Monday, 27 December 2010
In search of quality evidence for lifestyle management and glycemic control in children and adolescents with type 2 diabetes: A systematic review
Steve T Johnson email, Amanda S Newton email, Meera Chopra email, Jeanette Buckingham email, Terry T-K Huang email, Paul W Franks email, Mary M Jetha email and Geoff DC Ball email
BMC Pediatrics 2010, 10:97doi:10.1186/1471-2431-10-97
There is no high quality evidence to suggest lifestyle modification improves either short- or long-term glycemic control in children and youth with T2D. Additional research is clearly warranted to define optimal lifestyle behaviour strategies for young people with T2D.
Tuesday, 21 December 2010
Phys Ed: The Benefits of Exercising Before BreakfastBy GRETCHEN REYNOLDS
The holiday season brings many joys and, unfortunately, many countervailing dietary pitfalls. Even the fittest and most disciplined of us can succumb, indulging in more fat and calories than at any other time of the year. The health consequences, if the behavior is unchecked, can be swift and worrying. A recent study by scientists in Australia found that after only three days, an extremely high-fat, high-calorie diet can lead to increased blood sugar and insulin resistance, potentially increasing the risk for Type 2 diabetes. Waistlines also can expand at this time of year, prompting self-recrimination and unrealistic New Year’s resolutions.
But a new study published in The Journal of Physiology suggests a more reliable and far simpler response. Run or bicycle before breakfast. Exercising in the morning, before eating, the study results show, seems to significantly lessen the ill effects of holiday Bacchanalias.
For the study, researchers in Belgium recruited 28 healthy, active young men and began stuffing them with a truly lousy diet, composed of 50 percent fat and 30 percent more calories, overall, than the men had been consuming. Some of the men agreed not to exercise during the experiment. The rest were assigned to one of two exercise groups. The groups’ regimens were identical and exhausting. The men worked out four times a week in the mornings, running and cycling at a strenuous intensity. Two of the sessions lasted 90 minutes, the others, an hour. All of the workouts were supervised, so the energy expenditure of the two groups was identical.
Their early-morning routines, however, were not. One of the groups ate a hefty, carbohydrate-rich breakfast before exercising and continued to ingest carbohydrates, in the form of something like a sports drink, throughout their workouts. The second group worked out without eating first and drank only water during the training. They made up for their abstinence with breakfast later that morning, comparable in calories to the other group’s trencherman portions.
The experiment lasted for six weeks. At the end, the nonexercising group was, to no one’s surprise, super-sized, having packed on an average of more than six pounds. They had also developed insulin resistance — their muscles were no longer responding well to insulin and weren’t pulling sugar (or, more technically, glucose) out of the bloodstream efficiently — and they had begun storing extra fat within and between their muscle cells. Both insulin resistance and fat-marbled muscles are metabolically unhealthy conditions that can be precursors of diabetes.
The men who ate breakfast before exercising gained weight, too, although only about half as much as the control group. Like those sedentary big eaters, however, they had become more insulin-resistant and were storing a greater amount of fat in their muscles.
Only the group that exercised before breakfast gained almost no weight and showed no signs of insulin resistance. They also burned the fat they were taking in more efficiently. “Our current data,” the study’s authors wrote, “indicate that exercise training in the fasted state is more effective than exercise in the carbohydrate-fed state to stimulate glucose tolerance despite a hypercaloric high-fat diet.”
Just how exercising before breakfast blunts the deleterious effects of overindulging is not completely understood, although this study points toward several intriguing explanations. For one, as has been known for some time, exercising in a fasted state (usually possible only before breakfast), coaxes the body to burn a greater percentage of fat for fuel during vigorous exercise, instead of relying primarily on carbohydrates. When you burn fat, you obviously don’t store it in your muscles. In “our study, only the fasted group demonstrated beneficial metabolic adaptations, which eventually may enhance oxidative fatty acid turnover,” said Peter Hespel, Ph.D., a professor in the Research Center for Exercise and Health at Catholic University Leuven in Belgium and senior author of the study.
At the same time, the fasting group showed increased levels of a muscle protein that “is responsible for insulin-stimulated glucose transport in muscle and thus plays a pivotal role in regulation of insulin sensitivity,” Dr Hespel said.
In other words, working out before breakfast directly combated the two most detrimental effects of eating a high-fat, high-calorie diet. It also helped the men avoid gaining weight.
There are caveats, of course. Exercising on an empty stomach is unlikely to improve your performance during that workout. Carbohydrates are easier for working muscles to access and burn for energy than fat, which is why athletes typically eat a high-carbohydrate diet. The researchers also don’t know whether the same benefits will accrue if you exercise at a more leisurely pace and for less time than in this study, although, according to Leonie Heilbronn, Ph.D., a professor at the University of Adelaide in Australia, who has extensively studied the effects of high-fat diets and wrote a commentary about the Belgian study, “I would predict low intensity is better than nothing.”
So, unpleasant as the prospect may be, set your alarm after the next Christmas party to wake you early enough that you can run before sitting down to breakfast. “I would recommend this,” Dr. Heilbronn concluded, “as a way of combating Christmas” and those insidiously delectable cookies.
after multiple warnings from the watchdogs, the final study by the epidemiologists from Villejuif hospital has confirmed that around 2000 people in France have died after taking the medication, Mediator..
This particular drug had been banned in the USA but the French kept them on despite mounting evidence of deaths and the doctors continued to prescribe them.
I wonder why two such pharamaceutically advanced countries differ from each other: Avandia is banned in France but allowed to be prescribed in the USA.. in general USA seems to have a more publicized approach to the drugs..
In any case, one by one many of the new touted miracle drugs are getting the exit sign..perhaps it is like describing all the beaches in every country as Paradise on earth, there are just few outstanding beaches... there are drugs which are extraordinary such as Aspirin and the concocted ones which treat an array of symptoms and some people get better. Most of the Oral Anti Diabetes drugs and including injectable drugs such as Byetta (but not insulin ) fall into this category.. In the end, what is new may not be the best, what is tried and proven may be.. such as Insulin introduced 70+ years ago and Aspirin introduced in the 19th century? French scientist Gerhardt 1853!
Friday, 17 December 2010
If there were no Indians in Cuba in 1903 where did they suddenly appear from in 1983 when Cuban born European researchers from Camaguey living in the USA and Mulattos raised in Puerto Rico and New York began "researching" the Indians in Cuba with local cultural prostitutes or jinateros?
Why dont these people come to Cuba and meet up with the Ministry of Culture and present their case for the presence of the Indians in Cuba and solve this questions once and for all? The current minister of Culture in Cuba is Mr Abel Prieto a well educated and well traveled Cuban with an extremely open mind and I am sure he will be willing to listen to these New Indians.
I shall wait to hear of such a meeting so that I can myself correct my understanding or confirm it.
Monday, 29 November 2010
When we talk about Poverty and diseases of Civilization, we are mainly talking about the West and wannabee West countries like Malaysia and Singapour.. It is well known that degenerative diseases such as Diabetes and Hypertension affect the poor more than the rich. Epidemiologists have done disservice to the public and the propagation of Health in general by perfecting their tools to find the answer they want. That is why currently up to 90 per cent of the scientific articles have to be scrutinized for truth because most of them have assumed false circumstances and thus produce false results. Few years ago they found out that taking calcium supplements are useless in preventing osteoporotic fractures that is before we found out that almost every one living in the west is low in Vitamin D and thus lacking an absorption mechanism for Calcium.
I have always maintained that Cholesterol is a marker of Inflammation in the body and that Statins the expensive medications that do bring the levels of cholesterol have also an antiinflammatory effects but we dont hear about new anti inflammatory drugs since there is profit in statin medications. there is a lawsuit pending against Pfizer the manufacturer of anti cholesterol medication Lipitor for falsifying some tabulative procedures by bribing the researchers and national organizations... oh what a world we are living in.. surrounded by vultures feeding on the carrions..
when I began my work with American Indians, truly one of the last of the colonized people on the earth, many elders got up to speak at a Prevention of Diabetes symposium at their Lakota Reservation.. Give us Jobs, that would take care of Diabetes the elders intoned.. and you can look at the employment figures and diabetes rates all through the Indian Country, one of the best is the example given in the book Diabetes: The Sugar coated Crisis by that tireless crusader, David Spero, two bands of the Cuahuilla nation, the Morongo and the Torres-Martinez. The latter has four times the rate of Diabetes than the former who is fairly well off due to a well run Casino in their Reservation.. Most everyone working with the First Nations know of the Epidemiological Hijacking of the Pima Nation of the USA and very little attention paid to the fact that their relatives the Pima of Mexico suffer from much less (incredibly much less) of the Diabetes and other metabolic disorders which the researchers have made them famous for.
Suffering among human beings cannot be objectified to certain physiological phenomenon. Whenever you see fantastic claims of a medical breakthrough or a magic of a single nutritional ingredient, be skeptical.
