Joint guideline contains new recommendations for diabetes, CVD.


New guidelines on diabetes, prediabetes and CVD unveiled at the ESC Congress 2013 recommend diagnosis using HbA1c, less-strict BP targets and optimal use of revascularization.

The guidelines were developed as a collaboration between the ESC and the European Association for the Study of Diabetes (EASD).

“The growing awareness of the strong biological relationship between diabetes and CVD rightly prompted these two large organizations to collaborate to generate guidelines relevant to their joint interests, the first of which were published in 2007,” the statement reads.

Among the notable updates is the recommendation to use HbA1c for the diagnosis of diabetes. If HbA1c is elevated, the patient is diagnosed with diabetes; if not elevated, patients with CVD should receive an oral glucose tolerance test.

“We have simplified diagnosis because many patients may be disclosed with HbA1c, limiting the numbers who need the lengthier test. But a normal HbA1c does not rule out diabetes in high-risk patients, who need to have an oral glucose tolerance test,” ESC chairperson Lars Rydén, MD, PhD, of the cardiology unit at Karolinska Institute, Sweden, stated in a press release.

The guidelines also simplify CV risk assessment and no longer advocate the use of risk engines. “Risk engines which accumulate risk factors and produce a low-, medium- or high-risk score are less useful for patients with diabetes,” EASD chairperson Peter J. Grant, MD, from the division of cardiovascular and diabetes research at University of Leeds, U.K., stated in the release.

Patients with diabetes are considered at high CV risk. Patients with diabetes and CVD, including MI, angina or peripheral vascular disease, are considered at very high risk for recurrent CVD, according to the release.

Recommendations on revascularization have also changed since the previous guidelines. Medical therapy is now recommended before intervention for patients with stable CAD and no complex coronary lesions. “In former days, we were quick to do coronary interventions, but based on new trial data we now do not advocate bypass surgery and coronaryangioplasty until medical therapy has been tried,” Rydén stated.

Another addition is the recommendation that patients with several or complex coronary artery stenoses should be offered bypass surgery before percutaneous coronary dilatation. This change was based on new trial data that show superior morbidity and mortality with bypass surgery as compared with coronary dilatation, according to the release.

The guidelines also individualize targets for BP and glycemic control. The general BP target for patients with diabetes is <140/85 mm Hg; in the 2007 version, the target was 130/80 mm Hg. In patients with diabetes and kidney disease, the target is <130/85 mm Hg. Stricter BP control is also urged for patients at risk for stroke. Younger patients with a recent diagnosis of diabetes and no CVD history have lower recommended glycemic control targets, while those who are older and have longstanding diabetes and CVD have more modest targets.

Other changes in the new guidelines include the prioritization of weight stabilization over reduction, recommendations against drugs to increase HDL levels and aspirin use in patients with diabetes and no CVD, and a new chapter on patient-centered care with emphasis on shared decision-making.

Source: Endocrine Today.

Unique Brain Pattern May Explain Superior Math Skills in Autism.


A unique pattern of brain organization may explain why children with autism spectrum disorder (ASD) often possess superior math skills.

A small brain imaging study showed that children between the ages of 7 and 12 years with ASD had significantly superior numerical problem-solving abilities, including the use of more sophisticated strategies to figure out single-digit addition questions, than their age-, sex-, and IQ-matched healthy peers.

In addition, participants with ASD showed different activation patterns in the ventral temporal-occipital cortex (VTOC), the posterior parietal cortex, and the medial temporal lobe during mathematical problem solving — with activation patterns in the VTOC region actually predicting these superior abilities.

“Our findings suggest that altered patterns of brain organization in areas typically devoted to face processing may underlie the ability of children with autism to develop specialized skills,” lead author Teresa Iuculano, PhD, from the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine, in California, and from the Stanford Cognitive and Systems Neuroscience Laboratory, said in a release.

She told Medscape Medical News that because children with ASD are often bad at recognizing faces, this particular area was recruited instead for math abilities in this patient population.

“However, this isn’t a universal finding, and we know that the spectrum is very broad. So there could be many different talents discovered, including music and drawing, and should be assessed on a case-by-case basis,” said Dr. Iuculano.

“If a parent sees that a child is strongly interested in something, they should help them to follow their passion. This is important for all children, but especially those with autism. It can be used as a relaxation tool and to help them to enjoy life more.”

The study was published online August 19 in Biological Psychiatry.

Mostly Anecdotal Evidence

The investigators note that although past research has suggested that individuals with ASD often have high mathematical skills, the evidence has been “mostly anecdotal and descriptive.”

For the current study, they sought to assess both the cognitive and neural characterizations of these skills.

“We thought that because math is such a concrete discipline, and with many rules, it could represent a good way to look at superiorities in a group of children on the spectrum,” said Dr. Iuculano.

The researchers enrolled 18 children with ASD (78% boys) and 18 children without the disorder, who were considered the “control group” (also 78% boys).

Standardized tests given during the study’s recruitment stage showed that all of the participants had IQs considered to be in the normal range; and those with ASD had “normal” verbal and reading skills. Standardized math tests were also administered.

While undergoing functional magnetic resonance imaging (fMRI) scans, all children were asked to solve addition problems, one at a time.

During the scans, the researchers also interviewed the participants to determine which of the following types of problem-solving strategies were being used: remembering an answer already known (retrieval), counting on fingers or in their heads, or decomposition.

The latter strategy is a comparatively sophisticated method and consists of breaking down a problem into several components.

Significant Differences

Results showed that the group with ASD had significantly higher scores on the numerical operations subscale of the Weschsler Individual Achievement Test–Second Edition for mathematics (WIAT-II) than the control group (P= .012).

They also displayed significantly greater use of decomposition (P = .033), “suggesting that more analytic strategies, rather than rote memory, were the source of their enhanced abilities,” the investigators note.

There were no between-group differences in use of counting or retrieval strategies or on any of the 4 working memory measures assessed.

The MRI scans showed “several cortical regions where arithmetic complexity-related activity patterns differed significantly” between the 2 groups.

“Notably, high cross-validation classification accuracies (80% to 90%) were in [VTOC], including bilateral inferior lateral occipital cortex and fusiform gyrus, as well as posterior parietal cortex, including the left intraparietal sulcus, angular gyrus, and the left precuneus,” write the researchers.

Significant differences in activity patterns were also found in medial temporal lobe regions.

Finally, “numerical abilities in the ASD group were predicted by the pattern of neural activity in an area of the left VTOC encompassing the left fusiform gyrus and lateral occipital cortex,” whereas numerical abilities in the control group were predicted by activity patterns in the left dorsolateral prefrontal cortex.

Not Universal

Overall, “there appears to be a unique pattern of brain organization that underlies superior problem-solving abilities in children with autism,” senior author Vinod Menon, PhD, professor of psychiatry and behavioral sciences at Stanford and from the Child Health Research Institute at the Lucile Packard Children’s Hospital, said in a release.

He added that although instant recall of calendar dates (a skill often found in individuals with ASD) is not likely to help with academic and professional success, “developing good mathematical skills could make a big difference in the life of a child with autism,” including possibly leading to future employment.

“Our study supports the idea that the typical brain development in autism can lead not just to deficits but also to some remarkable cognitive strengths. We think this can be reassuring to parents,” said Dr. Menon.

