by S.L. Baker
It’s well-established that exposure to ionizing radiation can trigger mutations and other genetic damage and cause normal cells to become malignant. So it seems amazing how mainstream medicine frequently dismisses the idea that medical imaging tests from mammograms to CT scans could play much of a role in causing breast cancer. Take this example from the web site for Cornell University’s Program on Breast Cancer and Environmental Risk Factors:
In answer to the question “Is ionizing radiation a cause of breast cancer?”, the Cornell experts say “Yes” and note “.. female breast tissue is highly susceptible to radiation effects.” But then they pooh-pooh the possible hazard from mammography x-rays saying the risk …”should not be a factor in individual decisions to undergo this procedure. The same is true for most diagnostic x-ray procedures.”
If that’s not confusing enough, they turn around and state: “Nonetheless, unnecessary radiation exposures should be avoided and continued vigilance is required to ensure that the benefits associated with specific procedures outweigh the future risks.”
Why radiation causes breast cancer
Common sense suggests there is plenty of reason to be worried about radiation causing breast cancer. And now there’s a new reason to be concerned. Researchers at the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have discovered that radiation exposure can alter cells’ microenvironment (the environment surrounding cells). And that greatly raises the odds future cells will become cancerous.
The reason is that signals from a cell’s microenvironment, altered by radiation exposure, can cause a cell’s phenotype (made up of all its biochemical and physical characteristics) to change by regulating or de-regulating the way a cell uses its genes. The result can be a cell that not only becomes pre-cancerous but that passes this pre-malignant condition on to future cells.
“Our work shows that radiation can change the microenvironment of breast cells, and this in turn can allow the growth of abnormal cells with a long-lived phenotype that have a much greater potential to be cancerous,” Paul Yaswen, a cell biologist and breast cancer research specialist with Berkeley Lab’s Life Sciences Division, said in a statement to the press.
“Many in the cancer research community, especially radiobiologists, have been slow to acknowledge and incorporate in their work the idea that cells in human tissues are not independent entities, but are highly communicative with each other and with their microenvironment,” he added.
For their study, Yaswen and his research teams used human mammary epithelial cells (HMECs), the cells that line breast ducts, where most breast cancers start. When placed in a culture dish, the vast majority of HMECs display a phenotype that allows them to divide between five and 20 times until they become what is known as senescent, or unable to divide. However, there are also some variants of these cells which have a phenotype that allows them to continue dividing for many weeks in culture. Known as a vHMEC phenotype, this type of breast cell arises spontaneously and is more susceptible to malignancy because it lacks a tumor-suppressing protein dubbed p16.
To find out what radiation exposure does to the cellular environment and how it could impact the future of cell behavior, the Berkeley Lab scientists grew sets of HMECs from normal breast tissue in culture dishes for about a week. Then they zapped each set with a single treatment of a low-to-moderate dose of radiation and compared the irradiated cells to sets of breast cells that had not been irradiated.
The results, just published in the on-line journal Breast Cancer Research, showed that four to six weeks after the radiation exposure, the normal breast cancer cells had stopped dividing far earlier than they would have normally — and this premature cell senescence had accelerated the outgrowth of vHMECS.
“However, by getting normal cells to prematurely age and stop dividing, the radiation exposure created space for epigenetically altered cells that would otherwise have been filled by normal cells. In other words, the radiation promoted the growth of pre-cancerous cells by making the environment that surrounded the cells more hospitable to their continued growth,” Yaswen explained in the press statement.
The researchers pointed out that the levels of radiation used in their experiments were not as much as a woman would be exposed to during a single routine mammogram but were comparable to those a woman could receive during a CT scans or radiotherapy “and could represent sources of concern.”
Of course, women are often pushed to get annual mammograms, raising their overall radiation exposure through the years. And, as NaturalNews has reported, previous research has already provided compelling evidence linking mammography to breast cancer.
May 17, 2010
By Jonathan Leake
SCIENTISTS have discovered the “Methuselah” genes whose lucky carriers have a much improved chance of living to 100 even if they indulge in an unhealthy lifestyle.
The genes appear to protect people against the effects of smoking and bad diet and can also delay the onset of age-related illnesses such as cancer and heart disease by up to three decades.
No single gene is a guaranteed fountain of youth. Instead, the secret of longevity probably lies in having the right “suite” of genes, according to new studies of centenarians and their families. Such combinations are extremely rare — only one person in 10,000 reaches the age of 100.
The genes found so far each appear to give a little extra protection against the diseases of old age. Centenarians appear to have a high chance of having several such genes embedded in their DNA.
“Long-lived people do not have fewer disease genes or ageing genes,” said Eline Slagboom of Leiden University, who is leading a study into 3,500 Dutch nonagenarians. “Instead they have other genes that stop those disease genes from being switched on. Longevity is strongly genetic and inherited.”
Slagboom and her colleagues recently published studies showing how the physiology of people in long-lived families differs from normal people. Other studies, showing the genetic causes of those differences, are due for publication soon.
“People who live to a great age metabolise fats and glucose differently, their skin ages more slowly and they have lower prevalence of heart disease, diabetes and hypertension,” she said.
“These factors are all under strong genetic control, so we see the same features in the children of very old people.”
The so-called Methuselah genes — named after the biblical patriarch who lived to 969 — are thought to include ADIPOQ, which is found in about 10% of young people but in nearly 30% of people living past 100. The CETP gene and the ApoC3 gene are found in 10% of young people, but in about 20% of centenarians.
