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Fasting,ketosis and cancer

ketosis cancer thomas seyfried fasting

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102 replies to this topic

#91 theconomist

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Posted 15 April 2013 - 10:49 AM

Not to cut you guys from a very interesting discussion but we've kinda moved away from the initial question without really finding an answer.
It seems that neither fasting nor a ketogenic diet can ''cure'' cancer once it's diagnosable.
A ketogenic diet may significantly slow down tumor growth in some type of cancers; brain,prostate... however it seems and based on anecdotal reports that fasting does not induce the same benefits as the tumor growth accelerates once the fast is over.
Hypothetically one could fast long enough to kill the cancer cells however we don't know how long it would take ; 10,30,60 days?
If I was facing cancer I'd personally go on a fast from the moment I get diagnosed under a doctor's watch unless it's one of the cancers that feed almost exclusively on glucose; I'd simply switch to a fully ketogenic diet.
It's true that a 60 day keto diet is much easier to implement than a 60 day water fast. Anyhow I think this is an interesting area of research; the treatment of cancer as a metabolism related disease.

My take home message is that one should limit his consumption of carbs to the bare necessities (green veggies, nuts and the beneficial fruits) and in case one is fighting cancer in the hypothesis were an extened fast is impossible one should go on a ketogenic diet with as low protein as possible without inducing muscle wastage.


Sorry for my tangential questions. I am indeed interested in a prostate cancer treatment via ketosis. My relative has prostate cancer and I am also trying to figure out whether it's better to suggest he eat more to support his immune system or to induce ketotic metabolism. He's taking hormonal ejections of some kind.

Are you saying that a ketogenic diet is more effective than fasting outright for someone who has already been diagnosed with prostate cancer?


A fast will be superior to a ketogenic diet for all types of cancer there's no doubt in my mind that if one were to fast long enough and kill all the cancer cells you'd be ''cured''. However this is impractical for many reasons; the health of a cancer patient, the unknown duration of the fast (does it take 30,60,90 days? more? we simply don't know the studies haven't been done)...
A keto diet works very well for some cancers (checkout the first page of this thread where this is discussed further) and is implementable on the long term; a person diagnosed with a brain tumor could fast for a week prior to chemo/radiation and implement a ketogenic diet for the rest of his life en théorie, idem for someone who's been diagnosed with prostate cancer.

#92 Mind

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Posted 16 April 2013 - 05:20 PM

the unknown duration of the fast (does it take 30,60,90 days? more? we simply don't know the studies haven't been done


A water fast for 30 days or more....sounds dangerous to me.

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#93 theconomist

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Posted 17 April 2013 - 07:07 AM

the unknown duration of the fast (does it take 30,60,90 days? more? we simply don't know the studies haven't been done


A water fast for 30 days or more....sounds dangerous to me.


Under medical supervision it's actually rather safe.

Here is a paper which has fascinated me for a while now.
http://www.ncbi.nlm....les/PMC2495396/

382 days fast.

Some forums dedicated to water fasts have many reports of members fasting for that long and even longer with very little side effects.
I would still consult with a doctor and have blood tests every week but it's definitely doable.

#94 xEva

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Posted 18 April 2013 - 07:20 PM

Under medical supervision it's actually rather safe.

Here is a paper which has fascinated me for a while now.
http://www.ncbi.nlm....les/PMC2495396/

382 days fast.

Some forums dedicated to water fasts have many reports of members fasting for that long and even longer with very little side effects.
I would still consult with a doctor and have blood tests every week but it's definitely doable.


Many reports of members fasting 380 days and even longer?

The links please.

#95 theconomist

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Posted 18 April 2013 - 08:09 PM

Under medical supervision it's actually rather safe.

Here is a paper which has fascinated me for a while now.
http://www.ncbi.nlm....les/PMC2495396/

382 days fast.

Some forums dedicated to water fasts have many reports of members fasting for that long and even longer with very little side effects.
I would still consult with a doctor and have blood tests every week but it's definitely doable.


Many reports of members fasting 380 days and even longer?

The links please.


I was refering to 30 day fasts.

#96 alecnevsky

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Posted 25 April 2013 - 07:11 AM

Non-glucose metabolism in cancer cells--is it all in the fat?


http://www.ncbi.nlm....pubmed/22706846

"10 Conclusion and clinical translational opportunities
Cancer cells demonstrate an a priorireprogramming of fatty
acid metabolism, which in concert with an upregulation of
glycolytic proteins can cause the induction and maintenance
of a Warburg-ian effect in cancer cells. Non-glucose cancer
cell metabolism is a recent discovery which has revolutionized our understanding of cancer biology [1]. We are beginning to understand that glucose is not the only carbon
skeleton for cellular biosynthesis and ATP production [1,
10, 72] and that certain types of cancer cells seem to have a
greater “addiction” to fatty acids than to glucose, potentially
providing therapeutic opportunities for tumor-specific therapeutic interventions. Furthermore, given that the development of metastasis in cancer patients is frequently
accompanied by significant changes in whole body organ
metabolism, careful preclinical testing of compounds that
perturb FA metabolism in preclinical models would be essential, such that a systems biology approach using in silico
computational models in addition to noninvasive functional
imaging techniques in xenograft models would be required.
Furthermore, in vivo preclinical models could also be used
to determine whether the metabolic signature of primary
tumors differs from their metastasis and whether metabolic
switching of carbon skeletons (e.g., from glucose to fatty
acids), or upregulation of FA metabolism per se, accompanies tumor progression. Similarly, the contribution of FA
metabolism in premalignant cells to tumorigenesis remains
to be elucidated."