In this world of human exploitation, be very cynical about its messengers who are now Professors at Medical Schools in USA and their lackeys in UK and Australia. If they are pushing drugs, that is what they are: Drug pushers. and there are many who have made a name for themselves while harming immense number of women, by trying to make Menopause a disease and let us hope that we wont allow them to do the same by making Menarche a disease by objectifying it into physiology without taking into consideration the social and economic impacts.
Thursday, 25 November 2010
Analysis of sex and gender-specific research reveals a common increase in publications and marked differences between disciplines
BMC Medicine 2010, 8:70doi:10.1186/1741-7015-8-70
|Published:||10 November 2010|
The incorporation of sex and gender-specific analysis in medical research is increasing due to pressure from public agencies, funding bodies, and the clinical and research community. However, generation of knowledge and publication trends in this discipline are currently spread over distinct specialties and difficult to analyze comparatively.
Using a text-mining approach, we have analyzed sex and gender aspects in research within nine clinical subspecialties - Cardiology, Pulmonology, Nephrology, Endocrinology, Gastroenterology, Haematology, Oncology, Rheumatology, Neurology - using six paradigmatic diseases in each one. Articles have been classified into five pre-determined research categories - Epidemiology, Pathophysiology, Clinical research, Management and Outcomes. Additional information has been collected on the type of study (human/animal) and the number of subjects included. Of the 8,836 articles initially retrieved, 3,466 (39%) included sex and gender-specific research and have been further analyzed.
Literature incorporating sex/gender analysis increased over time and displays a stronger trend if compared to overall publication increase. All disciplines, but cardiology (22%), demonstrated an underrepresentation of research about gender differences in management, which ranges from 3 to 14%. While the use of animal models for identification of sex differences in basic research varies greatly among disciplines, studies involving human subjects are frequently conducted in large cohorts with more than 1000 patients (24% of all human studies).
Heterogeneity characterizes sex and gender-specific research. Although large cohorts are often analyzed, sex and gender differences in clinical management are insufficiently investigated leading to potential inequalities in health provision and outcomes.
Tuesday, 23 November 2010
They found that testosterone concentrations dropped about 1.2% per year, or about 17% overall, from 1987 to 2004. The downward trend was seen in both the population and in individuals over time.
The decline is consistent with other long-term trends in male reproductive health, including decreases in sperm quality and increases in testicular cancer, hypospadias and cryptorchidism.
The strongest association was observed in same-aged men from different sampling years. For example, a 65-year-old in 2002 had lower testosterone levels than a 65-year-old in 1987.
Lower concentrations of testosterone can increase a man’s risk for age-related diseases, depression and infertility.
Also, the younger and older men in the study experienced similar hormone declines that dropped faster than would be predicted by normal aging.
Context: In men, the hormone testosterone guides behavior and reproduction. It controls growth and development of sex organs and other typically male characteristics, such as facial hair and a deep voice.
Normally, levels fluctuate from conception through puberty then level out during adulthood before declining as men age. Some chronic health problems typically seen in older adults, such as diabetes, depression and obesity, are associated with lower testosterone levels.
Recent studies have that found environmental impacts on testosterone levels. For example, testosterone levels were lower in US Air Force veterans exposed to dioxins while spraying Agent Orange during the Vietnam War, as well as in men exposed to phthalates at work.
What did they do?
Travison et al. used blood hormone data and personal information collected from men living in Boston, MA, as part of the Massachusetts Male Aging Study (MMAS). The MMAS examined men’s health and endocrine function. Data were gathered during three home visits from 1987-89 (T1), 1995-97 (T2), and 2002-04 (T3). Total testosterone (TT) and serum sex hormone-binding globulin were measured in the blood and available testosterone (BT) was calculated. The men self-reported such things as basic demographics, health status, and smoking and alcohol use.
In this study, Travison et al. analyzed data from 1,532 men (1,383, 955, and 568, respectively, from T1, T2 and T3) that met age and birth year requirements. Participants ranged from 45 to 79 years old and were born between 1916 and 1945. The researchers excluded high and low T levels, missing data, and unidentified prostate cancer treatment. Within the sample, they calculated and compared three separate but related associations among concentration, age, and time. They looked at changes in testosterone concentrations in the group of men at different years and ages associated with T1, T2, and T3; testosterone declines in individual men as they aged during the study; and testosterone concentrations of men of the same age but in different years (age-matched).
What did they find?
Travison et al. found strong evidence of a decline of more than 1% per year in men’s blood testosterone levels during the last two decades. The graph to the right shows average levels for each for men of different ages in each of the three measurement periods (T1-T3).
Dotted lines are 95% confidence bands. Adapted from Travison et al.
The first comparison to make is that within a cohort, older men tend to have lower testosterone levels. Compare, for example, 80 yr old men in T3 compared to 60 yr old men.
The crucial comparison to make is from one cohort to the next, comparing men of the same age. For example, 60 yr old men during the first measurement period (red line, 1987-1989) had total testosterone levels over 500 ng/dL. Men aged 60 yrs old in the third cohort (blue line, measured 2002-2004) had TT below 450 ng/dL. There is no overlap between the confidence bands of T1 vs T3: T3 (measured 2002-2004) is always lower than T1.
The trend holds regardless of the men’s age. Similar declines over the 17 years were seen in all ages of men in the study.
Travison et al. note that the decline within the cohorts related to age is less than the decrease observed across cohorts. For example, men aged 70 in T1 had TT only 6% less than men aged 45 in the same cohort. But 60 yr old men in T3 had TT concentration approximately 13% lower than men the same age in T1.
To illustrate this point another way, Travison et al. compared the average decline of testosterone levels in T1 vs T2 as a function of age, and then contrast that with differences in testosterone between men of the same age in T1 vs T2. Note that T1 and T2 were only separated by 9 years. The average declines in T1 and T2 per decade of life were 17 and 20 ng/mL, respectively. But 65 yr old men in T2 had total testosterone levels 50 ng/mL lower than those in T1, even though the samples were separated by less than a decade.
Travison et al. then estimated the decline over time, from the first cohort to the third, for men of the same age (what they called the age-matched decline). They found that testosterone declined by 1.2% per year (95% CI 1.0% to 1.4%).
Bioavailable testosterone (BT) also showed similar declines over time. The strongest associations again held for age-matched trends with declines of 1.3% per year (95% CI 1.7% - 1.1%).
None of the health and lifestyle factors examined were associated with either age-matched declines in either TT or BT: The age-matched declines remained essentially the same after controlling for chronic illness, general health, medications, smoking, body mass index, employment, marital status, and other indicators.
Finally, the trends held when analyzing the data in a number of different ways, including by interview date, study cohort, restricting to men of certain ages or birth cohorts, and considering incomplete versus complete data.
What does it mean?
Travison et al. find that testosterone levels declined in Massachusetts men by approximately 1.2% per year from the late 1980s through 2004, controlling for the age of the men and other possible confounding variables.
This study is important because of its large sample size and long duration. Few studies have looked directly at testosterone levels over time.
The results are surprisingly consistent with another set of long-term human epidemiology studies. Those studies also show a long-term decline in male reproductive functions, such as decreased sperm health and increased infertility, which are highly associated with or controlled by testosterone and other androgen hormones. The rate of decline reported in this study is roughly comparable to the rate of decline of sperm count reported first by Carlson et al. in 1992 and then reanalyzed by Swan et al.in 2000.
In commentary accompanying Travison et al.'s study in the Journal of Clinical Endocrinology and Metabolism, Dr. Shalender Bhasin (Boston Medical Center) writes: The data in this study are "important because they provide independent support for the concerns raised earlier about the reproductive health of men." ... "it would be unwise to dismiss these reports as mere statistical aberrations because of the potential threat these trends-- if confirmed-- pose to the survival of the human race and other living residents of our planet."
Faced with performance problems, menopause blues and an increased mismatch of expectations between the sexes, middle-aged Americans are the unhappiest people of all when it comes to making love, a new Associated Press-LifeGoesStrong.com poll shows.
Only 7 percent of people between 45 and 65 describe themselves as extremely satisfied with their sex lives. And nearly a quarter of the middle-aged Americans say they are dissatisfied. Even among seniors, fewer are dissatisfied.
"Older people can learn new tricks," said Ruth Westheimer, the sex therapist better known as Dr. Ruth. Aging men and women need to work on being "sexual literate - to really know what they need, what their partner needs and how to pleasure each other," she said in an Associated Press interview.
The findings represent a stark turnaround for the group of Americans who spearheaded the sexual revolution, coming of age as birth control became readily available, premarital sex gained wider acceptance and abortion was legalized. The many of the first victims of the AIDS epidemic were in this group.
Younger and older people report better feelings about their sex lives.
