Annual Flu Vaccine May Weaken Kids Resistance to Other Viruses

November 28th, 2011 by Admin No comments »

November 28, 2011 — The annual flu vaccine can weaken children’s resistance to other types of influenza virus, including those that could cause a pandemic, according to a study published in the November issue of the Journal of Virology.

“Annual vaccination against influenza is effective but may have potential drawbacks that have previously been underappreciated and that are also a matter of debate,” write lead author Rogier Bodewes, DVM, from Erasmus Medical Center in Rotterdam, the Netherlands, and coauthors.

They don’t suggest that annual childhood vaccinations should be halted, but they call for research into better vaccines that eliminate this adverse effect.

To study the effects of seasonal immunization, the researchers collected blood samples from 27 healthy unvaccinated children (median age, 6.0 years; range, 2.0 to 8.8) and 14 children with cystic fibrosis who had received annual influenza vaccinations (median age, 6.2 years; range, 3.1 to 9.0). In the Netherlands, only special populations of children, such as those with cystic fibrosis, are routinely vaccinated against influenza.

Of the unvaccinated children, 24 of 27 (89%) had antibodies against at least 1 A/H3N2 virus, and 20 (74%) had antibodies against at least 1 A/H1N1 virus. All vaccinated children had antibodies against at least 1 influenza virus, including A/H1N1(2009). However, unvaccinated children had significantly higher geometric mean titers for several viruses, including the influenza A/Panama/07/99 (H3N2) and A/Solomon Islands/3/2006 (H1N1) viruses (P = .04 and P = .01, respectively).

They found that the percentage of virus-specific ICD8+ T cells — that is, T cells with a memory for influenza viruses — ranged from 0.00% to 2.32% in unvaccinated children and from 0.06% to 1.56% in vaccinated children.

They noted an age-dependent increase in the virus-specific CD8+ T cell response in the unvaccinated children (P = .040), but not in the vaccinated children (P = .714).

Finally, in children older than 5 years, the investigators found a significantly higher percentage (P = .038) of CD8+ T cells in the unvaccinated group (mean, 0.86%; standard deviation [SD], 0.67%) than in the vaccinated group (mean, 0.37%; SD, 0.45%).

The study results are consistent with the team’s previous mouse experiments. In those studies, Dr. Bodewes and colleagues found that vaccination against the seasonal influenza A virus prevented the development of influenza A virus-specific CD8+ T cell immunity, which would otherwise be induced by infection.

During the 2009 pandemic, Canadian children who had been vaccinated against the seasonal flu were more likely to be infected with A/H1N1 than those who had not been vaccinated. (These results were not confirmed by studies in other countries.)

It is a small study, so the results have to be taken with a grain of salt, Christopher Harrison, MD, director of the Infectious Disease Research Laboratory at Children’s Mercy Hospitals and Clinics in Kansas City, Missouri, who was not involved with the study, told Medscape Medical News. But, he said, it lends weight to the argument that children should be immunized with the live virus instead of the killed virus.

“We have known for a long time that most vaccines given in the muscle don’t produce the ideal response,” said Dr. Harrison.

Killing the virus changes key proteins, which immune cells must recognize to prepare for another influenza infection, he explained. In addition to probably providing better protection against unexpected flu viruses, immunization with the live virus is 10% to 15% more effective than immunization with the killed virus against the seasonal flu, he added.

But Walter Orenstein, MD, a member of the American Academy of Pediatrics Committee on Infectious Diseases, said there isn’t enough evidence yet to make changes in the US Centers for Disease Control and Preventionguidelines for vaccinations, which explicitly state no preference for live or killed vaccines.

This study only shows a difference in biomarkers for immunity, not in immunity itself, Dr. Orenstein emphasized. “We have to look at the actual disease,” he said. “Do people who get repeated vaccination have as much disease as people who don’t? That’s the ultimate question.”

The study was supported in part by TI Pharma. The study authors and Dr. Orenstein have disclosed no relevant financial relationships. Dr. Harrison reports receiving research support from GlaxoSmithKline.

Journal of Virology. 2011;85:11995-12000. Abstract

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Vitamin K2 as Menaquinone=7 is Essential for Healthy Bone Growth & Development in Children

October 24th, 2011 by Admin No comments »

Findings of a new study published in British Journal of Nutrition 2009 by van Summeren and colleagues demonstrated that even modest supplementation with menaquinone-7 in children increases activation of osteocalcin, the bone-building protein; and in that way supports healthy bone growth and development. This is an important finding as the greater bone mineral established during childhood and early adult years, culminating in peak bone mineral density around 30 years of age, allows for better maintenance of bone health as we age and lose bone mass.

The present study is a double-blind randomized placebo-controlled study examining the effect of 45 mcg natural vitamin K2 as menaquinone-7 (MK-7) on the circulating levels of the vitamin K-dependent protein Osteocalcin. Active osteocalcin is required for bone-building cells (osteoblasts) to optimally utilize calcium for building and maintaining a healthy bone matrix. 8 weeks of MenaQ7 supplementation in healthy prepubertal children increased blood levels of vitamin K2 as MK-7 and significantly increased the amount of active osteocalcin.

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According to Professor Cees Vermeer at the VitaK research center, “Non-supplemented people are generally insufficient in vitamin K. It has been demonstrated that children are far more vitamin K deficient than adults. We explain this by the rapid growth of their bones and consequently the high vitamin K demand by the bones for the production of osteocalcin. The present study is the first one to demonstrate that increased vitamin K intake by supplement improves the osteocalcin activity in children. The next step must be that also an effect of MenaQ7 on bone strength or fracture risk is demonstrated in this age group. There is a growing awareness that maximizing bone strength at childhood is an important strategy to prevent osteoporosis at later age.”

Osteocalcin – the potent protein
Osteocalcin is a protein responsible for utilization of calcium within bone tissue – it has the ability to bind calcium to the matrix of bones, which makes them stronger and less susceptible to fractures. Without sufficient amounts of vitamin K in the diet, or in cases of Vitamin K deficiency, inactive osteocalcin is not able to bind calcium properly, and thus the bones weaken and become fragile.

Strong bones – best investment for the future
Children have the greatest requirement for active osteocalcin and thus for K vitamins because bone tissue grows and develops most intensively during childhood and adolescence. The higher peak mass young bones achieve, the lower the risk of osteoporotic changes in the elderly. Hence, the optimal pubertal status of bone is important to prevent disorders in later life.

Benefits scientifically proven
Results of the new study clearly confirm outcomes of previous laboratory experiments, population-based (i.e., epidemiological) studies and clinical trials that have tightly linked better vitamin K status in children to the achievement of a healthy, strong bone-structure. Simplified, improving vitamin K status in children results in stronger and denser bones. Additional K vitamins intake might also improve bone geometry and positively influence gain in bone mass. That contributing effect has been recently reported by O’Connor et al , who, while conducting a study in a cohort of 223 healthy girls (11-12 years old), found better K vitamin status related to higher bone mineral density.

Warfarin, a commonly prescribed blood-thinning medication, inhibits vitamin K activity. A study of children with long-standing vitamin K deficiency induced by this drug were shown to have a significantly reduced bone mass, which illustrates the potential consequences of K vitamins deficiency in growing bones.