Some of those genes were discovered by a research group at Albert Einstein College of Medicine in New York, led by Prof Nir Barzilai, following an analysis of the genes of over 500 centenarians and their offspring.
The studies show that tiny mutations in the make-up of particular genes can sharply increase a person’s lifespan. Nonetheless, environmental factors such as the decline in infectious diseases are an important factor in the steady rise in the number of centenarians. The human genome contains about 28,000 genes, but they are controlled by a tiny number of so-called regulator genes.
Dr Barzilai told a Royal Society conference that the discovery of such genes gave scientists clear targets for developing drugs that could prevent or delay the onset of age-related diseases, potentially lengthening people’s lives and keeping them healthier for longer.
Dr David Gems, a longevity researcher at University College London, believes that treatments to slow ageing will become widespread.
“If we know which genes control longevity then we can find out what proteins they make and then target them with drugs. That makes it possible to slow down ageing. We need to reclassify it as a disease rather than as a benign, natural process,” he said.
“Much of the pain and suffering in the world are caused by ageing. If we can find a way to reduce that, then we are morally obliged to take it.”
An anti-ageing drug which might be taken by millions of people, perhaps from middle age onwards, could be the ultimate blockbuster for the pharmaceutical industry.
Michelle Mitchell of Age UK said: “Ageing is a natural part of life. The key is to ensure that we do not simply extend life but extend the years of healthy life so that people can enjoy, not endure, their later years.”
March 3, 2010
By Maggie Fox
Can’t lose weight on a low-fat diet? Maybe you need to cut carbs instead, and a new genetic test may point the way, maker Interleukin Genetics Inc reported on Wednesday.
The small study of about 140 overweight or obese women showed that those on diets “appropriate” for their genetic makeup lost more weight than those on less appropriate diets, researchers told an American Heart Association meeting.
“The potential of using genetic information to achieve this magnitude of weight loss without pharmaceutical intervention would be important in helping to solve the pervasive problem of excessive weight in our society,” Christopher Gardner at Stanford University in California, who worked on the study, said in a statement.
Massachusetts-based Interleukin’s $149 test looks for mutations in three genes, known as FABP2, PPARG and ADRB2.
The company says 39 percent of white Americans have the low-fat genotype, 45 percent have the type that responds best to a diet low in processed carbohydrates and an unlucky 16 percent have gene mutations that mean they have to watch both fat and processed carbohydrates.
The researchers randomly assigned around 140 women to one of four diets — the low-carb Atkins diet, the ultra low-fat Ornish diet, the very low-fat LEARN diet or the more balanced Zone diet.
Interleukin went back and tested about 100 of the women for their DNA by using a cheek swab and then looked to see if the women on the “right” diets lost more weight.
MOST EFFECTIVE MATCHES
Over a year, people on diets appropriate to their genetic makeup, as determined by the test, lost 5.3 percent of body weight. People on mismatched diets lost 2.3 percent, the Stanford researchers told the meeting.
Cholesterol levels improved in line with weight loss, they said.
The company said the test looks for genes that affect metabolism.
“One of the gene variations affects absorption of fats from the intestine,” Ken Kornman, chief scientific officer at Interleukin, said in a telephone interview. He said people with that particular mutation absorb more fat from their food and thus should avoid fat if they want to lose weight.
Another of the variations affects insulin response — the body’s production of insulin to metabolize sugar, he said. Simple carbohydrates such as sugar and processed flour stimulate people with that particular gene type to store more of the energy as fat.
Ten percent to 16 percent of people have both mutations, and must watch both carbs and fat, Kornman said.
“What we don’t know is if they are on the right diet for their genotype whether it affects satiety or feeling full,” he said. He said the company planned broader studies to ask these questions.
Interleukin markets the test under the brand name Inherent Health. It also can test who might best lose weight in response to exercise.
November 25, 2009
By Stefanie McIntyre
China must be alert to any mutation or changes in the behavior of the H1N1 swine flu virus because the far deadlier H5N1 bird flu virus is endemic in the country, a leading Chinese disease expert said.
Zhong Nanshan, director of the Guangzhou Institute of Respiratory Diseases in China’s southern Guangdong province, said the presence of both viruses in China meant they could mix and become a monstrous hybrid — a bug packed with strong killing power that can transmit efficiently among people.
“China, as you know, is different from other countries. Inside China, H5N1 has been existing for some time, so if there is really a reassortment between H1N1 and H5N1, it will be a disaster,” Zhong said in an interview with Reuters Television.
“This is something we need to monitor, the change, the mutation of the virus. This is why reporting of the death rate must be really transparent.”
The World Health Organization warned on Tuesday that H5N1 had erupted in poultry in Egypt, Indonesia, Thailand and Vietnam, posing once again a threat to humans.
“First, it places those in direct contact with birds — usually rural folk and farm workers — at risk of catching the often-fatal disease. Second, the virus could undergo a process of “reassortment” with another influenza virus and produce a completely new strain,” it said.
“The most obvious risk is of H5N1 combining with the pandemic … (H1N1) virus, producing a flu virus that is as deadly as the former and as contagious as the latter.”
Zhong told the Chinese media last week that China may have had more H1N1 flu deaths than it has reported, with some local governments possibly concealing suspect cases.
The doctor is known for his candor and work in fighting Severe Acute Respiratory Syndrome in 2003, when nationwide panic and international alarm erupted after it emerged that officials hid or underplayed the spreading epidemic.
Cover-ups by local governments in 2003 during the SARS epidemic led to the sackings of several officials. More than 300 people died in that outbreak.