However, he noted that it is important to realize that not all children with ASD have superior math skills. So future research should examine the neural basis of variations in problem-solving abilities.

Dr. Iuculano added that she is excited about the current study’s findings on both research and clinical levels.

“As a scientist, it’s great that we’re understanding how the brain works in children with autism. And on a practical level, it’s important because it can raise awareness of the fact that these individuals can be contributing in a very good way to society,” she said.

Not Limited to Math

“I think this is not new as such, but it’s a very good study and important because it extends some things we already know,” Laurent Mottron, MD, PhD, professor of psychiatry at the University of Montreal, Quebec, Canada, and scientific director of the University’s Center of Excellence in Pervasive Development Disorders, toldMedscape Medical News.

He added that mathematic cognition has not been really studied before in ASD; but the take-away message is not that these findings are specific only to mathematics.

“This overactivation of the occipital region, and specifically the fusiform gyrus, is found in all tasks involving any visual information,” said Dr. Mottron, who was not involved with this research.

As reported at the time by Medscape Medical News, his investigative team published findings from a meta-analysis in Human Brain Mapping 2 years ago. Their analysis of 26 fMRI studies and more than 700 individuals showed that those with ASD had higher activity in the temporal and occipital regions in relation to visual-based tasks than those without the disorder.

“As scientists, we are happy when something is replicated. Here it’s more than replication, it’s specification. But I think if you want to see the big picture, you need to realize this isn’t only related to mathematics. Because autistics, when reasoning in general, use more of their perceptual expertise than other people,” he said.

“And I’m quite happy that now it’s become a kind of consensual message about autistic intelligence.”

Source: Medscape.com

 

Cocoa, Even With Few Flavonoids, Boosts Cognition.


Drinking cocoa, whether rich in flavonoids or not, appears to boost the effect of blood flow on neuronal activity in the brain, known as neurovascular coupling (NVC).

A new study shows not only that drinking flavonoid-rich or flavonoid-poor cocoa improves NVC but also that higher NVC is associated with better cognitive performance and greater cerebral white matter structural integrity in elderly patients with vascular risk factors.

As researchers search for ways to detect dementia at the earliest possible stage, the study results could pave the way for using NVC as a biomarker for vascular function in those at high risk for dementia, said lead author Farzaneh A. Sorond, MD, PhD, Department of Neurology, Stroke Division, Brigham and Women’s Hospital, Boston, Massachusetts.

“Our study shows that NVC is modifiable and can be enhanced with cocoa consumption,” said Dr. Sorond.

Tight Correlation

The double-blind proof-of-concept study included 60 community-dwelling participants, mean age 72.9 years. About 90% of the participants were hypertensive, but with well-controlled blood pressure, and half had diabetes mellitus type 2 with reasonably good control. Three quarters were overweight or obese.

Participants were randomly assigned to 2 cups a day of cocoa rich in flavonoids (609 mg per serving) or cocoa with little flavonoids (13 mg per serving). Diets were adjusted to incorporate the cocoa, each cup of which contained 100 calories. Participants were also asked to abstain from eating chocolate.

Researchers measured cerebral blood flow in these participants using transcranial Doppler ultrasonography. Among other things, they documented changes in the middle cerebral artery and blood flow velocity at rest and in response to cognitive tasks (NVC).

The study showed that NVC was tightly correlated with cognition; scores for Trail making Test B, a test of executive function, were significantly better in those with intact NVC (89 seconds vs 167 seconds; P = .002). Participants with intact NVC also had significantly better performance on the 2-Back Task, a test for both attention and memory (82% vs 75%; P = .02).

“The higher you increase your blood flow during a cognitive task, the better your cognitive performance,” commented Dr. Sorond, adding that this is something that has never been shown before.

NVC was also correlated with cerebral white matter structural integrity. Higher NVC was associated with overall less white matter macro- and micro-structural damage. In general, those with intact NVC had a greater volume of normal white matter and smaller volume of white matter hyperintensities, higher fractional anisotropy, and lower mean diffusivity in the normal white matter and WMH.

Therapeutic Target

These results suggest that NVC could be an important therapeutic target. But before NVC can be considered a biomarker, it has to be shown to be changeable, and the clinical importance of the modification must be shown.

To that end, the study authors opted to use cocoa. They could have chosen many other potential modifiers but chose cocoa because the literature has shown the beneficial effects of cocoa on brain health and also because it’s something that many people enjoy, said Dr. Sorond.

The study found that blood pressure, blood flow, and change in NVC were not significantly different between the 2 cocoa groups. In the combined cocoa groups, 30-day blood pressures were not significantly different from baseline (P > .5).

In contrast, response to cocoa differed significantly depending on NVC status. Cocoa had a significant effect on NVC in those with impaired (<5%) coupling at baseline. Of those with impaired NVC, 89% responded to 30 days of cocoa consumption and increased NVC compared with only 36% of those with intact NVC (P = .0002). In those with impaired baseline coupling, cocoa consumption was associated with an 8.3% (P < .0001) increase in NVC at 30 days.

The effect of cocoa consumption on Trail B scores was also significantly dependent on NVC status.

The authors were surprised at the lack of effect of flavonoids because previous research had indicated a dose-response with respect to cognitive performance. It could be something other than flavonoids in the cocoa, possibly caffeine, that improves NVC, or it could be that the 13 mg in the low-flavonoid cocoa group was enough to have an effect.

“I think there are effects of flavonol on brain blood flow no matter how low it is,” said Dr. Sorond, adding that perhaps only a tiny amount is needed to activate an enzyme or some other trigger.

It’s important to identify the component or mechanism, whatever it is, because just telling patients to drink cocoa could be risky, said Dr. Sorond. “Patients with diabetes or hypertension really don’t need the extra sugar, extra calories, and extra fat that come with it.”

Dr. Sorond thinks NVC could be measured in high-risk patients seen in the clinic. “I think this could be an easy, in-clinic quick test of vascular brain function that pertains to cognitive performance.”

The ideal next step would be to carry out a larger study in patients with mild cognitive impairment that includes more detailed cognitive profiles and more control groups. “We need a cocoa arm; we need a caffeine arm; we need maybe other arms, to make sure that we understand this, and maybe look at some of the metabolites in the blood as a result of cocoa consumption that correlates with these things,” said Dr. Sorond.

Remarkable First Step

In an accompanying editorial, Paul B. Rosenberg, MD, associate professor of psychiatry and behavioral sciences, Johns Hopkins School of Medicine, Baltimore, Maryland, and Can Ozan Tan, PhD, Harvard Medical School, Boston, write that in many ways, the study represents a “remarkable first step.”

For one thing, it demonstrates the practical utility of a simple, inexpensive, and noninvasive technique for measuring NVC that has several advantages over functional MRI and other means of measuring blood brain flow during cognitive tasks.

In demonstrating a link between NVC and cerebral white matter structural integrity, the study provides an important validation for the association between vascular and cognitive function, according to Dr. Rosenberg.

The study demonstrates that NVC “hangs together” as a measure of vascular function, which could be used in studies targeting vascular interventions, said Dr. Rosenberg in an interview with Medscape Medical News. In this way, he added, the study is “promising for the development of new treatments for vascular dementia.”

The study suggests that the vascular effects of cocoa are not due to its flavonol content, noted Dr. Rosenberg.”It could be a placebo effect.”