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Pure Scientific’s E3MV for Children is the first kids multi-vitamin to include the therapeutic dose of 45cmg ofVitamin K2 (MK-7) for health bones and cardiovascular health.  Learn more here:  E3MV.

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Study Strengthens Vitamin K1’s Heart Benefits

October 24th, 2011 by Admin No comments »

Abstract

Background: Coronary artery calcification (CAC) is an independent predictor of cardiovascular disease. A preventive role for vitamin K in CAC progression has been proposed on the basis of the properties of matrix Gla protein (MGP) as a vitamin K–dependent calcification inhibitor.

Objective: The objective was to determine the effect of phylloquinone (vitamin K1) supplementation on CAC progression in older men and women.

Design: CAC was measured at baseline and after 3 y of follow-up in 388 healthy men and postmenopausal women; 200 received a multivitamin with 500 ?g phylloquinone/d (treatment), and 188 received a multivitamin alone (control).

Results: In an intention-to-treat analysis, there was no difference in CAC progression between the phylloquinone group and the control group; the mean (±SEM) changes in Agatston scores were 27 ± 6 and 37 ± 7, respectively. In a subgroup analysis of participants who were ?85% adherent to supplementation (n = 367), there was less CAC progression in the phylloquinone group than in the control group (P = 0.03). Of those with preexisting CAC (Agatston score > 10), those who received phylloquinone supplements had 6% less progression than did those who received the multivitamin alone (P = 0.04). Phylloquinone-associated decreases in CAC progression were independent of changes in serum MGP. MGP carboxylation status was not determined.

First published April 22, 2009, doi: 10.3945/?ajcn.2008.27338 Am J Clin Nutr June 2009 vol. 89 no. 6 1799-1807

Full text article available at no charge: http://www.ajcn.org/content/89/6/1799.abstract.

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Diet Soda Linked to Stroke, Myocardial Infarction & Vascular Death

October 21st, 2011 by Admin No comments »

Soda with line through itFebruary 9, 2011 (Los Angeles, California) — Diet soda may not be the healthier alternative many had hoped. A new study suggests that the popular drinks may increase the risk for stroke, myocardial infarction, and vascular death.

“People who had diet soda every day experienced a 61% higher risk of vascular events than those who reported drinking no soda,” lead investigator Hannah Gardener, ScD, an epidemiologist from the University of Miami Miller School of Medicine in Florida, told reporters attending a news conference here at the International Stroke Conference.

The risk persisted after controlling for metabolic syndrome, peripheral vascular disease, and cardiac disease history (relative risk, 1.48; 95% confidence interval, 1.03 – 2.12).

“This is the first report of this association,” said American Stroke Association national spokesperson Larry Goldstein, MD. “I think that it’s always good to do things in moderation. People should look at this information and consider it in the context of their other risk factors.”

The researchers looked at more than 2500 people from the multiethnic Northern Manhattan Study. Participants were asked to report how much and what kind of soda they drank.

During an average follow-up of 9.3 years, 559 vascular events occurred, including ischemic and hemorrhagic stroke.

The researchers also observed a marginally significant increased risk for vascular events among those who consumed diet soda daily and regular soda once or more a month (adjusted relative risk, 1.74; 95% confidence interval, 0.96 – 3.16).

As reported by Medscape Medical News, previous studies have suggested a link between diet soda consumption and the risk for metabolic syndrome and diabetes. But this is the first time diet drinks have been associated with vascular events.

“This is an observational study and not a prospective randomized trial,” Dr. Goldstein, from the Duke Stroke Center, in Durham, North Carolina, pointed out. “This is an association and not yet a proven causal relationship.”

The investigators acknowledge that additional studies are needed. The potential mechanisms for the association between diet soda and vascular events remain unknown.

What should clinicians advise patients on the basis of the information we have today? Steven Greenberg, MD, from Harvard Medical School in Boston, Massachusetts, suggests that patients start by concentrating on a healthy diet and regular exercise. “Once the metabolic syndrome is under control and any risk of diabetes, then we can consider cutting back on soda consumption.” Dr. Greenberg is the vice chair of the International Stroke Conference Committee, and during an interview he suggested that patients shouldn’t rush to eliminate diet drinks.

“I do think this is a wake-up call, though,” he said, “and we need to start paying closer attention.”

This study was funded by the Javits award from the National Institute of Neurological Disorders and Stroke and the Evelyn McKnight Brain Institute. The researchers have disclosed no relevant financial relationships.

American Stroke Association International Stroke Conference. Abstract # P55. News conference February 9, 2011.

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Diet Appears to Modulate Alzheimer’s Biomarker

June 20th, 2011 by Admin No comments »

June 17, 2011 — Results of a new study provide more evidence that diet may modulate the risk for Alzheimer’s disease.

In a 4-week diet intervention study, healthy cognitively intact older adults who stuck to a low-saturated-fat, low-glycemic-index diet experienced decreases in cerebrospinal fluid (CSF) levels of ?-amyloid 42, a biomarker of Alzheimer’s disease risk.

But in a group of older adults with amnestic mild cognitive impairment (aMCI), the healthy diet had the opposite effect, raising CSF levels of this protein.

These observations “made sense to us,” Suzanne Craft, PhD, of the Veterans Affairs Puget Sound Health Care System in Seattle, Washington, who worked on the study, told Medscape Medical News.

“That’s because in patients with Alzheimer’s disease,” she explained, “?-amyloid 42 sticks in the brain and so levels are lower in the CSF, and something that is going to reverse that process is going to raise levels in the spinal fluid.”

“But for a healthy adult,” she said, “it looks like levels get higher and higher over the course of life until, for some people, they reach a tipping point where [?-amyloid 42] begins to stick in the brain. In healthy adults, having levels decrease is actually a healthy pattern.”

“It looks like a healthy diet that contains a lot of fruits and vegetables and healthy fats would be important for people who have Alzheimer’s disease or conditions that put them at risk for developing Alzheimer’s disease,” Dr. Craft said.

The study appears in the June issue of the Archives of Neurology.

Mounting Evidence That Diet Matters to the Brain

There is a “fair amount” of evidence starting to accrue in the epidemiologic literature looking at what patterns of diet seem to both be protective and alternatively place someone at greater risk for Alzheimer’s disease, Dr. Craft noted.

“That evidence,” she said, “is suggesting that a diet like the Mediterranean diet seems to have a protective effect and a diet that has a lot of saturated fat and sugar seems to place you at greater risk.”

“Those studies are very important for setting the stage, but what’s different about our study is that we actually placed people on a very specific diet and provided every piece of food that they ate for an entire month,” the researcher said.

The high-saturated-fat/high-glycemic-index diet included 45% fat (25% saturated fat), 35% to 40% carbohydrates (glycemic index > 70), and 15% to 20% protein. The low-saturated-fat/low-glycemic-index diet included 25% fat (< 7% saturated fat), 55% to 60% carbohydrates (glycemic index < 55), and 15% to 20% protein.

Participants included 20 healthy adults with a mean age of 69.3 years and 29 adults with aMCI and a mean age of 67.6 years. For 4 weeks, 24 participants followed the high-fat diet (9 healthy adults and 15 with aMCI) and 25 followed the low-fat diet (11 healthy adults and 14 with aMCI).

