probably iodine and skin d (aka my special lamp) are the most significant for promoting cell differentiation working against somatic evolution
Bodily breakdown explained: How cell differentiation patterns suppress somatic evolution
Natural selection can occur at the cellular level, where it is detrimental to health. Fortunately it is normally controlled by a well-known pattern of ongoing cell differentiation in the mature tissues of animals, according to a new study published December 14 in PLoS Computational Biology.
The failure of normal cell differentiation patterns may explain cancer and senescent decline with aging, say researchers at the University of Arizona, the Santa Fe Institute, the University of Pennsylvania, and the Wistar Institute.
Darwinian natural selection and evolution is usually studied in populations of organisms, but it also applies to cellular populations; this is called “somatic” evolution. Such somatic evolution tends to reduce cooperation among cells, thus threatening the integrity of the organism.
In this study the authors proposed that a well-known pattern of ongoing cell differentiation in the mature tissues of animals functions to suppress somatic evolution, which is essential to the origin and sustainability of multicellular organisms.
The team, lead by Dr. John Pepper, tested this hypothesis using a computer simulation of cell population dynamics and evolution. The results were consistent with the hypothesis, suggesting that familiar patterns of ongoing cell differentiation were crucial to the evolution of multicellular animals, and remain crucial as a bodily defense against cancer.
We discovered that levels of several key autophagy pathway members are reduced in Drosophila (fruit fly) neural tissue as a normal part of aging,” says senior author Kim Finley, Ph.D., a scientist in the Cellular Neurobiology Laboratory, Salk institute “which suggests there is an age-dependent suppression of autophagy that may be a contributing factor for human neurodegenerative disorders like Alzheimer’s disease.”
All cells undergo autophagy — literally self-eating, — which requires the assembly of specialized vesicles called autophagosomes. These vesicles surround or engulf damaged cellular proteins or structures and then traffic the “bagged garbage” to a second group of vesicles, which disposes of the trash with the help of digestive enzymes. This process can be enhanced when animals are placed on a calorie-restricted diet, a regime known to extend lifespan.
“The activation of autophagy facilitates the removal of damaged molecules that accumulate during cellular aging,” says Finley. “This may be particularly important in the nervous system since neurons produce damaged molecules at a much higher rate than most cell types.” Keeping cells free of damaged molecules is critical for neurons because unlike many cells, they do not divide or replace themselves once created at birth. “They rely on autophagy together with other clearance and detoxification pathways to keep themselves healthy and functioning for decades,” explains Finley.
For their studies, the Salk researchers turned to the fruit fly Drosophila, a powerful model organism, whose genetics can easily be manipulated. When initial experiments indicated that the expression of several autophagy genes decreased over the normal lifespan of fruit flies, the Salk researchers focused on one particular protein, Atg8a. This protein is an essential component needed for the formation of new autophagosomes. Finley and her team found that levels of Atg8a were significantly reduced by four weeks of age, a time when the flies are considered middle aged. At the same time, protein aggregates were not efficiently cleared by the cellular clean-up crew and started to accumulate.
Without Atg8a, things went from bad to worse. Damaged proteins tagged for degradation started to pile up early and life expectancy plummeted. “The abnormal accumulation of protein aggregates had striking similarities to those seen in the most common human neurodegenerative diseases,” says first author Anne Simonsen, Ph.D., a visiting scientist from the University of Oslo, Norway.
When the researchers kept the neuronal levels of Atg8a high, the genetically engineered flies were spared the ravages of time. Promoting the pathway not only prevented the accumulation of protein aggregates but also significantly extended the average lifespan. “Our experiments show for the first time genetically that autophagy can sequester and eliminate misfolded and damaged proteins, which accumulate in neurons as normal part of the aging process,” says Simonsen, “but most importantly they demonstrate that enhancing the clearance of damaged proteins and protein aggregates increases longevity.”
Insulin signaling and caloric restriction are two major determinants of longevity and they also impact the activity level of autophagy. Therefore, regulating autophagy, the pathway that directly does the cleanup work, may be the key factor in controlling the aging process, the researchers say. “By maintaining the expression of a rate-limiting autophagy gene in the aging nervous system there is a dramatic extension of lifespan and resistance to age-associated oxidative stress,” says Finley.
Since its initial discovery in the 1960s, programmed cell death has been a primary focus of studies for investigators across a wide array of scientific disciplines. An essential mechanism in development and homeostasis, programmed cell death allows for the clean intracellular destruction of unnecessary or damaged cells. While apoptosis is the most understood type of programmed cell death, recently scientists have begun to take a closer look at autophagy— a highly regulated, catabolic process that essentially allows a cell to eat itself. Paradoxically, autophagy is not only a major mechanism by which a starving cell reallocates nutrients to ensure survival, scientists are now demonstrating that autophagy also provides cells that cannot undergo apoptosis with an alternate form of self-destruction.
In “Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila,” published in the December 14 2007 issue of Cell, Eric Baehrecke, PhD, UMMS Associate Professor of Cancer Biology, and colleagues examined fruit fly salivary glands, which contain all of the machinery required to dismantle and recycle their own cellular components and thus provide a genetic model system for elucidating the complex functions of autophagy. The paper describes the cellular components required for autophagic cell death and defines multiple pathways that cooperate in the clearance of cells during fly development. Further, their findings demonstrate a critical relationship between growth and this form of cell death.
“When cells keep growing, they don’t die well,” Dr. Baehrecke explained. “We show that an arrest of growth preceded the death of these cells. If we maintain growth by turning on certain genes, we can block the death of these cells, and this has potential clinical implications. Therapies directed at apoptotic mechanisms have resulted in limited success; we hope that further studies of autophagy could lead to new approaches to the treatment of human disease.”
I realize that this is a bit odd of a thing to ask....
I was wondering if anyone on this or neighboring lists has ever tried or has been successful growing their own cell lines at home....like your own probiotics?
pretty weird, ...I know. Any comments are appreciated.
yup thats as weird as the stuff i write, congratulations ;o)
i actually understand what you are saying , the genetic clock has to be turned backwards
i do it differently, not being able to grow my own cell lines or being able to implant the cell lines if i could grow them
basically you need to encourage a higher rate of degenerated DNA cell apoptosis (apoptosis = cell death) and also encourage new cell formation by nutrition
in english u need to encourage cells with bad dna to kill themselves
also this is a very effective anti cancer approach
metafolin and my dual selenium protocol and retinyl acetate encourage apoptosis, my general supplement approach covers the growth factor side
also vit and skin d's i think for cell differentiation
i think some of the herbal anti cancer lore like essiac also is able to force higher rates of cell apoptosis
bloodroot may be a bit aggressive and uncontrolled in this respect
but basically adult cell differentiation being what it is, results are a bit limited. though worthwhile.