ttystikk
Well-Known Member
Don't be callous.
Please Help! Stage 4 Liver and Pancreatic Cancer
- Thread starter Joe Arsenault
- Start date
ttystikk
Well-Known Member
I know little about cancer other than that as an American I'm at relatively high risk of getting it in one form or another.
What can be done to help prevent it in the first place?
Healthy diet and exercise, yadda yadda, I get that, but are there any specific things one can do to reduce risk- that actually have some objective track record of success?
heckler73
Well-Known Member
Do not be so quick to presume my motives or intent, please. That's naively arrogant.
Pancreatic is vicious. The reason I pointed out the OP's absence is because something may have drastically changed his mind, perhaps a grim realization. There is a video(s?) of a gentleman, that I watched a while back, who had pancreatic cancer and also tried using RSO.
I think you can guess the outcome, but what struck me was his lament, if not regret, for taking so much. IIRC he made that video regarding that about a couple weeks before he changed his address for a place in the Cosmos. When I noticed the OP's absence since posting, I remembered that vid and wondered if he perhaps watched it, too. I believe a colloquial term for it is "black-pilled", unless I am taking liberties with the definition.
Considering the time that has passed, I can only hope the OP is at least at peace, regardless of present physical state.
abe supercro
Well-Known Member
Any updates on your brother's wife?
How you doing easy-d... I know oil has helped you with your symptoms.
You still kickin and feelin ok?
Tangerine_
Well-Known Member
There are varying forms. Some the result of genetics - some lifestyle choices. Healthy diet/lifestyle can certainly reduce the risks, but as @Indacouch pointed out, it doesn't discriminate. Early detection is key. With the US healthcare system, unfortunately, many fall through the cracks. I've never worked oncology but I continue to tell ppl to just know your body and listen to your instincts. Its been a few yrs since I've worked in healthcare, but at the time, there were amazing advances happening in genetic testing...especially for breast cancer.
Even with all my training, my sons cancer advanced because action wasn't taken quickly. We were repeatedly told it was an "infection". When I questioned this, I was quickly shut down. I took it upon myself to make his referral/fax records. Within 24 hrs of seeing an oncologist he was in surg. But at this point the cancer had advanced and spread up through his lymph chain. This is why I'm against all the anecdotal studies that attempt to show "false cures". Time is not a luxury that can be afforded. My training proved to be a blessing and curse. To this day I shake my head, wondering how I missed all the signs.
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Indacouch
Well-Known Member
Not sure why you quoted me ...infact seems like were actually on the same page mostly ....I replied in this thread due to my own experiences and feelings towards cancer ......I know all about the ups and downs of cancer ((trust me)) ...I didn't or wouldn't say anything negative on OPs thread ....all I can say is I agree I hope he's at peace ,,regardless...
heckler73
Well-Known Member
I wasn't quoting you in the first part.
Sorry if that confused you.That's one of the risks of "multi-quote".
Indacouch
Well-Known Member
I was falling asleep last night ....no worries .I wasn't quoting you in the first part.
That's one of the risks of "multi-quote".
Heisenberg
Well-Known Member
I don't know how many of you want to take the time to read this, but here's an excerpt from an article written by my partner. It's an attempt to explain cancer to the layperson in a way that makes it simple without "dumbing" it down. IOW, she intended to acknowledge that the average reader is actually pretty smart, but that cancer is an extremely complicated subject with many misconceptions behind it. Also, she is British, hence the English spelling of some words.
"I think the best place to start is to consider normal body cells. Unlike free-living cells, such as bacteria, the cells of our body do not compete with each other for their own ‘selfish’ genetic propagation. On the contrary, they co-operate on a huge scale, through a vast network of elaborate communication mechanisms, dividing and assuming designated roles in adherence to instruction and signals, and even committing suicide, on cue, for the interests of the aggregate. This non-rebellious behaviour is of course explained by the fact that body cells are a collection of clones. Co-operative behaviour contributes to the propagation of their genes.