Dr. Rosenberg pointed out several strengths of the study, including its relatively large size for a pilot study and its “well-chosen” measures.

Among its weaknesses are that it’s not a placebo-controlled study and the hypothesis that flavonoid-rich cocoa would work better than flavonoid-poor cocoa didn’t pan out. The study may also not have been long enough, said Dr. Rosenberg. “It’s nice to see a drug work for 30 days, but you really need a longer study.”

The study didn’t include patients with mild cognitive impairment who are at risk of developing dementia, which Dr. Rosenberg sees as another weakness. “It’s one thing to show an effect in cognitively healthy older people; it’s a very different thing to show an effect in people who have a brain disease,” he said.

The Alzheimer’s Association also sees weaknesses in the study. Not only is it a very small and very preliminary study, but it was also not well designed as a test of an intervention or therapy because it didn’t include a control group for comparison with the group that drank cocoa, said Maria Carrillo, PhD, Alzheimer’s Association vice president of medical and scientific relations.

Further, said Dr. Carrillo, it didn’t appear that other factors that could possibly affect brain blood flow and/or cognition were controlled for, tracked, or accounted for in the study.

“There is no information on what else the 18 people with impaired cerebral blood flow did during the trial that might have improved their cerebral blood flow or cognitive performance: exercise, for example. A well-designed intervention trial anticipates, tracks, and accounts for these possible confounding factors to help ensure the credibility of the findings.”

Source: Neurology

 

Obestity Epidemic.


Obesity is associated with nearly 1 in 5 US deaths, according to a study published online August 15 in the American Journal of Public Health. The new data suggest obesity’s toll on Americans is more than 3 times previous estimates.

In research that counters previous studies of the effect of obesity on American life spans, Ryan K. Masters, PhD, a Robert Wood Johnson Foundation Health and Society Scholar at Columbia University’s Mailman School of Public Health in New York City, and colleagues report that overweight and obesity were associated with 18.2% of all deaths among adults from 1986 through 2006 in the United States. Previous estimates of the effect of obesity on mortality, published in Demography in 2009, established an obesity-related death rate of approximately 5%.

In the current study, obesity appears to have a particularly strong effect among black women, with 26.8% (95% confidence interval [CI], 7.3% – 47.4%) of deaths associated with a body mass index (BMI) of 25 kg/m2 or higher. In white women, 21.7% (95% CI, 14.4% – 29.3%) of deaths were associated with overweight or obesity. Among black men, 5.0% (95% CI, −6.8 – 18.3) of deaths were associated with overweight or obesity, and among white men, 15.6% (95% CI, 8.6 – 22.9) were.

The study also showed that the more recent the birth year, the greater effect obesity has on mortality rates. Further, contrary to claims in much public health literature, obesity is not protective for the elderly.

“Obesity has dramatically worse health consequences than some recent reports have led us to believe,” Dr. Masters said in a university news release.

The authors write that prior estimates ignored various factors such as low participation in public health surveys by obese people. In addition, previous studies often relied on average obesity rates, even though such averages blur the substantial differences among various age groups.

Using data from 19 consecutive waves of the National Health Interview Survey covering 1986 through 2004, and linking those data with mortality information in the National Death Index through 2006, the researchers analyzed obesity and mortality among 290,383 white men, 41,710 black men, 324,131 white women, and 61,344 black women, all aged between 40 and 84.9 years.

The authors excluded people aged 85 years and older to avoid biases induced by the National Health Interview Survey coding of 85+ years. They also excluded the 1% of the sample with a BMI less than 18.5 kg/m2, which can be an indicator of illness, frailty, or mortality risk, according to the authors.

The investigators followed federal guidelines, setting normal BMI as 18.5 to 24.9, overweight as 25.0 to 29.9, and obese as 30.0 kg/m2 and higher. Further, obesity was stratified as grade 1 for a BMI between 30.0 and 34.9 kg/m2 and grade 2/3 for a BMI of 35.0 kg/m2 or higher.

Obesity-Associated Morality Growing

Grade 1 obesity accounted for an increasing number of deaths in each successive age group. For example, an analysis of population-attributable fractions (PAFs) showed that those born in the 1960s experienced higher obesity-related mortality than those born in the 1930s or 1920s. PAF is a calculation of the proportional reduction in mortality that would occur if the risk factor under consideration, such as obesity, were replaced with the ideal alternative, such as a normal-range BMI.

Among white men born from 1915 to 1919, 3.4% of all deaths at age 66 years could be attributed to grade 1 obesity. Men born just 10 years later saw obesity-related mortality rise to 4.5%, and for those born 10 years after that (ie, men born from 1935 to 1939), 5.8% of deaths at age 66 years were attributable to obesity. “These steady rises in PAF for class 1 obesity as a cause of adult mortality reflect more recent cohorts’ greater exposure to obesity across their respective life courses,” the authors write.

The data further reveal rising hazard ratios (HRs) for mortality and obesity as age increases. For instance, among white women, the HR for obesity at age 45 years is about 1.25, but by age 65 years, obesity increases the risk for mortality about 2-fold. Among black women, the HR for obesity at age 45 years is about 0.7, but by age 65 years, it rises to roughly 1.5.

“We believe that it is imperative for the US public and those who construct policy for that public to recognize that population health and more than a century of steady gains in life expectancy are being jeopardized by the obesity epidemic. Indeed, evidence has already implicated high rates of obesity as a significant contributor to the United States’ relatively low life expectancy among high-income countries,” the authors write.

Source: Medscape.com

HKDC1, BACE2 could predict gestational diabetes before pregnancy.


Data collected from the Hyperglycemia and Adverse Pregnancy Outcomes Study have led researchers to identify variants in two novel genes which they said are associated with measures of glucose and insulin levels among pregnant women.

 “With additional study and verification of these and other risk genes, we could one day have genetic risk profiles to identify individuals at elevated risk for developinggestational diabetes,” M. Geoffrey Hayes, PhD, from the division of endocrinology, metabolism, and molecular medicine at Northwestern University Feinberg School of Medicine, said in a press release.

 

Hayes and colleagues conducted a discovery genome-wide association study in a large cohort of pregnant mothers from various ancestries from the Hyperglycemia and Adverse Pregnancy Outcomes Study (n=4,437). The women were administered an oral glucose tolerance test at approximately 28 weeks gestation to determine genetic loci linked to measures of maternal metabolism, researchers wrote.

The researchers identified two novel genome-wide significant associations in glucose metabolism and HKDC1 and insulin secretion and BACE2 within two genes. Researchers wrote that these data suggest the genes’ underlying roles could play a significant role in hypoglycemia during pregnancy compared with women who are not pregnant.

“Together with the results of earlier studies, our findings suggest that the roles of HKDC1 in glucose metabolism and BACE2 in insulin secretion are more important during pregnancy than in the nongravid state,” researchers wrote.

Source: Endocrine Today

 

Absurd Study Claims Omega-3 Fats Raise Prostate Cancer Risk.