#97 theconomist

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Posted 25 April 2013 - 08:08 AM

Non-glucose metabolism in cancer cells--is it all in the fat?


http://www.ncbi.nlm....pubmed/22706846

"10 Conclusion and clinical translational opportunities
Cancer cells demonstrate an a priorireprogramming of fatty
acid metabolism, which in concert with an upregulation of
glycolytic proteins can cause the induction and maintenance
of a Warburg-ian effect in cancer cells. Non-glucose cancer
cell metabolism is a recent discovery which has revolutionized our understanding of cancer biology [1]. We are beginning to understand that glucose is not the only carbon
skeleton for cellular biosynthesis and ATP production [1,
10, 72] and that certain types of cancer cells seem to have a
greater “addiction” to fatty acids than to glucose, potentially
providing therapeutic opportunities for tumor-specific therapeutic interventions. Furthermore, given that the development of metastasis in cancer patients is frequently
accompanied by significant changes in whole body organ
metabolism, careful preclinical testing of compounds that
perturb FA metabolism in preclinical models would be essential, such that a systems biology approach using in silico
computational models in addition to noninvasive functional
imaging techniques in xenograft models would be required.
Furthermore, in vivo preclinical models could also be used
to determine whether the metabolic signature of primary
tumors differs from their metastasis and whether metabolic
switching of carbon skeletons (e.g., from glucose to fatty
acids), or upregulation of FA metabolism per se, accompanies tumor progression. Similarly, the contribution of FA
metabolism in premalignant cells to tumorigenesis remains
to be elucidated."


I wonder what Thomas Seyfried has to say about this.
There is more to the subject than what we know it seems; some cancerous cells definitely rely on glucose as the only source of fuel(brain), others rely mainly on fat(leukemia). I guess it would be too easy to just say switch to a keto/no fat diet depending on the cancer you have... Our best hope is to stay healthy until all cancers are treatable. It's a race against the clock for us.

#98 alecnevsky

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Posted 26 April 2013 - 07:30 AM

Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.

http://www.ncbi.nlm....pubmed/18042933

"

Abstract




BACKGROUND:

Prior research suggested that energy balance and fat intake influence prostate cancer progression, but the influence of dietary carbohydrate on prostate cancer progression has not been well characterized. We hypothesized that hyperinsulinemia resulting from high intake of refined carbohydrates would lead to more rapid growth of tumors in the murine LNCaP xenograft model of prostate cancer.
METHODS:

Athymic mice were injected subcutaneously with LNCaP human prostate cancer cells and, when tumors were palpable, were randomly assigned (n = 20 per group) to high carbohydrate-high fat or low carbohydrate-high fat diets. Body weight and tumor volume were measured weekly. After 9 weeks, serum levels of insulin and insulin-like growth factor 1 (IGF-1) were measured by enzyme immunoassay. AKT activation and the levels of the insulin receptor in tumor cells were determined by immunoblotting. The in vitro growth response of LNCaP cells to serum from mice in the two treatment groups was measured based on tetrazolium compound reduction. All statistical tests were two-sided.
RESULTS:

After 9 weeks on the experimental diets, mice on the high carbohydrate-high fat diet were heavier (mean body weight of mice on the high carbohydrate-high fat diet = 34 g versus 29.1 g on the low carbohydrate-high fat diet, difference = 4.9 g, 95% CI = 3.8 to 6.0 g; P = .003), experienced increased tumor growth (mean tumor volume in mice on high carbohydrate-high fat diet = 1695 versus 980 mm3 on low carbohydrate-high fat diet, difference = 715 mm3, 95% CI = 608 to 822 mm3; P<.001), and experienced a statistically significant increase in serum insulin and IGF-1 levels. Tumors from mice on the high carbohydrate-high fat diet had higher levels of activated AKT and modestly higher insulin receptor levels than tumors from mice on the low carbohydrate-high fat diet. Serum from mice on the high carbohydrate-high fat diet was more mitogenic for LNCaP cells in vitro than serum from mice fed the low carbohydrate-high fat diet.
CONCLUSION:

A diet high in refined carbohydrates is associated with increased tumor growth and with activation of signaling pathways distal to the insulin receptor in a murine model of prostate cancer."


It's difficult to say. Here for example they tested prostate cancer cells specifically and found a totally different effect in mice.


