Drinking soft drinks is associated with higher blood pressure, according to a study of over 2,500 people reported this week in the journal Hypertension. High blood pressure is a major risk factor for heart disease, which is the leading cause of death worldwide. Someone with a blood pressure level in millimetres of mercury (mmHg) of 135 over 85 is twice as likely to have a heart attack or stroke as someone with a reading of 115 over 75.
The new research shows that for every extra can of soft drink consumed per day, participants on average had a higher systolic blood pressure by 1.6 mmHg and a higher diastolic blood pressure by 0.8 mmHg. This difference was statistically significant even after adjusting for factors such as weight and height. The study did not examine the mechanism that might link soft drinks with blood pressure. However, the researchers suggest that raised uric acid, which has been linked to soft drink consumption, might raise blood pressure by reducing the levels of nitric oxide, a chemical that relaxes the lining of the blood vessels.
The association between soft drinks and higher blood pressure was especially strong in people who consumed a lot of salt as well as sugar. Diet drinks were linked with lower blood pressure levels in some analyses, but the association was not consistent or strong. Professor Paul Elliott, senior author of the study, from the School of Public Health at Imperial College London, said: “It’s widely known that if you have too much salt in your diet, you’re more likely to develop high blood pressure. The results of this study suggest that people should be careful about how much sugar they consume as well.”
The researchers analysed data from 2,696 volunteers aged between 40 and 59, in eight areas of the US and two areas of the UK. On four separate occasions over a period of three weeks on average, the participants reported what they had eaten in the preceding 24 hours, as well as giving urine samples and having their blood pressure measured. The volunteers were taking part in INTERMAP, the International Study of Macronutrients, Micronutrients and Blood Pressure.
The researchers also found that people who drink more soft drinks tended to have more unhealthy diets in general. As well as consuming more sugar, those consuming more than one soft drink a day consumed more calories by 397 kilocalories per day on average, and less fibre and minerals. Those who did not consume soft drinks had a lower body mass index (BMI) on average than those who consumed more than one drink per day. “Individuals who drink a lot of sugar-sweetened beverages appear to have less healthy diets,” said Dr Ian Brown, the study’s first author, also from the School of Public Health at Imperial College London. “They are consuming empty calories without the nutritional benefits of real food. They consume less potassium, magnesium and calcium.” “This is a population study,” Dr Brown added. “It can’t say definitively that sugary drinks raise your blood pressure, but it’s one piece of the evidence in a jigsaw puzzle that needs to be completed. In the meantime, we would advise people who want to drink sugar-sweetened beverages should do so only in moderation.”
New research may help explain why multiple sclerosis rates have risen sharply in the U.S. and some other countries among women, while rates appear stable in men.The study could also broaden understanding of how environmental influences alter genes to cause a wide range of diseases. The causes of multiple sclerosis (MS) are not well understood, but experts have long suspected that environmental factors trigger the disease in people who are genetically susceptible. In the newly published study, researchers found that women with MS were more likely than men with MS to have a specific genetic mutation that has been linked to the disease.
Women were also more likely to pass the mutation to their daughters than their sons and more likely to share the MS-susceptibility gene with more distant female family members. If genes alone were involved, mothers would pass the MS-related gene to their sons as often as their daughters, said researcher George C. Ebers, MD, of the University of Oxford. Ebers’ research suggests that the ability of environmental factors to alter gene expression — a relatively new field of genetic study known as epigenetics — plays a key role in multiple sclerosis and that this role is gender-specific.
The theory is that environmental influences such as diet, smoking, stress, and even exposure to sunlight can change gene expression and this altered gene expression is passed on for a generation or two. “The idea that the environment would change genes was once thought to be ridiculous,” Ebers says. “Now it is looking like this is a much bigger influence on disease than we ever imagined.”
The study by Ebers and colleagues included 1,055 families with more than one person with MS. Close to 7,100 genes were tested, including around 2,100 from patients with the disease. The researchers were looking for MS-specific alterations in the major histocompatibility complex (MHC) gene region. They found that women with MS were 1.4 times more likely than men with the disease to carry the gene variant linked to disease risk. A total of 919 women and 302 men had the variant in the MHC region, compared to 626 women and 280 men who did not have it.
The study appeared in the Jan. 18 issue of Neurology.
