Bruce Lipton : Internationally Recognized Leader In Bridging Science And Spirit

An Intimate Interview with Author Bruce H. Lipton, Ph.D.

“When I first recognized that the brain of the cell was the cell membrane, rather than genes, I was blown away, for the mechanism revealed that life was controlled by signals from the “environment.” The significance of this finding is that the identity of the “self,” distinguishing one individual from another, would also represent an environmental (external) signal.”

What is it like for you to be pressing the edges of the conventional, entrenched wisdom of the medical/health care field?

I am on an amazing journey that is filled with exhilarating life experiences expressing both sweet and sour consequences. On the sweet side is the fact that I am having the most exciting time of my life!! My research revealed a revolutionary understanding of how life “worked” twenty years ago and this awareness is now beginning to be recognized by leading edge science. The beautiful part is that with a twenty year head start over my former colleagues, I have not only benefited by applying this empowering awareness in creating the joyous life I am experiencing, but I have been able to extend that knowledge to reveal how the world can thrive and evolve.

The sweetness of that knowledge is also where the “sour” part comes in to the picture. Our conventional world is engaged in a ruthless survival of the fittest competition, based upon science’s endorsement of Darwinian theory, a belief that emphasizes, “life is a struggle for survival.” In contrast, the new biology reveals a completely different understanding of our place in the world. Science is now recognizing that we are an integral part of a giant living community, collectively referred to as Gaia. The new science underscores the fact that our survival is based upon the cooperation of all the organisms in the biosphere. Unfortunately, our social consciousness, shaped by Darwinian science, is so destructive to the environment that it has already precipitated the planet’s sixth mass extinction—which of course threatens the survival of humanity.

Yet there is also good news. Just as some terminal cancer patients undergo a spontaneous remission, the living Gaia can do the same. As with those cancer patients, all we need to do to save our world is change our beliefs, and this is precisely the consequence of the evolving new science. My book, The Biology of Belief: Unleashing the Power of Consciousness, Matter and Miracles, provides an easy to understand explanation of how our thoughts and mind create both our internal (biological) and external (social) life experiences.

What about your discoveries has most profoundly affected your life and the way you live it?

In the first instant of acquiring my new insights into how cells worked, I was completely transformed. As a conventional scientist, I taught my students that genes controlled life and that we were essentially “victims” of our heredity. When I first recognized that the brain of the cell was the cell membrane, rather than genes, I was blown away, for the mechanism revealed that life was controlled by signals from the “environment.” The significance of this finding is that the identity of the “self,” distinguishing one individual from another, would also represent an environmental (external) signal.

If the cell (organism) dies, its identity signal is still present in the environment. At that moment of awareness, I realized that we have an externalized “identity” (spirit) and are immortal. The realization of a transcendent “identity” brought an amazing sense of peace into my life, for I had truly lost the greatest of all fears…death. It was the most profound experience for me, a non-spiritual scientist that wasn’t even looking for that particular understanding.

Subsequently, my life was transformed when I realized how my developmental experiences programmed my genes and behaviour. With this knowledge I was able to rewrite limiting, self-sabotaging beliefs that were keeping me from experiencing the health, love and joy we all seek. I have actively created a wonderful healthy, fulfilling life and supporting environment. I love my days, sleep like a baby and enjoy life without the necessity of taking a single pharmaceutical drug!

One of the most important things I learned through my research was that human beings were biologically modelled after the anatomy and physiology of single cells. Cells are in a sense, miniature people. My research provided insight into understanding how the fifty trillion cells that comprise the human body can live in health and harmony under the skin. I was able to apply the fundamental principles of cellular life to the way I was living my life with great success. In the words of old hippie philosophy, I was “cleaning up my own backyard before cleaning up the world.” I learned to live better and healthier on less money, not only through modelling my efficiency upon cellular life, but also because my personal joy and satisfaction in life was no longer linked to consumerism. My pleasures are now directly derived through my appreciation of Gaia, my family and my community.

If you were to choose one area that you feel is your greatest challenge in sharing your discoveries, what would that be?