The number of times participants were nonadherent to their assigned diet was “small and comparable among groups,” the authors note. The mean nonadherent incidents per week ranged from 1.23 to 1.80 per group.

Effects on ?-amyloid “Striking”

As expected, in both groups, the high-fat diet produced unhealthy changes in serum cholesterol and insulin profiles, while the low-fat diet produced healthy changes in these measures.

Notably, the investigators say, the 4-week diet intervention had “striking effects” on ?-amyloid 42 concentrations in CSF, the primary outcome measure, and the effects differed by diet and by cognitive status.

In the healthy adults, the high-fat diet increased CSF ?-amyloid 42 levels, essentially moving them “in a direction that may characterize a presymptomatic stage of Alzheimer’s disease before plaque deposition,” the investigators note in their report. The high-fat diet also increased concentrations of the oxidative stress marker F2-isoprostane and lowered insulin levels.

Conversely, in the participants with aMCI, ?-amyloid 42 levels were nearly unchanged by the high-fat diet, “possibly because more extreme intervention is needed to exacerbate already-extant pathologic processes,” the investigators suggest.

The low-fat diet had beneficial effects in both the healthy participants and the participants with aMCI.

In the aMCI group, it increased ?-amyloid 42 concentrations in the CSF, contrary to the pathologic pattern of lowered CSF ?-amyloid 42 typically observed in Alzheimer’s disease.

In the healthy adults, the healthy diet decreased CSF ?-amyloid 42 levels, which may help move them away from the “tipping point” that corresponds with the start of ?-amyloid brain deposition, leading eventually to cognitive impairment.

In both groups, the low-fat diet reduced F2-isoprostane concentrations; increased apolipoprotein E, which aids with ?-amyloid clearance; and was associated with improved delayed memory, a hallmark cognitive deficit in aMCI and Alzheimer’s disease.

In their paper, the researchers say their study provides “converging support” for recent epidemiologic investigations of dietary patterns and Alzheimer’s disease risk.

The results, they conclude, support further investigation into the “possibility that consumption of a diet high in saturated fat and simple carbohydrates may contribute to pathologic processes in the brain that increase the risk of Alzheimer’s disease, while a diet low in saturated fat and simple carbohydrates may offer protection against dementia and enhance brain health.”

The study was supported by grants from the National Institute on Aging and by funding from the Nancy and Buster Alvord Endowment. The authors have no disclosed no relevant financial relationships.

Arch Neurol. 2011;68:743-752. Abstract

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Early Childhood Diet Linked to IQ

May 16th, 2011 by Admin No comments »

A diet high in fats, sugars, and processed foods in early childhood may result in lower IQ scores, while a diet rich in healthy foods packed with vitamins and nutrients may work in reverse, suggests new research.

The study, published in BMJ’s Journal of Epidemiology and Community Health, reports a “weak but novel” association between dietary patterns in early childhood, and general intelligence assessed at eight and a half years of age.

The results of the study suggest that the eating habits in early childhood – particularly up until the age of three – may play a role in shaping the development of the brain, and thus affect behaviour, learning performance and IQ in later life.

“In this population of contemporary British children, a poor diet, associated with increased intake of processed foods, fat and sugar, in early childhood may be associated with lower IQ at the age of 8.5 years. In addition, a concurrent healthy diet may be associated with higher IQ,” said the researchers, led by Dr Kate Northstone from the Department of Social Medicine at the University of Bristol, UK.

The importance of healthy diets

Commenting on the new study, Barbara Gallani director of food safety and science at the UK’s Food and Drink Federation told FoodNavigator that it would not be surprising if a healthy, balanced diet is important in IQ development, “just like it is generally for children’s health and growth.”

She added that it is important for everyone, not just children, to eat a wide variety of foods, noting that it is possible eat a healthy diet and still include some ‘treat’ foods.

Gallani said that food manufacturers are leading the way when it comes to providing clear labelling on foods, as well as changing recipes to make old favourites healthier, which “makes it even easier for parents to choose a balanced diet that’s right for their families.”

An intelligent diet

Northstone and her colleagues noted that previous research investigating possible associations between nutrition and IQ in children have tended to focus on the use of dietary supplements or on intakes of specific nutrients.

For example, several studies have examined the effects of vitamin supplementation on IQ in children, with mixed results.

However, the authors said that studies investigating the long-term effects of nutrition on intelligence are sparse and conflicting. “In particular …there appears to be little known about the effects of the diet in early childhood on general intelligence later in life,” they said.

“We do not eat foods in isolation, rather consuming combinations of foods in meals and snacks,” explained the authors.

“Assessing dietary patterns as opposed to individual foods or nutrients allows to us take into account these intercorrelations, which may otherwise be overlooked,” they said.

The new cross sectional study, based on the Avon Longitudinal Study of Parents and Children (ALSPAC), examined the links between dietary patterns through early and mid-childhood (3 to 8.5 years) and IQ assessed at 8.5 years of age.

Study details

The researchers measured dietary patterns using principal-components analysis (PCA), which provide overall summaries of dietary intake. The diet data, measured at the ages of 3, 4, 7 and 8.5 was then examined for any associations between diet and IQ in nearly 4,000 children.

Three consistent dietary patterns were found from PCA at each time point: a ‘processed’, ‘traditional’ and ‘health conscious’ pattern.

The ‘processed’ pattern was illustrated by foods containing high fat and sugar content and by higher intakes of processed and convenience foods. The ‘traditional’ pattern was associated with consumption of generally home cooked meat, poultry, potato and vegetables, whilst the ‘health-conscious’ pattern was predominantly made up from high intakes of salads, fruit, vegetables, fish, pasta and rice.

“On minimal adjustment, all dietary pattern scores were associated with IQ with the exception of the ‘traditional’ pattern,” said the authors.

Before adjustment for confounding factors (such as parental influence, social and economic status, and other environmental factors) the researchers observed that the ‘processed’ food pattern was negatively associated with IQ at all ages, while the ‘health-conscious’ pattern at all ages were positively associated with IQ.

However, after adjustment for a wide variety of potential confounding factors, they reported that many associations between IQ and dietary pattern were lost, and those that remained (‘processed’ pattern at three years and ‘health-conscious’ patterns at 8.5 years) “were markedly attenuated”, according to the authors.

For the remaining relationships (after full adjustment) the ‘processed’ food pattern at 3 years was found to be such that a one point increase in the PCA score resulted in an almost two-point decrease in IQ at 8.5 years. Whilst the ‘health-conscious’ pattern was associated with an increased in IQ of 1.20 points per one point increase in PCA pattern score.

Interpretation

Northstone and colleagues said that the results of the study suggest a more “long-term effect of diet on the child’s ability to ‘learn’,” they noted that this could be in part be explained by favourable growth of the brain in early childhood – They noted that it is known that the brain grows at its fastest rate during the first 3 years of life.

“Studies have shown that head growth during this time is associated with cognitive outcome, and it is possible that good nutrition during this early period may encourage optimal brain growth,” said the authors.

However, they added that given the levels of attenuation seen in the effect sizes when adjusted for confounding factors, “we cannot exclude the possibility of residual confounding.”

