Hi
Diagnosed in 2013 and on W&W but blood tests not so good and expecting to get some sort of treatment soon. Trying out using Hyperbaric Chamber, will do 20 sessions and then drop to 1 per week as advised so will be interesting to compare blood results before and after. Any body had similar experience I wonder?
Rob (surname edited out by Admin to protect identity)
I tried the hyberbaric chamber during W&W, without any change in condition. May have done 20 treatments. Did not seem to be effective for me.
Thank you for sharing that hyberbaric chamber therapy didn't help you. That fits with the replies in this post on this topic:
healthunlocked.com/cllsuppo...
Neil
I was curious about the science involved, a Gpogle search found these articles
mayoclinichealthsystem.org/...
oxfordrecoverycenter.com/wp...
ncbi.nlm.nih.gov/pmc/articl...
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Len
Hi there, I asked the group the same question 3 years ago, see Aussie Neil's link to my original post. I went there quite regularly during W&W. I also went after ITP (low platelets) and it is hard to know whether it was just the medication or the combination with hyperbaric which helped the platelets to increase. I continued with hyperbaric until a bit before starting on V&O (Venetoclax and Obintuzamab) about a month ago. I dare not carry on with hyperbaric in case it would make the treatment work too well. It is impossible to know whether the hyperbaric delayed needing treatment or not...Sorry not been much help but very interested in this discussion.
How are you tolerating the V & O treatment?
Hi thanks for asking. I put some brief notes on my profile.
I was sick from the trial dose of Obinituzumab but since then I have taken an anti sickness tablet and I have been fine. I had intravenous Piriton for the first 3 doses to protect against an allergic reaction, which made me quite tired but they have stopped giving that now and I have been fine.
I started with 20mg Venetoclax about 10 days ago and am now on 50mg. Not really any side effects at all so far, thank G-d except for the cramps last week which I mentioned before, but they are not happening at the moment. Basically so far so good.... wondering if the ramp up to 400mg will make a big difference to how I feel.
HBOT research on cancer generally is interesting. My summary of the research is IF?? it has something to offer it will be in conjunction with other therapies such as Professor Thomas Seyfrieds metabolic approach which you can learn about here-youtu.be/KusaU2taxow BUT despite it being very interesting and I am starting his approach CLL shows a lot of metabolic flexibility and hence I would suggest you find a Integrative Doctor to guide you as its very tricky and may not work especially for low grade CLL which is is not as responsive to high grade CLL that has a positive PET scan which suggests its more glucose dependent.
and so HBOT alone lacks research but could be useful in other conditions such as head trauma and early Alzheimers
I suspect CLL's preference of lipids along with its metabolic flexibility are likely to undermine such efforts. Based on heavy waters studies, we know that CLL cells do undergo apoptosis, but have long survival times. How do you starve slowly dividing CLL, while not hurting faster dividing and or less resilient body cells?
Of more relevance, according to the below analysis by Dr David Gorski, an American surgical oncologist, Dr Seyfried's enthusiasm is based on mouse studies where even the way that these are done, indicates that poorer outcomes in human brain tumour trials are likely.
"Throughout his talks, both here and elsewhere, Dr. Seyfried presents mouse studies that are interesting and suggestive that there might be something to this whole ketogenic diet thing, at least in brain tumors, such as this one. However, this is what we in the oncology biz would call pretty preliminary data, worthy of further investigation but not supporting the grandiose claims that Dr. Seyfried makes.
We need more beef. We need clinical studies. Unfortunately, they’re in short supply."
More specifically, with respect to the mouse model studies, "This cell line has the property of metastasizing quickly and widely when implanted under the skin and allowed to grow, which actually makes it not very much like brain tumors, which seldom metastasize and usually kill through local invasion and taking up increasing volume in the closed space of the skull, something the brain most definitely does not like. The results showed that a ketogenic diet increased mean survival time by over 56%, while a combination of a ketogenic diet and hyperbaric oxygen therapy (HBOT) increased survival time 78%. The result is interesting, but it is a mouse tumor model, not a human tumor model, and that makes its applicability to humans tenuous, particularly given the nature of the murine tumor, but probably worth investigating further."
sciencebasedmedicine.org/ke...
