Smokers ‘will die 10 years early’

Smoking cigarettes cuts an average of 10 years off a person’s life, a landmark study suggests. But it also shows that quitting at any age reduces the risks of dying from smoking-related diseases. The findings, published in the British Medical Journal, are the culmination of a 50-year study involving 34,439 men. The study, which began in 1951, was the first to confirm the link between smoking and lung cancer exactly 50 years ago. All of those involved in the study were born between 1900 and 1930 and all worked as doctors.

 

They were each asked about their smoking habits at the start of the study in 1951. Researchers contacted them periodically over the next 50 years to see if those habits had changed. Since the study began in 1951, tobacco has killed around 100 million people Professor Alex Markham, Cancer Research UK They also gathered information on those who died during the period. They have now analysed that data. They found that men who have never smoked lived on average 10 years longer than those who smoked for most of their lives. Men who smoked were at least twice as likely to die before the age of 70 as non-smokers. They were up to three times more likely to die before they were 90 compared to those who never took up the habit. The average age of these men when they started smoking was 18. On average, they said they smoked around 18 cigarettes a day.

 

It was already known that about half of all persistent cigarette smokers are killed by their habit, a quarter while still in middle age (35-69 years). The biggest killers are cancer, heart disease and stroke. But the study also revealed that giving up cigarettes at any age has major health benefits. It found that men who had stopped smoking by the time they were 30 lived as long as those who never smoked. Those who quit at 40, lived just one year less than those who had never smoked. Those who stopped smoking at 50 added six years onto their lives, while those who kicked the habit at 60 added an extra three years to their life.

Genes and bladder cancer

Arylamines are known bladder carcinogens and are an important constituent of tobacco smoke. The handling of arylamines in the body is complex and includes metabolism by NAT1 and NAT2, enzymes that play a role in both activation and detoxification of arylamines and their congeners. Both NAT1 and NAT2 are polymorphic, with alleles that have been shown to correlate with higher or lower enzyme activity. To explore the combined role of these genes and exposure on bladder cancer risk, we examined the NAT1 and NAT2 genotype in a case-control study of bladder cancer in which detailed exposure histories were available on all 230 cases and 203 frequency-matched controls. Using PCR-RFLP genotyping, we determined NAT2 genotype for the five most common alleles, NAT2*4, NAT2*5, NAT2*6, NAT2*7, NAT2*14 (frequently referred to as WT, M1, M2, M3, and M4, respectively).

 

Similarly, the NAT1 genotype was determined for the four most common alleles NAT1*3, NAT1*4, and NAT1*11, and the putative high-activity allele, NAT1*10. No association between NAT2 genotype and bladder cancer risk was found whether genotype was considered alone or in combination with smoking, in either stratified or logistic regression analysis that adjusted for age, sex, and race. Stratified and logistic regression analysis both demonstrated an increased risk for individuals carrying the NAT1*10 allele among smokers. There was evidence of a gene-dosage effect, such that those who were homozygous for the NAT1*10 allele had the highest risks.

 

There was also evidence of a statistically significant gene-environment interaction, such that bladder cancer risk depends on both NAT1 genotype and smoking exposure. Interestingly, although NAT2 genotype did not influence risk either alone or in combination with smoking exposure, there was evidence of a statistically significant gene-gene-environment three-way interaction. Bladder cancer risk from smoking exposure is particularly high in those who inherit NAT2 slow alleles in combination with one or two copies of the NAT1*10 allele. A biological mechanism for this finding is suggested.

Appeal to the Tobacco Industry to Fund Cancer Research

The Tobacco settlement with the states ($246 billion over 25 years) went to the states, which are pissing it away on everything except cancer research. What the petition advocates is for the Tobacco Industry to fund *its own* carefully focused effort to find a cure for cancer, i.e., eliminate the government middlemen. I bet that if the Tobacco Industry spent 10 billion/year over 5 years, it would find a cure for cancer in 5 years.

 

They could do this by starting a Celera like corporation. If the tobacco industry spent 10 billion a year fighting cancer the damage to its image would be so grave that it soon wouldn’t -have- 10 billion a year. This is like advocating that the best cure for lung cancer would be for the tobacco industry to voluntarily cease to exist. Sure it would, but they aren’t going to die quietly. My personal belief is that selling tobacco is a crime against humanity comparable with genocide, and deserves the death penalty if anything does, but I am also a realist. I am afraid I don’t believe in ordering dogs to pick up their own poop, or the Mafia to fund the FBI.

 

This is a war, much more real than the so called war on terrorism. Cancer industry, in its own way, is just as bad as tobacco industry. Never have so many spent so much money and so much time to achieve so little! Of course, I am talking about cancer researchers. And, all currently established cancer treatments are based on their puny achievements. Only expensive cancer treatments are explored. A highly effective, entirely scientific, treatment is being shunned because it won’t bring big bucks.

