicken, duck and fish for me. But as a result of that, when I do eat a steak, I treat myself its a good one. That means marbling, fat is flavor. But no doubt lean meat is better for us.
I also tried my hand at a traditional Bolognese sauce, compared to the usual spaghetti sauce we have. I used ground beef and ground pork, but not lean beef, and it was amazing.
I have concluded Italian food is the best in the world, better than even cajun and creole, I hate to admit. But our food is influence by Italian food I think.
Cajuns start many dishes with the holy trinity of vegetables: chopped onions, celery and bell pepper. I learned while cooking my bolognese that Italians start with a sofrito: Chopped onions, celery and carrots.
I never thought of cooking with carrots as a base. It makes for a bit sweeter taste than the peppers. It was delicious.
I'm definitely adding some rosemary every day. I just discovered a test tube study from 2014 which found that RA (Rosmarinic Acid from rosemary) when combined with EA (anardana and bramble family) and EGCG (green tea) can prevent myeloid leukemia cells from proliferating. Thus rosemary could make EA and EGCG more effective:
Essential oils are abrorbed into the body through the skin and also through the olfactory system. They don't just sit on the skin . If they did they wouldn't be of any use. I think I shall add some rosemary oil to my body oil. Can't do any harm. Rosemary oil is also very good for memory.
My question regarding the lipid article would be where do the lipid droplets come from. Normally there should be no lipid droplets in the plasma. Lipids are transported in cholesterol molecules, not as free floating lipid particles. If there are such in the plasma, they are the result of high carbohydrate diets which at extremes lead to the so called fatty blood where the plasma is milky white from the abundance of free floating fat globules. This is the same as very high triglyceride levels in the blood. High fat diets reduce triglyceride levels drastically. That's my personal experience too. There are only 2 sources of energy (let's omit proteins which can't provide the daily energy needs, they are toxic in large amounts over 30% of daily energy needs or so and their consumption is tightly regulated by the body) carbohydrates and fat. A low fat diet is by definition a high carbohydrate diet. Which produces excess free floating lipids in the plasma. Are these the ones collected by the CLL cells? Per Prof. Seyfried lymphoma cells have damaged mitochondria. Hence the random gene damage in CLL cells variable from person to person. Such cells can't use the Oxfos pathway to produce energy. They can't burn ketones for energy. Even if there was enough oxygen in the marrow and nodes, which likely isn't. So where does the energy come from? The only possible answer is substrate level phosphorylation. Good luck with your experiment which I'll be interested to compare to mine as I go the other way hoping to get to the same destination.
I enjoyed your insights on this topic. My reading of the lipid 2018 meeting report (not a peer reviewed manuscript) reference is that, relative to normal B-cells, abnormal levels of "lipid droplets" are found intracellularly (within the cytoplasm) of CLL cells. I don't think the authors reported differences in lipid levels in CLL patients' blood plasma vis a vis controls. The authors present data that support their hypothesis that CLL cells rely on lipids uptake and synthesis as their energy source, which is rather unique feature of cancer cells that has been reported by other scientists too. Whether this abnormality can be significantly influenced (or exploited for treatment) can be influenced by by diet is an open question.
Thank you. Yes, it's an open question. Many of those who tried it and saw good results are quite convinced that it was the diet that helped. Can they prove it? No. Is it worth a try? I think so. What's there to lose? If it does not seem to work I can always go back to eating like I did most of my life 😁 Though I sure won't. I'd have to unlearn a lot of what I learned about nutrition and that's not possible.
Another thought. If CLL cells were scavenging lipids out of cholesterol molecules somehow, then I suppose those patients who eat a low fat diet, vegans and similar perhaps, would have a very low serum cholesterol content but high triglycerides at the same time. Them CLL cells eating out all the fat from the cholesterol molecules. Is that the case? Low fat eaters pls chime in. BTW most of the cholesterol in the body is made in the liver. 25% of the brain is made of cholesterol if I remember correctly. If one does not eat enough of it the liver will promptly step in and ramp up production. It belongs in the blood. What does not belong there is high levels of triglycerides.