Source: Journal of Epidemiology and Community Health
Published online ahead of print, doi: 10.1136/jech.2010.111955
“Are dietary patterns in childhood associated with IQ at 8 years of age? A population-based cohort study”
K. Northstone, C. Joinson, P. Emmett, A. Ness, T. Paus

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Low Vitamin D in Kids Associated with Insulin Resistance

May 16th, 2011 by Admin No comments »

Children with low serum vitamin D levels are at risk for diabetes and increasing insulin resistance, according to a new study published online ahead of print, Feb. 22, in the Archives of Disease in Childhood journal.

Researchers from the Children’s Hospital of Philadelphia (CHOP) looked at the relationship between serum 25-hydroxyvitamin D (25-OH-D) and fasting glucose, insulin and insulin sensitivity in obese and non-obese children. The cross-sectional design involved 85 kids age four to 18 years from the local community and sleep center. Researchers measured the fasting blood glucose, insulin and 25-OH-D levels of these children, and calculated insulin resistance using homeostasis model assessment (HOMA). In addition, they measured body-mass index (BMI-z) standard deviation and determined pubertal stage of the children.

Median vitamin D levels were 52 nmol/l, with 26 percent of subjects showing sufficient D levels (higher than 70 nmol/l), 27 percent having intermediate levels (50 to 75 nmol/l) and 47 percent having insufficient (25 to 50 nmol/l) or “frankly deficient” 25-OH-D levels (under 25 nmol/l). In the multivariate model used to determine the association of vitamin D levels with HOMA, children older in age, with higher BMI-z and of African-American race were all negatively associated with 25-OH-D levels—summertime saw slight increases in D levels among these children. Overall, lower D levels were associated with higher fasting blood glucose, insulin and HOMA after adjusting for puberty and BMI-z.

Researchers concluded low 25-OH-D levels are common in children, putting them at risk for diabetes and increasing insulin resistance.

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Study: Being Overweight in Mid-Life Linked to Dementia

May 13th, 2011 by Admin No comments »

Being overweight or obese in midlife increases the risk for dementia independent of a history of diabetes and vascular disease, a new study suggests.

overweight on the scaleGiven that 1.6 billion adults around the world are overweight, the study results highlight the need to control body weight, at least in midlife, to prevent dementia later on, the researchers say.

“Several studies have already shown an association between midlife obesity and dementia, but for overweight, the association has been controversial,” said lead author Weili L. Xu, MD, PhD, a postdoctoral researcher in the Aging Research Center, Karolinska Institute, Stockholm, Sweden. “But from this twin study, we demonstrated that both overweight and obesity increases the risk of dementia in later life.”

The study was published in the May 3 issue of Neurology.

Swedish Twin Registry

The study used data from the nationwide Swedish Twin Registry. Between 1998 and 2001, twins in this registry age 65 years and older were invited to participate in the research. Of these, 13,723 twins completed cognitive screening tests and 8534 were included in this study.

The protocol included a neuropsychological assessment, including the Mini Mental State Examination (MMSE). Researchers calculated body mass index (BMI) at midlife (mean age, 43.4 years) using self-reported weight in kilograms divided by self-reported height in meters squared and categorized BMI into 4 groups: underweight (BMI < 20), normal weight (20-25), overweight (26-30), and obese (>30).

Dementia was diagnosed in 350 of the 8534 participants (4.1%), including 232 with Alzheimer’s disease and 74 with vascular dementia; 114 (1.3%) had what was considered questionable dementia.

Compared with those without dementia, twins with confirmed or questionable dementia were older; had lower levels of education and current BMI; and were more likely to have diabetes, stroke, and heart disease.

The study showed a strong link between dementia and midlife BMI. In the model adjusted for age, sex, education, diabetes, hypertension, stroke, and heart disease, both overweight and obesity at midlife were associated with increased dementia risk compared with normal BMI.

Risk for Dementia Associated With Midlife Overweight and Obesity

Group Odds Ratio (95% CI)
Overweight 1.71 (1.30 – 2.25)
Obesity 3.88 (2.12 – 7.11)

CI = confidence interval

In this study, 29.8% (2541) of the twins were overweight or obese at midlife, a percentage much lower than the over 50% who are currently considered overweight or obese in the United States and Europe. This, said Dr. Xu, is because the data are from 30 years ago, before the global obesity epidemic.

Dementia-Discordant Twins

In a matched case-control analysis of 137 dementia-discordant twin pairs, the association of midlife overweight and obesity with dementia was no longer significant. A comparison of high BMI among the unmatched and matched controls showed a statistically significant difference (odds ratio, 1.62; 95% confidence interval, 1.12 – 2.66; P = .019).

Because twins share the same genes and early life environment, these 2 factors might help explain the link between body weight and dementia, said Dr. Xu.

In the case of only 1 twin developing dementia, that sibling might have been exposed to a trigger in early life that turned on a gene that increased the risk for obesity or dementia, she added. Dr. Xu and her colleagues have shown that the FTO gene, for example, is associated with both obesity and Alzheimer’s disease.

In addition to the contribution of genes, the link between body fat and dementia could involve a vascular pathway, said Dr. Xu. “High body fat is associated with diabetes and vascular disease, which in turn are related to dementia risk.” However, this study controlled for lifespan vascular disease, suggesting that the pathway may be nonvascular.

If that’s the case, the pathway may involve metabolism. High adiposity is associated with an altered metabolic status, including hyperglycemia, hyperlipidemia, and high blood pressure. This can contribute to the metabolic syndrome, which other studies have linked to cognitive decline, said Dr. Xu.

Or, the association could also involve a hormonal pathway or inflammation, said Dr. Xu. “Adipose tissue is the largest endocrine organ and it secretes inflammatory cytokines and growth hormones such as interleukin-6 and C-reactive protein, and also leptin, which is associated with obesity.”

Whatever the mechanism, the important message is that overweight and obese people need to lose weight. Dr. Xu emphasized that even though the study looked at midlife body weight, “it’s never too late” to shed excess pounds.

She added that physical activity can reverse the risk for dementia due to obesity. “This is part of our ongoing study, but preliminary results already show that if you do more physical activity, you can reduce your risk of dementia.”

Association, Not Causation

Asked to comment on this research, John Hart, MD, professor of neurology, Southwestern Medical Center, Dallas, Texas, and member of the American Academy of Neurology, emphasized that the study shows correlation between obesity and dementia and does not prove cause and effect. He noted that other studies have not found a positive association between obesity and dementia.

Dr. Hart also speculated whether the association between obesity and dementia would remain if obese people lost weight and got their blood pressure, blood glucose, and cholesterol under control.

He pointed out that the analysis didn’t include overweight people who did not live long enough to develop dementia because they died of a stroke or other vascular disease. “What would have happened to those people if they had lived long enough? That’s a sort of missing piece of the puzzle.”

As for the contribution of environmental factors, Dr. Hart agreed that twins share genes, but they don’t necessarily share the same experiences that might trigger a genetic reaction. For example, one twin may have had a severe infection or a head injury that the other twin didn’t.

Funded by the National Institute on Aging, the Swedish Research Councils, and the Swedish Brain Power. Also supported in part by funds from the Gamla Tjänarinnor, the Bertil Stohnes Foundation, the Demensfonden, the Loo and Hans Ostermans Foundation, and the Foundation for Geriatric Diseases at Karolinska Institute. Dr. Xu has disclosed no relevant financial relationships. For information on other authors, see original article.