Milk linked to ovarian cancer

Consuming large amounts of milk may increase the risk of developing ovarian cancer, research suggests. A study of more than 60,000 women found drinking more than two glasses of milk a day significantly upped the risk of the most serious form of the disease. Dairy products have previously been linked to cancers, including those of the breast and prostate. The research, by Sweden’s Karolinska Institute, is published in the American Journal of Clinical Nutrition. The researchers followed 61,084 women aged 38 to 76 for around 13 years. During this time a total of 266 women were diagnosed with ovarian cancer, of whom 125 had serious ovarian cancer.

 

The researchers found women who consumed more than four servings of dairy products a day had twice the risk of serious ovarian cancer than women who had fewer than two. They found that milk had the strongest link with ovarian cancer – those women who drank two or more glasses a day were at double the risk of those who did not consume it at all, or only in small amounts. The reason why milk may increase the risk of ovarian cancer is unclear, but one theory is that lactose, a type of sugar found in milk, may overstimulate production of hormones which encourage tumour growth. Dr Kate Law, of Cancer Research UK, said it was not yet clear how nutrients, or the amount and distribution of body fat affected the risk of developing cancer. She said: “Previous research has also suggested that a diet rich in whole milk, yogurt and cheese may put women at higher risk of ovarian cancer.

 

“But the picture is far from clear, as other evidence suggests that women who drink skimmed or low-fat milk might have a lower risk of ovarian cancer.” Dr Law a major study, involving 500,000 people, was currently underway to try to assess the impact on diet on cancer. “Until more is known about the specific components of diet that influence cancer risk, the best advice is to emphasize a balanced diet which includes plenty of fresh fruit and vegetables.” Around 6,700 women in the UK are diagnosed with ovarian cancer each year.

Genetic Breast Cancer

While there is no proof that these foods do what is claimed here, they can help in achieving a well-rounded diet. Good nutrition and diet are important to a cancer patient. – Tomatoes – These tasty spheres are bursting with the powerful antioxidant vitamin C and lycopene. Vitamin C bolsters the immune system and fends off cancer-causing free radicals, and lycopene is instrumental in cutting the risk of stomach, mouth, bladder, cervical, colon and prostate cancer. – Cruciferous Vegetables – Broccoli, red cabbage, cauliflower, kale, red beets and brussels sprouts all belong to this veggie family. All are amply fortified with cancer-fighting phytochemicals, including sulforaphane, beta-carotene and indolcarbinol. – Spinach – Popeye knew his nutrition. This dark, leafy vegetable is chock-full of antioxidants such as glutathione, vitamin C, beta-carotene, folic acid and carotenoids. Bright orange carrots are also an excellent source of beta-carotene and carotenoids — chemicals known to curb various cancers. – Beans – Beans, beans, they’re good for … beating digestive and breast cancer! Soybeans are stocked with protease inhibitors that don’t let cancer cells invade the body, and also contain isoflavones instrumental in protecting against breast cancer.

 

Fava beans fight carcinogens, reducing the risk of cancer in the digestive tract. – Hot red peppers – Biting into these zesty peppers may set off a fire in your mouth, but the capsaicin inside snuffs out harmful carcinogens emitted by cigarettes and some foods. These hot chilies rate number one in protecting against lung cancer. Caution: Capsaicin, is believed to have blood-thinning properties (natural blood thinner), a minor nuisance for some of us, but for some who have blood problems or already on blood thinners for other reasons, may need to check with their doctors before consuming capsaicin. – Garlic – This member of the onion family isn’t only powerful in flavor and scent. Garlic effectively thwarts carcinogens with organosulfides and allicinthus, helping to protect the body from breast cancer.

 

Oranges – Jam-packed with cancer-fighting bioflavonoids and immune system-boosting vitamin C, oranges also contain 170 photochemicals, including carotenoids. In addition, limonoids found in oranges and other citrus fruit fuel the immune system to fight cancer. – Berries – Strawberries, blueberries, cranberries, raspberries, blackberries and red and purple grapes boast more than a sweet taste. These bite-sized fruits get their dark hue from anthocyanins that can neutralize carcinogens. Plus, berries are bursting with flavonoids, a powerful group of cancer-fighting antioxidants.