As mentioned, the new science reveals that our preoccupation with competition and consumerism is compromising our species and our environment. There is a lot of money trying to keep us from evolving. Corporate and government interests, playing on our Darwinian fears, are undermining our civilization and environment. Simply, self-empowerment is not in the interest of those whose focus is to “control” civilization.

Wars, social and moral decay, faltering education, famine and much of our disease will be eliminated when the new science becomes common knowledge. The self-empowerment offered by the new science is a threat to those organizations that profit from war and ill health. Among others, these organizations include the military-industrial complex, the larger biomedical-pharmaceutical industry and those fundamentalist religions that encourage violence and self-limitation in seeking their ends.

Presently, these organizations are spending vast sums of money, enough to solve civilization’s problems, to “control” and limit our abilities via the news, magazines and television programming. Consequently, it is a difficult endeavour to fight the tide of self-limiting, self-defeating propaganda sponsored by the moneyed interests. Yet, in recent years I have noticed vast changes in consciousness by people who intuitively know we are on the wrong track and are looking for a course correction. Fortunately, books like The Biology of Belief, as well as a number of other new works of science, are aimed at introducing the mass reading audience to the life-changing power of their conscious mind. I believe we are approaching a threshold, like the notion of the hundredth monkey, where the new science will appear to spontaneously change the direction of civilization and save us from our excesses.

When you consider your existing science and what other discoveries undoubtedly lie ahead, who do you believe human beings are capable of becoming?

We will learn that if there is a “heaven,” it is right here on Earth. We will learn how to recreate the proverbial Garden of Eden. In this new awareness we will be able to guide our own stem cells to renew our lives, without the use of pharmaceutical agents. Like breathairian’s, we will also learn to capture energy directly from the environment and will no longer be dependent upon the massive quantities of food we now think we need to eat. This awareness should provide us with a natural lifespan of at least 120-140 years, while simultaneously taking the pressure off the environment to feed us. Interestingly, current research reveals that we can double the life of laboratory organisms by simply curtailing their metabolic intake.

The new science provides insight into how we manifest our reality. Since most people are looking for happiness, joy and health, their collective vision can create such a reality. Such a culture would be one that does not encourage disharmony and disease. That’s already a good start in revitalizing Eden.

When you witness the range of responses to your material - from great joy to outrage, no doubt! - what is it that keeps you moving forward?

The simplest answer is that I have found Heaven on Earth by personally applying the principles of the new science to the way I carry out my own life. I love my job of bringing this new science to the public, for in my travels, I have seen many people use this information to “taken control” of their own lives. There is nothing more joyous than to see an individual overcome physical and emotional adversity through self-empowerment. And on a more self-serving level, the more people create harmony in their world, the more harmony I experience in my world.

Books and media by Dr. Lipton can be found in our store on our website at www.2012survivornet.com

Bruce Lipton : Internationally Recognized Leader In Bridging Science And Spirit

Backgrounder: Epigenetics and Imprinted Genes

 

Backgrounder: Epigenetics and Imprinted Genes

There is far more to genetics than the sequence of building blocks in the DNA molecules that make up our genes and chromosomes. The "more" is known as epigenetics.

What is epigenetics?

Epigenetics, literally "on" genes, refers to all modifications to genes other than changes in the DNA sequence itself. Epigenetic modifications include addition of molecules, like methyl groups, to the DNA backbone. Adding these groups changes the appearance and structure of DNA, altering how a gene can interact with important interpreting (transcribing) molecules in the cell's nucleus.

How do epigenetic modifications affect genes?
Genes carry the blueprints to make proteins in the cell. The DNA sequence of a gene is transcribed into RNA, which is then translated into the sequence of a protein. Every cell in the body has the same genetic information; what makes cells, tissues and organs different is that different sets of genes are turned on or expressed.

Because they change how genes can interact with the cell's transcribing machinery, epigenetic modifications, or "marks," generally turn genes on or off, allowing or preventing the gene from being used to make a protein. On the other hand, mutations and bigger changes in the DNA sequence (like insertions or deletions) change not only the sequence of the DNA and RNA, but may affect the sequence of the protein as well. (Mutations in the sequence can prevent a gene from being recognized, amounting to its being turned off, but only if the mutations affect specific regions of the DNA.)