In each somatic cell (that means all cells except sperms and eggs), there is a copy of the body’s genome. Your genome is the sum of all your body’s genetic information, which is organised into 46 chromosomes – 22 pairs of “autosomes” and one pair of sex chromosomes (“XX” or “XY”, depending on whether you are a girl or a boy). Far from being an inaccessible “blueprint”, as it is often dubbed, each cell’s genome is a dynamically active factory, churning out myriad different proteins in response to incoming demands, which are communicated via precise chemical signals that either come from within the cell itself, or originate elsewhere in the body. These signals work by selecting specific stretches of gene sequence (“written” in DNA) to be read off and converted into corresponding protein sequences (which are “written” in amino acids). The number of different proteins produced by cells in the body is estimated to be somewhere in the realms of a couple of million. Each of them coils, bends and folds into its own unique shape, according to the signature of physical interaction that occurs between its constituent amino acids, all of which have slightly different distributions of electrical charge and molecular bonds.
Some of these protein shapes act as building blocks for structures such as muscle and skin, whereas others function as tools for breaking things apart, or putting things together. Some act as vehicles, carrying important stuff around the body, while others work to neutralise germs and viruses that get into us. Yet another class of proteins works in communication, as chemical signals (like those mentioned above), to trigger the production of yet more proteins, perhaps in cells some distance away from the ones in which they themselves were put together. In some cases, a protein’s communication errand entails recognising a certain sequence on a certain chromosome, and sticking to it in order to deactivate a gene, or perhaps cause it to go into programmed hyperactivity, which would result in a concentrated outflow of another specific protein.
So, each copy of the genome (in every cell) acts like a mini factory, and The Genome, in its singlular, more abstract sense, is responsible for matching supply and demand in a vast supersystem of interconnected production, maintenance, communication, and transport subsystems.
The growth and maintenance of this supersystem depends on cells’ ability to make copies of themselves, which is itself based on DNA’s ability to self-duplicate, since every new cell needs its own copy of The Genome. As with any copying system, DNA replication has an inherent, unavoidable error-rate. In the course of a human lifetime, some 10,000,000,000,000,000, (ten thousand million million) cell divisions take place. It is estimated that the probability of an error being made is approximately 0.000001 per gene, per cell division, under normal circumstances (i.e. in the absence of mutagens – substances which promote mutation). It follows that any given gene in The Genome can be expected to have experienced mutation around one million times in one lifetime. Unsurprisingly, evolution has stumbled across a number of mechanisms to fix errors as they arise. Occasionally, however, things do slip through the net. And it is at these moments of accidental neglect that cancer has its chance to begin laying the groundwork for infiltration.
So, what is cancer?
Cancer is the product of a collection of genetic alterations that promote “selfish” behaviour in cells, at the expense of the body in which they live. A situation is set up in which natural selection, fuelled by a building momentum of newly-acquired mutations, works (unintentionally, of course), to cultivate an increasingly deviant population of cells that “compete” with their neighbours to proliferate their own mutant genotypes, a phenomenon which begins to manifest as a tumour. In the sense that they are subject to natural selection, tumour cells have started to look quite like unicellular organisms such as bacteria, which, as we know all-too-well, can evolve extremely quickly, thanks to the exponentiating speed with which a cell population can multiply. So, in the case of cancer, what kind of accidentally-acquired traits could flip a perfectly respectable, law-abiding body cell into the realms of cancerous activity? And what “skills” might then be “useful” for it in its selfish accrual of control?
The most obvious power that must be acquired by a somatic (body) cell, via a change in its genome, is that of overcoming restraints on cell division. Cells that begin breaking the rules like this are, in most cases, eventually detected by patrolling immune surveillance mechanisms and sentenced to death by apoptosis, which consists in a signal that commands the cell to digest itself. Thus, by the time detection occurs, for the trajectory of cancer development to continue, another “ability” must have been acquired: that of evading such a signal. A mutation conferring this ability may arise before or after uncontrolled cell division was allowed to begin, but of course one of the numerical implications of increased division is that the absolute rate of copying error is increased, so it follows that an already illegitimately dividing cell lineage has an enhanced likelihood of chancing upon a signal-evasion mutation.