New Cancer Therapy from Europe

A new method of treating cancer is proving to be 80% successful at stimulating the natural reduction and elimination of tumors. This process has been developed and perfected over the last five years in Europe. It is called BioResonance Tumor Therapy and it has an effect similar to stimulating spontaneous remission. As with all great breakthroughs in science, the best are based on insights that are penetratingly simple. Such is the case with this new therapy. It is based on the understanding of how cells naturally die. Every cell in the human body has a gene called the P53 gene. This gene tracks the degeneration of the cell and when it finds that the cell is damaged beyond repair, it triggers its self-destruction. This active, controlled process of cell death is happening all the time in all of us. 95% of the cells that are in your body now weren’t there 2 years ago. The old cells died through this natural self-destruction process that is triggered by the P53 gene. New cells are then created through cell division. What about tumor cells? In tumor cells the function of the P53 gene gets suppressed. The tumor cells lose the ability to die naturally. This insight about the P53 gene has led to the development of a new way to re-enliven the function of the suppressed P53 gene and bring back its ability to naturally self-destruct the cell upon recognizing that the cell is degenerate.

 

What this means is that malignant tumors can be reduced and/or eliminated from the body by re-activating the cells’ suppressed P53 function. The technique for re-enlivening the P53 function is through a process known as BioResonance Therapy. Mr. Keymer’s brilliant insight was to shift the thinking from seeing the tumor cells as the enemy that has to be aggressively killed, to seeing the tumor cells as weakened normal cells. The therapy that he devised was to re-energize the tumor cells in order to re-activate the function of the suppressed P53 gene. With this function re-energized, the tumor cells recognize their own degenerate state and naturally die on their own. There are other factors involved in addition to this underlying principle. In the surrounding tissue there is another gene called the Myg gene that sends signals to the surrounding cells to stay alive.

 

In the tissue surrounding the tumors the Myg gene becomes overactive. Its activity must be reduced which is also accomplished through BioResonance Therapy. There are also background toxic stresses that have initially caused the suppression of the P53 gene. These toxic stresses must be identified and eliminated also through BioResonance Therapy. Some of these include viruses, parasites, bacteria, mold, fungus, mercury and other heavy metals, environmental toxins, electro-magnetic field stresses, etc. The body’s organs, glands and the immune system must also be strengthened and detoxified. Inevitably, there are emotional or psychological stresses underlying every tumor. These factors have also responded very well to BioResonance Therapy.

Anticancer Mechanisms for Endostatin

Endostatin, currently in Phase I clinical trials at three centers in the U.S., has been shown in earlier studies to shrink a variety of tumors in mice without developing drug resistance over time. Until now, its mechanism of action at the molecular level was poorly understood. EntreMed’s scientists presented an abstract entitled: “Tropomyosin Identified as a Potential Modulator of the Antiangiogenic Activity of Endostatin Protein,” that established a role for tropomyosin, a molecule involved in endothelial cell movement, as a molecular target for Endostatin. This is the first report in the scientific literature addressing a possible mechanism of action for the antiangiogenic effects of Endostatin in cancer.

 

Another abstract entitled, “2-methoxyestradiol Inhibits Proliferation and Induces Apoptosis Independently of Estrogen Receptors Alpha and Beta,” provides mechanistic information on EntreMed’s orally-available small-molecule inhibitor of angiogenesis, 2ME2. On March 31st, EntreMed announced that patients with metastatic breast cancer began receiving oral dosing of 2ME2 in Phase I studies at Indiana University in Indianapolis. The biologic mechanisms by which 2ME2 acts to inhibit tumor growth were poorly understood until these findings were revealed. We now know that 2ME2 acts by non- estrogen mechanisms to stimulate cellular “suicide”, or apoptosis, causing the death of rapidly proliferating cancer cells and the endothelial cells that feed them. EntreMed scientists Drs. Kim Lee Sim and Nicholas MacDonald collaborated with Dr. Therese Visted of Norway on the abstract, “Release of Angiostatin From Alginate-Encapsulated Producer Cells; A New Approach for the Treatment of Malignant Brain Tumors,” for which Dr. Visted won an AACR Young Investigator Award.

 

This prestigious award is given to scientists whose abstracts have been highly rated by the AACR Annual Meeting Program Committee. These preclinical studies potentially represent a new therapeutic strategy for the treatment of brain tumors by combining cell-encapsulation technology with Angiostatin genes for the local production of Angiostatin protein at the site of the brain tumor. EntreMed was recently authorized by the FDA to initiate clinical trials with Angiostatin protein in Phase I studies with cancer patients; these studies will begin at the Thomas Jefferson Cancer Center in Philadelphia, PA, within the next few weeks.

Telomerase inhibitors

Telomerase, the ribonucleoprotein enzyme maintaining the telomeres of eukaryotic chromosomes, is active in most human cancers and in germline cells but, with few exceptions, not in normal human somatic tissues. Telomere maintenance is essential to the replicative potential of malignant cells and the inhibition of telomerase can lead to telomere shortening and cessation of unrestrained proliferation.