Hi LeoPa, I admit to being less than careful about fat intake, freely consuming full fat dairy products, and I probably tend to overdo the carbs a bit (though very little sugar or processed foods). Being slowed down with CLL fatigue I have noticed a rise in blood sugar levels. But my cholesterol levels have always been low and remain so. I guess we're all different.
Hi bennevisplace, mixing carbs and fat in the same meal I'd advise against. That's the way to produce the harmful kind of cholesterol Apo Lipo B. I mean the transport molecule not the lipid of course. High fat meals are ok only as long as there's little to no carb in them. If you must have sweet fruit etc. the best way is to have a fruit and veggie only meal. But given we are in the same boat on somewhat elevated sugar levels if not careful, I decided to cut them out completely. I eat only whipped cream and sauer cream since dairy protein especially casein is said to promote tumour proliferation. I used to eat cheese like others eat bread but no more.
It’s interesting LeoPa because if you’d written that on a Diabetes forum, many of the members would have thrown their hands up in horror! Following a diet rich in monounsaturated or polyunsaturated fat instead of meals high in carbohydrates or saturated fat helps improve blood sugar control. Fat slows down the glucose uptake which is essential to avoid hyperglycaemia but the key message is fats are not all created equal.
If I had a bowl of strawberries, my glucose level would be higher than if I’d had them with full fat cream.
It’s a hard balance and some of us are fighting different conditions which don’t respond equally to the same nutritional response.
Hi Newdawn, I guess they are on the diabetes forum exactly for the reason of not knowing about these things 🤔 As for the fats, we're half on the same page Polyunsaturated fats easily oxidise and promote inflammation especially when heated (cooking on corn oil? oh no). Extra virgin cold pressed olive oil is what I use on salads and that's the only one I use. On the other hand saturated fats do not oxidise and thus are much safer. Coconut oil is the most saturated plant based fat, contains no cholesterol (not that cholesterol as a lipid is dangerous because it's not, but as a transport molecule it can be, think Apo Lipo B) , can be heated to 220 deg. Celsius before it burns. I use it almost exclusively for cooking. Mono unsaturated are the good guys too,like most in the olive oil. Strawberries are tasty and sweet 😋 But I go only as far as a tomato on that front. And only once in a while. Is such food fanaticism going to help me? No idea. But I have to try because what if... Best wishes!
Your first sentence hints at a diabetes blame culture LeoPa and that sadly demonstrates lack of understanding of the subject.
Sadly much of the standard nutritional advice type 2 diabetics receive on dx does little to control and even reverse hyperglycaemia. What demonstrably works is the high fat, low carb diet but the type of fat is important. It’s not food fanaticism because I can’t be bothered with all of that but eating by the meter teaches you an awful lot about how the body responds to different foods.
Newdawn, no blame culture whatsoever. How can a patient be blamed for not knowing these things if most diabetologists don't? If there's blame to be laid somewhere, it's at their doorstep. I know more about the subject than I'd wish to as my mom had type 2 for 25 years and it was me who got her condition under control not the doctors.
Per this medical news article, "This was a study into lung and esophageal cancers in mice, not blood cancers, let alone CLL, in people. Further, 'The combination of the diet and diabetes drug didn’t shrink the lung and esophageal cancers in the mice."
Finally, "The research is in the extremely early stages. It’s unclear if these results could be replicated in humans."
Even if they were, per the earlier discussion above, given CLL cells derive their energy from fat lipids, rather than glucose, there may not be the benefit anticipated.
Howard, on another note, did you think about a low fat high carb diet could set the stage for rapid advancement of a secondary cancer, given all we know about solid tumor metabolism? Just something to think about. Possibly could be fixed by keeping such diet hypo caloric, aka starvation diet. For a few. weeks or months you could pull it off, but not for the long run.
LeoPa, You may be on to something. CLL cells love lipids, but other cancer calls love sugars. So if you increase sugars and reduce lipids, you could be encouraging a secondary cancer. As far as I know, I don't have a secondary cancer right now, so I'm not going to worry about this.