Story at-a-glance

  • A recent case-cohort study found that men with higher blood concentrations of omega-3 fat had a 44 percent increased risk of developing low-grade prostate cancer compared to those with the lowest levels
  • Specifically, higher blood levels of the omega-3 fat DHA correlated to higher prostate cancer risk, while no correlation was found for EPA and ALA. They also had a 71 percent higher risk of developing high-grade prostate cancer
  • The elevated blood levels of DHA found in the featured study is not necessarily indicative of higher fish consumption. In fact, low-fat diets can increase DHA levels in much the same way omega-3 supplementation can
  • While the researchers warn that fish oil supplements may be dangerous based on their findings, this study cannot show causation. Furthermore, no fish oil supplements were actually given as part of this study
  • Foods rich in omega-3 fats have previously been shown to prevent prostate cancer from spreading, and one recent meta-analysis found that fish consumption was associated with a 63 percent reduction in prostate cancer-specific mortality.
  • omega3

Omega-3 rich fish oil is one of the most well-researched substances on the market. Its wide ranging health benefits have been repeatedly proven, and animal-based omega-3 is one of the few supplements I recommend for virtually everyone to improve overall health.

But omega-3 fat, naturally found in salmon and krill, which are both excellent sources, has received some undeservedly bad press coverage lately. You may have seen some of the following headlines:

  • Link Between Omega-3 Fatty Acids and Increased Prostate Cancer Risk Confirmed (Science Daily1)
  • Omega-3 Supplement Taken By Millions ‘Linked to Aggressive Prostate Cancer’ (Huffington Post2)
  • Men who take omega-3 supplements at 71% higher risk of prostate cancer (NY Daily News3)
  • Omega-3 supplements may trigger prostate cancer (Nursing Times4)
  • Hold the salmon: Omega-3 fatty acids linked to higher risk of cancer(Time Magazine5)

These headlines are perfect examples of gross misreporting of science by the media, and it is instances like this that demonstrate why you cannot trust the conventional press to keep you informed about health. In the words of Jonny Bowden,6 PhD, CNS, the media’s reporting on this particular study is “disgraceful, incompetent, and scientifically illiterate.” I couldn’t agree more.

‘Omega-3 Fats Involved in Prostate Tumorigenesis,’ Researchers Claim

The study raising all this hoopla was published in the Journal of the National Cancer Institute7 on July 10. This case-cohort study8 examined associations between omega-3 levels in blood and prostate cancer risk among participants in the “Selenium and Vitamin E Cancer Prevention Trial,” also known as SELECT.9

The researchers concluded that men with higher blood concentrations of animal-based (marine-derived) omega-3s had a 44 percent increased risk of developing low-grade prostate cancer compared to those with the lowest levels.

Specifically, higher blood levels of the omega-3 fat DHA correlated to higher prostate cancer risk, while no correlation was found for EPA and ALA. They also had a 71 percent higher risk of developing high-grade prostate cancer.

The “grade” refers to the level of abnormality found in the cancer cells.10 The more abnormal the cells appear, the higher the grade of the cancer. Based on these correlations, the researchers concluded that “these fatty acids are involved in prostate tumorigenesis.” But just how did they reach that conclusion?

According to Time Magazine:11

“The study measured omega-3 blood levels in the participating men, and did not include information on the volunteers’ eating habits, so researchers could not differentiate between the effects of fatty acids from fish from those of supplements. However, the overwhelming majority of the participants did not take fish oil supplements.

Based on the results, [lead author, Theodore] Brasky says that men with a family history of prostate cancer should discuss with their doctor whether fish oil supplements are safe for them, since these pills tend to contain concentrated doses of omega-3.

Supplements contain between 30% to 60% of a serving of fish, and if a fish oil supplement is taken every day, that adds up to a lot of daily fish oil. Brasky also suggested that men cut down on their fatty fish intake, though not eliminate it entirely.”

Folks, this is some of the most absurd advice I’ve seen in a long time. How they could possibly come to the conclusion that omega-3 supplements might be dangerous based on this study is a mystery in and of itself. Correlation is not the same as causation, first of all.

Secondly, no omega-3 supplements were actually given in this study. In fact, most participants reportedly did not take them. Another immediate tip-off that something’s awry is the finding that participants who had the highest levels oftrans fats in their blood had the lowest risk for prostate cancer… As Dr. Bowden writes in his Huffington Post12 rebuttal:

“How do you explain the fact that reporter after reporter and news outlet after news outlet conveniently equated higher blood levels of DHA with ‘fish oil supplement taking?’

There’s almost no other explanation other than a strong anti-supplement bias and a desire for shocking headlines. And any doubt about the objectivity of the researchers should have been abandoned after one of them—Dr. Alan Kristy—told reporters,13 ‘We’ve shown once again that use of nutritional supplements may be harmful.’”

Indeed, Dr. Kristy sounds like a spokesperson for Senator Durbin’s hypocritically idiotic supplement bill, which threatens the supplement industry by granting the FDA more power to regulate supplements as if they were drugs, potentially putting supplement companies out of business.

Do Omega-3s Raise Men’s Prostate Cancer Risk? Hardly!

Foods rich in omega-3 fats have previously been shown to prevent prostate cancer from spreading. One such clinical study (opposed to the featured study, which was observational and therefore cannot establish causality) was published in the British Journal of Cancer14 in 2006. This study found that while omega-6 fats (the kind found in most vegetable oils) increased the spread of prostatic tumor cells into bone marrow, the spread of cancer cells was blocked by omega-3 fats, suggesting that a diet rich in omega-3 fats could potentially inhibit the disease in men with early stage prostate cancer.

A more recent meta-analysis15 of available research, published in 2010, found that fish consumption was associated with a 63 percent reduction in prostate cancer-specific mortality, even though no association between fish consumption and a significant reduction in prostate cancer incidence could be found. GreenMedInfo.com16 recently discussed this topic as well, listing a number of additional studies that have shown fish/fish oil/omega-3 to be beneficial against prostate cancer.

As pointed out by Denise Minger,17 previous research18 has shown that the higher blood levels of DHA found in the featured study is not necessarily indicative of higher fish consumption. In fact, low-fat diets can increase DHA levels in much the same way omega-3 supplementation can. According to previous research:

“Plasma phospholipid fatty acids have the potential to function as a surrogate measure of the potential effects of diet on a whole range of cell membrane lipids… This difference in fatty acid levels after the consumption of similar proportions but varied content of fatty acids suggests competition among the lipid series [(n-3), (n-6), (n-7) and (n-9)] for the enzymes of elongation and desaturation.

When the relative supply of (n-3) fatty acids is abundant, these fatty acids are preferentially desaturated and elongated relative to (n-6) fatty acids)…

In summary… free fatty acid compositions are responsive to total dietary fat content. Specifically, the consumption of a low fat diet promotes an increase in the level of total and highly unsaturated long-chain (n-3) fatty acids and a decrease in the total (n-6) content of plasma phospholipid and cholesteryl ester fatty acids. The observed modifications in phospholipid and cholesteryl ester fatty acids in response to a low fat diet are similar to those observed when (n-3) fatty acids of plant or animal origin are fed.”

Why DHA Levels in Featured Study May Be Meaningless…

Furthermore, the featured study reported DHA levels based on percentage of total fatty acids rather than the absolute value, which in and of itself can be quite misleading,19 as it actually obscures any real differences. Dr. Bowden illustrates the dilemma well with the following analogy:

“Would you like 90 percent of all the money Mr. Jones has or 10 percent of all the money Mr. Smith has?”