Neurology. 2011;76:1568-1574. Abstract

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Girls’ Early Puberty: Causes & How to Avoid It

May 12th, 2011 by Admin No comments »

I’m posting this relevant article by Dr. Joel Furhman because of the much younger ages at which puberty starts.  Share this information with parents who can benefit from the tips near the end of the article.

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By Joel Fuhrman, MD

Today in the U.S., about 16% of girls enter puberty by the age of 7, and about 30% by the age of 8. A recent study determined that the number of girls entering puberty (defined by breast development) at these early ages has increased markedly between 1997 and 2010.[1]

Trends in Age at Menarche
The average age at menarche in Western countries began declining during the early part of the 20th century due to increased consumption of animal products and increasing calorie intake; the decline slowed in the 1960s, and now in the U.S. there has been a more recent surge in early puberty starting in the mid-1990s.[2]

In Europe, in 1830, the average age at menarche was 17. Similarly in the 1980s in rural China, the average age at menarche was 17.3 In the U.S. in 1900, the average was 14.2. By the 1920s, average age at menarche in the U.S. had fallen to 13.3 and by 2002, it had reached 12.34.[4] Similar trends are occurring in other Western nations.[5,6] For example, age at menarche in Ireland has declined from 13.52 in 1986 to 12.53 in 2006.[7] In Italy, a recent study showed that girls’ age at menarche was on average 3 months earlier than their mothers’.[8]

Taking all this data together, we can estimate that the normal, healthy age at menarche under conditions of excellent nutrition without caloric excess would probably fall somewhere between 15 and 18. But today in the U.S., about half of girls begin developing breasts before age 10, and the average age at menarche is less than 12 ½ and still declining.

Why Is this happening?
The neurological and hormonal systems that regulate pubertal timing are complex, but research has identified a number of environmental factors that may be contributing to the decline in age at puberty:

Increasing rates of childhood overweight and obesity
Several studies have found associations between higher childhood BMI and earlier puberty in girls.[4,9-11] Excess body fat alters the levels of the hormones insulin, leptin, and estrogen, and these factors are believed to be responsible for the acceleration of pubertal timing by obesity. Also, physical inactivity may decrease melatonin levels, which can also affect signals in the brain that trigger pubertal development.[4, 12]

Increased animal protein intake
Higher total protein, animal protein, and meat intake in children age 3-7 have been associated with earlier menarche in multiple studies.[13-15] In contrast, higher vegetable protein intake at age 5-6 is associated with later menarche.[15] High protein intake elevates IGF-1 levels and promotes growth, which could accelerate the onset of puberty – IGF-1 contributes to pubertal development on its own and in part by its involvement in estradiol signaling.[4,16] Meat and dairy consumption in children may also reflect ingestion of environmental endocrine-disrupting chemicals (EDCs) that have accumulated in animal tissues (see EDCs below).

Other dietary factors:
High dairy consumption is associated with earlier than average menarche.[17] Soft drink consumption is associated with early menarche.[18]

Children with lower nutrient diets (based on analysis of macronutrients, vitamins, minerals, and certain whole foods) tend to enter puberty earlier.[19] Overall our modern diet rich in processed foods, dairy, processed meats and fast food is disruptive to normal development and aging. Early puberty is an early sign of premature aging.

Exposure to endocrine-disrupting chemicals (EDCs)
EDCs are hormonally active synthetic chemicals that either mimic, inhibit, or alter the action of natural hormones. These chemicals are ubiquitous in our environment, and are considered by scientists to be a significant public health concern. Although EDCs are thought to pose a threat to adults as well, children’s bodies are more sensitive to exposure to exogenous hormones.[20]

Chemicals are not currently tested for their endocrine disruption potential before they are approved for use and enter our environment, and there are endocrine disruptors in a vast array of products we come into contact with every day, including organochlorine pesticides, plastics, fuels, and other industrial chemicals.[21]

The substances of most concern currently are BPA and phthalates. BPA is one of the highest volume chemicals produced in the world. It is used in the manufacture of polycarbonate plastics, such as rigid cups, water bottles and food storage containers; BPA is also found in the linings of food cans and dental sealants. BPA can leach from containers into food and beverages, especially during heating and washing.[4] BPA exposure is associated with early puberty in girls.[22]

Phthalates are chemicals used to make PVC plastics more flexible, and are found in a variety of products including toys, food packaging, hoses, raincoats, shower curtains, vinyl flooring, wall coverings, lubricants, adhesives, detergents, nail polish, hair spray, and shampoo. Phthalates are associated with early breast development in girls.[22, 23] They are considered chemicals of concern to the EPA and may be phased out — some phthalates have already been removed from children’s toys and cosmetics. [24]

Additional EDCs that have been associated with dysregulation of pubertal timing include industrial chemicals such as PCBs, pesticides such as DDT and endosulfan, the flame retardant PBB, and dioxins and furans, which are formed during incineration of waste, chlorine bleaching of paper, and chemical manufacturing. [22,23,25,26]

It is important to note that EDCs break down very slowly and accumulate in the fatty tissues of animals, so animal foods contain higher levels of these chemicals than plant foods.

Why is this troublesome?
The most significant and alarming consequence of early maturation is an increased risk for breast cancer in adulthood. Early menarche is an established risk factor for breast cancer, and this is believed to be due to the extended lifetime exposure to ovarian hormones.[10,27,28] Similarly, exposure to EDCs during childhood is associated with hormonal cancers, such as breast and testicular cancers.[29-31]

Girls of 7, 8 or 9 years old are not emotionally or psychologically equipped to handle puberty. As such, earlier puberty is also associated with a higher risk of psychological problems during adolescence such as anxiety, depression, and eating disorders. Girls who mature earlier are also more likely to take part in risky behaviors like smoking and alcohol use.[4,12]

What can parents do to protect their children?

  • Children’s diets should focus on whole plant foods rather than animal foods — this will keep protein intake in a safe range and reduce their consumption of EDCs.


  • Minimize dairy products in children’s diets — use almond and hemp milks instead of cows’ milk


  • Encourage children to exercise and exercise with them.


  • Minimize processed foods — these are calorie-dense and nutrient-poor, and they promote obesity and other diseases.


  • Children’s diets should include a wide variety of natural plant foods as possible including, green vegetables, squashes, corn, carrots, tomatoes, onions, mushrooms, nuts, seeds, avocados, beans, fruits and whole grains. This means that healthy eating is a lifetime event.


  • Buy organic produce when possible to avoid synthetic pesticides.


  • Minimize children’s exposure to BPA: Avoid using of rigid polycarbonate plastics (recycling label #7) whenever possible; Do not use plastic water bottles if they are old or scratched; Do not microwave in plastic containers; Minimize the use of canned foods and avoid canned infant formulas.32


  • Minimize children’s exposure to phthalates:Avoid plastics marked with recycling label #3 (PVC) whenever possible; Check ingredient lists on personal care products for phthalates. Also be aware that “fragrance” listed as an ingredient often means that the products contains phthalates. For more information, visit the Environmental Working Group’s guide to children’s personal care products.

