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

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/