Women consuming too much red meat may have a higher risk of stroke than women eating less, says a new study. Red meat is high in saturated fat and cholesterol; both are risk factors for cardiovascular disease, heart attack, and stroke. The United States Centers for Disease Control and Prevention suggests lowering saturated fat intake and eating more fresh fruits and vegetables to help reduce your risk of stroke. Writing in the journal Stroke, researchers examined nearly 35,000 Swedish women, ages 39 to 73. None of the women had heart disease prior to the start of the study in 1997.
After ten years, results showed 4% of the study participants, 1,680 women, had a stroke. Those consuming the most red meat had the highest risk of stroke. Women in the top tenth of red meat intake, consuming at least 3.6 ounces each day, were 42% more likely to have a stroke, compared to women who ate just under one ounce of red meat daily.
Eating processed meat also increased stroke risk. Women eating 1.5 ounces of processed meat each day were 24% more likely to suffer a cerebral infarction, compared to woman consuming less than half an ounce of processed meat each day. Processed meat was not linked to any other form of stroke. Cerebral infarction is a type of stroke caused by a disturbance in the blood vessels supplying blood to the brain. Other types of stroke involve a rupturing of a blood vessel, called hemorrhagic strokes.
The scientists blame red meat and processed meat’s effect on raising blood pressure for the increased stroke risk. According to the World Health Organization (WHO), every year an estimated 17 million people die due to cardiovascular diseases, most notably stroke and heart attack. The WHO lists physical inactivity and unhealthy diet as the main risk factors for heart disease and major cardiac events.
Women suffering from diabetes plus depression have a greater risk of dying, especially from heart disease, a new study suggests.In fact, women with both conditions have a twofold increased risk of death, researchers say. “People with both conditions are at very high risk of death,” said lead researcher Dr. Frank B. Hu, a professor of medicine at Harvard Medical School. “Those are double whammies.” When people are afflicted by both diseases, these conditions can lead to a “vicious cycle,” Hu said. “People with diabetes are more likely to be depressed, because they are under long-term psychosocial stress, which is associated with diabetes complications.”
People with diabetes plus depression are less likely to take care of themselves and effectively manage their diabetes, he added. “That can lead to complications, which increase the risk of mortality.” Hu stressed that it is important to manage both the diabetes and the depression to lower the mortality risk. “It is possible that these two conditions not only influence each other biologically, but also behaviorally,” he said.
Type 2 diabetes plus depression are often related to unhealthy lifestyles, including smoking, poor diet and lack of exercise, according to the researchers. In addition, depression may trigger changes in the nervous system that adversely affect the heart, they said.
The report is published in the January issue of the Archives of General Psychiatry.
Commenting on the study, Dr. Luigi Meneghini, an associate professor of clinical medicine and director of the Eleanor and Joseph Kosow Diabetes Treatment Center at the Diabetes Research Institute of the University of Miami Miller School of Medicine, said the findings were not surprising.
“The study highlights that there is a clear increase in risk to your health and to your life when you have a combination of diabetes and depression,” he said. Meneghini noted there are many diabetics with undiagnosed depression. “I am willing to bet that there are quite a number of patients with diabetes and depression walking around without a clear diagnosis.” Patients and doctors need to be more aware that depression is an issue, Meneghini added.
For the study, Hu’s team collected data on 78,282 women who were aged 54 to 79 in 2000 and who were participants in the Nurses’ Health Study. Over six years of follow-up, 4,654 women died, including 979 who died of cardiovascular disease, the investigators found. Women who had diabetes had about a 35 percent increased risk of dying, and those with depression had about a 44 percent increased risk, compared with women with neither condition, the researchers calculated. Those with both conditions had about twice the risk of dying, the study authors found.
When Hu’s team looked only at deaths from heart disease, they found that women with diabetes had a 67 percent increased risk of dying and those with depression had a 37 percent increased risk of death. But women who had both diabetes and depression had a 2.7-fold increased risk of dying from heart disease, the researchers noted.
In the United States, some 15 million people suffer from depression and 23.5 million have diabetes, the researchers say. Up to one-fourth of people with diabetes also experience depression, which is nearly twice as many as among people who don’t have diabetes, they added. “The combination of diabetes and depression needs to be addressed,” Meneghini concluded. He added that patients need to tell their doctors if they are feeling depressed, and doctors also need to be on the lookout for signs of depression in their diabetic patients.