Some 24 percent of middle-aged group say they are dissatisfied, compared with only 12 percent of 18- to 29-year-olds, 20 percent of those 30-44 and 17 percent of those over 65.
Perhaps the middle-aged group have given up on experimenting.
A surprising number of them feel they have learned just about all there is to know about sex - nearly three in five women and half of men.
But if women are wiser, men are more disgruntled. Twenty-eight percent of men between 45 and 65 are dissatisfied, and more than two in five say their sex lives got worse in the last decade.
Part of the explanation seems to lie in different sexual expectations.
Men are often more eager - at least mentally, if not physically - as more women become uninterested. Nearly half of the men say their partners do not want sex often enough, while only 17 percent of women feel similarly let down.
The story is different when it comes to action, as men are the underperformers.
The poll finds two in five men between 45 and 65 having problems with sexual functioning. Only 19 percent of women in the same age group say the same. For both genders, less than half received treatment.
Still, a slim majority of boomers say they can have a strong relationship without sex.
It is true that nationaly the testosterone levels have been declining.. perhaps it could explain for this lack of satisfaction with sex?
more on another post..
Can’t Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
I came across the following article when I was browsing MSN the other day. It’s full of great information that may open your eyes to facts of which you haven’t been aware.
The following article originally appeared on MSN Health.
The New American Diet
It’s not just about calories in versus calories out.
If that were all it took to lose weight—eating a little less and exercising a little more—then weight loss would be as simple as grade-school math: Subtract Y from Z and end up with X.
But if you’ve ever followed a diet program and achieved less than your desired result, you probably came away feeling frustrated, depressed, and maybe a bit guilty. What did I do wrong?
Instead of X, it’s XXL.
Because there’s probably more at work here than just calories in/calories out. More and more research is indicating that America’s obesity crisis can’t be blamed entirely on too much fast food and too little exercise. (Or on these seven habits of highly obese people.) A third factor may be in play: a class of natural and synthetic chemicals known as endocrine-disrupting chemicals (EDCs), or as researchers have begun to call them, obesogens.
Muffintop Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
The new weight-gain threat
Obesogens are chemicals that disrupt the function of hormonal systems; many researchers believe they lead to weight gain and, in turn, numerous diseases that curse the American populace. They enter our bodies from a variety of sources—natural hormones found in soy products, hormones administered to animals, plastics in some food and drink packaging, ingredients added to processed foods, and pesticides sprayed on produce. They act in a variety of ways: by mimicking human hormones such as estrogen, by misprogramming stem cells to become fat cells and, researchers think, by altering the function of genes.
Endocrine disruptors are suspected of playing a role in fertility problems, genital malformation, reduced male birth rates, precocious puberty, miscarriage, behavior problems, brain abnormalities, impaired immune function, various cancers, and cardiovascular disease. “We have data linking environmental chemicals to practically every major human disease, from cardiovascular disease to attention-deficit disorder,” says Jerry Heindel, Ph.D., an expert on EDCs at the National Institute of Environmental Health Sciences (NIEHS).
Now new research is finding that some EDCs, the obesogens, may be helping to make us fat. This field of research is dominated by animal and test-tube studies. And while researchers note that the known effects of many obesogens are more potent in the unborn and newly born, some suspect a similar impact on adults.
This combination of factors, along with our growing tendency to put on weight, is what we call the obesogen effect. Understanding it could be the key to freeing ourselves from weight gain and the other hazards of these chemicals.
Why traditional diets don’t work
Decades ago, before big, soft guts were the norm in the United States, we referred to overweight people as having “glandular problems.” Their weight was not their fault, doctors explained; their bodies just didn’t have the ability to fight off weight gain like most people’s bodies did.
We don’t use that polite phrase any longer. What changed? Now that about two-thirds of American adults are overweight or obese, did those folks with “glandular problems” disappear? No; it’s just that many others have caught the same disease. Thanks to the obesogen effect, we may all be at risk for some glandular problems.
magnuson fat family Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
The average American family.
Because it’s probably been a while since you took high-school anatomy, here’s a quick refresher: Your endocrine system is the contingent of glands producing the hormones that regulate your body. Growth and development, sexual function, reproductive processes, mood, sleep, hunger, stress, metabolism—they’re all controlled by hormones. And the pancreas, hypothalamus, adrenal glands, thyroid, pituitary gland, and testes are all part of that system. So whether you’re male or female, tall or short, hirsute or hairless, lean or heavy—that’s all determined in a big way by your endocrine system.
Your endocrine system is a finely tuned instrument that can easily be thrown out of kilter. “Obesogens are thought to act by hijacking the regulatory systems that control body weight,” says Frederick vom Saal, Ph.D., curators’ professor of biological sciences at the University of Missouri. “And any chemical that interferes with body weight is an endocrine disruptor.”
That’s why obesogens seem to be good at making us fat—and why researchers are so bent on uncovering the truth about these chemicals. The NIEHS is funding studies that target them. The Endocrine Society, the largest organization for hormone research and clinical endocrinology, has also noted the connection. “The rise in the incidence in obesity matches the rise in the use and distribution of industrial chemicals that may be playing a role in generation of obesity,” it stated in a recent report, “suggesting that EDCs may be linked to this epidemic.”
That’s one reason weight-loss advice may not always work. In fact, even strictly following the smartest traditional advice won’t lower your obesogen exposure. See, an apple a day may have kept the doctor away 150 years ago. But if that apple now comes with chemicals believed to promote obesity, then that advice is way out of date. In fact, apples have been named one of the most pesticide-laden produce choices out there.
The obesogen effect may be part of the reason why traditional dieting practices—choosing chicken over beef, eating more fish, loading up on fruits and vegetables—may not work anymore.
But as we began researching our book, The New American Diet, we found some good news: There’s no reason why our favorite foods—steak, burgers, pasta, ice cream—can’t be part of a reasonable weight-loss program. We just need to move past the old thinking, and adopt some new laws of leanness.
Leanness Law 1: Know when to go organic
Every day the average American is exposed to an estimated 10 to 13 different pesticides and/or their metabolites (breakdown products) through food, beverages, and drinking water.
Some of those chemicals can mimic estrogen during development, which can lead to weight gain later in life. Others can spur unnecessary fat-cell formation at any age. At the University of California at Irvine, Bruce Blumberg, Ph.D., recently reported that prenatal exposure to obesogens among mice can predispose them to weight gain later in life. The effect is likely the same in humans. In one study, the adult daughters of women who had the highest levels of DDE (a breakdown product of the pesticide DDT) in their blood during childbearing years were found to be 20 pounds heavier, on average, than daughters of women who had the least.
And the evidence continues to accumulate.
* Researchers have noted a link between organochlorine pesticides and impaired thyroid function. According to the Endocrine Society’s 2009 report on EDCs, changes in thyroid function can result in metabolic effects. Indeed, the authors of a 2009 Thyroid Research article cited hypothyroidism, a symptom of which can be weight gain, as a possible effect of organochlorines on the thyroid.
* The authors of a study in the journal BioScience found that tributyltin, a fungicide, activates components in human cells known as retinoid X receptors, which are part of the metabolic pathway necessary for fat-cell formation. They also found that tributyltin causes the growth of fat cells in mice exposed to it. Although tributyltin is no longer used on crops, experts suspect that a similar compound still used on produce, fenbutatin, is at least as potent.
* The authors of a recent study in Molecular and Cellular Endocrinology note that organophosphates and carbamates, two common classes of pesticides, cause obesity in animals.
But there is some hopeful research; a study in the journal Environmental Health Perspectives found that children who ate fruits and vegetables free of organophosphorous pesticides for just five days reduced their urine concentrations of those pesticides to undetectable levels.
organic summer fruit basket 1 main Full Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
According to the Environmental Working Group, you can reduce your pesticide exposure by nearly 80 percent simply by choosing organic versions of the 12 fruits and vegetables shown in its tests to contain the highest pesticide load. The group calls them the Dirty Dozen: In order of pesticide load, they are peaches, apples, bell peppers, celery, nectarines, strawberries, cherries, kale, lettuce, imported grapes, carrots, and pears.
There’s a Clean Fifteen, too, a group of conventionally grown fruits and vegetables with the least pesticide residue: onions, avocados, sweet corn, pineapples, mangoes, asparagus, sweet peas, kiwis, cabbages, eggplants, papayas, watermelons, broccoli, tomatoes, and sweet potatoes.
Leanness Law 2: Stop eating plastic
You’re thinking, “Well, I don’t generally eat plastic.”
Ah, but you do.
Chances are you’re among the 93 percent of Americans with detectable levels of bisphenol A (BPA) in their bodies, and you’re also among the 75-plus percent of Americans with detectable levels of phthalates in their urine. Both of these synthetic chemicals, found in plastics, mimic estrogen. And like some pesticides, these chemicals can predispose your body from an early age to gain fat.