There are different kinds of epigenetic "marks," chemical additions to the genetic sequence. The addition of methyl groups to the DNA backbone is used on some genes to distinguish the gene copy inherited from the father and that inherited from the mother. In this situation, known as "imprinting," the marks both distinguish the gene copies and tell the cell which copy to use to make proteins.

 

What is "imprinting?"

"Imprinted genes" don't rely on traditional laws of Mendelian genetics, which describe the inheritance of traits as either dominant or recessive. In Mendelian genetics, both parental copies are equally likely to contribute to the outcome. The impact of an imprinted gene copy, however, depends only on which parent it was inherited from. For some imprinted genes, the cell only uses the copy from the mother to make proteins, and for others only that from the father.

Imprinting in genetics is not new, but it is gaining visibility as it is linked to more diseases and conditions that affect humans. Centuries ago, mule breeders in Iraq noted that crossing a male horse and a female donkey created a different animal than breeding a female horse and a male donkey. In the modern scientific era, however, the initial evidence for parent-of-origin effects in genetics didn't appear until the mid 1950s or so.

Then, in the mid 1980s, scientists studying mice discovered that inheritance of genetic material from both a male and a female parent was required for normal development. The experiments also revealed that the resulting abnormalities changed depending on whether the inherited genetic material was all male in origin or all female.

Around the same time, others discovered that the effects of some transgenes in mice differed when they were passed from the male or female parent. The first naturally occurring example of an imprinted gene was the discovery of imprinting in the IGF-2 gene in mice in 1991, and currently about 50 imprinted genes have been identified in mice and humans.

Why should it matter which parent donated the gene copy?
Why imprinting evolved in animals is unclear, but one hypothesis is that imprinting represents a genetic "battle of the sexes," since many imprinted genes regulate embryonic growth. Maternally-expressed imprinted genes (for which the copy from mom is always used) usually suppress growth, while paternally expressed genes usually enhance growth.

The "battle of the sexes" hypothesis is partly based on studies in animals that suggest growth-promoting imprinted genes help ensure the continuation of the father's genes, a particularly important issue for species in which more than one male can contribute to a single litter of offspring. The mother, however, is more interested in maintaining her own health, biologically speaking, and hence her genes "fight" the paternal genes and limit the size of the embryo or fetus.

What role does imprinting play in disease?
Because of their growth-related aspects, imprinted genes likely play a major role in the development of cancer and other conditions in which cell and tissue growth are abnormal. Imprinted genes in which the copy from the mother is turned on (maternally expressed) usually suppress growth, while paternally expressed genes usually stimulate growth (see above).

In cancer, some tumor suppressor genes are actually maternally expressed genes that are mistakenly turned off, preventing the growth-limiting protein from being made. Likewise, many oncogenes -- growth-promoting genes -- are paternally expressed genes for which a single dose of the protein is just right for normal cell proliferation. However, if the maternal copy of the oncogene loses its epigenetic marks and is turned on as well, uncontrolled cell growth can result.

In the collection of birth defects known as Beckwith-Wiedemann syndrome (BWS), abnormal epigenetics leads to abnormal growth of tissues, overgrowth of abdominal organs, low blood sugar at birth and cancers. Similiarly, in the imprinting disorder Prader-Willi syndrome, abnormal epigenetics causes short stature and mental retardation as well as other syndromic features.

There's also evidence in mice that some imprinted genes may play a role in behavior, particularly in nurturing and social situations.

How does imprinting get messed up?
Just as mutations in the sequence of DNA can be acquired as a cell copies its DNA, changes in a cell's epigenetics can be acquired as well, although how those errors occur isn't as well understood. Scientists do know that epigenetic alterations can be caused by environmental changes, such as the laboratory conditions used for growing cells, but the details are murky.

For example, researchers are still trying to understand the process by which cells maintain or change their gene's imprinting marks. In sperm and egg, for instance, imprinted gene copies have to be re-imprinted. Imagine one copy of a paternally imprinted gene passed from a father to his daughter (the copy is paternally inherited and will be "on") and then to her child (it's now a maternally inherited copy and will be "off").