To conclude, the earlier occurrence of puberty is an ominous event that we can stop. We can even win the war on breast cancer in America and prevent millions of young females from developing it. The answer however, must begin in the way we feed ourselves and our children. The most effective type of health care is vigilant and excellent self care.


References:
1. Biro FM, Galvez MP, Greenspan LC, et al: Pubertal Assessment Method and Baseline Characteristics in a Mixed Longitudinal Study of Girls. Pediatrics 2010.
2. Biro FM, Khoury P, Morrison JA: Influence of obesity on timing of puberty. Int J Androl 2006;29:272-277; discussion 286-290.
3. Gates JR, Parpia B, Campbell TC, et al: Association of dietary factors and selected plasma variables with sex hormone-binding globulin in rural Chinese women. Am J Clin Nutr 1996;63:22-31.
4. Steingraber S: Tha Falling Age of Puberty in U.S. Girls: What We Know, What We Need To Know. In Breast Cancer Fund; 2007.
5. McDowell MA, Brody DJ, Hughes JP: Has age at menarche changed? Results from the National Health and Nutrition Examination Survey (NHANES) 1999-2004. J Adolesc Health 2007;40:227-231.
6. Anderson SE, Must A: Interpreting the continued decline in the average age at menarche: results from two nationally representative surveys of U.S. girls studied 10 years apart. J Pediatr 2005;147:753-760.
7. O’Connell A, Gavin A, Kelly C, et al: The mean age at menarche of Irish girls in 2006. Ir Med J 2009;102:76-79.
8. Rigon F, Bianchin L, Bernasconi S, et al: Update on age at menarche in Italy: toward the leveling off of the secular trend. J Adolesc Health 2010;46:238-244.
9. Aksglaede L, Juul A, Olsen LW, et al: Age at puberty and the emerging obesity epidemic. PloS one 2009;4:e8450.
10. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.
11. Kaplowitz PB: Link between body fat and the timing of puberty. Pediatrics 2008;121 Suppl 3:S208-217.
12. Burt Solorzano CM, McCartney CR: Obesity and the pubertal transition in girls and boys. Reproduction 2010;140:399-410.
13. Berkey CS, Gardner JD, Frazier AL, et al: Relation of childhood diet and body size to menarche and adolescent growth in girls. Am J Epidemiol 2000;152:446-452.
14. Rogers IS, Northstone K, Dunger DB, et al: Diet throughout childhood and age at menarche in a contemporary cohort of British girls. Public Health Nutr 2010:1-12.
15. Gunther AL, Karaolis-Danckert N, Kroke A, et al: Dietary protein intake throughout childhood is associated with the timing of puberty. J Nutr 2010;140:565-571.
16. Veldhuis JD, Roemmich JN, Richmond EJ, et al: Endocrine control of body composition in infancy, childhood, and puberty. Endocr Rev 2005;26:114-146.
17. Wiley AS: Milk intake and total dairy consumption: associations with early menarche in NHANES 1999-2004. PloS one 2011;6:e14685.
18. Vandeloo MJ, Bruckers LM, Janssens JP: Effects of lifestyle on the onset of puberty as determinant for breast cancer. Eur J Cancer Prev 2007;16:17-25.
19. Cheng G, Gerlach S, Libuda L, et al: Diet quality in childhood is prospectively associated with the timing of puberty but not with body composition at puberty onset. J Nutr 2010;140:95-102.
20. Aksglaede L, Juul A, Leffers H, et al: The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Hum Reprod Update 2006;12:341-349.
21. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, et al: Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev 2009;30:293-342.
22. Roy JR, Chakraborty S, Chakraborty TR: Estrogen-like endocrine disrupting chemicals affecting puberty in humans–a review. Med Sci Monit 2009;15:RA137-145.
23. Den Hond E, Schoeters G: Endocrine disrupters and human puberty. Int J Androl 2006;29:264-271; discussion 286-290.
24. Chemical Families: Phthalates. In Environmental Working Group.
25. Schell LM, Gallo MV: Relationships of putative endocrine disruptors to human sexual maturation and thyroid activity in youth. Physiol Behav 2010;99:246-253.
26. Massart F, Parrino R, Seppia P, et al: How do environmental estrogen disruptors induce precocious puberty? Minerva Pediatr 2006;58:247-254.
27. Leung AW, Mak J, Cheung PS, et al: Evidence for a programming effect of early menarche on the rise of breast cancer incidence in Hong Kong. Cancer Detect Prev 2008;32:156-161.
28. Pike MC, Pearce CL, Wu AH: Prevention of cancers of the breast, endometrium and ovary. Oncogene 2004;23:6379-6391.
29. Cohn BA, Cirillo PM, Christianson RE: Prenatal DDT exposure and testicular cancer: a nested case-control study. Arch Environ Occup Health 2010;65:127-134.
30. Cohn BA, Wolff MS, Cirillo PM, et al: DDT and breast cancer in young women: new data on the significance of age at exposure. Environ Health Perspect 2007;115:1406-1414.
31. Maffini MV, Rubin BS, Sonnenschein C, et al: Endocrine disruptors and reproductive health: the case of bisphenol-A. Mol Cell Endocrinol 2006;254-255:179-186.
32. Consumer tips to avoid BPA exposure. In Environmental Working Group.

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The Promise of the Red Wine Polyphenol Stent

May 11th, 2011 by Admin No comments »

‘Red-Wine’ Polyphenol Stent Shows Promise

By Reed Miller

April 29, 2011 (Chicago, Illinois) — Polyphenols found in red wine may one day be used in antirestenosis compounds for drug-eluting stents, results of early trials in animals suggest [1].

At the American Heart Association Arteriosclerosis, Thrombosis and Vascular Biology 2011 Scientific Sessions, PhD-candidate Jim Kleinedler (Louisiana State University Health Sciences Center, Shreveport, LA) presented data that showed a “red-wine” polyphenol-eluting stent reduces neointimal hyperplasia and promotes reendothelialization in a rat model of angioplasty.

Previous research has shown that resveratrol, found in the skin of red grapes and in high concentrations in red wine, reduced restenosis, accelerated reendothelialization, and reduced inflammatory cell activation in animals. Earlier studies have also shown that quercetin, also found in wine grapes, is a strong antioxidant that inhibits platelet activation and vascular smooth-muscle-cell proliferation, Kleinedler explained.

Data from drug-eluting-stent trials suggest the antiproliferative compounds loaded onto the stents inhibit smooth-muscle-cell proliferation but also act nonselectively in the vessel wall and delay the reformation of functional endothelium. “By delaying or prolonging that endothelialization, you can increase the risk of thrombosis, so part of the impetus for our research stemmed from that dichotomy. We need something that’s going to inhibit restenosis but still promote reendothelialization, and we were encouraged by the vascular protective effects of red-wine polyphenols,” said Kleinedler. “You’d have to give a lot of these polyphenols orally to see an effect after a local injury like that, but by providing local delivery we can achieve high concentrations directly at the time of injury.”

Current drug-eluting stents “are still limited as far as pharmacologic targets. These polyphenols may lead us to explore other targets because they are hitting so many different things . . . that increase reendothelialization,” he said.