How do they end up inside you? Mostly through what you eat and drink: Phthalates can be found in food packaging, plastic wraps, and pesticides, as well as children’s toys, PVC pipe, and medical supplies. Each year, about 18 billion pounds of phthalate esters are created worldwide, and they can easily leach into your body.
More than 6 billion pounds of BPA, found in polycarbonate plastics and epoxy resins, is produced every year; it leaches from food and drink packaging, baby bottles, cans, and bottle tops. Pop the top off a jar of tomato sauce and check out the resin on the inside of the cap—that’s where the BPA comes from. A recent study published on BPA’s effects on humans found that workers exposed to BPA at Chinese factories had more than four times the risk of erection difficulties. (Japan reduced the use of BPA in cans between 1998 and 2003; as a result, measures of BPA in some Japanese populations dropped more than 50 percent.)
According to the Environmental Working Group, canned chicken soup, infant formula, and ravioli have BPA levels of the highest concern. And your sturdy reusable water bottle? After people drank out of a polycarbonate bottle (usually stamped with a 7 on the bottom) for just one week, their BPA levels jumped by nearly 70 percent, according to a seminal study from Harvard University and the Centers for Disease Control and Prevention.
ChickenBroth 400 Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
It may look innocent...
Here’s how you can limit your exposure.
* Follow vom Saal’s rule: “No plastic item ever goes into the oven or the microwave.” Heat can damage plastic and increase leaching.
* Avoid plastic-wrapped meat. “The plastic wrap used at the supermarket is mostly PVC, whereas the plastic wrap you buy to wrap things at home is increasingly made from polyethylene,” vom Saal says. PVC contains phthalates that, according to animal studies, may lower testosterone levels. In humans, lower testosterone leads to weight gain as well as a decrease in muscle mass and sex drive. Go to a butcher who uses paper instead.
* Cut down on canned goods like tuna, and buy frozen vegetables in bags instead of canned produce. Consider buying Eden Foods canned beans and jarred foods, which are in BPA-free packaging.
* Use a nonplastic mug whenever you can. And for good measure, avoid drinking coffee or other hot beverages out of Styrofoam, which can leach styrene, a compound linked to cancer.
Leanness Law 3: Don’t eat the Viking
When was the last time you took a dose of weight-promoting hormones?
OK, when was the last time you ate a burger?
The answer to both questions may well be the same. Every time you eat conventionally grown beef, there’s a chance you’re eating weight-gain hormones—a potential cocktail of natural and synthetic obesogens. In fact, a report in the International Journal of Obesity by researchers at 10 universities, including Yale, Johns Hopkins, and Cornell, notes that the use of hormones in meat could be a contributing factor to the obesity epidemic.
A 1999 European study concluded that people who eat meat from cattle treated with growth hormones are taking in hormones and their metabolites: estrogens in the range of 1 to 84 nanograms per person per day, progesterone (64 to 467 ng), and testosterone (5 to 189 ng).
filetsteak1 Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
If it's not grass fed and organic, just say no!
A nanogram is a billionth of a gram: That’s tiny. But it may be enough to disrupt the way your hormone system operates, research indicates. Some experts believe that certain obesogens exert influence at below 1 part per billion. And small amounts from many sources add up over time.
Perhaps even more worrisome are the potent synthetic steroids we ingest from beef. Trenbolone acetate is an anabolic steroid estimated to be eight to 10 times as potent as testosterone, which is an endocrine-disrupting chemical by definition. “This cocktail of hormones given to beef has huge consequences,” vom Saal says. We know what happens to the body when it receives large doses of steroids over a short period of time, but there is no research on the effects of small doses over years.
To bring this all home, imagine you’ve been in a terrible plane crash in the Andes, like those poor souls depicted in the movie Alive. The only way to survive is to pick one of the dead folks to eat. You’re given the choice of an obese, grotesquely muscled, man-boob-toting Minnesota Vikings lineman with shrunken testicles who’s been injecting himself with hormones for a dozen years, or someone of normal size and body type and hormonal function. (One of the Kardashian sisters, maybe.) Which would you choose?
Well, every time you eat conventionally raised beef, you’re choosing the Viking.
There’s a better way. Organic beef has none of the weight-promoting steroid hormones of conventional beef, while grass-fed beef has been found to have more omega-3s and more conjugated linoleic acid (CLA). CLA is a fatty-acid mixture that’s been linked to protection against cardiovascular disease and diabetes; it can also help you lose weight, according to a meta-analysis in the American Journal of Clinical Nutrition.
Similarly, conventionally raised dairy cows are often given hormones to produce more milk, which may lead to some nutrient dilution. Grass grazing, however, may increase omega-3 content in milk. By choosing to eat and drink more omega-3s, more CLA, and more nutrients, you’re choosing to fill your body with more nutrition—feeding your brain, fueling weight loss, and keeping hunger at bay.
Leanness Law 4: Beware of the sneaky saboteurs
Ingesting pesticides, growth hormones, and plastic-based chemicals obviously isn’t a good idea. But other, sneakier obesogens are at work. We’re talking about high-fructose corn syrup (HFCS) and soy, which are added into your diet and the diet of the animals you eat, and which carry or are converted into natural obesogens.
But wait: Isn’t soy good for your heart? Not necessarily. A review in the American Heart Association’s journal Circulation notes that soy protein can lower LDL cholesterol, but only a measly 3 percent. You’d have to eat the equivalent of 2 pounds of tofu a day to reap that benefit. As a result, the AHA withdrew support for definitive health claims for soy protein and coronary heart disease. Yet soy is in hiding in everything from cookies to french fries to salad dressing.
soy Cant Lose Fat? Endocrine Disrupting Chemicals May Be to Blame
Still eating soy? You may want to reconsider.
The result of all that extra soy could be—get ready for it—more fat. This is particularly true for people who were given soy-based formula as infants. You see, soy contains two naturally occurring chemicals, genistein and daidzein, both of which are estrogenics, which can spur the formation of fat cells.
But wait! Guess who else is on a soy diet? Elsie, Wilbur, and Chicken Little—the animals we depend on for food. (Many fish, too, are chowing down on soy.) Chickens that once ate natural grasses and forage now feed on a high-energy diet of which soybean meal is a large component.
According to British researchers, this type of diet is partly to blame for the fact that some modern chickens contain two to three times as many calories from fat as from protein. (That’s right: The chicken’s proportion of muscle is dropping, just like ours! Sounds like the obesogen effect.)
So when you eat modern, supermarket chicken and beef you’re eating more fat, less protein, and more obesogens.
High-fructose corn syrup, too, has been fingered by some experts as a possible player in the obesity crisis. HFCS is found in countless items, from bread to ketchup to Life Savers to cough medicine. Recent research indicates that a diet high in HFCS may trick your brain into craving more food even when you don’t need it. And preliminary research indicates that HFCS may even play a role in disrupting the endocrine system, says Robert Lustig, M.D., a pediatric endocrinologist at UCSF. In overweight people, it interferes with leptin, a hormone that regulates appetite.
Is all this a bit disturbing? You bet. Depressing? Not at all. Because you can reconsider the old weight-loss advice—the “diet wisdom” that told you to stop eating burgers, pasta, and ice cream—and go back to eating what you love. Of course, you should eat reasonably-sized portions. But the key is to eat natural, obesogen-free versions. Do this while keeping up your exercise program and over time you’ll see results. Your waistline, your tastebuds, and even your muscles and libido will thank you.
Adapted from The New American Diet (Rodale 2009), available at bookstores and at NewAmDiet.com.
News Author: Caroline Cassels
CME Author: Désirée Lie, MD, MSEd
CME Released: 11/15/2010; Valid for credit through 11/15/2011
November 15, 2010 — Women who experience physical or sexual abuse as children or adolescents are at significantly increased risk of developing type 2 diabetes, a large, longitudinal cohort study suggests. Furthermore, investigators found there is a dose-response relationship such that the more severe the abuse, the greater the risk.
The latest findings from the Nurses' Health Study II show moderate or severe physical abuse was associated with a 26% to 54% higher risk for diabetes in adulthood. Unwanted sexual touching was associated with a 16% higher risk for the disease. Forced sexual activity before adulthood carried a 34% increased risk if it occurred once and but carried a 69% greater risk if it occurred more frequently.
"Although there was no evidence of a multiplicative, synergistic impact of experiencing both physical and sexual abuse, women who experienced both types of abuse had higher absolute risks of diabetes than expected from physical or sexual abuse alone.
"Girls who experience both types of abuse may suffer more severe abuse, more emotionally damaging abuse, or more chronic abuse than girls who experienced abuse of one type," the researchers, led by Janet Rich-Edwards, ScD, director of developmental epidemiology at the Conners Center for Women's Health, Brigham and Women's Hospital, Boston, Massachusetts, write.
The study was published online November 9 in the American Journal of Preventive Medicine.