How could you possibly tell how much money those percentages of total represent, unless you know how much money Mr. Jones and Mr. Smith each have to begin with? As explained in a 2009 commentary published in the American Journal of Clinical Nutrition,20 the only time percentage of total might be meaningful is when the total fatty acid content is identical for all subjects, which it undoubtedly was not in this case.

As stated by Dr. Bob Roundtree, MD:21

“Considering the extensive body of literature that supports the anti-inflammatory effects of omega-3 fatty acids, there is no credible biological mechanism, nor is one suggested in the article, that would explain why these essential fatty acids might increase tumorigenesis.”

Confounding Factors Ignored

Another problem with studies looking at correlations only, is that the factor you’re looking at may only be a minor player, or completely irrelevant, compared to other factors. For example, in this case:22

  • 53 percent of the subjects with prostate cancer were smokers
  • 64 percent of the cancer subjects regularly consumed alcohol
  • 80 percent of the cancer subjects were overweight or obese

According to a 2011 study published in PLoS One,23 aggressive prostate cancer was associated with obesity. More recently, a cohort study published in Cancer Epidemiology, Biomarkers & Prevention24 in April of this year found that men who were overweight or obese increased their risk of prostate cancer by 57 percent—a percentage that falls right smack in the middle of that 44-71 percentage range attributed to high DHA serum levels in the featured study. And this association between obesity and prostate cancer held for all cases— low-grade and high-grade, early stage and late, nonaggressive and aggressive prostate cancer.

Krill Oil vs. Fish Oil: What’s the Better Source?

From my perspective, based on medical experience and overwhelming scientific evidence, making sure you’re getting enough omega-3 in your diet, either from wild Alaskan salmon or a high-quality omega-3 supplement like krill oil, is absolutely crucialfor your optimal health. While a helpful form of omega-3 can be found in flaxseed, chia, hemp, and a few other foods, the most beneficial form of omega-3 — containing two fatty acids, DHA and EPA, which are essential to fighting and preventing both physical and mental disease — can only be found in fish and krill.25

Unfortunately, nearly all fish, from most all sources, are now severely contaminated with toxic mercury, which is why I have amended my previous recommendations to consume fish on a routine basis. It’s simply not advisable for most people any longer. About the only exception to this rule is wild-caught Alaskan salmon. This is really the ONLY fish I’ll eat on a regular basis, and the only one I feel comfortable recommending as a good source of healthful fats. AVOID farmed salmon, as they contain only about half of the omega-3 levels of wild salmon. Farmed salmon may also contain a range of harmful contaminants, including environmental toxins, synthetic astaxanthin, and genetically engineered organisms from the grain feed they’re given.

My latest recommendation for a source of high quality omega-3 fats is krill oil. The omega-3 in krill is attached to phospholipids that increase its absorption, which means you need less of it, and it won’t cause belching or burping like many other fish oil products. Additionally, it naturally contains astaxanthin, a potent antioxidant—almost 50 times more than is present in fish oil. This prevents the highly perishable omega-3 fats from oxidizing before you are able to integrate them into your cellular tissue. In laboratory tests, krill oil remained undamaged after being exposed to a steady flow of oxygen for 190 hours. Compare that to fish oil, which went rancid after just one hour. That makes krill oil nearly 200 times more resistant to oxidative damage compared to fish oil!

When purchasing krill oil, you’ll want to read the label and check the amount of astaxanthin it contains. The more the better, but anything above 0.2 mg per gram of krill oil will protect it from rancidity.

Source: mercola.com

Migraine associated with brain artery defect..


The network of arteries supplying blood flow to the brain is more likely to be incomplete in people who suffer migraine, a new study by researchers in the Perelman School of Medicine at the University of Pennsylvania reports. Variations in arterial anatomy lead to asymmetries in cerebral blood flow that might contribute to the process triggering migraines.

The arterial supply of blood to the brain is protected by a series of connections between the major arteries, termed the “circle of Willis” after the English physician who first described it in the 17th century. People with migraine, particularly migraine with aura, are more likely to be missing components of the circle of Willis.

migraine-aura-1

Migraine affects an estimated 28 million Americans, causing significant disability. Experts once believed that migraine was caused by dilation of blood vessels in the head, while more recently it has been attributed to abnormal neuronal signals. In this study, appearing in PLOS ONE, researchers suggest that blood vessels play a different role than previously suspected: structural alterations of the blood supply to the brain may increase susceptibility to changes in cerebral blood flow, contributing to the abnormal neuronal activity that starts migraine.

“People with migraine actually have differences in the structure of their blood vessels; this is something you are born with,” said the study’s lead author, Brett Cucchiara, MD, Associate Professor of Neurology. “These differences seem to be associated with changes in blood flow in the brain, and it’s possible that these changes may trigger migraine, which may explain why some people, for instance, notice that dehydration triggers their headaches.”

In a study of 170 people from three groups—a control group with no headaches, those who had migraine with aura, and those who had migraine without aura—the team found that an incomplete circle of Willis was more common in people with migraine with aura (73 percent) and migraine without aura (67 percent), compared to a headache-free control group (51 percent). The team used magnetic resonance angiography to examine blood vessel structure and a noninvasive magnetic resonance imaging method pioneered at the University of Pennsylvania, called Arterial spin labeling (ASL), to measure changes in cerebral blood flow.

“Abnormalities in both the circle of Willis and blood flow were most prominent in the back of the brain, where the visual cortex is located. This may help explain why the most common migraine auras consist of visual symptoms such as seeing distortions, spots, or wavy lines,” said the study’s senior author, John Detre, MD, Professor of Neurology and Radiology.

Both migraine and incomplete circle of Willis are common, and the observed association is likely one of many factors that contribute to migraine in any individual. The researchers suggest that at some point diagnostic tests of circle of Willis integrity and function could help pinpoint this contributing factor in an individual patient. Treatment strategies might then be personalized and tested in specific subgroups.

In addition to Dr. Cucchiara and Dr. Detre, the research team at Penn includes Scott Kasner, MD, Ritobrato Datta, PhD, Geoffrey Aguirre, MD, PhD from Neurology, and Ronald Wolf, MD, PhD, from Radiology. Radiologists Lidia Nagae, MD, from the Children’s Hospital of Philadelphia, and Quan Zhang, PhD, from Tianjin Medical University in Tianjin, China, contributed to the study.

Source: http://machineslikeus.com

Faster optical fibre breakthrough.


A Monash PhD student has presented the next step in creating superfast internet through the optimisation of optical fibre at a prestigious conference in Kyoto.

Md. Monir Morshed of the Optical Communications Group in the Department of Electrical and Computer Systems Engineering presented his findings in a post-deadline session at the 18th OptoElectronics and Communications Conference/ Photonics in Switching (OECC) earlier this month.

yienkeat_OpticFibres_shutterstock

Post-deadline sessions are reserved for late-breaking innovations and are usually dominated by industrial research laboratories.

Mr Morshed said he was thrilled to present at the largest optical communications conference in the Asia Pacific.

“Attending the conference was a wonderful opportunity to hear from the leading researchers in the field. The paper was a great achievement for our group,” Mr Morshed said.

Mr Morshed’s research aims to increase the data capacity of optical fibre, in terms of both speed and distance by mitigating a feature known as nonlinearity. Impressively, he demonstrated data speeds of more than one terabit per second over more than 800 kilometres. This is more than 10 times the capacity of current systems and could lay the groundwork for superfast inter-city networks.

