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  #196   ^
Old Thu, May-30-19, 11:12
JEY100's Avatar
JEY100 JEY100 is offline
To Good Health!
Posts: 11,202
 
Plan: IF Fung/LC Westman/Primal
Stats: 222/171/169 Female 5' 9"
BF:45%/25.3%/24%
Progress: 96%
Location: NC
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Quote:
Originally Posted by JEY100
Exciting news...D. Colin Champ has written a summary article for DietDoctor and appears he will be writing more on the topic of cancer.
Long article at:

https://www.dietdoctor.com/low-carb/diet-and-cancer


Exciting news in Dr. Colin Champ's newsletter today (maybe more so for me a half hour away, but merely the fact his job will be researching diet, exercise and cancer is very encouraging:

Quote:
New Adventures Ahead

I am excited to let you all know that we will be moving to North Carolina in the next several months. I will be starting a new position at Duke University, where I will continue my clinical care of patients with a focus on the treatment of breast cancer and lymphoma. However, my new position will strongly focus on nutrition and exercise research and its impact on cancer care. The hope is to really advance the field in this important, albeit under-emphasized, area of healthcare.

Furthermore, I can neither confirm nor deny whether I will be using my remaining three years of NCAA eligibility to replace Zion Williamson on the basketball team. [ ]

I was born and raised in Pittsburgh, so needless to say this is a bittersweet move. It will be tough to leave our family, but we are excited at the opportunities that await us down south and the hope that important diet and exercise research will be produced to help further the field.

Lastly, once these distractions end, you can all expect me to be more engaged with my posts and newsletters. Thank you for all the nice messages and kind words of encouragement in the meantime.


Last edited by JEY100 : Fri, May-31-19 at 04:04.
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  #197   ^
Old Thu, May-30-19, 12:20
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Plan: atkins
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Thanks for posting Janet. Good to see someone working on this angle. I cannot talk to local oncologists are they seem to be in the dark ages. Even at DF.
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  #198   ^
Old Fri, May-31-19, 03:27
JEY100's Avatar
JEY100 JEY100 is offline
To Good Health!
Posts: 11,202
 
Plan: IF Fung/LC Westman/Primal
Stats: 222/171/169 Female 5' 9"
BF:45%/25.3%/24%
Progress: 96%
Location: NC
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Quote:
Originally Posted by JEY100
New podcast interview with Dr. Thomas Seyfried.



Some of his claims about standard of care are quite upsetting, and not just for brain cancer.

http://2ketodudes.com/show.aspx?episode=169


A study he was referencing in this interview published yesterday, summary here from Science Daily: https://www.sciencedaily.com/releas...90530154220.htm
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  #199   ^
Old Sun, Jun-09-19, 13:10
teaser's Avatar
teaser teaser is offline
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https://www.sciencedaily.com/releas...80531114606.htm

Might seem a little contrary posting this here--but really I think it could be seen as an aspect of cancer as a metabolic disease.

Quote:
Lipid molecules can be used for cancer growth

Cancer cells can when the blood supply is low use lipid molecules as fuel instead of blood glucose. This has been shown in animal tumour models by researchers at Karolinska Institutet in Sweden in a study published in Cell Metabolism. The mechanism may help explain why tumours often develop resistance to cancer drugs that inhibit the formation of blood vessels.

Tumour growth and spread rely on angiogenesis, a process of growing new blood vessels that supply the cancer cells with nutrients and hormones, including glucose (sugar). Treatment with antiangiogenic drugs reduces the number of blood vessels in the tumour as well as the blood glucose supply. Many such drugs have been developed and are now used in human patients for treating various cancer types. However, the clinical benefits of antiangiogenic drugs in cancer patients are generally low and the cancers treated often develop a resistance to drugs, especially cancer types that grow close to fat tissues such as breast cancer, pancreatic cancer, liver cancer and prostate cancers.