According to investigators there is a considerable amount of research examining the psychological sequelae of childhood abuse but few studies examining lifelong physical consequences, with 1 exception.
The researchers note that there has been a consistently reported link between child abuse and adult obesity and evidence indicating that child abuse leads to overweight.
The study authors add that because obesity is a major risk factor for type 2 diabetes, it may be that early abuse may lead to the disease via this pathway. They also note that experimental and observational research suggests that "early trauma may cause lasting dysregulated stress responsivity, which may link child abuse with diabetes through physiologic pathways independent of adiposity."
According to investigators, earlier studies examining childhood trauma and diabetes have been limited by small sample sizes, cross-sectional design, unvalidated or nonspecific metabolic outcomes, or cursory assessments of abuse history.
To examine the extent to which child physical or sexual abuse is associated with type 2 diabetes, the researchers examined data from 67,853 women participating in the Nurses' Health Study II.
Established in 1989, the cohort has been followed by biennial mailed questionnaires asking about risk factors and disease incidence. In 2001 a Violence Questionnaire was sent to 91,297 study participants and 67,853 individuals responded. The investigators then examined reported lifetime abuse in 2001 and corresponding risk for diabetes from 1989 through 2005.
More than half (54%) of participants reported mild to severe physical abuse as a child or teen and 34% reported experiencing sexual abuse. Adjusted analyses revealed that compared with women who reported no physical abuse, the hazard ratios (HRs) were 1.03 (95% confidence interval [CI], 0.91 – 1.17) for mild physical abuse, 1.26 (95% CI, 1.14 – 1.40) for moderate physical abuse, and 1.54 (95% CI, 1.34 – 1.77) for severe physical abuse.
Compared with women who reported no childhood or adolescent sexual abuse, the HRs were 1.16 (95% CI, 1.05 – 1.29) for unwanted sexual touching, 1.34 (95% CI, 1.13 – 1.59) for a single episode of forced sexual activity, and 1.69 (95% CI, 1.45 – 1.97) for repeated forced sex.
"The more severe the reported abuse, the higher the woman's risk of developing type 2 diabetes as an adult," Dr. Rich-Edwards said in a statement.
The investigators report that adult body mass index accounted for 60% of the association of child and adolescent physical abuse and 64% of the association of sexual abuse with diabetes.
"Interpersonal violence is a prevalent and understudied threat to women's health," said Dr. Rich-Edwards. "Since child abuse predicts later obesity, and obesity is one of the primary causes of chronic disease, our study demonstrates just one of many potential health risks associated with childhood abuse."
The investigators note that there is a need for further investigation of potential associations between abuse of girls and women with health issues.
The study authors have disclosed no relevant financial relationships.
Am J Prev Med. Published online November 9, 2010.
A total of 52% of US women have been physically assaulted, and 15% have been raped in their lifetime. There is evidence that links childhood abuse, but not childhood sexual abuse, to adult type 2 diabetes, mediated by an increased body mass index.
This is a longitudinal study within the Nurses' Health Study II to examine the association between childhood physical and sexual abuse and the risk for adult diabetes.
* The Nurses' Health Study II is a cohort of 116,430 registered nurses aged 25 to 42 years in 1989 who were followed up by mailed biennial questionnaires.
* In 2001, a Violence Questionnaire was mailed to 91,297 participants; 68,376 participants returned their questionnaires.
* Participants contributed person-time from 1989 until their last returned questionnaire, diabetes diagnosis, or follow-up in 2005.
* All 2074 cases of women with type 2 diabetes were examined from 1989 to 2005.
* Excluded were women with baseline diabetes diagnosis and those with diabetes secondary to other treatments.
* Diabetes was confirmed with use of the responses to the biennial questionnaire.
* The Violence Questionnaire covered 3 periods: childhood up to age 11 years, adolescence aged 11 to 17 years, and adulthood.
* Childhood and adolescent physical abuse were assessed through an adaptation of the revised Conflict Tactics Scale.
* Physical abuse during childhood was categorized as no physical abuse; being "pushed, grabbed, or shoved" at any frequency; being "kicked, bitten, or punched once"; being "hit with something" once; or being subjected to any of these abuses more than once.
* Severe physical abuse included being choked or burned.
* Participants were categorized by the most severe violence event.
* Child and adolescent sexual abuse were measured by questions regarding unwanted sexual touching and forced sexual activity.
* Exposure was classified as no sexual abuse, unwanted sexual touching only, forced sexual activity once, and forced sexual activity more than once.
* Covariates considered included race/ethnicity, birth weight and family history of type 2 diabetes, childhood adiposity, depression, and school diet.
* 54% of participants reported physical abuse in childhood or adolescence, including 9% who reported severe physical abuse.
* One third (34%) reported sexual abuse in childhood or adolescence, including 12% with forced sexual activity, half of whom reported this happening more than once.
* There was a dose-response association between physical abuse and the risk for type 2 diabetes; adjustment for covariates attenuated the association.
* Adjusted analyses revealed that compared with women who reported no physical abuse, the HRs were 1.03 (95% CI, 0.91 - 1.17) for mild physical abuse, 1.26 (95% CI, 1.14 - 1.40) for moderate physical abuse, and 1.54 (95% CI, 1.34 - 1.77) for severe physical abuse.
* Mild physical abuse in childhood was not associated with adult type 2 diabetes, but moderate and severe physical abuse were associated with a 26% and 54% higher risk for diabetes, respectively.
* Physical and sexual abuse history were correlated (P < .0001).
* Moderate and severe physical abuse predicted an increased risk for type 2 diabetes, whether women had experienced sexual abuse.
* Women who experienced unwanted sexual touching had a 16% increased risk for adult type 2 diabetes.
* Women who had experienced forced sexual abuse once vs repeatedly had a 34% to 69% high risk for adult type 2 diabetes vs women who experienced no sexual abuse.
* The HRs were 1.16 (95% CI, 1.05 - 1.29) for unwanted sexual touching, 1.34 (95% CI, 1.13 - 1.59) for a single episode of forced sexual activity, and 1.69 (95% CI, 1.45 - 1.97) for repeated forced sex.
* Most girls had experienced both physical and sexual abuse.
* Among girls who experienced sexual but not physical abuse, the risk for type 2 diabetes was 56% higher.
* Physical and sexual abuse interacted on an additive, but not multiplicative, scale indicating that the absolute, but not relative, risk for type 2 diabetes was higher among women who had experienced both forms of abuse.
* There was a 29% increased risk for type 2 diabetes for moderate physical abuse and a 49% increased risk for severe physical abuse isolated to childhood or adolescence.
* For isolated sexual abuse, there was a 19% increased risk for sexual touching, 32% for forced sex once, and 86% for repeated forced sex.
* Adult body mass index accounted for 60% of the association for physical abuse and 64% of the association for sexual abuse with the risk for adult diabetes.
* The authors concluded that childhood physical and sexual abuse both correlated positively with the risk for adult type 2 diabetes and that more than 60% of this effect was mediated through increased body mass index. Also, between 10% and 30% of the effect was accounted by the abuse itself.
* The estimated proportion of women with type 2 diabetes attributed to childhood physical or sexual abuse is 9%.
* There is a dose-response association between childhood and adolescent physical abuse and the risk for adult type 2 diabetes; this effect is partly mediated by increased body mass index.
* There is a dose-response association between childhood and adolescent sexual abuse and the risk for adult type 2 diabetes; this effect is partly mediated by increased body mass index.
Sunday, 21 November 2010
I remember the Cuna Indians whom I visited many times and I was amazed at the fact that none of them had any levels of Blood pressure near the well accepted 130/80... I measured hundreds of Cuna for BP and Blood Sugar and sure enough Diabetes also was very rare.
Many theories were put forward by the epidemiologists who look at numbers and not at societies and they came up with Potassium, Sea Food etc as the cause of such healthy BP numbers.It must have been an anthropologist who had noticed the fact that the Cuna drank ground up cocoa powder made into a drink many times during the day. Studying the ingredients in that drink.. started up this story of their benefits..
Yet another contribution to the Western Civilization by the Native Indians..
Chocolate as we are familiar with in the west, was the product of chemical imagination of a swiss, who learned to solidify it and make it into tablet forms. In the ancient Maya ceremonies depicted in pictographs you would see them drinking chocolate and not eating it..The bad press for Chocolate arrived when they started calling everything with a whiff of chocolate in it Chocolate, such as Hersheys Bar and other "candy" in the USA which has only about 10 per cent chocolate in them.
Eat Dark Chocolate and make sure that it has at least 70% Cacao..
By Sara Novak, Planet Green
Once in a blue moon, I'll hear some positive news on the healthy eating front and dark chocolate has time and time again come out on top. This along with the antioxidants in wine is enough to make you jump for joy. We know that this delectable sweet treat provides a wealth of health benefits, but how much is too much?