“Internet users increasingly demand more and more bandwidth. We are working out how to optimise existing infrastructure to create next generation optical systems,” Mr Morshed said.

Leader of the Optical Communications Group and Australian Laureate Fellow, Professor Arthur Lowery, praised Mr Morshed’s research.

“Monir has made tremendous progress in his PhD, with theoretical and experimental innovations that are globally competitive. I am extremely proud of my group and its achievements in tackling the nonlinear capacity limit in optical fibres,” Professor Lowery said.

Source:  http://sciencealert.com.au

 

The PD-1 Immune Checkpoint Emerges as a Promising Therapeutic Target in NSCLC.


Several new studies presented at the American Society of Clinical Oncology (ASCO) 2013 annual meeting provide additional support for the growing interest in programmed cell death 1 (PD-1), a key immune-checkpoint receptor, as a therapeutic target in NSCLC and other tumor types.

“We now have a new pillar of treatment for cancer patients,” said Padmanee Sharma, MD, PhD, of the MD Anderson Cancer Center in Houston, Texas, a discussant in the session on developmental immunotherapy. “We have standard chemotherapy, targeted therapies, radiation therapy, surgery—and I propose now that immune-checkpoint therapy is really here.”

Under normal physiologic conditions, immune checkpoints such as PD-1 maintain self-tolerance and prevent autoimmunity by limiting T cell effector functions within tissues. Tumor cells can upregulate various ligands for PD-1, including PD-L1 and PD-L2, as a mechanism of evading antitumor immune responses in the tumor microenvironment. Therapeutic strategies for targeting the PD-1 pathway to restore tumor-specific T cell immunity include direct inhibition of the PD-1 receptor and PD-L1 blockade.

Nivolumab is an anti-PD-1 antibody with activity in advanced solid tumors, including melanoma, NSCLC, and renal cell carcinoma (RCC). In a phase I study, treatment with intravenous nivolumab induced an overall response rate of 16% in 122 patients with heavily pretreated, advanced NSCLC, and was associated with a median overall survival of 9.6 months (Topalian SL et al.). In the total study population of 304 patients with melanoma, NSCLC, and RCC, 10 patients (3%) developed drug-related pneumonitis, resulting in 3 deaths. Additional grade 3-4 adverse events were reported in 15% of patients.

Additional phase I trials demonstrated the utility of nivolumab in previously treated patients with advanced NSCLC (Brahmer JR et al.) and in combination with platinum-based doublet chemotherapy in chemotherapy-naïve patients with stage IIIB/IV NSCLC (Rizvi NA et al.). Based on these promising results, nivolumab is currently being evaluated in two phase III trials versus docetaxel for the second-line treatment of NSCLC, as well as a phase II trial of third-line therapy in patients with squamous cell histology.

MPDL32802 is a human monoclonal anti-PD-L1 antibody that contains an engineered Fc-domain designed to optimize efficacy and safety. Treatment with MPDL32802 yielded a 21% response rate in a phase I study of 171 patients with locally advanced or metastatic tumors, including NSCLC, melanoma, colorectal cancer, gastric cancer, and RCC (Herbst RS et al.). The highest response rates were in patients with NSCLC and melanoma. Intravenous treatment with MPDL32802 every 3 weeks was well tolerated, with no dose-limiting toxicities and no pneumonitis-related deaths.

Biomarker studies show that higher levels of PD-L1 tumor expression predict better response rates to PD-1 checkpoint inhibitors (Herbst RS et al.Powderly JD et al.). The investigational PD-1 checkpoint inhibitors are being developed with companion diagnostic assays to measure tumor PD-L1 expression by immunohistochemistry (IHC). Each agent, however, uses a different antibody to detect PD-L1 expression and a different IHC staining threshold to define PD-L1 positivity. Although some ongoing trials will include patients with any PD-L1 IHC status, others will require PD-L1 positivity for enrollment.

“Selection by PD-L1 expression may enhance response, but there is activity seen in PD-L1-negative tumors,” saidNatasha B. Leighl, MD, MMSc, of the University of Toronto, Canada, a discussant in the session on new agents for metastatic NSCLC. “I think it is far too early to close the door on this group.”

Several other agents targeting the PD-1 checkpoint are currently under development. Other direct inhibitors of PD-1 include the humanized monoclonal antibodies pidilizumab (CT-011) and lembrolizumab (MK-3475), and AMP-224, a recombinant fusion protein. Investigational monoclonal antibodies targeting PD-L1 include BMS-936559, Medl-4736, and MPDL-3280A 

Source: The oncologist

 

ght:1K�p;# 0 d:white’>Because of the very low doses of pollutants used in the mixture, these findings may have strong implications in terms of understanding the potential role of environmental contaminants in food in the development of metabolic diseases.”

 

Endocrine-Disrupting Chemicals Likely to Cause Harm Even at Low ‘Safe’ Doses

The chemical contaminants used in the study were chosen not only because they’re pervasive in the food supply, but also because they’re known endocrine disruptors. The glands of your endocrine system and the hormones they release influence almost every cell, organ, and function of your body. It is instrumental in regulating mood, growth and development, tissue function, metabolism, as well as sexual function and reproductive processes.

Endocrine disrupters are substances or mixtures that alter the functions of your endocrine system and consequently cause adverse health effects, either in your body or in your offspring. These types of chemicals can exert their effects by:

  • Mimicking the biological activity of your hormones by binding to a cellular receptor. This can initiate your cell’s normal response to the naturally-occurring hormone at the wrong time or to an excessive extent (agonistic effect).
  • Binding to the receptor but not activating it. Instead the presence of the chemical on the receptor prevents binding of the natural hormone (antagonistic effect).
  • Binding to transport proteins in your blood, thus altering the amounts of natural hormones that are present in your blood circulation.
  • Interfering with the metabolic processes in your body, affecting the synthesis or breakdown rates of your natural hormones.

The strongest evidence showing that exposure to these types of environmental chemicals can lead to disruption of endocrine function comes from the bizarre changes seen in a number of wildlife species, such as male fish transforming into females, frogs developing a variety of defects like multiple testes or ovaries, and hermaphrodite bears, just to name a few.  

Yet, it’s commonly stated that these chemicals are not dangerous to humans because they exist at such low levels, even as research suggests otherwise. For instance, of 115 published animal studies, 81 percent found significant effects from even low-level exposure to BPA.

And the latest study only adds to this undeniable knowledge:

“With this study, we have succeeded in providing proof-of-concept that low doses of contaminants, even at levels normally considered to be without health impacts in humans, do in fact affect humans when subjected to chronic exposure, and when the contaminants are combined with a high-calorie diet,” the researchers said.2

What Are the Long-Term Health Risks from Exposure to Common Food Contaminants?

A typical American comes in regular contact with some 6,000 chemicals and an untold number of potentially toxic substances on a less frequent basis. There are about 75,000 chemicals regularly manufactured and imported by US industries, so you could be exposed to any number of them. Disturbingly, many of them have never been fully tested for safety, and virtually none have been studied in combination with one another, which is how real-world exposure occurs and where their toxicities can be amplified exponentially.