Now, any additional increase in tendency toward DNA mutation represents another “advantageous” trait for a cancer cell in-the-making and, therefore, any mutation that deactivates DNA repair mechanisms, or tampers with DNA copying mechanisms themselves, become favoured. (As a quick aside, when we talk of a “favoured” mutation in this context, we mean one that boosts a cell’s probability of reproducing more prolifically, relative to cells lacking the mutation, and thus becoming increasingly over-represented as a proportion of the population, as this population grows.)
The next barrier a potential cancer cell in a growing mass must overcome is the stringy matrix of proteins that surrounds it, keeping it stationary and contained within its designated area of body tissue. Without the ability to do this, a cell can spawn a mass of abnormal offspring, but this localised tumour can be easily surgically removed. Such a tumour is considered “benign”. Conversely, a tumour whose cells have undergone mutations that allow them to invade and colonise surrounding tissues is considered malignant. Fugitive cells are said to have metastasised, escaping through blood or lymphatic vessels to form secondary tumours, or metastases, in other parts of the body. Once this has happened, it can be very difficult, and often impossible, to eradicate the disease."
Full article here: Confronting Cancer Quackery
"I think the best place to start is to consider normal body cells. Unlike free-living cells, such as bacteria, the cells of our body do not compete with each other for their own ‘selfish’ genetic propagation. On the contrary, they co-operate on a huge scale, through a vast network of elaborate communication mechanisms, dividing and assuming designated roles in adherence to instruction and signals, and even committing suicide, on cue, for the interests of the aggregate. This non-rebellious behaviour is of course explained by the fact that body cells are a collection of clones. Co-operative behaviour contributes to the propagation of their genes.
In each somatic cell (that means all cells except sperms and eggs), there is a copy of the body’s genome. Your genome is the sum of all your body’s genetic information, which is organised into 46 chromosomes – 22 pairs of “autosomes” and one pair of sex chromosomes (“XX” or “XY”, depending on whether you are a girl or a boy). Far from being an inaccessible “blueprint”, as it is often dubbed, each cell’s genome is a dynamically active factory, churning out myriad different proteins in response to incoming demands, which are communicated via precise chemical signals that either come from within the cell itself, or originate elsewhere in the body. These signals work by selecting specific stretches of gene sequence (“written” in DNA) to be read off and converted into corresponding protein sequences (which are “written” in amino acids). The number of different proteins produced by cells in the body is estimated to be somewhere in the realms of a couple of million. Each of them coils, bends and folds into its own unique shape, according to the signature of physical interaction that occurs between its constituent amino acids, all of which have slightly different distributions of electrical charge and molecular bonds.
Some of these protein shapes act as building blocks for structures such as muscle and skin, whereas others function as tools for breaking things apart, or putting things together. Some act as vehicles, carrying important stuff around the body, while others work to neutralise germs and viruses that get into us. Yet another class of proteins works in communication, as chemical signals (like those mentioned above), to trigger the production of yet more proteins, perhaps in cells some distance away from the ones in which they themselves were put together. In some cases, a protein’s communication errand entails recognising a certain sequence on a certain chromosome, and sticking to it in order to deactivate a gene, or perhaps cause it to go into programmed hyperactivity, which would result in a concentrated outflow of another specific protein.
So, each copy of the genome (in every cell) acts like a mini factory, and The Genome, in its singlular, more abstract sense, is responsible for matching supply and demand in a vast supersystem of interconnected production, maintenance, communication, and transport subsystems.
The growth and maintenance of this supersystem depends on cells’ ability to make copies of themselves, which is itself based on DNA’s ability to self-duplicate, since every new cell needs its own copy of The Genome. As with any copying system, DNA replication has an inherent, unavoidable error-rate. In the course of a human lifetime, some 10,000,000,000,000,000, (ten thousand million million) cell divisions take place. It is estimated that the probability of an error being made is approximately 0.000001 per gene, per cell division, under normal circumstances (i.e. in the absence of mutagens – substances which promote mutation). It follows that any given gene in The Genome can be expected to have experienced mutation around one million times in one lifetime. Unsurprisingly, evolution has stumbled across a number of mechanisms to fix errors as they arise. Occasionally, however, things do slip through the net. And it is at these moments of accidental neglect that cancer has its chance to begin laying the groundwork for infiltration.
So, what is cancer?