In collaboration with Japanese and Chinese scientists, a research group at Karolinska Institutet in Sweden has discovered a new mechanism by which cancers can evade antiangiogenic treatment and become resistant.

The reduction of tumour blood vessels results in low oxygenation in tumour tissues -- a process called hypoxia. In the current study, the researchers show that hypoxia acts as a trigger to tell fat cells surrounding or within tumour tissues to break down the stored excessive lipid energy molecules. These lipid energy molecules can when the blood supply is low be used for cancer tissue expansion.

"Based on this mechanism, we propose that a combination therapy consisting of antiangiogenic drugs and drugs blocking lipid energy pathways would be more effective for treating cancers. In animal tumour models, we have validated this very important concept, showing that combination therapy is superior to monotherapy," says Yihai Cao, Professor at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet, who led the study.

Professor Cao's group now plans to work with drug companies and clinical oncologists to explore whether such a new combination therapy would improve the quality of life and lifespan in human cancer patients.


Sort of addresses the question of how to address a tumour turning to an alternate fuel, once glucose has been restricted, here by reducing blood supply rather than dietary glucose. Would be interesting to know what difference in the tumour's response there would be if glucose was just low due to diet, versus low oxygen etc.
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  #200   ^
Old Wed, Jul-03-19, 07:13
teaser's Avatar
teaser teaser is offline
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https://www.sciencedaily.com/releas...90627114056.htm


Quote:
New basic understanding of how lung cancer spreads: antioxidants implicated


Lung cancer cells use antioxidants, endogenous or dietary, to spread in the body by activating a protein called BACH1 and increasing the uptake and use of sugar, Swedish and American researchers report in two independent studies. The studies, which are published in the eminent scientific journal Cell, pave the way for new therapeutic strategies for lung cancer.

It is a known fact that cancer cells, owing to their special metabolism, are exposed to oxidative stress caused by free oxygen radicals. It is also well-known that cancer cells are characterised by the high uptake and use of glucose, or sugar, and that this is one of many factors that govern their ability to divide and metastasise. Studying mice and human tissue, two independent research teams have now discovered how these circumstances interact when cancer cells metastasise to other parts of the body.

The process begins when the cancer cells manage to reduce their oxidative stress, which can happen in one of two ways: the cancer cells can either obtain antioxidants, such as vitamins A, C or E, from the diet, or synthesise their own. In about one in every three cases of lung cancer, the tumour cells have special mutations, linked to the NRF2 and KEAP1 genes, which enable them to start producing their own antioxidants.

It is when the oxidative stress has subsided that the fundamental process of the new discovery occurs: the protein BACH1 is stabilised and accumulates in the cancer cells. This protein presses several start buttons in the cancer cell which stimulates metastasis mechanisms, including one that orders the cancer cell to increase both the metabolism of glucose into cell fuel and lactic acid, and the stockpiling of glucose from the blood stream. The higher rate of glucose use then greatly boosts the ability of the cancer cells to spread.

"There is nothing to suggest, however, that the amount of glucose in the blood has anything to do with this; rather, it is the tumour cells' ability to utilise glucose that is essential to the accelerating metastasis," says Martin Bergo, professor at the Department of Biosciences and Nutrition at Karolinska Institutet, who led the Swedish study.

Lung cancer is the leading cause of cancer-related deaths worldwide. The most life-threatening aspect of lung cancer is metastasis.

"We now have important new information on lung cancer metastasis, making it possible for us to develop new treatments, such as ones based on inhibiting BACH1," says Professor Bergo. "In this present study, we show that the aggressive metastasising induced by antioxidants can be blocked by stopping the production of BACH1 or by using drugs that suppress the breakdown of sugar. Our American colleagues show how inhibiting another enzyme, heme oxygenase, which is linked to BACH1, can also curb the metastasis process."