Upwards of 20 environmental chemicals, most of them endocrine-disrupting chemicals, have been shown to cause weight gain when exposure occurs during fetal and infant development, although some are also linked to adult exposures. Others, including BPA, PCBs, phthalates and agricultural pesticides can lead to health problems including:

Non-descended testes in young males

Breast cancer in women

Prostate cancer in men

Developmental effects on the nervous system in children

Attention deficit hyperactivity in children

Thyroid cancer

 

According to a World Health Organization (WHO) and United Nations Environment Program (UNEP) report:3

“The diverse systems affected by endocrine-disrupting chemicals likely include all hormonal systems and range from those controlling development and function of reproductive organs to the tissues and organs regulating metabolism and satiety. Effects on these systems can lead to obesity, infertility or reduced fertility, learning and memory difficulties, adult-onset diabetes or cardiovascular disease, as well as a variety of other diseases.”

Specifically, health problems linked to some of the most common food contaminants include:

  • BPA: Plasticizing chemicals like BPA, found in plastics and canned food linings, disrupt embryonic development and are linked to heart disease and cancer. Beware that many manufacturers of ‘BPA-free’ products have simply replaced BPA with bisphenol-S (BPS), an equally toxic chemical. More recently, research has found that other bisphenols used in the production of consumer products, namely, bisphenols M, AP and P, are actually more toxic to DNA than BPA.4
  • Phthalates: Phthalates dysregulate gene expression and cause genital anomalies, especially in baby boys, that may pass down several generations. Phthalates are found in vinyl flooring, detergents, automotive plastics, soap, shampoo, deodorants, fragrances, hair spray, nail polish, plastic bags, food packaging, garden hoses, inflatable toys, blood-storage bags, and intravenous medical tubing.
  • Dioxins: Dioxins are a byproduct of industrial processes, such as chlorine bleaching of paper products and the manufacturing of some pesticides. Because they are persistent environmental pollutants, they accumulate in the food chain and more than 90 percent of human exposure is through foods like meat, dairy products and fish. According to WHO, “Dioxins are highly toxic and can cause reproductive and developmental problems, damage the immune system, interfere with hormones and also cause cancer.”5
  • PCBs: Like dioxins, PCBs are persistent organic pollutants (POPs) that persist in the environment and resist breaking down, accumulating in the food chain and posing serious risks to human health and the environment. For instance, even though PCBs have been banned in the US for decades, they are still present in your environment. PCBs and other POPs have caused birth defects and other abnormalities among wildlife, along with damage to virtually every human bodily system.

Tips for Finding the Purest Foods Possible

When it comes to staying healthy, avoiding processed foods and replacing them with fresh, whole foods is the “secret” you’ve been looking for. The more steps your food goes through before it reaches your plate, the greater your chances of contamination becomes. If you are able to get your food locally, you eliminate numerous routes that could expose your food to contamination with not only disease-causing pathogens but also with the chemical contaminants noted above, which often exist in food packaging.

It’s also important to choose your fresh foods wisely, as you’ll want to focus on those grown in non-polluted areas using organic farming methods. Whatever food you’re looking to eat, whether organic or locally grown, from either your local supermarket or a farmer’s market, the following are signs of a high-quality, healthy food. Most often, the best place to find these foods is from asustainable agricultural group in your area. You can also review my free nutrition plan to get started on a healthy eating program today:

It’s grown without pesticides and chemical fertilizers (organic foods fit this description, but so do some non-organic foods)

It’s not genetically engineered

It contains no added growth hormones, antibiotics, or other drugs

It does not contain artificial anything, nor any preservatives

It is fresh (if you have to choose between wilted organic produce or fresh conventional produce, the latter may still be the better option as freshness is important for optimal nutrient content)

It was not grown in a concentrated animal feeding operation (CAFO)

It is grown with the laws of nature in mind (meaning animals are fed their native diets, not a mix of grains and animal byproducts, and have free-range access to the outdoors)

It is grown in a sustainable way (using minimal amounts of water, protecting the soil from burnout, and turning animal wastes into natural fertilizers instead of environmental pollutants)

 

 

Source: mercola.com

Treatment With a Next-Generation ALK Inhibitor Results in High Response Rates Following Crizotinib Failure in Advanced, ALK-Positive NSCLC.


A majority of patients with advanced non-small cell lung cancer (NSCLC) whose tumors harbor mutations in the anaplastic lymphoma kinase (ALK) gene responded to treatment with a novel ALK inhibitor despite progressing on earlier ALK inhibitor therapy, according to new results from a phase I study (Shaw AT et al.). The trial highlights the potential role of second-line ALK-targeted therapy in the treatment of ALK-positive NSCLC.

Approximately 3% to 7% of patients with NSCLC have ALK rearrangements, which occur more commonly in nonsmokers, younger patients, and adenocarcinomas. ALK-mutated tumors become dependent on ALK signaling, and as a result, are highly susceptible to ALK inhibition. Crizotinib, a first-generation ALK inhibitor, can induce response rates of 60% in patients with advanced ALK-positive NSCLC, but most patients develop resistance to crizotinib within one to two years.

In general, ALK rearrangements do not overlap with other oncogenic drivers such as EGFR and KRAS mutations in patients with NSCLC (Gainor JF et al.). New options for ALK-targeted therapy, therefore, expand treatment options for patients who are not candidates for other targeted therapies, and for those who progress on current ALK inhibitor therapy.

Alice T. Shaw, MD, PhD, Assistant Professor at Harvard Medical School in Boston, presented findings from a multicenter, open-label, single-arm study of 122 patients with locally advanced or metastatic ALK-positive NSCLC. Of these, 63% had progressed on prior crizotinib therapy, and 31% were ALK-inhibitor naïve. All patients received LDK378, an oral next-generation ALK inhibitor that has shown 20-fold greater potency against ALK compared with crizotinib.

Response rates to LDK378 400-750 mg once daily were high in 114 evaluable patients, with 75% demonstrating some degree of tumor regression. The complete response rate was 58% for all patients, with no apparent differences between those with crizotinib resistance (57%) and those with no prior exposure to an ALK inhibitor (60%). Responses were durable, with a prolonged median duration of response (8.2 months) and median progression-free survival (8.6 months). Imaging studies also demonstrated the activity of LDK378 against central nervous system (CNS) metastases.

“CNS relapses are a major cause of morbidity and mortality in patients treated with crizotinib, so establishing the CNS activity of LDK378 is extremely important,” Dr. Shaw said.

Treatment with LDK378 was generally well tolerated. The most common adverse events included mild gastrointestinal symptoms in 58%-73% of patients. Grade ≥3 adverse events included elevated ALT (19%), elevated AST (10%), diarrhea (8%), and elevated lipase, hypokalemia, and nausea in 5% of patients. Three patients (2%) discontinued LDK378 due to adverse events. No treatment-related deaths were reported.

The current gold standard for detecting ALK rearrangements is fluorescence in situ hybridization (FISH). Many institutions, however, are exploring the use of immunohistochemistry screening with ALK-specific antibodies, reserving ALK FISH to confirm ALK positivity (Tsao MS et al.Lantuejoul S et al.).

Based on early findings from this trial, the FDA recently designated LDK378 as a breakthrough therapy, a designation intended to expedite the development and review of new therapies for serious or life-threatening conditions. LDK378 is currently under evaluation in phase II and III trials of patients with advanced NSCLC who have received prior chemotherapy and crizotinib and in patients who are crizotinib-naïve.