Epigenetics is not evolution. Genetic alterations linked to environmental assaults can be passed down for a generation or two, but DNA usually rights itself over time, Ebers says. “This may explain why we hardly ever see MS in families over more than three generations,” he says. Earlier studies by Ebers and colleagues suggest that vitamin D deficiency may be the environmental stressor that triggers the MS-linked gene alterations. Rates of the disease are highest among people living farthest from the equator, and there is widespread speculation that lack of vitamin D due to low sun exposure may explain this. Other than Ebers’ research team, Orhun Kantarci, MD, of the Mayo Clinic in Rochester, Minn., is one of the few researches studying epigenetics as it relates to multiple sclerosis.
Kantarci calls the new research a potentially important piece of the puzzle to explain the gender difference in MS, but he adds that the research must be replicated. “This study provides more questions than answers, but it is very interesting,” he says. “We are learning that inheritance isn’t as simple as [Gregor] Mendel described.”
In research described as “a stark warning” to those tempted to start smoking, scientists are reporting that cigarette smoke begins to cause genetic damage within minutes — not years — after inhalation into the lungs. Their report, the first human study to detail the way certain substances in tobacco cause DNA damage linked to cancer, appears in Chemical Research in Toxicology, one of 38 peer-reviewed scientific journals published by the American Chemical Society.
Stephen S. Hecht, Ph.D., and colleagues point out in the report that lung cancer claims a global toll of 3,000 lives each day, largely as a result of cigarette smoking. Smoking also is linked to at least 18 other types of cancer. Evidence indicates that harmful substances in tobacco smoke termed polycyclic aromatic hydrocarbons, or PAHs, are one of the culprits in causing lung cancer. Until now, however, scientists had not detailed the specific way in which the PAHs in cigarette smoke cause DNA damage in humans.
The scientists added a labeled PAH, phenanthrene, to cigarettes and tracked its fate in 12 volunteers who smoked the cigarettes. They found that phenanthrene quickly forms a toxic substance in the blood known to trash DNA, causing mutations that can cause cancer. The smokers developed maximum levels of the substance in a time frame that surprised even the researchers: Just 15-30 minutes after the volunteers finished smoking. Researchers said the effect is so fast that it’s equivalent to injecting the substance directly into the bloodstream.
“This study is unique,” writes Hecht, an internationally recognized expert on cancer-causing substances found in cigarette smoke and smokeless tobacco. “It is the first to investigate human metabolism of a PAH specifically delivered by inhalation in cigarette smoke, without interference by other sources of exposure such as air pollution or the diet. The results reported here should serve as a stark warning to those who are considering starting to smoke cigarettes,” the article notes. The authors acknowledged funding from the National Cancer Institute.
A new study shows that adolescents who take acetaminophen, better known as Tylenol, have a higher risk of asthma, allergic nasal conditions and the skin disorder eczema.
Acetaminophen is widely viewed as a very safe drug—one reason why hospitals use it routinely as a painkiller instead of aspirin or ibuprofen. The major problem associated with it is liver damage caused by overdoses. Recently, however, there has been a growing drumbeat about possible dangers from the drug. One study, for example, found that acetaminophen increased the risk of hearing loss in men. And some others have hinted that the drug is linked to asthma in newborns whose mothers used the drug during pregnancy and in young children exposed to it.
The new findings were reported in the American Journal of Respiratory and Critical Care Medicine by researchers in the International Study of Asthma and Allergies in Childhood. The team, headed by epidemiologist Richard Beasley of the Medical Research Institute in Wellington, New Zealand, gave written questionnaires to 322,959 13- and 14-year-olds in 50 countries exploring their use of acetaminophen, other drugs, and asthma symptoms. They were also shown a video containing five scenes of clinical asthma and asked whether they had experienced any symptoms similar to those shown. About 73% of the teens said they had used acetaminophen at least once in the previous year and 30% said they had used it monthly.
Taking into account maternal education, smoking, diet and siblings, the team found that those subjects who had used the drug at least once per year were 43% more likely to have asthma, while those who used it at least monthly were 2.5 times as likely to suffer from the condition. The risk of rhinoconjunctivitis (a severe nasal congestion) was 38% higher for those who used it once per year and 2.39 times as high for those who used it at least monthly. The comparable increases in risk for eczema were 31% and 99%, respectively.
Overall, the increased risk of asthma associated with acetaminophen was 41%, the authors found. That could, at least in part, explain why there has been an increase in the prevalence of asthma in the 50 years since the drug was introduced. Given the widespread use of the drug, it could also represent a large public health problem.
