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Eating Processed Meat Causes Cancer

One Brow said:
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.
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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.
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One Brow said:
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.
Click to expand...

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.
 
Howard said:
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.
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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.
 
Just found this useful diagram...

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ONE LOVE said:
Says the World Health Organisation...

https://money.cnn.com/2015/10/26/news/red-meat-processed-cancer-world-health-organization/




You are what you eat!!!
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pretty sleazy science here. No controlled study determining the levels of antibiotics or other cattle/pig/chicken risk factors, or feedlot practices/ or processing procedutes. . . . and c'mon, an 18% increased incidence does not justify a headline of "causation". It seems to be risk factor, but the exact reason for that increased risk is unevaluated. Alarmist idiots running the science asylum.
 
Howard said:
If we just eliminate colons and old age, cancer will drop by approximately 95%. Get to work society.
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Henry E. Eyring, who presided over quite a lot of cancer research, said "If you don't die of something else first, you will die of cancer."

We are actually doing pretty good at eliminating a lot of other causes of death, something to consider when declaring our technology or modern diet is "causing cancer".
 
Siro said:
Yep. Can't wait for the AI world government managing the affairs of the immortal post-humans.
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oughtta rep you for this, honesty and wit combined.

the reason I can wait well enough is because I realize AI, when it "crosses the line" into self-willed self-sufficient self-replicating jackbooted thugs, they will still be far inferior to even the ordinary politician in terms of the whole spectrum of human values essential to our civilization. . . .

materialism isn't all it's cracked up to me, my friend.
 
babe said:
oughtta rep you for this, honesty and wit combined.

the reason I can wait well enough is because I realize AI, when it "crosses the line" into self-willed self-sufficient self-replicating jackbooted thugs, they will still be far inferior to even the ordinary politician in terms of the whole spectrum of human values essential to our civilization. . . .

materialism isn't all it's cracked up to me, my friend.
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I guess we'll see. :)
 
Siro said:
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:
Click to expand...

I get what you're saying and am familiar with SENS but I think you're being overconfident(I don't even think the people @ SENS are that confident). That's their theory and strategy but it is by no means a forgone conclusion that they are right. I think what they are doing is important and exciting but I'm glad there are others investigating "programmed" aging theories too.

Here's a pretty decent breakdown of aging theories.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995895/
 
♪alt13 said:
I get what you're saying and am familiar with SENS but I think you're being overconfident(I don't even think the people @ SENS are that confident). That's their theory and strategy but it is by no means a forgone conclusion that they are right. I think what they are doing is important and exciting but I'm glad there are others investigating "programmed" aging theories too.

Here's a pretty decent breakdown of aging theories.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995895/
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OB's comment about stopping aging simply by turning genes off is not possible with current level of knowledge. And it is extremely unlikely to ever be sufficient to stop aging all together.

There is no question in gerontology that aging is the result of damage. Now there is a faction of researchers who believe that damage mitigation mechanisms are genetically programmed to gradually switch off with age. I wouldn't be surprised at all if this turns out to be true at some level. But we currently have little idea if/to what extent this is true.

The details of SENS theory might turn out to be wrong. I was simply presenting an overview of the types of damage that cause aging, and SENS model happen to include pretty much all of them.
 
Siro said:
OB's comment about stopping aging simply by turning genes off is not possible with current level of knowledge. And it is extremely unlikely to ever be sufficient to stop aging all together.

There is no question in gerontology that aging is the result of damage. Now there is a faction of researchers who believe that damage mitigation mechanisms are genetically programmed to gradually switch off with age. I wouldn't be surprised at all if this turns out to be true at some level. But we currently have little idea if/to what extent this is true.

The details of SENS theory might turn out to be wrong. I was simply presenting an overview of the types of damage that cause aging, and SENS model happen to include pretty much all of them.
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It sounds like we agree for the most part. Except, I think gene therapy is promising and could stop aging all together. The range of lifespans for animals and the existence of animals that naturally exhibit negligible senescence suggests, I think, that there are genes that could defeat aging. That we are programmed to start sucking at repairing ourselves. I do think though that those advancements may be too far off for us to enjoy them without a set of rejuvenation therapies in the meantime.
 
One Brow said:
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.
Click to expand...

Siro said:
OB's comment about stopping aging simply by turning genes off is not possible with current level of knowledge.
Click to expand...

That's not quite what I meant. I believe we have knockout mice that age much more slowly than normal mice, but many of them do not have longer lifespans, because they still get cancers.
 
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