The Joie de Vivre (mindful happiness) Rejuvenation Special
In this three days retreat, we focus on the epigenetic clock that governs 2 percent of our DNA, the eukaryotic genes, as well as on telomere biology as these two mechanisms are decisive in terms of switching off the suicide-death genes (inflammation, senescence, misfoldment of proteins etc) and switching on the youthful life happy genes that govern cell repair, autophagy, methylation, neuropeptides and many other pathways. (1)
Thanks to mindful “joie de vivre” meditation, breathing and exercises, as well as the Center’s other holistic techniques, three full days of deep “now” consciousness is enough to start modulating one’s joie de vivre and healthy lifespan potential via neural, hormonal and cellular change. (2)
In this perspective, the emerging evidence that rejuvenation is a function of frequencies and signaling is accumulating. Three researcher groups (at Stanford Harvard, Berkeley) have shown that injecting blood plasma from a young mouse into an old mouse makes the old mouse healthier and younger. The blood plasma contained no cells, only signal molecules that are the product of gene expression. And yes, as we will show via power point presentation, an enriched environment of mindful “joie de vivre” consciousness and meditation does rejuvenate. (3) The Science that this above-mentioned epigenetic clock either erodes or enhances a healthy lifespan is compelling. (4) Supercentenarians like Jeanne Calment who lived to 122 years remind us that epigenetics is key insofar as rejuvenation is concerned.
For those who need more than five days, workshopees can enroll in the Center’s other longer retreats where these and other “joie de vivre” techniques are practiced on a daily basis.
Reference and Precision notes
(1). Epigenetics is a new science in the 21st century. All the cells in one body have the same DNA (Source), but differernt genes are “expressed” (translated into proteins) in different tissues and at different times, and this is what controls the body’s metabolism. In fact, only 2% of our DNA is genes, and 98% determines how the DNA is folded and spooled, opened and closed at particular times and places, and this in turn controls gene expression. We are 2% genetic and 98% epigenetic. There is a language called the “genetic code” which determines how genes are translated into proteins. It was decoded by Francis Crick and others in the 1950s. It is as simple as it can be, and is completely understood. There is another language, the “epigenetic code” that determines gene expression.
(2). The body is programmed to die, and its suicide plan is laid out in the form of transcribing an unhealthy combination of genes. This idea flies in the face of traditional evolutionary theory. (How could natural selection prefer a genome that destroys itself and cuts off its own reproduction?) Nevertheless, the evidence for this hypothesis is robust. With age, most of the genes that are turned on don’t protect the body. Genes for inflammation are dialed up. Genes for the body’s defense against free radicals are dialed down. Cell turnover is dialed down. DNA repair is dialed down. The mechanisms of programmed cell death (apoptosis) are strengthened in healthy cells, at the same time that they are perversely weakened in cells that are a threat to the body, like infected cells and cancer cells.
(3). For evidence, see the blog’s “mechanisms” section.
(4). A variety of epigenetic alterations affects all cells and tissues throughout life (Talens et al., 2012) (Figure 2B). Epigenetic changes involve alterations in DNA methylation patterns, posttranslational modification of histones, and chromatin remodeling. Increased histone H4K16 acetylation, H4K20 trimethylation, or H3K4 trimethylation, as well as decreased H3K9 methylation or H3K27 trimethylation, constitute age-associated epigenetic marks (Fraga and Esteller, 2007; Han and Brunet, 2012). The multiple enzymatic systems assuring the generation and maintenance of epigenetic patterns include DNA methyltransferases, histone acetylases, deacetylases, methylases, and demethylases, as well as protein complexes implicated in chromatin remodeling. (See the Optimal Longevity Institute for corroboration).
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