Recently, Mehmet Oz and Mike Roizen, authors of YOU: On a Diet, answered some important questions on the specifics of dark chocolate consumption. According to the article in the Sun Setinel, you don't need a whole bar to get a healthy dose of antioxidants. The flavonoids in dark chocolate are so powerful that a daily piece the size of a Hershey's kiss can lower your blood pressure.
While this is an ideal size comparison, it's not a good quality comparison because the chocolate cannot be milk chocolate. The chocolate should be fair trade, organic, and at least 70 percent cocoa. Avoid any filling like peanut butter, which could be laced with hydrogenated oils.
Dark chocolate and heart disease
According to a study published in the European Heart Journal and reported on CBS News, German researchers found people who had an average of six grams of chocolate per day (one square of a chocolate bar) had a 39 percent lower risk of either a heart attack or stroke.
Dark chocolate and stroke protection
I wrote about another study published in the Journal of Cerebral Blood Flow and Metabolism. This new study found that dark chocolate can provide protection after a stroke has already occurred.
A specific chemical found in dark chocolate called epicatechin appears to do the trick. We already know that it can prevent strokes from happening and now we know that it can provide protection against stroke damage.
Wednesday, 17 November 2010
Western Medicine is practiced without empathy and understanding of the person, in a totally un-holistic way in all the five countries mentioned.
The Cardiologist in Miami was friendly, the Cardiologist in France was efficient, the Neurologist in Bangalore did a brief exam and the ENT doctor in KL was humourous but dismissed my queries as being not important. No body could help me with information about how to remain healthy, but all of them had a tendency to convey the information that one can expect wear and tear, as one gets older. All of them had cursory advice like: Take care of the nutrition.
Thus the experience with Western Medicine has been a robotic one. It is as if I was a car needing some replacement for worn out parts and the mechanic could take care of it: a CT of the lower back, Stress test, Echocardiogram, MRI of the sinuses.
Objectification of symptoms, mechanization of thought, dismissal of the patient’s explanatory models, and in general a disregard for the knowledge of the patient.
My respect for western medicine is at its lowest level at the moment after the encounter with the Cuban Doctor. Secretly I had hoped that the Cubans with a formation within the society which is far more egalitarian and socialist would have a point of view slightly different from the money driven medical practice of Miami, or the Meat Market Shopping of Manipal Medical Center in Bangalore or controlled National Health Service of France. No, it was not to be. He was overbearing, middle aged and obese, with no bedside manners, and his examination of my limbs took him less than one minute. There was no comforting words but only some paternalistic advice (I did tell him that I knew a fair bit about nutrition and that the advice to take care of my nutrition was a little superficial).
The consultation fees differed by the country regardless of the service or the results.
USA 235 usd France 75 Euros Bangalore 300 INR Cuba 25 cuc and the doctor in KL did not charge me as I was a friend of his faithful patient and the normal charge would have been about 30 usd.
Dissatisfaction at any price!
My connection with Cuba has been in the fields of Psychology and Anthropology and I have been impressed with the quality of their thinking and caring. Cira Garcia is a fee for service system set up in Cuba to serve foreigners and many Caribbean islanders come here since the services are cheap compared to the other alternative, which is Miami. I wish the clinic financial success as there is a need for tertiary advice but my advice to you is:
Doctors are not helpful when your problem is not acute or simple that they need to think about it. They are good at acute situations and vague when it comes to prevention with no interest at all in Health but with all the interest in the world in Disease. Cuban doctors have the same mentality as the western doctors trained in the Cartesian model of division of body and mind.
My friend is a professor of Psychology, can with her comprehension about human feelings; take care of a lot of medical problems even though she is not a medical doctor. When my blood pressure was fluctuating, the cardiologist in Miami suggested that I take medications, while the cardiologist in France did not see the need for medication. The neurologist in Bangalore after seeing that my CT of lower back and Nerve Conduction studies were normal, said in a plain voice, I am not quite sure what to advice you. The humourous ENT physician suggested that my decreased hearing might indicate my decreased desire to hear! The psychologist in Cuba was the first one to alert me, her first question to me was: what has happened in your life in the past year? And then suggested a way to go around the stress of the times and take care of my body thus.
2009 had been an eventful year for me; I had traveled 13 times from Paris to Miami to oversee the medical treatment and the surgical removal of the cancer in the lung of my sister. I was her counselor and translator of the medical world. For those of you who have watched a dear one undergoing chemotherapy with the likes of Taxol or Neulasta (to increase the white cells), and the excruciating pain as well as the general sense of being totally unwell, can understand the stress of being a care provider. In addition, I had to think in terms of prevention of any complications. Since her medications could give her hemorrhagic cystitis, we had to set up alarm to make sure that she emptied her bladder once every three to four hours at night and was well hydrated.
So the psychologist’s advice to me was not to take any medications, but to cut the frequency of my visits to my sister now that she was free of the disease.
I am a Medical Anthropologist and take the doctor-patient relationship seriously and see it much more than just a mechanical transaction the kind a car mechanic has with your car. Every person lives in the context of their lives and no two lives are the same, so this idea that a general consensus exists about the treatment or an algorithm of treatment exists is sheer nonsense. I had written earlier how one has to navigate very carefully through clinical studies done since up to 90 per cent of them are without value outside their contexts.
I am concluding my anthropological study of the observation of doctors practicing western medicine in five different countries: two in the Americas, one in Europe and two in Asia, with the following warnings.
Doctors and Western Medicine, to reiterate what Ivan Illich has said thirty or forty years ago, is dangerous to your health.
Western Medicine is excellent when you are having an acute problem such as multiple fractures after an accident or a myocardial infarction. It is not helpful and actually may harm you if you have a chronic problem such as Hypertension or Diabetes.
Western medicine is incapable of prevention of diseases since the thinking behind the treatment if detrimental to the process of prevention. None of the doctors I talked to were in a position to give advice to prevent diseases whereas they were able to suggest various mechanical resolutions such as CT, Gastroscopy, Sinus Surgery, all invasion of the body. None of the doctors I interviewed were capable of giving any sort of psychological or socially related counseling or advice.
But this is the world we live in, whether it is Cambodia or Cuba. At least in most societies you are not paying for your medical care so you can be a little bit more expansive in your choices. It is in the societies where the medical care is fee for service that the dominance of the western medicine usually quashes the appearance of alternative or complementary medicine. Even the nomenclature Alternative Medicine assumes the supremacy of Western Medicine. I am sure they don't consider Chinese Medicine in China, Alternative?
But great diversity exists in the healing systems all over the world. After the brisk encounter with the mechanistic world of Western Medicine in Cuba, I drove to the house of the longest practicing Yoga teacher in Cuba! Western Medicine is just one part of the spectrum of what is available and I believe that in the care of patients, western medicine including their lackeys Doctors, Nutritionists, Exercise Persons, Pharmaceuticals consist no more than 25 per cent of the efforts necessary to heal the suffering person.
American Indians have taught me that, to achieve a balanced life, there has to be equal attention to many parts in ones life. Using the model I have come to following conclusion:
For a person who is suffering from a chronic condition or illness:
25 % western medicine, including the clinic and Physiotherapy etc, all the western accouterments
25% has to be family oriented counseling
25% spiritually oriented counseling
25% is the changes in the lives of the patients in understanding the social responsibility of their lives.
Western Medical trained people can take care of you; they are the complimentary medicine to the 75% of the caring. Healing comes from counselors and persons who can educate you about the context in your lives and that is the major part. Western medicine interested in curing plays a minor part.
American Heart Association Scientific Sessions 2010
CHICAGO — Low serum vitamin D levels appear to be independently associated with the development of prehypertension, new data suggest.
Researchers conducted a cross-sectional study of 9,215 participants included in the National Health and Nutrition Examination Survey (NHANES) III who were free of hypertension at baseline. Participants were divided into quartiles based on serum vitamin D levels. The main outcome of interest was prehypertension (n=3,712), which was defined as systolic blood pressure of 120 mm Hg to 139 mm Hg or diastolic BP of 80 mm Hg to 89 mm Hg.
According to the results, low serum vitamin D levels were associated with the development of prehypertension, independent of risk factors such as age, sex, race, smoking, alcohol intake, BMI, physical inactivity, diabetes, HDL ratio, C-reactive protein and glomerular filtration rate.
When compared with the highest quartile of serum vitamin D (>32.4 ng/mL), the odds of developing prehypertension were increased in the lowest quartile (≤17.7 ng/mL; OR=1.48; 95% CI, 1.16-1.90). On continuous analysis, each standard deviation decrease in vitamin D was associated with an odds ratio of 1.14 (95% CI, 1.05-1.24) of prehypertension.
“These findings are largely consistent with previous studies that examine the association [between low vitamin D levels] and prehypertension,” Charumath Sabanayagam, MD, PhD, of West Virginia University, said during his presentation.