In collaboration with Nanocopoeia (St Paul, MN), Kleinedler’s group implanted stents loaded with their polyphenol compound into the carotid arteries of rats. The study compared the endothelial cell proliferation of rats treated with a high-dose version of the stent, a low-dose version, a bare-metal stent, or no stent. The results showed that local, stent-based delivery of both the low- and high-dose polyphenol compound promoted faster reendothelialization after stenting injury compared with bare-metal stents. The rat study also showed that the polyphenols migrated to the site of injury faster than the rates shown for drug coatings in previous studies. Resveratrol was also found to promote endothelial cell wound closure under laminar shear stress.

Kleinedler owns a stake in this technology’s intellectual property. Disclosures for the coauthors are listed in the abstract.

References

  1. Kleinedler J, Foley JD, Hebert V, et al. Red wine polyphenol-eluting stent reduces neointimal hyperplasia and promotes re-endothelialization in a rat model of stenting angioplasty. American Heart Association Arteriosclerosis, Thrombosis and Vascular Biology 2011 Scientific Sessions; April 29, 2011; Chicago, IL. Abstract 93.

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Forgiveness & Improved Immune Response

May 9th, 2011 by Admin No comments »

Could forgiveness lead to enough beneficial physiological change to improve immune function in people whose immune status is already compromised?

A new study conducted in people living with HIV shows individuals who truly forgave someone who had hurt them in the past showed positive changes in their immune status.

The study was presented here at the Society of Behavioral Medicine 32nd Annual Meeting and Scientific Sessions.

Amy Owen, PhD, Duke University Medical Center, Durham, North Carolina, found that greater forgiveness significantly correlated with higher CD4 cell percentages (P = .042). Unlike the CD4 cell count, which is a measure of how many functional CD4 T cells are circulating in the blood, the CD4 cell percentage represents the percentage of total lymphocytes that are CD4 cells.

In regression analyses, the relationship of forgiveness and CD4 cell percentages remained significant even when controlling for variables that could affect CD4 cell counts, including age, race, sex, level of education, years with HIV, adherence, substance use, and viral load (P = .034).

“We hypothesized that higher levels of forgiveness would be associated with higher CD4 cell percentages controlled for demographic and behavioral variables as well as viral load,” Dr. Owen told Medscape Medical News. “And none of these variables accounted for the relationship between forgiveness and CD4 cell percentages. So there is something special going on between forgiveness and CD4 cell counts.”

Beneficial Effect

The study involved 78 individuals living with HIV and receiving antiretroviral medications. Subjects had been taking anti-HIV medications for at least 1 year, and 67% of them had undetectable viral loads. Eighty-one percent were nonwhite. Medication adherence was assessed by calculating the mean number of missed doses during the past 4 days. Subjects were also asked about tobacco, alcohol, marijuana, and cocaine use.

Forgiveness was measured by the Enright Forgiveness Inventory, a tool that assesses positive and negative feelings, thoughts, behaviors, or imagined behaviors toward an individual who caused the subject hurt.

Dr. Owen also defined forgiveness strictly as being a freely made choice to move away from negative cognitive, emotional, and behavioral responses toward a person who caused a hurt and work towards developing positive cognitive emotional and behavioral responses toward that person.

“For my study, I compared the relationship of forgiveness of another person and CD4 cell percentages both without controlling for any other factors (using a bivariate correlation), and then I tested whether this relationship would hold up when I controlled for other possible factors linked to CD4 percentage levels that could account for an observed relationship between forgiveness and CD4 percentages (using a hierarchical linear regression).”

In bivariate correlations, results showed that greater forgiveness was significantly associated with higher CD4 percentages, whereas linear regression analyses found that this relationship remained significant after controlling for the potential influence of other factors.

“Results support our hypothesis and reflect previous findings on relationships of psychosocial factors with immune makers in people living with HIV/AIDS, and findings indicate that forgiveness of another person may be beneficial for their health,” said Dr. Owen.

Understanding Forgiveness is Key

She also noted that helping people who have been violated in the past come to a place of peace can be done, but it has to be done well.

“If psychiatrists want to counsel patients about forgiveness, they first need to understand very deeply what forgiveness is and what it is not,” she said. “If there isn’t a good therapeutic relationship between a physician and the patient, “what patients can hear from you when you are suggesting forgiveness is, ‘I don’t want to hear about it anymore and what’s wrong with you that you are not just fine with it.’ But that can be extremely violating and potentially retraumatize the person who has already been deeply hurt.”

It’s also very important to respect a patient’s anger, she added, because sometimes that is all a person has.

“If you threaten that by suggesting that the patient shouldn’t be so angry, it can be disrespectful, so if a psychiatrist wants to engage with a patient on the topic of forgiveness, it’s essential they understand the definitions of forgiveness and be willing to journey with that person over time. Patients will struggle with it; it’s not a linear process, but it is very transformative.”

Emotional Pain Common

Reverend Michael Barry, PhD, Cancer Treatment Centers of America, Philadelphia, Pennsylvania, told Medscape Medical News that unforgiveness is a state where a person retains negative emotions, including anger and hatred, for a perpetrator of harm.

“This creates a state of chronic anxiety, and chronic anxiety has a predictable impact on a wide range of bodily functions, including the reproductive system, the digestive system, and the immune system,” he said.

For example, stress hormones, including cortisol and adrenalin, have been shown to reduce the production of natural killer cells — the “foot soldiers” in the fight against cancer, he noted.

Dr. Barry’s own research has shown that almost two-thirds of cancer patients identified forgiveness as a personal issue for them, and 1 in 3 of them indicated they had severe forgiveness issues, “so we are aware of the emotional pain that many of our patients are in.

“There is a direct correlation between unforgiveness and our immune system, which directly affects our healing processes. We teach people what we have learned about the process of forgiveness in a short-term forgiveness intervention program that works,” he added.

Dr. Owen has disclosed no relevant financial relationships. Dr. Barry is the author of The Forgiveness Project. He also developed a forgiveness program, entitled Release! The Healing Power of Forgiveness.

Society of Behavioral Medicine (SBM) 32nd Annual Meeting and Scientific Sessions: Abstract 4010. Presented April 30, 2011.

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Why Vitamin D Supplementation in Children is Important

May 5th, 2011 by Admin No comments »

The Importance of Vitamin D Supplementation in ChildrenOverweight Boy Cropped

The majority of obese adolescents are vitamin D deficient, which increases their  risk of diabetes, hypertension, cancer, cardiovascular disease, according to new study published online ahead of print in the Journal of Adolescent Health.

Researchers at Hasbro Children’s Hospital who conducted the study also said vitamin D status is significantly associated with muscle power/force, and a deficiency may interfere with the obese adolescent’s ability to increase physical activity. They called for increased surveillance of vitamin D levels in adolescents and further studies to determine if normalizing vitamin D levels will help to lower the health risks associated with obesity.

The researchers examined the prevalence of low vitamin D status among 68 obese adolescents and examined the impact of treatment of low vitamin D status in the patients. They found low vitamin D status was present in all of the girls (72% deficient & 28% insufficient) and in 91 percent of the boys (69% & 22% insufficient).

Of those with vitamin D deficiency or insufficiency, 43 patients had a repeat measurement of vitamin D level after treatment. While there was a significant increase in vitamin D levels following treatment, serum vitamin D levels normalized in only 28% of the patients. Repeat multiple courses of vitamin D treatment in the patients who did not normalize their vitamin D levels after initial course, failed to normalize their low vitamin D status.