Many scientists believe that "incorrect" epigenetic changes to tumor suppressor genes and oncogenes are some of the first steps in cancer initiation. Determining when and how imprinting marks get re-written during egg and sperm development is crucial in figuring out whether imprinting abnormalities could be corrected in cancer.

What's next for imprinting research?
As more is learned about what role abnormal imprinting plays in biology and disease, it's important to continue learning about exactly how imprinting works. What marks distinguish maternal and paternal gene copies, and are they the same for all imprinted genes? How and when during conception or formation of sperm and egg are the tell-tale marks changed? Can epigenetics be manipulated to return normal control to cells in tumors?

To find answers to these and other questions, imprinting in early stage embryos will need to be studied. Hopkins researchers recently created a mouse model in which the paternal and maternal gene copies are easily distinguished in order to help answer these questions. The true test will be one day evaluating the questions in humans, although such experiments are not currently permitted.

Backgrounder: Epigenetics and Imprinted Genes

Epigenetics? - Dining for your descendants - Epigenome NOE

An expectant mother might well logically reason that what she eats will affect her unborn child. But the evidence is mounting that not only her children, but her grandchildren and subsequent generations will be affected by her nutrition. What she eats may not only affect her descendants as they develop, but potentially throughout their adult lives.

Brona McVittie reports :: November 2008
The early environment of a developing child can talk to its genome by epigenetic means. Environmental cues trigger changes to epigenetic tags on our genome, which shape the way genes are expressed. These tags on the genome can be carried through from cell to cell as we replace damaged body tissue. When such changes occur inside egg or sperm cells, they can pass through to the next generation. So, we don’t just inherit our genes, but potentially also their modes of expression.
A recent study published in Diabetes by Josep Jimenez–Chillaron and colleagues on 19th November adds further strength to this argument.  Based on recent research, which indicates that low birth weight is associated with increased risk of obesity, diabetes and cardiovascular disease during adult life, the team wanted to know whether such disease risks might be passed on to future generations.
They bred mice with low birth weight by starving pregnant mothers during the last week of pregnancy.  Animals with low birth weight were mated and compared to the offspring from normal crosses. The experimental results indicated that starving pregnant mothers “programs” a low birth weight not only in her infants, but those of the next generation.
Coupled with this, males from the first-generation crosses were found to be glucose intolerant, which increased with age. All of the subsequent generation developed glucose intolerance by four months. Other studies have confirmed that diabetes can pass through more than a single generation through the maternal line, but this is the first study that shows inheritance of glucose intolerance through the male line.
Exactly how such changes manifest at the molecular level remains to be fully elucidated, although the team pinpointed a gene called Sur1, which could be linked to the glucose intolerance. While the researchers haven’t yet established the epigenetic basis of this inheritance, further studies will investigate changes to epigenetic tags that might be responsible. Such research has important medical implications, but will also cast light on the role of epigenetics in evolution.

Epigenetics? - Dining for your descendants - Epigenome NOE

Bruce Lipton, PhD | The Living Matrix

 

The Living Matrix – The Science of Healing, uncovers new ideas about the intricate web of factors that determine our health.

Tapping into the power of information

Leaders in science are examining the body through the lens of quantum physics. They’ve discovered that we're far more than biochemical machines

Instead, our cells are senders and receivers of information, controlling our health in ways we never imagined.

Renowned cell biologist, former University of Wisconsin Medical School professor and Stanford University researcher Dr. Bruce Lipton has turned his scientific exploration to the integration of mind, body and spirit. In short, he studies how our beliefs affect our health.

In 1982, Dr. Bruce Lipton began exploring quantum physics to more fully explain the cell’s information processing systems. His breakthrough studies on the cell membrane revealed its function as essentially an organic computer chip, the cell’s equivalent of a brain.

A decade later, Dr. Bruce Lipton made a discovery that ran counter to everything scientists believed about the role of genes in the body. His research showed that environmental forces outside the cell control its behavior and physiology, turning genes on and off. This idea opened the door to a new and important field, the science of epigenetics.