PS you really need exposure to the Sun to receive Vitamin D naturally..
Tuesday, 16 November 2010
I have read the weekly magazine The Economist ever since I began my university studies and each and every issue contains something of interest. the name is misleading, you may think it is only about economics but as you can see in the following article published, interesting and earth shattering news in the field of science gets attention long before the lay press picks it up
Obesity, malnutrition and gestation
Evidence that the problem of obesity starts in the womb
Nov 11th 2010 | Lausanne
Hiding from the future
IN THE late 1980s David Barker, a British doctor, suggested that what a woman eats when she is pregnant shapes her child’s physiology for life. He called the idea fetal programming. Such programming would allow an individual to make optimum use of available nutrients, on the assumption that his own diet will be similar to his mother’s. If it was not similar, though, there could be problems. Dr Barker speculated that fetal programming—in mesalliance with the spread of fatty, sugary foods over recent decades—might explain the epidemic of obesity, heart disease and late-onset diabetes that plagues many rich countries.
It is a neat theory, but hard to prove. On October 29th, though, Sir Peter Gluckman, an endocrinologist and evolutionary biologist at the University of Auckland, in New Zealand, presented evidence to support it at a conference organised in Lausanne by Nestlé, a Swiss food company. Dr Gluckman carried out his study in Jamaica, in collaboration with Terrence Forrester, of the University of the West Indies. He picked Jamaica because malnutrition is endemic there. That allows the theory of fetal programming to be tested by finding out whether those who experienced malnutrition in the womb respond differently to food than those who were properly fed.
Dr Gluckman and Dr Forrester began their study by looking at people who had survived childhood malnutrition. Symptoms normally manifest themselves in one of two ways, known as marasmus and kwashiorkor. Children with marasmus are simply emaciated. The abdomens of those with kwashiorkor, however, distend in a way that is distressingly familiar from televised appeals for famine relief. One significant difference between the two syndromes is that children with marasmus are twice as likely to survive malnutrition as those with kwashiorkor.
Dr Gluckman and Dr Forrester looked at 240 people aged between 25 and 40 who had survived one syndrome or the other as children, and found a systematic difference between them. The marasmus survivors tended to have had low birthweights. The kwashiorkor group had normal birthweights. Low birthweight is an indication of a malnourished mother. Dr Gluckman and Dr Forrester thus hypothesise that the capacity for a marasmus-style response to malnutrition, with its higher survival rate, is programmed into fetuses by maternal malnourishment. Fetuses carried by well-nourished mothers do not, as it were, anticipate the risk of malnutrition, and thus respond to it less well.
That suggests fetal programming is a real phenomenon. But can it help explain obesity, diabetes and so on? To investigate this, the two researchers then offered their volunteers foods that were either high in protein and low in fat, or low in protein and high in fat—but which, crucially, tasted the same, so that they did not know what they were eating.
They found that those who had survived marasmus ate differently from those who had survived kwashiorkor. The bodies of marasmus survivors seemed to demand more protein in their food. When offered a diet low in protein and high in fat, they consumed more of it. That kept their protein intake constant, but meant they were eating 500 calories a day more than a normal maintenance diet (2,000 calories for women and 2,500 for men). Kwashiorkor survivors did not overeat in this way.
This, then, may be the key that unlocks the puzzle. Diets of the past would tend to have been lean (that is, to have favoured protein and complex carbohydrates like starch over fats and sugars). Anticipating scarcity by overeating in times of plenty would be no bad thing if times of scarcity were a real risk. Bodies that expected food to be plentiful, by contrast, should ration themselves to avoid the consequences of chronic overeating. An inability to do that is the price paid for protection from famine by those predisposed to marasmus.
This study thus makes a prediction: as diets become high in sugar and fat in places where malnutrition was once common, those who suffered marasmus as children will become overweight more rapidly than those who suffered kwashiorkor. If that turns out to be the case, it will be evidence that Dr Barker was right. What is not yet clear is whether the children of today’s overfed westerners will experience programming in the opposite direction, and have their appetites restricted.
Saturday, 6 November 2010
U.S. Obesity Rate May Hit 42% by 2050
By Kathleen Doheny
HealthDay Reporter by Kathleen Doheny
healthday Reporter Fri Nov 5, 11:48 pm ET
FRIDAY, Nov. 5 (HealthDay News) -- Despite reports that the rate of obesity among U.S. adults might be slowing down, a new projection from Harvard University and MIT suggests otherwise.
Instead, using a sophisticated model that views obesity like an infectious disease, the team predicts that adult obesity rates will rise for another 40 years before leveling out. And before reaching that plateau, 42 percent of adults will be obese, the team predict.
For the last few years, the U.S. Centers for Disease Control and Prevention has placed the adult obesity rate at 34 percent, with another 34 percent of Americans overweight but not obese.
"It's definitely true that the percent of obese people has slowed down," said study author Alison Hill, a graduate student in Harvard's Program for Evolutionary Dynamics, Biophysics Program. "But our results suggest it is not the end."
The study is published this week in the journal PLoS Computational Biology.
The prediction is a ''best-case'' scenario, said Hill and Dr. David Rand, a research scientist at Harvard who was also involved in the study. That means the obesity rate might rise even higher than 42 percent.
Obesity is defined as having a body-mass index (BMI) of 30 or higher. For instance, a person 5-feet-5 inches tall who weighs 200 pounds has a BMI of 33 and is considered obese.
The modeling was done after examining the spread of obesity via "social networks" in the long-running Framingham Heart Study Network. In the analysis, a social network includes family, co-workers, friends and neighbors. The spread of obesity among U.S. adults in recent decades due to social contacts can't be ignored, Hill and Rand said. That idea is based on the ''social contagion'' theory of obesity.
Under this theory, a normal weight person has a 2 percent chance of becoming obese in any given year, according to the researchers.
That number increases by 0.4 percent with each obese social contact a person has, meaning that a person with five obese contacts doubles his or her risk for obesity.
On the other hand, when it comes to losing weight, an obese adult has a 4 percent chance of losing enough to become just overweight in any given year, the team found.
But they didn't find that weight loss had much to do with social contacts. So an obese person who hangs out with normal-weight friends won't necessarily lose pounds because of those contacts.
Other factors play into the spread of obesity, Hill and Rand explained, including the rate of ''non-social transmission" of obesity, such as easier access to unhealthy foods, and the rate of ''recovery" from obesity, or a weight loss that puts people below a BMI of 30.
While the non-social transmission factors are still most important in the spread of obesity, Rand said, the role of social transmission has expanded in the past four decades.
Exactly why hanging out with obese people boosts one's risk of becoming obese isn't fully understood. One speculation, Rand said, is that over time, as we have become more and more connected via emails, Internet and social networking, the social transmission factor has naturally played a larger role. It could be, he said, that what is appropriate and ''normal" to eat changes if you have obese friends.
The findings have some public health implications -- suggesting ways policy makers might attack the obesity epidemic -- but also a message for individuals, said Hill.
"One good take-home point is it's actually in your best interest to help your friends lose weight," Hill said. "The more obese friends you have, the more likely you are to gain."
Another expert, James O. Fowler, professor of medical genetics and political science at the University of California San Diego, said the study, even with its dismal 42 percent obesity prediction, has some bright news.
"The good news here is that we may be reaching a high point in the obesity epidemic, and the authors' model is a useful framework for understanding how we can bring the rate of obesity back down," he said.
Fowler co-wrote a book on social connections with Dr. Nicholas Christakis, who is another co-author of the new modeling study with Hill and Rand.
To learn more about overweight and obesity, visit the U.S. Centers for Disease Control and Prevention.
IF YOU ADD CANADIAN STATISTICS, SIX OUT OF THE SEVEN THINNEST STATES WOULD BE IN CANADA..
Sunday, 31 October 2010
A method of assessing a newborn's health.
[After anesthesiologist Virginia Apgar (1909-1974) who devised it.]
This is a judging world and we get evaluated right from birth (Apgar score) to death (how many people came to the funeral). In 1953, Dr. Virginia Apgar devised a quick way to measure the health of a newborn child. She assigned 0, 1, or 2 points for each of the five criteria: heart rate, respiration, muscle tone, skin color, and reflex response. The Apgar score is typically calculated at one minute and five minutes after birth. Ten years after the debut of the Apgar score, Dr. L. Joseph Butterfield introduced an acronym as a mnemonic aid for the term: Appearance, Pulse, Grimace, Activity, Respiration. Also see backronym.
"The baby, a 6-pound, 14-ounce boy, appeared so healthy that doctors who delivered him gave him an Apgar score of 9 on a scale of 1 to 10."
Delthia Ricks; Congenital Malaria Case is First For NY; Newsday (New York); Apr 23, 2005.
