Eating Processed Meat Causes Cancer

[Jazz Spazz]

Your risk of colon cancer is 5%. Raising 5% by 18% makes your risk of getting colon cancer something like 5.89%.


OH NO!!!!!!!

Pass the bacon please.

******** article.

2 slices of bacon will raise it by 18%. 6 slices of bacon, a large steak, and 2 burgers a day will increase it by what %, and what will the resulting cancer risk be then?

 

[green]

2 slices of bacon will raise it by 18%. 6 slices of bacon, a large steak, and 2 burgers a day will increase it by what %, and what will the resulting cancer risk be then?

I dunno. 6%?

Let's be honest here. We are talking about colon cancer. They type of cancer that a yearly checkup and a couple polyp snips cure.

This is blatant making something out of nothing journalism.

 

[♪alt13]

A while ago I read what I thought was a pretty convincing study about colon cancer. According to the study people who have a colon are much more likely to develop colon cancer. In fact a colonless person has never been diagnosed with colon cancer.

 

[RandyForRubio]

A while ago I read what I thought was a pretty convincing study about colon cancer. According to the study people who have a colon are much more likely to develop colon cancer. In fact a colonless person has never been diagnosed with colon cancer.

If we just eliminate colons and old age, cancer will drop by approximately 95%. Get to work society.

 

[BabyPeterzz]

Science won't let me and my kids be fat.

****.

 

[Siro]

If we just eliminate colons and old age, cancer will drop by approximately 95%. Get to work society.

We're working on it...

 

[moevillini]

If we just eliminate colons and old age, cancer will drop by approximately 95%. Get to work society.

LOL!!! This reminds me of a humorous birthday card I have. It shows a drawing of an old geezer playing Wheel of Fortune and saying to Pat Sajak "I'd like to buy a bowel."
Inside it makes some quip about getting older...

cracks me up even now, just thinking about it!

 

[One Brow]

If we just eliminate colons and old age, cancer will drop by approximately 95%. Get to work society.

Actually, the problem seems to be long life as opposed to old age, if I recall the studies on mice where genes that cause aging were deactivated.

 

[Miggs]

We're working on it...

I'm not trying to incite, I'm genuinely curious. Are you an atheist? Or agnostic?

 

[Siro]

Actually, the problem seems to be long life as opposed to old age, if I recall the studies on mice where genes that cause aging were deactivated.

It isn't possible to stop aging in mice currently... That would be an incredible breakthrough. Aging is not "programmed" into us through genetics. It is the result of accumulation of damage.

https://en.wikipedia.org/wiki/Strategies_for_Engineered_Negligible_Senescence

from that page:

Types of aging damage and treatment schemes

Nuclear mutations/epimutations—OncoSENS

These are changes to the nuclear DNA (nDNA), or to proteins which bind to the nDNA. Certain mutations can lead to cancer.

This would need to be corrected by a cure for cancer, if any is ever found. SENS focuses on a strategy called "whole-body interdiction of lengthening telomeres" (WILT), which would be made possible by periodic regenerative medicine treatments.

Mitochondrial mutations—MitoSENS

Mitochondria are components in our cells that are important for energy production. Because of the highly oxidative environment in mitochondria and their lack of the sophisticated repair systems, mitochondrial mutations are believed to be a major cause of progressive cellular degeneration.

This would be corrected by allotopic expression—copying the DNA for mitochondria completely within the cellular nucleus, where it is better protected. De Grey argues that experimental evidence demonstrates that the operation is feasible, however, a 2003 study showed that some mitochondrial proteins are too hydrophobic to survive the transport from the cytoplasm to the mitochondria.[24]

Intracellular junk—LysoSENS

Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can’t be digested accumulate as junk inside our cells, which is detected in the form of lipofuscin granules. Atherosclerosis, macular degeneration, liver spots on the skin and all kinds of neurodegenerative diseases (such as Alzheimer's disease) are associated with this problem.

Junk inside cells might be removed by adding new enzymes to the cell's natural digestion organ, the lysosome. These enzymes would be taken from bacteria, molds and other organisms that are known to completely digest animal bodies.

Extracellular junk—AmyloSENS

Harmful junk protein can accumulate outside of our cells. Junk here means useless things accumulated by a body, but which cannot be digested or removed by its processes, such as the amyloid plaques characteristic of Alzheimer's disease and other amyloidoses.

Junk outside cells might be removed by enhanced phagocytosis (the normal process used by the immune system), and small drugs able to break chemical beta-bonds. The large junk in this class can be removed surgically.

Cell loss and atrophy—RepleniSENS

Some of the cells in our bodies cannot be replaced, or can be only replaced very slowly—more slowly than they die. This decrease in cell number affects some of the most important tissues of the body. Muscle cells are lost in skeletal muscles and the heart, causing them to become frailer with age. Loss of neurons in the substantia nigra causes Parkinson's disease, while loss of immune cells impairs the immune system.

This can be partly corrected by therapies involving exercise and growth factors, but stem cell therapy, regenerative medicine and tissue engineering are almost certainly required for any more than just partial replacement of lost cells.

Cell senescence—ApoptoSENS

Senescence is a phenomenon where the cells are no longer able to divide, but also do not die and let others divide. They may also do other harmful things, like secreting proteins. Degeneration of joints, immune senescence, accumulation of visceral fat and type 2 diabetes are caused by this. Cells sometimes enter a state of resistance to signals sent, as part of a process called apoptosis, to instruct cells to destroy themselves.

Cells in this state could be eliminated by forcing them to apoptose (via suicide genes or vaccines), and healthy cells would multiply to replace them.

Extracellular crosslinks—GlycoSENS

Cells are held together by special linking proteins. When too many cross-links form between cells in a tissue, the tissue can lose its elasticity and cause problems including arteriosclerosis, presbyopia and weakened skin texture. These are chemical bonds between structures that are part of the body, but not within a cell. In senescent people many of these become brittle and weak.

SENS proposes to further develop small-molecular drugs and enzymes to break links caused by sugar-bonding, known as advanced glycation endproducts, and other common forms of chemical linking.

 

[RandyForRubio]

Actually, the problem seems to be long life as opposed to old age, if I recall the studies on mice where genes that cause aging were deactivated.

You ever met an old person that hasn't lived a long life?

If I remember right, we have chromosomes that continually replicate themselves, and the more they do it, the more likely it is we get a mutation, which leads to cancer. It's been a while since my last genetic class, but it's something like that.

 

[Siro]

You ever met an old person that hasn't lived a long life?

If I remember right, we have chromosomes that continually replicate themselves, and the more they do it, the more likely it is we get a mutation, which leads to cancer. It's been a while since my last genetic class, but it's something like that.

It is more than that. Various mechanisms that safeguard against cancer decline with age (immune system, telomere length, etc). It is most definitely about aging.