Dr. Bruce Lipton’s two major scientific papers based on these studies defined the molecular pathways connecting the mind and body. Subsequent papers by other researchers have validated his concepts.

A sought-after lecturer, Dr. Bruce Lipton has appeared on numerous TV and radio shows and speaks to audiences around the world.

 

Bruce Lipton, PhD | The Living Matrix

Cellular Aging: Telomeres | Cellular Aging: Telomeres Information | HighBeam Research - FREE Trial

 

CELLULAR AGING: TELOMERES

Aging is a complex process that occurs on multiple levels. The end result of aging is that life span is limited in multicellular organisms. The cells that make up multicellular organisms also have limited life spans. The limitation on cellular life span is comprised of two parts: (1) cells become unable to continue dividing but remain metabolically active, and (2) at some future time cell death occurs. Many cells in the human body are continually undergoing cellular division. Cellular division is a normal condition of certain tissues; examples include hair growth, the sloughing off of skin every several days, and the complete turnover and replacement of the cells of the immune systems every few months. In some instances, cellular division occurs in order to heal damaged tissues. Thus, having a limited number of cellular divisions available could contribute to aging by slowing down processes such as wound healing, as well as affecting general tissue maintenance.

In the 1960s, Leonard Hayflick first noted that human cells undergo a limited number of divisions when placed in culture. Furthermore, he noted that the number of divisions cells undergo is related to the number of prior divisions undergone by the cells. This observation suggested the existence of an intracellular clock that marked the division history of each cell. In addition, it suggested that once a predetermined number of divisions has occurred, a signal (or signals) is generated that prevents the cell from undergoing further divisions. The timing mechanisms underlying and regulating this process remained elusive until the end of the twentieth century. The first of these clocks to be identified and characterized, the telomere, is active in several human cell types.

Telomeres are chromosome caps

Telomeres are specialized structures present at the end of liner chromosomes; they serve the essential function of protecting and stabilizing chromosome ends. The telomere was first defined in the 1930s following observations that naturally occurring chromosome ends behave differently than chromosome breaks induced by damaging agents such as ionizing radiation. Both structures are ends of double-stranded DNA molecules. However, chromosome ends are stable, allowing accurate transmission of chromosomes from generation to generation without loss of genetic material, whereas induced breaks are very unstable, reacting with other chromosomes in the cell to create rearrangements and chromosome fusions. In addition, broken ends of DNA trigger cellular protective responses. These responses act either to allow the DNA damage to be repaired, or to remove the cell from the population by cellular suicide, called apoptosis. Even though telomeres are the physical end of a DNA molecule, they do not trigger these protective responses. These observations indicated that there is something special about naturally occurring chromosome ends.

Telomere structure

Telomeres are made up of short tandem repeats of a simple DNA sequence and associated proteins. In humans, and all other vertebrates, the telomeric DNA sequence is 5'(TTAGGG)3', oriented towards the end of one DNA strand, with the complimentary sequence 5'(CCCTAA)3' oriented towards the interior of the chromosome. The duplexed telomeric repeats are arranged in tandem and are present in more than a thousand copies at the end of each human chromosome. At the very end of the chromosome there is a single-stranded protrusion of the G-rich strand that extends for twenty or more repeats.

Cellular Aging: Telomeres | Cellular Aging: Telomeres Information | HighBeam Research - FREE Trial

Study provides direct evidence of the role of telomeres in disease development. - Cancer Weekly | HighBeam Research - FREE trial

 

Study provides direct evidence of the role of telomeres in disease development. - Cancer Weekly | HighBeam Research - FREE trial

Telomere shortening may be early marker of cancer activity. - Biotech Week | HighBeam Research - FREE trial

 

Telomere shortening may be early marker of cancer activity. - Biotech Week | HighBeam Research - FREE trial

ARE TELOMERES THE KEY TO AGING AND CANCER?

Inside the center or nucleus of a cell, our genes are located on twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide and hold some secrets to how we age and get cancer.