I saw nothing convincing about CLL cells loving lipids, anecdotal evidence suggests otherwise. Immune systems primary fuel is glutamine. But I'm unsure about this being true for CLL as well. It's highly counterintuitive that any cancer is fuelled by lipids. My train of thought goes like this: when a cell has healthy mitochondria, it can't become cancerous. In case of mutations in the nucleus the mitochondria initiates apoptosis and the cell dies. Out of control mutated cells have damaged mitochondria. Which can't use the oxidative phosphorylation pathway to produce energy, hence can't burn fats. That leaves us with sugar or glutamine as energy sources. Through fermentation. In the marrow or nodes probably. Where there's not much oxygen probably. CLL causes hemoglobin levels to go down at later stages. Hence the fatigue. Lack of oxygen in the tissues to produce energy. But does this slow CLL? No! How so? Other cells can't function normally due to lack of oxygen but CLL cells still can? And multiply like crazy? What do they have lesser oxygen needs? Probably yes. How? There in lies the response. I might be wrong of course. But I don't see how.
There are actually several studies that show that CLL cells are opposite to cancer cells in this way. I didn't know about them until about a week ago. when AussieNeil alerted me to them on this blog.
Here's one of them which says that CLL cells scavenge up lipids from the blood stream and then synthesize and metabolize them. It also says that lipids are especially involved with CLL metabolism within the oxygen-starved lymph nodes and bone marrow where CLL cells proliferate:
There's two things. First they say it's a hypoxic environment in the marrow and nodes, then they say lipid synthesis via beta oxidation for energy production? even though there's very little oxygen there? Even if that was true, how and what kind of lipids do the CLL cells collect from the serum? Triglycerides or cholesterol? Cholesterol is protective against cancers. First sign of liver cancer? Very low cholesterol for no apparent reason. Unlikely that it's the cholesterol molecules (which transport lipids as a vehicle.) Guess where triglycerides come from? Yep, high carb diets. Which are the mother of all catastrophies in the human body. This would be the one exception to the rule if its otherwise. How likely is that? Best way to reduce high levels of triglycerides? You guessed it. Very low carb diets, keto at the extreme end. Just my 2 cents. 😉
CLL cells are an exception to the rule! Most cancer cells show up in PET Scans due to the Warburg effect (i.e., they love sugar). CLL cells don't show up on PET scans. Here's a paper whose abstract begins by specifically stating that fact:
"Dysregulation of cancer cell bioenergetics is one of the hallmarks of cancer. The Warburg effect is one such documented change. However, glucose metabolism is not universally increased in cancer cells. Uptake of radiolabelled glucose in chronic lymphocytic leukaemia (CLL) fails as a marker of proliferation..."
Hi Howard, understood. But that does not change the fact that high carb consumption causes high triglyceride levels. That means fat in the blood. Eating carbs causes fatty blood while avoiding carbs and eating fat instead reduces the triglyceride levels dramatically. So counter intuitively the less carbs on the menu and more fat, the less fat in the blood. Cholesterol can't be much influenced through diet as the liver simply makes more if its level becomes sub optimal. Whichever way I slice it, low carb is the way to go. Nutritional fat is not the enemy. Except poly unsaturated vegetable oils, extracted via chemical processing. Try to squeeze fat from raw corn,if you know what I mean. And saturated fat isn't the enemy either. But I digress
"lipolysis is the breaking down of the triglycerides stored in the adipose tissues of the body into glycerol and free fatty acids"
This seems to support my suspicion that if there is lipolysis going on in CLL cells then it is the triglycerides in the blood that feed it ( fructose, in an indirect way).
But I still don't understand how beta oxidation can happen in a severely hypoxic environment and how can damaged CLL mitochondria ( I take it for a fact that monoclonal B cells have damaged mitochondria otherwise the cell would die since healthy mitochondria initiates apoptosis when it detects damaged genes in the nucleus) burn the released free fatty acids this way for energy.
Even if there is any beta oxidation there it could be a futile cycle which can't provide energy to CLL cells. And how much energy could it produce with oxygen levels that low?
So where do they take their energy from? Glutamine and sugars come to mind.
Since this is a chronic disease with slow progression maybe we don't need to see a severe increase in sugar consumption on account of substrate level phosphorylation like with solid tumors that grow like crazy. I mean when cancer cells double in numbers in 6 months (much less when one is on W&W), it is much different from them doubling in numbers in days with solid tumors. Can it be possible that they still use sugar as energy source but not in amounts that would be detected as abnormally high by PET scans?