But—and it is a very big but—the study shows only an association, not causality. That could only be determined by a randomized clinical trial, which the authors recommend. Furthermore, the study relies on the recall of teenagers. Recall is notoriously inaccurate in adults, and it is probably worse in adolescents, clouding the results. For the time being then, you can probably continue to feel comfortable giving the drug to your children.
In a statement, McNeil Consumer Healthcare, which manufactures Tylenol, said that the drug “has over 50 years of clinical history to support its safety and effectiveness” and that no clinical trial has demonstrated that the drug causes asthma.
The new data come from an ongoing National Institutes of Health-AARP study and involved more than 300,000 participants. Researchers found that those study participants who reported eating the most processed meat had about a 30 percent greater risk of bladder cancer than those who ate the least.
What's more, those whose diets were highest in nitrites and nitrates (from processed meat as well as other sources) were about 33 percent more likely to develop bladder cancer than those whose diets contained the smallest amounts of these compounds.
Bladder cancer is currently the 10th most common cancer in the US, with over 70,000 cases diagnosed each year.
Link to Bladder Cancer Needs Confirmation; Link to Colorectal Cancer Convincing
The evidence that consumption of processed meat is linked to colorectal cancer was judged convincing by the independent expert panel behind the major AICR/WCRF report, Food, Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective.
This same report, published in 2007, found the evidence linking red and processed meat to bladder cancer too sparse to make a judgment. Although this new study's findings need to be confirmed, it represents a major contribution to the scientific literature on diet's role in bladder cancer.
Higginbotham noted that the AICR/WCRF report's findings are continually updated; data from this and other studies will be added to AICR/WCRF's database and are scheduled to be reassessed by independent experts in the future.
Until that time, AICR reiterates that for people who are concerned about cancer, there is already good reason to limit consumption of red meat and avoid processed meat.
Source: American Institute for Cancer Research
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Since the 1960s, researchers have been studying how the water-soluble vitamin supports the healthy functioning of cells. They discovered that it's essential for cell division and replication, making it especially important for expectant mothers.
It's also important to proper replication of DNA and RNA — a lack of folate has been linked to genetic mutations that can lead to cancer.
Folate is commonly found in leafy green vegetables like spinach and turnip greens. Since 1998, the U.S. Food and Drug Administration has mandated that many foods, such as rice, flour and cornmeal, be enriched with a synthetic folate known as folic acid.
While folate deficiency is no longer a problem in the U.S., it remains widespread in developing nations and much of Europe, where enriching grain products is not widely practiced.
This new research, funded by the National Science Foundation and originally sparked by funding from the U.S. Department of Energy, links folate to the production or repair of compounds called iron-sulfur clusters through a recently discovered intermediary protein called COG0354.
These clusters are part of the mechanism cells use to produce energy and carry out other vital reactions. But they are also sensitive to a byproduct of the energy-producing process: highly reactive oxygen-based molecules, some of which are called free radicals.
The oxidative stress caused when these molecules pollute a cell has been linked to cell death and aging, as well as to conditions such as atherosclerosis, Parkinson's disease, heart disease, Alzheimer's, fragile X syndrome and many more.
Examining the folate-iron-sulfur cluster link required the team to pull experience from not only UF's microbiology and cell science and food science and human nutrition departments, but also the McKnight Brain Institute and the National High Magnetic Field Laboratory.
Expertise from the latter two institutions was needed because the researchers used nuclear magnetic resonance analysis to observe folate interacting with COG0354 protein — molecular-scale activity that could otherwise only have been shown indirectly, said Arthur Edison, the NHMFL's director of chemistry and biology and an associate professor with UF's biochemistry and molecular biology department.
The researchers have found that COG0354 is present in creatures from each of the six kingdoms of life, from mice and plants to one-cell organisms that may predate bacteria.
The findings will open new avenues of study into the overall mechanism of oxidative stress repair, and may someday lead to new medicines. For now, the researchers emphasize that this is another example of the vitamin's importance in one's diet.