Cancer is the product of a collection of genetic alterations that promote “selfish” behaviour in cells, at the expense of the body in which they live. A situation is set up in which natural selection, fuelled by a building momentum of newly-acquired mutations, works (unintentionally, of course), to cultivate an increasingly deviant population of cells that “compete” with their neighbours to proliferate their own mutant genotypes, a phenomenon which begins to manifest as a tumour. In the sense that they are subject to natural selection, tumour cells have started to look quite like unicellular organisms such as bacteria, which, as we know all-too-well, can evolve extremely quickly, thanks to the exponentiating speed with which a cell population can multiply. So, in the case of cancer, what kind of accidentally-acquired traits could flip a perfectly respectable, law-abiding body cell into the realms of cancerous activity? And what “skills” might then be “useful” for it in its selfish accrual of control?
The most obvious power that must be acquired by a somatic (body) cell, via a change in its genome, is that of overcoming restraints on cell division. Cells that begin breaking the rules like this are, in most cases, eventually detected by patrolling immune surveillance mechanisms and sentenced to death by apoptosis, which consists in a signal that commands the cell to digest itself. Thus, by the time detection occurs, for the trajectory of cancer development to continue, another “ability” must have been acquired: that of evading such a signal. A mutation conferring this ability may arise before or after uncontrolled cell division was allowed to begin, but of course one of the numerical implications of increased division is that the absolute rate of copying error is increased, so it follows that an already illegitimately dividing cell lineage has an enhanced likelihood of chancing upon a signal-evasion mutation.
Now, any additional increase in tendency toward DNA mutation represents another “advantageous” trait for a cancer cell in-the-making and, therefore, any mutation that deactivates DNA repair mechanisms, or tampers with DNA copying mechanisms themselves, become favoured. (As a quick aside, when we talk of a “favoured” mutation in this context, we mean one that boosts a cell’s probability of reproducing more prolifically, relative to cells lacking the mutation, and thus becoming increasingly over-represented as a proportion of the population, as this population grows.)
The next barrier a potential cancer cell in a growing mass must overcome is the stringy matrix of proteins that surrounds it, keeping it stationary and contained within its designated area of body tissue. Without the ability to do this, a cell can spawn a mass of abnormal offspring, but this localised tumour can be easily surgically removed. Such a tumour is considered “benign”. Conversely, a tumour whose cells have undergone mutations that allow them to invade and colonise surrounding tissues is considered malignant. Fugitive cells are said to have metastasised, escaping through blood or lymphatic vessels to form secondary tumours, or metastases, in other parts of the body. Once this has happened, it can be very difficult, and often impossible, to eradicate the disease."
Full article here: Confronting Cancer Quackery
Tangerine_
Well-Known Member
That was a good read, explaining the fundamentals of cellular structure/function. It reminded me I should've used the word "predisposed" with regard to genetics/cancer.
Has she written anything regarding genetic testing/early detection?
I'm afraid I really didn't answer @ttystikk question with any info he wasnt already aware of and should've deferred it to you.
I don't mean to hijack this thread, however, this is an excellent place to start a dialogue that could help expel myths and potentially help many MM patients/providers. After all, it was my sons illness that lead me on to cultivating cannabis which also lead me here, to RIU. Not as a cure, but to alleviate symptoms. (pharm co. charge obscene amounts for marinol which is lacking and hard to control dosage) My father grew for yrs on our farm which cut my learning curve, but it was a different time in the world of cannabis.
Perhaps a new thread would be more appropriate?
Has she written anything regarding genetic testing/early detection?
I'm afraid I really didn't answer @ttystikk question with any info he wasnt already aware of and should've deferred it to you.
I don't mean to hijack this thread, however, this is an excellent place to start a dialogue that could help expel myths and potentially help many MM patients/providers. After all, it was my sons illness that lead me on to cultivating cannabis which also lead me here, to RIU. Not as a cure, but to alleviate symptoms. (pharm co. charge obscene amounts for marinol which is lacking and hard to control dosage) My father grew for yrs on our farm which cut my learning curve, but it was a different time in the world of cannabis.
Perhaps a new thread would be more appropriate?
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RM3
Well-Known Member