I don't know but people much smarter than me do not know either, so I keep my mind open, my ears perked up and looking for answers.
BTW I am into another 40 hour fast and like last weekend, it is a breeze. No hunger at all. Can't say I'm looking fwd to the next multiday fast (I plan to do 4 days this time) though
Thank you for trying to sort this out. CLL cells release free fats when they are proliferating in the low oxygen environments of the lymph nodes and the bone marrow. Thus, as we both agree, they are engaging in beta oxidation.
You wrote, "But I still don't understand how beta oxidation can happen in a severely hypoxic environment." I don't understand this either.
By the way, I don't agree with your assumption that CLL cells have damaged mitochondria. There could be other reasons for why they don't engage as readily as normal cells in apoptosis.
There are chemicals (ibrutinib for example) that are able to induce apoptosis in CLL cells . [In an earlier draft of this post, I gave an incorrect example.] One possible explanation: ibrutinib prevents CLL cells from engaging in beta oxidation, forcing the mitochondria to engage in normal oxidation which induces apoptosis.
Thanks for the info! If they release fatty acids from the triglyceride molecules then no matter how they do it minimizing blood triglyceride content could be beneficial for CLL too. I know it's beneficial for a host of other conditions. So much so that pills are prescribed to lower it when too high. 👍
Howard, do you now have a reference for an in vitro study showing "the combo of EGCG (green tea), EA (brambles) and RA (rosemary) was able to induce apoptosis in CLL cells"? The study you previously referenced was for human HL-60 promyelocytic leukemia cells, from the myeloid, not lymphoid stem cell line: healthunlocked.com/cllsuppo...
The myeloid stem cell line produces red blood cells, platelets and most white blood cells, but not lymphocytes from which CLL cells originate. Hence research on human HL-60 cells is not relevant to CLL.
Thank you for the correction. My point was not to extol that study but to point out that there are studies which have found that drugs can induce apoptosis in CLL cells in the test tube. That point is true, even though my example was faulty. A better example would be the commonly used targeted thereapy [I mistakenly wrote chemotherapy in an earlier draft] drug ibrutinib which induces apoptosis in unmutated CLL cells. See:
Howard, this difference between the lymphoid and myeloid stem cell lines is extremely important, because the two stem cell lines have different cellular pathways. It's why for example Imatinib: en.m.wikipedia.org/wiki/Ima... works extremely effectively for Chronic Myeloid Leukaemia (CML), but not for CLL.
For evidence that something may work on CLL cells, you first need to find a study that shows apoptosis is triggered in B-lymphocytes, ideally close in the life cycle to when CLL develops. The reason that this is important is illustrated by the fact that all CLL treatments don't impact memory B cells and plasma cells, or our immunoglobulin production would plummet to zero during treatment. Active cellular pathways change during the B-lymphocyte life cycle.
Interestingly, there is a dearth of human CLL stem cell lines as it is difficult to get them to continue growing in a culture. That's why nearly all the in vitro research is about other lymphomas and leukaemias unless the CLL cells have been harvested from CLL patients. Unfortunately, such CLL cells lack the stromal protection that they have in their growth centres in our nodes and bone marrow, which is why proof of in vitro apoptosis is rarely translatable into in vivio success. CLL cells in vitro are very easily killed.
By the way, both ibrutinib and elagic acid (EA) are kinase inhibitors which can induce cell apoptosis. EA is found in pomegranates, strawberries, and all members of the bramble family. Here's a description of its effects in the test tube:
"Ellagic acid is a potent CK2 inhibitor, with an IC50 of 40 nM and a Ki of 20 nM. Ellagic acid also blocks other kinases such as LYN, PKA, SYK, GSK3, FGR and CK1, with IC50s of 2.9, 3.5, 4.3, 7.5, 9.4 and 13.0 μM, respectively, and shows no obvious effects on DYRK1a, CSK, NPM-ALK, RET and FLT3 (IC50s > 40 μM).... Ellagic acid with IR also induces cell apoptosis..."