Increased intakes of omega-3 fatty acids may decrease the risk of heart disease and heart attack in people with low fish intakes, says a new study from The Netherlands. Daily intakes of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) of about 240 milligrams was associated with a 50 per cent reduction in the risk of coronary heart disease (CHD), compared with intakes of about 40 milligrams, according to findings published in the Journal of Nutrition. Furthermore, the highest average intake of DHA and EPA was associated with a 38 per cent reduction in the heart attack, said researchers from Wageningen University following a study with over 21,000 people with low fish intakes.
The heart health benefits of consuming oily fish, and the omega-3 fatty acids they contain, are well-documented, being first reported in the early 1970s by Jorn Dyerberg and his co-workers in The Lancet and The American Journal of Clinical Nutrition. To date, the polyunsaturated fatty acids (PUFAs) have been linked to improvements in blood lipid levels, a reduced tendency of thrombosis, blood pressure and heart rate improvements, and improved vascular function.
Omega-3 fatty acids, most notably DHA and EPA, have been linked to a wide-range of health benefits, including reduced risk of cardiovascular disease (CVD) and certain cancers, good development of a baby during pregnancy, joint health, and improved behaviour and mood.
Intakes of EPA plus DHA, and fish were assessed in 21,342 people aged between 20 and 65. Fish intakes ranged from 1.1 to 17.3 grams per day. Over the course of an average of 11.3 years, the researchers documented 647 deaths, of which 82 were linked to coronary heart disease, with 64 of these being heart attack.
According to the results, the highest average intake of EPA plus DHA (234 milligrams per day) was associated with a 51 per cent reduction in the risk of fatal CHD, compared to the lowest average intake (40 mg per day).
“In conclusion, in populations with a low fish consumption, EPA+DHA and fish may lower fatal CHD and [heart attack] risk in a dose-responsive manner,” wrote the researchers.
Source: Journal of Nutrition
“Marine (n-3) Fatty Acids, Fish Consumption, and the 10-Year Risk of Fatal and Nonfatal Coronary Heart Disease in a Large Population of Dutch Adults with a Low Fish Intake”
Authors: J. de Goede, J.M. Geleijnse, J.M. A. Boer, D. Kromhout, W. M.M. Verschuren
In the current study, vitamin K2 — which study participants most frequently got through cheese — was linked to the odds of developing or dying from cancer, whereas vitamin K1 was not.
The findings are based on data from 24,340 German adults who were between the ages of 35 and 64, and cancer-free at the outset. The researchers estimated the participants' usual vitamin K intake based on a detailed dietary questionnaire. Over the next decade, 1,755 participants were diagnosed with colon, breast, prostate or lung cancers, of whom 458 died during the study period.
In general, the researchers found, the one quarter with the highest intakes of vitamin K2 were 28 percent less likely to have died of any one of the cancers than the one-quarter of men and women with the lowest intakes of the vitamin. That was with factors like age, weight, exercise habits, smoking and consumption of certain other nutrients, like fiber and calcium, taken into account.
Of the one-quarter of study participants who got the least vitamin K2, 156 — or 2.6 percent — died of one of the four cancers. That was true of 1.6 percent of participants with the highest intakes of the vitamin from food.
When Linseisin's team looked at the cancer types individually, there was no clear link between either form of vitamin K and breast cancer or colon cancer. However, greater consumption of vitamin K2 was linked to lower risks of developing or dying from lung cancer — a disease for which smoking is the major risk factor — or of developing prostate cancer.
Of the one-quarter of study participants with the lowest vitamin K2 intakes, 47 — or 0.8 percent — developed lung cancer, versus 0.4 percent of the one-quarter who got the most vitamin K2 in their diets. When it came to prostate cancer, there were 111 cases among the one-quarter of men with the lowest vitamin K2 intakes, and 65 cases in the group with the highest consumption.
In theory, vitamin K itself could offer some protection against cancer. It's often used to counteract too-high doses of blood thinners, although this does not have an obvious link to cancer. In lab research, however, Linseisin and his colleagues point out, the vitamin has been shown to inhibit cancer cell growth and promote apoptosis — a process by which abnormal cells kill themselves off.
But whether vitamin K intake itself is responsible for the lower cancer risks in this study is unclear, according to the researchers. One limitation is that they estimated vitamin K intake based on participants' reported eating habits; most of their vitamin K came from eating cheese, and it's possible, Linseisin and his colleagues note, that some other components of that food are related to cancer risk.
Future studies, the researchers say, should measure people's blood levels of vitamin K and look at the relationship of those levels with cancer risks.
SOURCE: American Journal of Clinical Nutrition