I agree with Dr. Seyfried that glioblastoma multiforme is a "devastating type of brain cancer". I've lost two close relatives to Glioblastoma multiforme. It's a very aggressive cancer, which is much like Richter's, not a slow growing, chronic cancer such as CLL. Resistance to chemotherapy typically develops quickly, limiting treatment/later palliative care, to maybe radiation therapy and/or operations. From observing what happened with those two cases I personally know of, I don't agree with Dr. Seyfried's hypothesized role of the ketogenic diet for this aggressive acute cancer. Maybe it might work with other cancers, but he isn't very convincing in my opinion.
Neil
Thanks Neal.... good info I will work through and I agree that Thomas might be overenthusiastic . It is very pleasing to see trials starting since dietary approaches often don't get support . Perhaps it turns out that keto-fasting works best in conjunction with traditional therapy as Prof Longo s work suggests but we await his trial of fasting in CLL which he wants to do but I have not been able to see it has got of the ground. His mouse CLL -Fasting approach was positive. It might be possible to block lipid metabolism in CLL with repurposed drugs but this is very experimental.
It seems CLL primarily prefers lipids and to a lesser degree sugar. Endogenous or exogenous? It would be nice to know more about this.
Exogenous, per the referenced research in this post:
healthunlocked.com/cllsuppo...
From 5 years ago with respect to brain cancers:
healthunlocked.com/cllsuppo...
Community discussion:
healthunlocked.com/cllsuppo...
Neil
I had a bunch of articles on this opened in my browser that I was looking at when it closed down. Didn’t bookmark. I did find some that are interesting.
This is an exogenous intake study from 2009-2013, clinicaltrials.gov/ct2/show....
A little blurb from Wikipedia (en.wikipedia.org/wiki/Lipop...), under Clinical significance regarding LPLs.
Clinical significance
LPL expression has been shown to be a prognostic predictor in Chronic lymphocytic leukemia.[39] In this haematological disorder, LPL appears to provide fatty acids as an energy source to malignant cells.[40] Thus, elevated levels of LPL mRNA or protein are considered to be indicators of poor prognosis.[41][42][43][44][45][46][47][48][49][50]
sciencedirect.com/science/a... (I don’t think they test for CD36, PLIN1, APOC1.)
Your science direct reference is reporting research from the same Flinders University research group I posted about, but as you've found, there is independent study and even a related clinical trial. The clinical trial was small, only 15 participants. They only measured changes in ALC, not the total tumour burden, so not much help in working out what, if anything resulted from the omega 3 supplement. No control group, so no randomisation possible either, but at least they reported some results!
References to your Google mail only work for you 
Thanks,
Neil
Oops. Here are the links.
pubmed.ncbi.nlm.nih.gov/311...
ncbi.nlm.nih.gov/pmc/articl...
Per your second reference, which is indeed interesting, despite it being a small study;
"Handling of LDLs is also heterogenous in CLL cells. For example, signaling processes in CLL cells appear less dependent on exogenous LDLs in a group of patients with more aggressive disease, indicated by higher circulating leukemia cell numbers and rapid doubling times in vivo (Fig. 6A, B). An interpretation of these findings may be that relatively early-stage CLL cells with indolent growth are more dependent on LDLs. However, as they become more aggressive in terms of rate of proliferation, they change their metabolism to become more like mitogen-activated normal lymphocytes (Owens et al., 1990) or acute leukemia cells, i.e. they become less responsive to exogenous cholesterol (Fig. 2, Fig. 6A, B) and decrease their intracellular cholesterol levels (Fig. 6C, D)."
:
Taken together, the observations in this manuscript suggest there is a cohort of CLL patients whose leukemia cells internalize LDLs and amplify signaling properties and for whom LDLs are tumor promoters. By lowering LDL levels, statins may reduce signaling and slow the growth of these cells, explaining their ability to slow time to first treatment and increase overall survival. (Chow et al., 2016, Mozessohn et al., 2016) However, statins may also have direct anti-tumor effects that are independent of plasma LDL-concentrations.
:
Appropriate therapeutic targets for LDL-cholesterol to prevent tumor progression are unknown, in contrast to target levels required to prevent cardiovascular disease.
So in summary, there's an unknown CLL population for which the researchers couldn't identify markers, where statins might extend the time to first treatment and overall survival, but only in early stage. Further, the therapeutic targets are unknown. I looked at the supplementary material in that reference and I couldn't see any patterns either. While a much larger study might be able to identify those with CLL who could benefit, you then have the challenge of finding an appropriate therapy and determining whether side effects and in particular adverse cardiovascular events from the treatment outweigh any advantages from the trial therapy.
Neil
CLL... Just tired of it all..
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