Oh to have a lodge in some vast wilderness. Where rumors of oppression and deceit, of unsuccessful and successful wars may never reach me anymore. -William Cowper, poet (1731-1800)
Magnolia Cardona-Morrell email, Lucie Rychetnik email, Stephen L Morrell email, Paola T Espinel email and Adrian Bauman email
BMC Public Health 2010, 10:653doi:10.1186/1471-2458-10-653
Published: 29 October 2010
The clinical effectiveness of intensive lifestyle interventions in preventing or delaying diabetes development in people at high risk has been established from randomised trials of structured, intensive interventions conducted over the past two decades in several countries. The challenge is to translate them into routine clinical settings. The objective of this review was to determine whether lifestyle interventions delivered to high-risk adult patients in routine clinical care settings are feasible and effective in achieving reductions in risk factors for diabetes.
Data sources: MEDLINE (PubMed), EMBASE, CINAHL, The Cochrane Library, Google Scholar, and grey literature were searched for English-language articles published from January 1990 to August 2009. The reference lists of all articles collected were checked to ensure that no relevant suitable studies were missed. Study selection: We included RCTs or before-and-after (with or without a control group) studies of lifestyle interventions with the stated aim of diabetes risk reduction or diabetes prevention conducted in routine clinical settings and delivered by healthcare providers such as family physicians, practice nurses, allied health personnel, or other healthcare staff associated with a health service. Outcomes of interest were weight loss, reduction in waist circumference, improvement of impaired fasting glucose or oral glucose tolerance test (OGTT) results, improvements in fat and fibre intakes, increased level of engagement in physical activity and reduction in diabetes incidence.
Twelve from 41 potentially relevant studies were included in the review. Four studies were suitable for meta-analysis. A significant positive effect of the interventions on weight was reported by all study types. The meta-analysis showed that lifestyle interventions achieved weight and waist circumference reductions after one year. However, no clear effects on biochemical or clinical parameters were observed, possibly due to short follow-up periods or lack of power of the studies meta-analysed. Changes in dietary parameters or physical activity were generally not reported. Most studies assessing feasibility were supportive of implementation of lifestyle interventions in routine clinical care.
Lifestyle interventions for patients at high risk of diabetes, delivered by a variety of clinical health care providers in routine clinical settings, are feasible but appear to be of limited clinical benefit one year after intervention. Despite convincing evidence from structured intensive trials, this systematic review showed that translation into routine practice has less effect on diabetes risk reduction.
Saturday, 30 October 2010
Vitamin D Has Retinopathy Link
By John Gever, Senior Editor, MedPage Today
Published: October 20, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
* Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
* Note that the study cannot determine causality, and that whether vitamin D supplementation can reduce the risk of diabetic complications is not known.
CHICAGO -- Diabetic retinopathy may be added to the list of conditions potentially related to vitamin D insufficiency, a researcher said here.
A study of 123 diabetic individuals with varying degrees of retinopathy, along with two groups of controls, showed that low vitamin D levels were significantly more common in those with the diabetic complication, according to John F. Payne, MD, of Emory University in Atlanta.
In a poster presentation here at the American Academy of Ophthalmology's annual meeting, Payne also reported that multivitamin use appeared to be helpful in preventing vitamin D insufficiency -- at least as currently defined.
"If you were taking a daily multivitamin, your mean vitamin D [25-hydroxyvitamin D] was about 31 [ng/mL] versus about 22 if you weren't taking a multivitamin," he told MedPage Today. Because 30 ng/mL was the cutoff Payne and colleagues had used to define insufficiency, "now you're up to the optimum level."
But he acknowledged that some researchers have begun to advocate for higher levels of daily vitamin D intake and serum levels of the 25-OH-D metabolite, relative to current norms, as necessary for health.
Payne and colleagues gathered a total of 221 individuals in five groups: 47 volunteers without diabetes or any eye disease; 51 without diabetes who had uveitis, macular degeneration, or other ocular diseases; 41 diabetics without eye disease; 40 diabetics with nonproliferative diabetic retinopathy; and 42 diabetics with proliferative disease.
Serum 25-OH-D levels were measured from December 2009 to March 2010, which eliminated seasonal effects on vitamin D levels.
Mean levels in the five groups were as follows (P<0.001 for diabetics versus nondiabetics):
* Healthy controls: 28.8 ng/mL
* Nondiabetics with eye disease: 24.7 ng/mL
* Diabetics without eye disease: 23.2 ng/mL
* Diabetics with nonproliferative retinopathy: 21.5 ng/mL
* Diabetics with proliferative retinopathy: 18.0 ng/mL
Vitamin D insufficiency was found in 81% of the proliferative retinopathy group and about 70% of the two other diabetic groups, versus 55% of the two nondiabetic groups (P=0.048).
Black participants, who made up about half the overall sample, had lower mean 25-OH-D levels than whites, at 23.7 versus 29.2 ng/mL -- a difference found in most studies, as melanin in the skin interferes with the vitamin D-boosting effect of sunlight.
But in multivariate analysis, which accounted for body mass index, glycated hemoglobin levels, and two measures of renal function, only the presence or absence of self-reported daily multivitamin use was significantly associated with 25-OH-D level (mean 31.1 versus 22.0 ng/mL).
Vitamin D insufficiency was seen in 44% of those taking daily multivitamins, versus 83% of those not taking them (P<0.001).
Payne said the big unanswered question remains whether vitamin D supplementation can reduce the risk of diabetic complications, or any of the wide range diseases that have been linked to vitamin insufficiency in previous studies. These have included breast cancer, heart failure, multiple sclerosis, GI infections, and age-related cognitive decline, among others.
He noted that in this cohort, there was not a significant relationship between reported multivitamin use and the presence or severity of diabetic retinopathy.
Payne added that a randomized, placebo-controlled trial of supplements might be impossible because withholding them from patients known to have vitamin insufficiency could be considered unethical.
"We may have to go about getting that data a bit differently than we normally would," he said.
Nevertheless, Payne recommended that patients and physicians should consider vitamin D supplements in the meantime, since they are safe and could very well be helpful.
The study was supported by Research to Prevent Blindness and the National Eye Institute.
Payne and colleagues declared they had no competing financial interests.
Primary source: American Academy of Ophthalmology
Payne J, et al "Vitamin D insufficiency in diabetic retinopathy" AAO 2010; Abstract PO223
According to a new study, regular consumption of sugar-sweetened beverages is linked with a clear and consistently greater risk of metabolic syndrome and Type 2 diabetes. Picture: Agency
Friday, October 29, 2010 - Page B02
A NEW study has found that regular consumption of soda and other sugar-sweetened beverages is associated with a clear and consistently greater risk of metabolic syndrome and Type 2 diabetes.
According to the Harvard School of Public Health (HSPH) researchers, the study provides empirical evidence that intake of sugary beverages should be limited to reduce risk of these conditions.
The study appears online Wednesday in the journal Diabetes Care and will appear in the November print edition.
"Many previous studies have examined the relationship between sugar-sweetened beverages and risk of diabetes, and most have found positive associations but our study, which is a pooled analysis of the available studies, provides an overall picture of the magnitude of risk and the consistency of the evidence," said lead author Vasanti Malik, a research fellow in the HSPH Department of Nutrition.
Consumption of sugary drinks, the majority of which are sodas, has increased substantially in the US and across the globe and previous scientific studies have shown consistent associations with weight gain and risk of obesity.
However, this study is the first meta-analysis to quantitatively review the evidence linking sugar-sweetened beverages with type two diabetes and metabolic syndrome.
Metabolic syndrome is a group of risk factors, such as high blood pressure and excess body fat around the waist, that increase the risk of coronary artery disease, stroke and diabetes.
The researchers, led by Malik and senior author Frank Hu, professor of nutrition and epidemiology at HSPH, did a meta-analysis that pooled 11 studies that examined the association between sugar-sweetened beverages and those conditions. The studies included more than 300,000 participants and 15,043 cases of Type 2 diabetes and 19,431 participants and 5,803 cases of metabolic syndrome.
The findings showed that drinking one to two sugary drinks per day increased the risk of Type 2 diabetes by 26 per cent and the risk of metabolic syndrome by 20 per cent compared with those who consumed less than one sugary drink per month.
Drinking one 12-ounce serving per day increased the risk of Type 2 diabetes by about 15 per cent.
"The association that we observed between soda consumption and risk of diabetes is likely a cause-and-effect relationship because other studies have documented that sugary beverages cause weight gain, and weight gain is closely linked to the development of Type 2 diabetes," said Hu.
While a number of factors are at work in the development of Type 2 diabetes and metabolic syndrome, sugar-sweetened beverages represent one easily modifiable risk factor that if reduced will likely make an important impact, say the researchers. "People should limit how much sugar-sweetened beverages they drink and replace them with healthy alternatives, such as water, to reduce risk of diabetes as well as obesity, gout, tooth decay, and cardiovascular disease," said Malik.