"Ibrutinib (formerly PCI-32765) is a potent, covalent inhibitor of Bruton's tyrosine kinase, a kinase downstream of the B-cell receptor that is critical for B-cell survival and proliferation. In preclinical studies, ibrutinib bound to Bruton's tyrosine kinase with high affinity, leading to inhibition of B-cell receptor signaling, decreased B-cell activation and induction of apoptosis."
Ellagic Acid (EA) has been specifically been found to induce apoptosis (natural cell death) in CLL cells (not AML cells) in the testube. Here's the study:
I can’t comment on your packaging nor can I see what country you are in. Janssen the European supplier states “ Imbruvica is an anti cancer medicine that contains the active substance Ibrutinib. It belongs to a class of medicines called protein kinase inhibitors “
If you are in the US mdanderson have an article online entitled “ the drug that may make Chemo a thing of the past “
The primary mechanism of action of Ibrutinib is the inhibition of "keep alive" B Cell Receptor signalling. Without that signalling, apopotosis naturally occurs: pharmacyclics.com/home/our-...
The genetic errors that can cause CLL are numerous and extremely complex. It will probably take decades to unravel all the causes, so that true personalised medicine can be successfully applied to most cases.
This paper just gives an inkling of what can be involved and how heterogeneous are the potential causes:
There may actually be something to my hypothesis (partly based upon your contribution to this discussion), when I wrote:
"One possible explanation: [Ibrutinib and EA] prevent CLL cells from engaging in beta oxidation, forcing the mitochondria to engage in normal oxidation which induces apoptosis."
I just carefully reread a study about why EA (Ellagic Acid which is in pomegranates, strawberries and the bramble family) causes CLL cell death in the testube. The reason: it directly affects the mitochondria in a way that induces cell death in CLL leukocytes (but not in normal leukocytes).
"Findings obtained in this study proved that EA selectively rises intracellular ROS formation in CLL B-lymphocytes (Fig. 4). The intrinsic pathway of cell death is especially susceptible to ROS [Reactive Oxygen Species]."
There are three hypotheses presented as to why this CLL cell death eventually occurs:
1. The extra oxygen has "an inhibitory effect on Na+/H+ exchanger activity resulting in cytosolic acidification, which creates a conducive environment for apoptosis."
2. Extra oxygen targets a mitochondrial protein called ANT which can possibly prevent apoptosis.
The third explanation may actually be a version of my hypothesis. Succinate dehydrogenase is an enzyme that participates in the citric acid cycle -- the beta-oxidation pathway used by cells to get energy from lipids.
If I am interpreting this study correctly, it could be saying that EA can force CLL cells to engage in normal oxidation, which eventually causes normal cell death. EA doesn't affect normal leukocytes because they already engage in normal oxidation and, like all other non-cancer cells, they eventually experience normal cell death.
CLL cells do not continue to accumulate, but do experience apoptosis, but at a slower rate than they are replenished by cell division. This was proven by tracking heavy water incorporation into CLL cells, per this overview. sciencedaily.com/releases/2... (The source paper is unfortunately behind a firewall).
In associated work, it has been determined that nearly all the CLL tumour growth happens in the lymph nodes, where the CLL cells establish a nurturing microenvironment which is responsible for the dramatic difference between in vitro and in vivo research results. "The LN was identified as the anatomical site harboring the largest fraction of newly born cells, compared to PB and BM. In fact, the calculated birth rate in the LN reached as high a 3.3% of the clone per day." At the birth rate of 3.3% per day, the tumour mass would double in a month if it wasn't for some degree of apoptosis.
Thank you for the link and the explanation! I haven't yet taken the time to read the studies that you linked to, but I will eventually do so.
One of the environmental characteristics of the lymph nodes is that they are oxygen-poor environments. It could be that CLL cells tend to engage in normal sugar-based oxidation which causes apoptosis when they they are in oxygen rich environments and beta-oxidation of lipids which doesn't cause apoptosis when they are in oxygen poor environments.
It looks like the oxygen poor environment only accentuates the difference between in vivo and in vitro results, per this paper, which found that CLL protective stromal cells thrive and multiply in low oxygen environments: ncbi.nlm.nih.gov/pmc/articl... Yet another reason why CLL is so very hard to eradicate.