Professor Bergo and his Swedish colleagues have previously shown that antioxidants, such as vitamin E, in dietary supplement doses accelerate tumour growth. When the first studies to show this were presented in 2014 they drew a great deal of media attention and sparked a fierce debate, since it was generally believed that antioxidant supplements had beneficial effects on cancer. What the researchers have done now is to explain how antioxidants go about expediting the course of the disease -- specifically, in the case of the present study, lung cancer.

"This is one of the most exciting findings we've made," says Volkan Sayin, assistant professor at the Department of Clinical Sciences, University of Gothenburg, and co-corresponding author. "Our results also provide a new explanation for how the so-called Warburg effect is activated. The Warburg effect describes how cancer cells absorb sugar and convert it into energy and lactic acid under normal aerobic conditions. Since this is one of the most well-known hallmarks of cancer, our results provide a crucial new piece in the oncological puzzle."

The Swedish study was conducted at Karolinska Institutet and Gothenburg University, whereas the American study was conducted at New York University. The pair of studies, as well as a "Preview" commenting on the new findings, are published at the same time in the journal Cell.
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  #201   ^
Old Wed, Jul-03-19, 07:34
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GRB5111 GRB5111 is offline
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Plan: Ketogenic (LCHFKD)
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So, among other things, will these findings regarding cancer cells use or production of antioxidants impact the antioxidant supplements industry? Much needs to be learned, but it's a reasonable question.
Quote:
"There is nothing to suggest, however, that the amount of glucose in the blood has anything to do with this; rather, it is the tumour cells' ability to utilise glucose that is essential to the accelerating metastasis," says Martin Bergo, professor at the Department of Biosciences and Nutrition at Karolinska Institutet, who led the Swedish study.
This statement got my attention, as a common belief among those who have eliminated sugar and minimize sugar production through low carb is that this could serve as a preventive measure for several diseases including cancer. Does cancer stimulate gluconeogenesis in any way to survive and spread when blood glucose is lower or glycogen is unavailable?
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  #202   ^
Old Wed, Jul-03-19, 09:18
teaser's Avatar
teaser teaser is offline
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https://www.sciencedirect.com/scien...022519378901790

Quote:
Abstract
Several theories have been proposed to account for the pathogenesis of cachexia in cancer patients. One of these is that the tumor's greater avidity for essential amino acids can result in an amino acid imbalance, which in turn can cause cachexia. In this paper it is shown how, by known biochemical mechanisms, a tumor caused amino acid imbalance can lead to cachexia, progressive weight loss, abnormal gluconeogenesis and lactate recycling. Cachexia leads to a decreased dietary intake, but the cachectic cancer patient, unlike normal man, is unable to adapt. The reason is that the changeover of metabolic fuels from the fed state (glucose) to the starved state (lipids) is hormone regulated, but gluconeogenesis and lactate recycling are substrate regulated. Because of this substrate regulation of gluconeogenesis, the host will be unable to effectively decrease gluconeogenesis as long as the tumor persists in causing an amino acid imbalance.


"By known biological mechanisms"--I'd prefer if this information was generated by more direct observation. I have seen suggestion that cancer cachexia fuels or may fuel gluconeogenesis in other places, but I'm not sure I've seen it looked at directly.
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  #203   ^
Old Wed, Jul-03-19, 10:01
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Plan: Ketogenic (LCHFKD)
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That's what I was thinking, but I know little about the mechanism. It stands to reason that cancer cells would attempt to create an environment in which they would thrive if it didn't already exist. A preventive lifestyle approach might still be a good measure. Much to learn.
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  #204   ^
Old Wed, Jul-03-19, 10:26
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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One branch of cancer research looks at fetal development. Genetic "programming" that allows rapid proliferation and cell migration, including fuel partitioning towards where it's most needed in that situation can be hijacked through mutation where it's inappropriately expressed etc. There's a process for instance where neighbouring tissue that's not directly involved in growth assists through changes in metabolism that produce organic molecules useful to the cancer, this is a theme that shows up in various areas where there's rapid proliferation, wound healing is another that comes to mind.
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