Another investigational ALK inhibitor, CH5424802, showed antitumor activity in in a phase I/II study of patients with ALK-positive NSCLC and no prior exposure to ALK-inhibitor therapy (Nakagawa K et al.). AP26113, a dual inhibitor of ALK and EGFR, is also under development for the treatment of ALK-positive NSCLC.

Source: The oncologist

 

 

ine-hei�j1.# 0 ground:white’>In females, there was a marked deterioration of glucose tolerance, which may be related to the 2-fold induction of estrogen sulfotransferase and reduced expression of estrogen receptor α (25%) and estrogen target genes (>34%).

 

Because of the very low doses of pollutants used in the mixture, these findings may have strong implications in terms of understanding the potential role of environmental contaminants in food in the development of metabolic diseases.”

Endocrine-Disrupting Chemicals Likely to Cause Harm Even at Low ‘Safe’ Doses

The chemical contaminants used in the study were chosen not only because they’re pervasive in the food supply, but also because they’re known endocrine disruptors. The glands of your endocrine system and the hormones they release influence almost every cell, organ, and function of your body. It is instrumental in regulating mood, growth and development, tissue function, metabolism, as well as sexual function and reproductive processes.

Endocrine disrupters are substances or mixtures that alter the functions of your endocrine system and consequently cause adverse health effects, either in your body or in your offspring. These types of chemicals can exert their effects by:

  • Mimicking the biological activity of your hormones by binding to a cellular receptor. This can initiate your cell’s normal response to the naturally-occurring hormone at the wrong time or to an excessive extent (agonistic effect).
  • Binding to the receptor but not activating it. Instead the presence of the chemical on the receptor prevents binding of the natural hormone (antagonistic effect).
  • Binding to transport proteins in your blood, thus altering the amounts of natural hormones that are present in your blood circulation.
  • Interfering with the metabolic processes in your body, affecting the synthesis or breakdown rates of your natural hormones.

The strongest evidence showing that exposure to these types of environmental chemicals can lead to disruption of endocrine function comes from the bizarre changes seen in a number of wildlife species, such as male fish transforming into females, frogs developing a variety of defects like multiple testes or ovaries, and hermaphrodite bears, just to name a few.

Yet, it’s commonly stated that these chemicals are not dangerous to humans because they exist at such low levels, even as research suggests otherwise. For instance, of 115 published animal studies, 81 percent found significant effects from even low-level exposure to BPA.

And the latest study only adds to this undeniable knowledge:

“With this study, we have succeeded in providing proof-of-concept that low doses of contaminants, even at levels normally considered to be without health impacts in humans, do in fact affect humans when subjected to chronic exposure, and when the contaminants are combined with a high-calorie diet,” the researchers said.2

What Are the Long-Term Health Risks from Exposure to Common Food Contaminants?

A typical American comes in regular contact with some 6,000 chemicals and an untold number of potentially toxic substances on a less frequent basis. There are about 75,000 chemicals regularly manufactured and imported by US industries, so you could be exposed to any number of them. Disturbingly, many of them have never been fully tested for safety, and virtually none have been studied in combination with one another, which is how real-world exposure occurs and where their toxicities can be amplified exponentially.

Upwards of 20 environmental chemicals, most of them endocrine-disrupting chemicals, have been shown to cause weight gain when exposure occurs during fetal and infant development, although some are also linked to adult exposures. Others, including BPA, PCBs, phthalates and agricultural pesticides can lead to health problems including:

Non-descended testes in young males Breast cancer in women Prostate cancer in men
Developmental effects on the nervous system in children Attention deficit hyperactivity in children Thyroid cancer

 

According to a World Health Organization (WHO) and United Nations Environment Program (UNEP) report:3

“The diverse systems affected by endocrine-disrupting chemicals likely include all hormonal systems and range from those controlling development and function of reproductive organs to the tissues and organs regulating metabolism and satiety. Effects on these systems can lead to obesity, infertility or reduced fertility, learning and memory difficulties, adult-onset diabetes or cardiovascular disease, as well as a variety of other diseases.”

Specifically, health problems linked to some of the most common food contaminants include:

  • BPA: Plasticizing chemicals like BPA, found in plastics and canned food linings, disrupt embryonic development and are linked to heart disease and cancer. Beware that many manufacturers of ‘BPA-free’ products have simply replaced BPA with bisphenol-S (BPS), an equally toxic chemical. More recently, research has found that other bisphenols used in the production of consumer products, namely, bisphenols M, AP and P, are actually more toxic to DNA than BPA.4
  • Phthalates: Phthalates dysregulate gene expression and cause genital anomalies, especially in baby boys, that may pass down several generations. Phthalates are found in vinyl flooring, detergents, automotive plastics, soap, shampoo, deodorants, fragrances, hair spray, nail polish, plastic bags, food packaging, garden hoses, inflatable toys, blood-storage bags, and intravenous medical tubing.
  • Dioxins: Dioxins are a byproduct of industrial processes, such as chlorine bleaching of paper products and the manufacturing of some pesticides. Because they are persistent environmental pollutants, they accumulate in the food chain and more than 90 percent of human exposure is through foods like meat, dairy products and fish. According to WHO, “Dioxins are highly toxic and can cause reproductive and developmental problems, damage the immune system, interfere with hormones and also cause cancer.”5
  • PCBs: Like dioxins, PCBs are persistent organic pollutants (POPs) that persist in the environment and resist breaking down, accumulating in the food chain and posing serious risks to human health and the environment. For instance, even though PCBs have been banned in the US for decades, they are still present in your environment. PCBs and other POPs have caused birth defects and other abnormalities among wildlife, along with damage to virtually every human bodily system.

Tips for Finding the Purest Foods Possible

When it comes to staying healthy, avoiding processed foods and replacing them with fresh, whole foods is the “secret” you’ve been looking for. The more steps your food goes through before it reaches your plate, the greater your chances of contamination becomes. If you are able to get your food locally, you eliminate numerous routes that could expose your food to contamination with not only disease-causing pathogens but also with the chemical contaminants noted above, which often exist in food packaging.

It’s also important to choose your fresh foods wisely, as you’ll want to focus on those grown in non-polluted areas using organic farming methods. Whatever food you’re looking to eat, whether organic or locally grown, from either your local supermarket or a farmer’s market, the following are signs of a high-quality, healthy food. Most often, the best place to find these foods is from asustainable agricultural group in your area. You can also review my free nutrition plan to get started on a healthy eating program today:

It’s grown without pesticides and chemical fertilizers (organic foods fit this description, but so do some non-organic foods) It’s not genetically engineered It contains no added growth hormones, antibiotics, or other drugs
It does not contain artificial anything, nor any preservatives It is fresh (if you have to choose between wilted organic produce or fresh conventional produce, the latter may still be the better option as freshness is important for optimal nutrient content) It was not grown in a concentrated animal feeding operation (CAFO)
It is grown with the laws of nature in mind (meaning animals are fed their native diets, not a mix of grains and animal byproducts, and have free-range access to the outdoors) It is grown in a sustainable way (using minimal amounts of water, protecting the soil from burnout, and turning animal wastes into natural fertilizers instead of environmental pollutants)  

 

Source: mercola.com