Unlike solid cancers, CLL doesn't form solid tumours where the cancer cells encourage the growth of nurturing blood vessels (angiogenesis), but infiltrates an existing structure. I'm not sure to what extent the nodes and spleen keep up with the extra oxygen demands due to increasing CLL infiltration, though it might occur in the bone marrow: nature.com/articles/2401825
I just read the first of the two studies you cited, the 2013 study which highlights the importance of MSC cell support of CLL cells in the bone marrow. (The article doesn't mention whether MSCs are also part of the lymph node environment - another oxygen-poor location where CLL proliferation takes place.)
Its point was that MSCs can't function in the normal 20% oxygen environment of the test tube, but they do well in 5% oxygen poor environments, which I presume to be the oxygen level of the bone marrow where they normally live.
I don't think that the 2015 EA & CLL study that I cited earlier included MSC cells in its test tubes. That study seemed to me to be examining CLL cells by themselves in part of the study and CLL cell mitochondria by themselves in another part.
But I am a novice at reading these papers. The EA & CLL study may have, by necessity, included MSC cells in the test tube culture. If so, in its conclusion it was ignoring a fourth possible explanation of its own results, the one suggested by the 2013 study you cited -- that high oxygen levels in the test tube caused the MSC support of CLL cells to enter senescence, resulting in CLL cell apoptosis.
We're discussing whether research evidence supports my ABCDE minus L diet. LeoPa knew a lot about lipids and thought that it doesn't make sense to reduce lipid consumption. We actually came to an agreement that I could possibly be right, though he is still doubtful.
AussieNeil knows that, of the supposedly therapeutic foods that I am eating, the only one supported by direct research evidence which shows that it helps CLL patients in a controlled experiment is EGCG from green tea, and he is correct. He thinks that I am making wild claims, but I am trying not to do so. Meanwhile, I am trying to get him to admit that I could possibly be correct about some of these foods. (EA, for example, has been found to be effective against CLL in a test tube study.)
Also, I am trying to learn as much as I can from AussieNeil while I still can as his health is deteriorating. He has immersed himself in this field of research for over a decade, while I am a social science researcher but new to this field.
News to me too! I needed treatment this time last year, but after 10 months on Acalabrutinib and Venetoclax, along with completing Obinutuzumab infusions back May, my blood counts are the best they have been for over a decade!
It's easy to get lost in the weeds. If we do reasonable things to improve our overall health, proactive as well as reactive, I think we have a better chance of living better and longer. EGCG extract gave me poorer liver markers. Do I want to help my CLL at the cost of my liver? The KETO diet dropped my high blood pressure and rid me of 40 pounds of fat. Is it supplying lipids to my CLL cells so they can proliferate? Not yet. After 6 months I am still UMRD thanks to Acalabrutinib. Am I healthier? Definitely. I also fast intermittently and have a KETO holiday about once a week. I eat lots of fresh salad with olive oil, some fish and animal protein and less than 20g of carbs.
I really do like the way you reach out and broaden your approach to deal better with our common enemy. Keep looking around and posting. Makes us think.
Why can't somebody please publish an article espousing the curative virtues of Belgian beers on CLL? Unfortunately, I think I know the answer. I appreciate your post and supporting references very much. I strongly believe there is much that thoughtful diet and exercise can do to improve health generally, as well as specifically for those with cancers such as CLL. I wish we could easily organize clinical trials to investigate such things, but doing a good trial is so costly that few would organize it absent overwhelming evidence it will work and/or government grant money. Please do let us know how it works for you!
I have not encountered this disease, but I think this diet can suit anyone, I want to try it. I've been using the ketogenic diet for a long time and I've been cooking with keto recipes from scottgoodingproject.com/rec... . I really like to cook with them, and the diet gave awesome results, but I didn't quite fit the increase in fat intake and reduction of carbohydrates. But in your diet, you just need to eat as little fat as possible. Perfect. I can definitely drink green tea and plenty of water, I love fruits and berries, but I doubt about broccoli and Brussels sprouts. I'll read about this diet on the Internet and find suitable products for myself.
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Whole food Plant based diet reversed cll.
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