SOURCES: HealthDay News; Frank B. Hu, M.D., Ph.D., professor, medicine, Harvard Medical School, Boston; Luigi Meneghini, M.D., associate professor, clinical medicine and director, Eleanor and Joseph Kosow Diabetes Treatment Center, Diabetes Research Institute, University of Miami Miller School of Medicine; January 2011, Archives of General Psychiatry
Treating obese women's depression may help them lose weight, a new study suggests. Although researchers couldn't determine which condition may cause the other, obesity and depression frequently strike together. Obese women who saw their depression lessened in a treatment program also lost more weight than women whose depression didn't improve or worsened, researchers said.
“I expect that the relationship between depression and physical activity goes in both directions,” said study researcher Dr. Gregory Simon, a senior investigator and psychiatrist at Group Health Research Institute in Seattle. “Increased physical activity leads to improvement in depression, and improvement in depression leads to increased physical activity.” “You can't prove which came first.”
The researchers evaluated 203 women, ages 40 to 65, who had an average body mass index of 38.3 at the study's start, and found that obesity increased a woman's risk of depression by 50 percent to 150 percent.
Participants were then split into two groups: one focused only on helping the women lose weight, and the other also treating the women's depression. The researchers held 26 group treatment sessions over 12 months, and checked in on the women six, 12 and 24 months after the study began.
Of those whose depression had loosened its grip — as measured by a small drop on a test called the Hopkins Symptom Checklist depression score — 38 percent had lost at least 5 percent of their body weight. Of those whose depression scores stayed the same or increased, 21 percent lost that much weight.
While the study's purpose wasn't to make recommendations about exercise, Simon said, it's advisable for people suffering from depression to seek more opportunities for physical activity. “There certainly is evidence that exercise alone is an effective treatment for depression, whether you're overweight or obese or not, or even if you're a normal weight,” he said.
The study was unusual because it focused on the sometimes-overlooked link between depression and obesity, without focusing solely on the role of weight loss, said Robert E. Thayer, a psychology professor at California State University in Long Beach who has researched how people regulate their moods with food and exercise.
“These findings suggest that, like other negative moods that motivate eating as a kind of self-medication, depression is no exception,” said Thayer, who was not involved with the study. “It's a useful addition to the scientific literature.”
Simon said future studies could focus on learning which antidepressants — many of which can bring on weight gain as a side effect — contribute most to that situation. “Losing weight can certainly have a positive effect on people's moods,” he said.
The research was published in the November/December issue of the journal General Hospital Psychiatry.
The idea that disease-causing genes can be beneficial is not new. The most clear-cut case involves a gene variant that, when present in two copies, causes sickle cell anaemia, which can result in severe pain, organ damage and death. Although it seems that natural selection would work to eliminate the disorder, the variant remains prevalent in some areas of Africa because people with just a single copy are less susceptible to malaria. Evolutionarily the trade-off is worth it: Far more people are protected from malaria than ever develop sickle cell anaemia even in today’s environment.
Unlike sickle cell anaemia, which is caused by a mutation in just one gene, many complex diseases are associated with several variants – specific locations in the DNA where the nucleotide ‘letters’ vary between individuals. These locations are known as SNPs, for single nucleotide polymorphisms. Some of these SNPs are associated with an increased disease risk, while others protect against developing the disease. When calculating an individual’s overall genetic risk, it’s necessary to consider the net effect of all of his or her variants.
Researchers at Stanford University picked seven well-known conditions to study: type-1 and type-2 diabetes, rheumatoid arthritis, hypertension, Crohn’s disease, coronary artery disease and bipolar disorder. Previous genome wide association studies have identified several hundred SNPs associated with each disorder. Corona found that of the top SNPs associated with type-1 diabetes, 80 have been recently increasing in prevalence, meaning that they underwent positive selection. Of these, a surprising 58 are associated with an increased risk of the disorder, while 22 appear protective. Similarly, SNPs associated with an increased risk for rheumatoid arthritis were found to be positively selected. In contrast to type-1 diabetes and rheumatoid arthritis, Corona found that we’re evolving away from a tendency to develop Crohn’s disease (that is, more protective SNPs than risky SNPs have been positively selected).