 

We describe novel chemical compounds which selectively inhibit telomerase in vitro and in vivo. Treatment of cancer cells with these inhibitors leads to progressive telomere shortening, with no acute cytotoxicity, but a proliferation arrest after a characteristic lag period with hallmarks of senescence, including morphological, mitotic and chromosomal aberrations and altered patterns of gene expression. Telomerase inhibition and telomere shortening also result in a marked reduction of the tumorigenic potential of drug-treated tumour cells in a mouse xenograft model.

 

This model was also used to demonstrate in vivo efficacy with no adverse side effects and uncomplicated oral administration of the inhibitor. These findings indicate that potent and selective, non-nucleosidic telomerase inhibitors can be designed as novel cancer treatment modalities.

Prostate cancer and dietary supplements

Researchers at the London Health Sciences Centre and London Regional Cancer Centre are looking for more than 3,000 men to test whether dietary supplements help prevent the disease. “Even (if the supplements have) a small effect (it) will translate into big results because this is such a common problem,” says Dr. John Radwan, a radiation oncologist at London Health Sciences Centre. London is one of eight Canadian cities participating in the 400-city study, the largest of its kind, with 32,000 participants drawn from Canada, the United States and Puerto Rico. Spearheaded by the National Cancer Institute and the Southwest Oncology Group, the study shows a new attitude toward alternative medicine, says Nancy Pus, research co-ordinator for the department of urology at London Health Sciences Centre. “The medical community is looking more at alternative therapies and the role of vitamins and nutrients in preventing diseases,” she says. Eighty per cent of Radwan’s patients are victims of prostate cancer. Prostate cancer is the second most deadly form of the disease next to lung cancer. One in every eight Canadian men will develop the disease. Dubbed SELECT, (Selenium and Vitamin E Cancer Prevention Trial) the study tests the effects of selenium and vitamin E. Both elements are found naturally in food. Researchers aren’t sure the supplements will work, but men should still get them, says John Blanchard, president of the Prostate Cancer Research Foundation of Canada. “Men ought to take some action, rather than saying the jury’s out. Within reason, (these supplements) can’t hurt you . . . we’re not talking about some dangerous medication here,” he says.

 

Vitamin E and selenium are both known antioxidants. Some doctors say they neutralize cancer-causing toxins that damage the genetic material of cells. Radwan says they definitely can’t hurt. “It seems to be a win-win situation, with antioxidants. They can only make things better,” he says. He advises individuals with high blood pressure to stay away from vitamin E, because it can thin the blood. Others excluded from the study are those who had cancer in the last five years, excluding non-melanoma skin cancer. Participants must be over age 55, if white, and 50 or older, if black. Radwan explained blacks are more susceptible to the disease, although it’s not yet known why. Study participants will take two capsules per day — a combination of either small doses of the supplements or placebos.

 

Participants will be tracked for seven years each — meaning the study could take up to 12 years to complete if recruitment takes an estimated five years. Radwan urges men at high risk — those with a family history of the disease — to seriously consider getting involved. The push for the study evolved from testing the supplements to see if they prevented other forms of cancer. In the case of a 1998 trial of vitamin E on 29,000 Finnish men, the supplement failed to prevent heavy smokers from developing lung cancer. Nonetheless, the clinical trial was successful in reducing the risk of prostate cancer among the heavy-smoking population by 32 per cent, Radwan said.

Anti-Cough Medicine fights cancer cells very effectively

Noscapine is used as a cough medicine in Europe and many countries worldwide. It is an opium derivative – a non-addictive one and not controlled by the DEA. A few years ago it was discovered at Emory University that noscapine induces apoptosis in cancer cells i.e. kills cancer cells with little or no toxicity to normal cells. Since noscapine has been on the market for 50 years, it is difficult to patent it. However, there is a process of patenting a drug for a new indication, and finally a few of months ago, Emory Univeristy was granted the patent. Until a patent is granted, human studies cannot be published as that will invalidate the patent.

 

Noscapine is a cough suppressant used widely throughout Europe. At higher doses, it has been shown to have anti-cancer activity in laboratory animals. Mice who were injected with human tumors had a significant shrinkage of their cancer after treatment with noscapine. Several anecdotal cases already exist of patients who have failed multiple standard chemotherapy agents and have responded to noscapine. At least one of the patients remains free of disease several years after taking noscapine. Potential Patient Impact: Non-Hodgkin’s lymphoma remains a difficult disease to cure; current treatments are highly toxic. Noscapine is a well-tolerated drug that may offer great potential for cure in patients who would otherwise die.

 

The dose being used in US human trials at present is 2 grams daily. In other countried people are using 1 gram – 2 grams daily according to their physician’s instructions. Side effects being seen are usually nausea in few cases. Noscapine can be purchased OTC in most European countries. Some don’t sell it alone, only in combination with other cough medications, but most countries i.e Holland, Belgiu, Italy, Sweden, Spain etc have it on its own. It comes in syrups, or tablets containing 15mg or 25mg.