Edited by alecnevsky, 26 April 2013 - 07:30 AM.


#99 theconomist

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Posted 26 April 2013 - 08:35 AM

Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.

http://www.ncbi.nlm....pubmed/18042933

"

Abstract




BACKGROUND:

Prior research suggested that energy balance and fat intake influence prostate cancer progression, but the influence of dietary carbohydrate on prostate cancer progression has not been well characterized. We hypothesized that hyperinsulinemia resulting from high intake of refined carbohydrates would lead to more rapid growth of tumors in the murine LNCaP xenograft model of prostate cancer.
METHODS:

Athymic mice were injected subcutaneously with LNCaP human prostate cancer cells and, when tumors were palpable, were randomly assigned (n = 20 per group) to high carbohydrate-high fat or low carbohydrate-high fat diets. Body weight and tumor volume were measured weekly. After 9 weeks, serum levels of insulin and insulin-like growth factor 1 (IGF-1) were measured by enzyme immunoassay. AKT activation and the levels of the insulin receptor in tumor cells were determined by immunoblotting. The in vitro growth response of LNCaP cells to serum from mice in the two treatment groups was measured based on tetrazolium compound reduction. All statistical tests were two-sided.
RESULTS:

After 9 weeks on the experimental diets, mice on the high carbohydrate-high fat diet were heavier (mean body weight of mice on the high carbohydrate-high fat diet = 34 g versus 29.1 g on the low carbohydrate-high fat diet, difference = 4.9 g, 95% CI = 3.8 to 6.0 g; P = .003), experienced increased tumor growth (mean tumor volume in mice on high carbohydrate-high fat diet = 1695 versus 980 mm3 on low carbohydrate-high fat diet, difference = 715 mm3, 95% CI = 608 to 822 mm3; P<.001), and experienced a statistically significant increase in serum insulin and IGF-1 levels. Tumors from mice on the high carbohydrate-high fat diet had higher levels of activated AKT and modestly higher insulin receptor levels than tumors from mice on the low carbohydrate-high fat diet. Serum from mice on the high carbohydrate-high fat diet was more mitogenic for LNCaP cells in vitro than serum from mice fed the low carbohydrate-high fat diet.
CONCLUSION:

A diet high in refined carbohydrates is associated with increased tumor growth and with activation of signaling pathways distal to the insulin receptor in a murine model of prostate cancer."


It's difficult to say. Here for example they tested prostate cancer cells specifically and found a totally different effect in mice.


Based on the study linked in the first page, prostate cancer was found to stop growing and even shrink on a ketogenic diet.

#100 tham

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Posted 26 April 2013 - 01:30 PM

Seyfried's theory is at least partially correct.


In Malaysia, the Malays, who are almost exclusively Muslims, fast a month a year.

Most of the Chinese don't. A certain proportion of the Indians do.


While genetics are the main factor, the overall cancer statistics some years ago were :

Malays - 1 in 7

Indians - 1 in 5

Chinese - 1 in 4



Malays in peninsular Malaysia may have the
lowest incidence of stomach cancer in the world.


http://www.ncbi.nlm....pubmed/19852334


Epidemiology of breast cancer in Malaysia.

http://www.ncbi.nlm....pubmed/17059323

#101 theconomist

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Posted 27 April 2013 - 04:51 PM

Seyfried's theory is at least partially correct.


In Malaysia, the Malays, who are almost exclusively Muslims, fast a month a year.

Most of the Chinese don't. A certain proportion of the Indians do.


While genetics are the main factor, the overall cancer statistics some years ago were :

Malays - 1 in 7

Indians - 1 in 5

Chinese - 1 in 4



Malays in peninsular Malaysia may have the
lowest incidence of stomach cancer in the world.


http://www.ncbi.nlm....pubmed/19852334


Epidemiology of breast cancer in Malaysia.

http://www.ncbi.nlm....pubmed/17059323


Fasting in Ramadan has it's drawback( people tend to overeat at night+risk of dehydration) but can definitely be used to one's benefit.
Fasting for 24 hours once a week is something I've always been in favor of.

Edited by theconomist, 27 April 2013 - 04:52 PM.


#102 Shepard

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Posted 19 May 2013 - 01:02 AM

NOTE: Many Off-Topic posts have been removed. Please keep discussion on the topic at-hand.
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#103 mag1

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Posted 26 September 2015 - 02:21 AM

Anyone know where you can buy ketone monoester. The below article notes that the FDA has deemed KME to be safe.

 

"Ketone monoester (KME), the reduced derivative of OBHB has undergone extensive animal  and human toxicity tests and was declared to be safe by Food and Drug Administration."

 

http://www.ncbi.nlm....les/PMC4509263/

 

"KME has undergone extensive animal and human toxicity tests and meets Food and Drug Administration generally recognized as safe standards."

 

http://www.alzheimer...(14)00032-6/pdf

 

Anyone know where this is sold?

 







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