Results for the other three disorders – type-2 diabetes, coronary artery disease and bipolar disorder – showed that protective and risky SNPs were positively selected in about equal proportions. ‘Now we’re starting to see little hints as to why this might be the case,’ said Butte. For example, a recent study in another lab showed that genetic variations in an antiviral response gene called IFIH1 that improve its ability to protect against enterovirus infection (and the resulting severe, potentially deadly, abdominal distress) also increase a carrier’s risk for type-1 diabetes. And scientists who study global disease patterns have long noted that the prevalence of tuberculosis varies inversely with that of rheumatoid arthritis.
‘It’s possible that, in areas of the world where associated triggers for some of these complex conditions are lacking, carriers would experience only the protective effect against some types of infectious disease,’ said Butte, who pointed out that the cumulative effect of many SNPs in a person’s genome may buffer the effect of any one variant, even if it did raise a person’s risk for a particular condition.
Regardless of the reason, some evolutionary tenets still apply. Healthier people are, presumably, more likely to reproduce and pass those same genes – be they protective or risky – to their offspring. When conditions changed because of differences in diet, exposures or location as populations move around the globe, carriers of the risky SNPs began to develop the conditions we struggle with today.
Corona and Butte are now expanding their investigation to include even more SNPs and diseases. They are also looking at the genetic profile of various types of tumours to see if there’s evidence for positive evolutionary pressure there as well.
‘Even though we’ve been finding more and more genetic contributions to disease risk,’ said Butte, ‘that’s not really an appealing answer. There have got to be some other reasons why we have these conditions.’
Source: Stanford University Medical Centre
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.
According to a new study by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Cancer Institute (NCI), and the USDA, conducted a study with 15,000 adults in the United States, and found that people who drink too many alcoholic beverages are more likely to eat less fruit and consume more calories from a combination of alcoholic beverages and foods high in unhealthy fats and sugar.
“Heavy drinking and dietary factors have independently been associated with cardiovascular disease, certain cancers, and other chronic health problems,” said NIAAA Acting Director Kenneth R. Warren, Ph.D. “This finding raises questions about whether the combination of alcohol misuse and poor diet might interact to further increase health risks.”
“We found that as alcoholic beverage consumption increased, Healthy Eating Index scores decreased, an indication of poorer food choices,” said first author Rosalind A. Breslow, Ph.D., an epidemiologist in NIAAA's Division of Epidemiology and Prevention Research.
A previous study by Dr. Breslow showed that the more alcohol people drink, the poorest quality diets they had. In addition to eating less fruits and vegetables, the researchers also found that increased alcoholic beverage consumption was associated with a decreased intake of whole grains and milk among men.
“Our findings underscore the importance of moderation for individuals who choose to consume alcoholic beverages, and a greater awareness of healthy food choices among such individuals,” says Dr. Breslow.
It is very important to control the amount of alcohol you consume. It could greatly affect you health.
The researchers analyzed data from the National Health and Nutrition Examination Survey (2003-2006) which consisted of 4,528 US adults 18 years of age or older that had no previous hypertension diagnosis. The survey asked about dietary habits and what foods and beverages that they consumed. The researchers said that those who ate 74 grams (about 2.5 cans of sugared soda) or more each day of fructose sugar, had shown an increased risk for developing hypertension. There was a 26 percent chance for these individuals to have high blood pressure reading at 135/85mmHg , a 30 percent higher risk to have high blood pressure measured at 140/90, and a 77 percent higher risk for having blood pressure measured at 160/100 mmHg. A normal blood pressure reading is under 120/80 mmHg.
The researchers point out that even though this shows a potential trigger for high blood pressure, a randomized clinical study would need to be conducted in order to prove that a low fructose diet would prevent hypertension.
According to UCSF Professor Michael German, MD, who is also the senior author of the paper, tryptophan hydroxylase (Tph1), the enzyme that produces serotonin from tryptophan increased by as much 1000-fold during the early pregnancy. The researchers found that inhibition of serotonin synthesis by restricting the intake of tryptophan in pregnant mice blocked beta cell proliferation and resulted in the development of glucose intolerance and gestational diabetes in the mice.
The research indicates that anything that affects the production of serotonin, such as drugs, diet or genetic inheritance may affect the risk of developing gestational diabetes and possibly the long-term risk of developing type 2 diabetes.
Serotonin has been widely studied as a neurotransmitter in the brain for its effects on appetite and mood, especially depression. Since it also influences the insulin production, this could explain why some patients with gestational diabetes experience depression. This would also explain the effect of some classes of psychiatric medications on diabetes.
