Prehypertension linked to low vitamin D

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..

The Origins of Obesity with Increasing Affluence

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
Slim pickings
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.

US of America set to become FATTER...Increasing Obesity in America

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.

More information

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..

how APGAR became a Backronym

Apgar score (AP-gar skor) noun

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.



X-Bonus
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)

Not very encouraging news for doctors in private practice

Reduction of diabetes risk in routine clinical practice: Are Physical Activity and Nutrition Interventions feasible and are the outcomes from reference trials replicable? A Systematic Review and meta-analysis

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
Abstract (provisional)

Background

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.
Methods

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.
Results

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.
Conclusion

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.

Vitamin D deficiency and Diabetic Retinopathy

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
Action Points

* 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
Source reference:
Payne J, et al "Vitamin D insufficiency in diabetic retinopathy" AAO 2010; Abstract PO223

Coke or Pepsi a day can bring on Diabetes

'Sugary beverages' increase risk of Type 2 diabetes


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
WASHINGTON
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.