The researchers said the association between obesity and low vitamin D status also may be due to obese individuals having fewer outdoor activities than lean individuals and therefore, less sun exposure.

They also theorized obese adolescents don’t eat enough vitamin D-rich foods such oily fish, eggs and fortified dairy products and breakfast cereals.

Posted in these publications:  News, Science & Research, Children, Vitamin D, Vitamins/Minerals, Healthy, Diet, Nutrition, Cancer, Heart Health, Cardiovascular, Diabetes, Egg, Fortification, Dairy, Breakfast Cereal, Bakery / Cereal, Cereal, Fish, Seafood, Obesity, Weight Management

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Patented E3MV provides 600IU of natural Vitamin D3 (Cholecalciferol) – the most up-to-date and recently increased recommendation by the National Institutes of Medicine.  E3MV is dispensed to thousands of US public school children daily as part of a comprehensive program called Eat, Exercise, Excel.  Administrators report improved academic performance, behavior, fitness, less absenteeism and dramatic improvement in standardized testing by children participating in the Eat, Exercise, Excel program.

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FDA to Weigh if Food Dyes Make Kids Hyperactive

March 30th, 2011 by Admin No comments »

Link to original article:  http://www.msnbc.msn.com/id/42273578/ns/health-kids_and_parenting/

By Lisa Richwine, Reuters

updated 3/25/2011

WASHINGTON — U.S. regulators are weighing a question parents have asked since the 1970s: do artificial food dyes make children hyperactive?

A consumer group has petitioned the government to ban blue, green, orange, red and yellow food colorings. The synthetic dyes are common in food and drinks ranging from PepsiCo’s Gatorade, Cheetos and Doritos to Kellogg’s Eggo waffles and Kraft’s Jell-O desserts.

Manufacturers say reviews by regulators around the world confirm the dyes are safe. The Center for Science in the Public Interest argues, however, there is plenty of data showing the dyes trigger hyperactivity in kids who are predisposed to it.

“There is convincing evidence that food dyes impair the behavior of some children,” said Michael Jacobson, head of the consumer group famous for exposing the fat and calories in movie-theater popcorn and fast food.

Jacobson and others will testify next week before a Food and Drug Administration advisory committee that will consider the question on Wednesday and Thursday. The FDA will hear the advisers’ views before deciding whether to take any action, which could take months or years.

FDA reviewers, in documents prepared for the advisory panel, said scientific research so far suggested some children with attention deficit and hyperactivity disorder (ADHD) may be affected by food coloring. The disorder affects up to 5 percent of U.S. children, according to government statistics.

“For certain susceptible children with ADHD and other problem behaviors, the data suggest their condition may be exacerbated” by substances in food including artificial colors, the FDA staff wrote in a preliminary analysis.

For the general population, the FDA “concludes that a causal relationship” between the dyes and hyperactivity “has not been established,” the agency staff said.

At the panel meeting next week, the FDA will ask outside experts if they agree with the agency’s conclusions or if they think more studies are needed.

Concerns about food dyes erupted in the 1970s when a pediatrician, Dr. Ben Feingold, claimed the colors were linked to hyperactive behavior and proposed a diet eliminating them.

Questions flared again after a 2007 British study of kids who drank fruit drinks with food colorings and preservatives.

The scientists concluded the colorings worsened hyperactive behavior and also affected kids not previously diagnosed with ADHD.

Other researchers said the study had limitations. A 2009 review by European authorities concluded all data available at the time did not support a link between food colorings and hyperactivity.

The 2008 petition from CSPI asked the FDA to ban all but one of the dyes, calling them “dangerous and unnecessary.” The exception, Citrus Red No. 2, is used only on orange skins. Companies could substitute natural colors, fruit or fruit juices, CSPI said.

Poll: Should food dyes be banned?

The group also asked the FDA to require a warning on products containing dyes until a ban takes effect.

The Grocery Manufacturers Association, which represents food producers and packagers, said “extensive review” by the FDA and European authorities showed the dyes were safe.  “All of the major safety bodies globally have reviewed the available science and have determined that there is no demonstrable link between artificial colors and hyperactivity among children,” the group said in a statement.

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This comes 4 years after a landmark study published in the British Medical Journal “The Lancet” proving that artificial colors and additives result in increased hyperactivity (www.ncbi.nlm.nih.gov/pubmed/17825405).  This double blind placebo-controlled crossover study is referenced in Pure Scientific’s  “Ingredients You Won’t Find in E3MV.”

E3MV does not contain artificial colors, artificial flavors, artificial preservatives or non-nutritionally necessary ingredients to ensure optimal purity for children.  Additionally, the natural superfruit & berry blend in E3MV is subjective to over 30 tests for agricultural pesticides, herbicides and a full panel of heavy metals to create the most tested, clean and pure supplement for children.

To learn more about the natural purity, potency and results of E3MV, please click here:  E3MV – Patented Nutrition for Academic Success.

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Prescribing Self Care

March 29th, 2011 by Asst to Dr.S No comments »

PHYSICIANS INTERESTED IN LEARNING MORE ABOUT SUPPLEMENTS

A study has found 57 to 75% of physicians use dietary supplements; and 66 to 91% recommend supplements to their patients.

Most doctors indicated their medical education had not included any formal training on dietary supplements and expressed an interest in continuing education regarding these products.

The study included 300 cardiologists, 300 dermatologists and 300 orthopedists; the percentage of each specialty that took dietary supplements occasionally was 57, 75 and 73%, respectively; the percentage of each specialty that took supplements regularly was 37, 59 and 50%, respectively.

The most common supplement taken by physicians was a multivitamin. Over 25% of doctors in each specialty took omega-3 fatty acids and over 20 percent reported they used botanical supplements.

Patients were advised to take specific supplements by 72% of cardiologists, 66% of dermatologists and 91% of orthopedists.

The main reasons given for recommending supplements were for heart health; skin, nail & hair health; and bone & joint health.

Most of us view supplements as a form of “self care” – which the medical community is beginning to adopt in everyday practice.

This study was released March 3, 2011 and will be published in a future issue of Nutrition Journal. It is available online now at http://bit.ly/hjL5mx without charge.

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Link Between Cholesterol & Infections

March 29th, 2011 by Admin No comments »

LOWERING CHOLESTEROL MAY FIGHT INFECTIONS

A study has found that when the body becomes infected with a virus, an immune system hormone sends a signal to the blood cells to curb the production of cholesterol, a waxy substance required by bacteria and viruses in order to grow; this suggests that lowering cholesterol may prove effective in fighting viral infections.

According to the findings, the body appears to have a built-in mechanism to reduce cholesterol production when it detects a viral or bacterial infection. Therapies that boost this effect could the help the body’s natural, anti-virus defenses. Currently, antibiotics are used to target serious bacteria directly while cholesterol-lowering therapies would target cholesterol metabolism and therefore, work in the same way as the immune system. This would be the first example of protecting against acute infection by targeting a metabolic pathway. But the challenge may be to develop strategies that slash cholesterol quickly.

This study was published March 8, 2011 by the journal, PLoS Biology. It is available online now at http://bit.ly/ho6xDB without charge.

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