Telomeres have been compared with the plastic tips on shoelaces because they prevent chromosome ends from fraying and sticking to each other, which would scramble an organism's genetic information to cause cancer, other diseases or death. Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell no longer can divide and becomes inactive or "senescent" or dies. This process is associated with aging, cancer and a higher risk of death. So telomeres also have been compared with a bomb fuse.

What are telomeres?

Like the rest of a chromosome and its genes, telomeres are sequences of DNA - chains of chemical code. Like other DNA, they are made of four nucleic acid bases: G for guanine, A for adenine, T for thymine and C for cytosine. Telomeres are made of repeating sequences of TTAGGG on one strand of DNA bound to AATCCC on the other strand. Thus, one section of telomere is a "repeat" made of six "base pairs."

In human blood cells, the length of telomeres ranges from 8,000 base pairs at birth to 3,000 base pairs as people age and as low as 1,500 in elderly people. (An entire chromosome has about 150 million base pairs.) Each time a cell divides, an average person loses 30 to 200 base pairs from the ends of that cell's telomeres.

Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent, die or sustain genetic damage that can cause cancer. Telomeres do not shorten with age in tissues such as heart muscle in which cells do not continually divide.

Why do chromosomes have telomeres?

Without telomeres, the main part of the chromosome - the part containing genes essential for life - would get shorter each time a cell divides. So telomeres allow cells to divide without losing genes. Cell division is needed so we can grow new skin, blood, bone and other cells when needed.

Without telomeres, chromosome ends could fuse together and degrade the cell's genetic blueprint, making the cell malfunction, become cancerous or die. Because broken DNA is dangerous, a cell has the ability to sense and repair chromosome damage. Without telomeres, the ends of chromosomes would look like broken DNA, and the cell would try to fix something that wasn't broken. That also would make them stop dividing and eventually die.

Why do telomeres get shorter each time a cell divides?

Before a cell can divide, the chromosomes within it are duplicated so that each of the two new cells contains identical genetic material. A chromosome's two strands of DNA must unwind and separate. An enzyme (DNA polymerase) then starts to make two new strands of DNA to match each of the two unwound strands. It does this with the help of short pieces of RNA. When each new matching strand is completed, it is a bit shorter than the original strand because of the room needed at the end by this small piece of RNA. It is like someone who paints himself into a corner and cannot paint the corner.

Does anything counteract telomere shortening?

An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age.

Telomerase remains active in sperm and eggs, which are passed from one generation to the next. If reproductive cells did not have telomerase to maintain the length of their telomeres, any organism with such cells soon would go extinct.

What role do telomeres play in cancer?

As a cell begins to become cancerous, it divides more often, and its telomeres become very short. If its telomeres get too short, the cell may die. It can escape this fate by becoming a cancer cell and activating an enzyme called telomerase, which prevents the telomeres from getting even shorter.

Studies have found shortened telomeres in many cancers, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.

Measuring telomerase may be a new way to detect cancer. If scientists can learn how to stop telomerase, they might be able to fight cancer by making cancer cells age and die. In one experiment, researchers blocked telomerase activity in human breast and prostate cancer cells growing in the laboratory, prompting the tumor cells to die. But there are risks. Blocking telomerase could impair fertility, wound healing, and production of blood cells and immune system cells.

What about telomeres and aging?

Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.

Rest of artickle here: http://learn.genetics.utah.edu/content/begin/traits/telomeres/

What YOUR Brain can do

Your Brain's Potential

In the brain there are 1,000,000,000,000 (a million million) individual neurons or nerve cells.

If each neuron can interact with anywhere between 1 and 100,000 other neurons then the brain's potential for pattern forming (the number of possible permutations) is a massive number that even in normal text would require 10.5 million kilometres of space to write one after the other!

That means that your brain has an almost infinite capacity for storing information.

What are you going to learn today to start realising your potential?

Prominence eruption from sun is seen

A prominence eruption from the sun is seen in this image taken by the Solar Dynamics Observatory (SDO) on March 30, 2010. NASA released the first publicimages from the SDO on April 21, 2010.

Source: http://news.yahoo.com/nphotos/NASA-releases-images-sun/ss/events/sc/042210nasasun#photoViewer=/100422/ids_photos_wl/r938069384.jpg