The study will be published in the upcoming issue of “Nature Medicine” and was published online on June 27, 2010.
The study was conducted in mice, some of which were fed a normal diet of rodent chow and some a 16-week diet of fructose and sucrose-enriched drinking water and trans-fat solids. Their liver tissue was then analyzed for fat content, scar tissue formation (fibrosis), and the biological mechanism of damage. This was done by measuring reactive oxygen stress, inflammatory cell type and plasma levels of oxidative stress markers, which are known to play important roles in the development of obesity-related liver disease and its progression to end-stage liver disease.
The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans-fat alone or a combination of trans-fat and high fructose) became obese and had fatty liver disease.
“Interestingly, it was only the group fed the combination of trans-fat and high fructose which developed the advanced fatty liver disease which had fibrosis,” says Dr. Kohli. “This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.”
Dr. Kohli hopes to further investigate the mechanism of liver injury caused by high fructose and sucrose enriched drinking water and study a therapeutic intervention of antioxidant supplementation. Antioxidants are natural defenses against oxidative stress and may reverse or protect against advanced liver damage, according to Dr. Kohli.
The investigators also would like to use this model to better understand human fatty liver disease and perform clinical trials using novel therapeutic and monitoring tools.
“Our data suggest that supplementation with pharmaceuticals agents should be tested on our new model to establish whether one is able to reverse or protect against progressive liver scarring and damage,” says Dr. Kohli.
The study was supported by grants from the National Institutes of Health and the Children's Digestive Health and Nutrition Foundation.
The paper directly compared findings from two separate studies: 'The Diets of British Schoolchildren' conducted by the Department of health (DH) in 1983 (Department of Health 1989); and the National Diet and Nutrition Survey (NDNS) from 1997 (Gregory & Lowe, 2000).
Gibson's analysis found that total sugar intake averaged at 115g/day in 1983, compared with 113g/day in 1997. Allowing for exclusions of low and high energy reporters, intake levels were 122g/day (1983) and 127g/day (1997), showing a marginal and insignificant increase over the study period. Contrastingly, mean body weight increased significantly during the period of the DH and NDNS surveys, showing a rise of 1.9kg for 10-11 year olds and 3.4kg among 14-15 year olds. BMI increased from 17.9 to 18.6 units in the younger group, and 20.2 to 21.3 units in the older group. According to these calculations, the prevalence of being overweight (plus obesity), as defined by the International Obesity Taskforce (IOTF) cut-offs (91st percentile) rose from 13% to 21-22% between surveys. Gibson concluded that the slight increase in consumption of total sugars did not account for the significant increase in BMI, equivalent to 2-3 kg over the review period.
During the same period, Gibson found that mean energy intake (EI) was 3% lower in 1997 than in 1983, mainly as a result of lower fat intake. This change in overall energy consumption meant that sugars represented a higher proportion of daily energy intake in 1997 (23.6% versus 22.3%), despite total sugar consumption remaining relatively static in comparison. The review surmises that the most likely cause for the increased BMI is a decline in energy expenditure.
In addition, Gibson's paper found that basal metabolic rate (BMR) increased by approximately 3% between surveys as a result of higher body weights, and it is estimated that EI in relation to basal requirements was even lower at 6%. Gibson found that the paradox of rising BMI, despite a 2-3% rise in BMR and an EI that is static or falling, pointed to declining energy expenditure as an important factor in the change.
The Gibson analysis showed that the key sources of sugars in the diet have changed with a marked shift away from table sugar and smaller falls in consumption of sugars through milk, biscuits and cakes, counterbalanced by a significant increase in sugars consumed in soft drinks and, to a lesser extent, fruit juice and breakfast cereals.
A conclusion of Gibson's reanalysis of data from the DH and NDNS studies, that consumption of total sugars remained relatively static during the period, providing an estimated 22% of energy, is supported by findings from a repeated cross sectional study of children's food and drink intake, conducted in Northumberland in 1989, 1990 and 2000 which looked at trends in children's food and drink intake.
Sigrid Gibson, the paper's author, said: “There are very few studies that have assessed trends in sugar intake over time and particularly over such an extended period. The findings of the reanalysis strongly contradict widespread assumptions that sugar levels in the diet are responsible for rising obesity levels. With dietary sugar intakes relatively static, and overall energy consumption showing decline, increased BMI levels cannot be attributed to sugar consumption.”