Archive for the ‘News’ Category

Issues on cholesterol: Diet, statins and genetics

May 15th, 2009 BMI

Conversely, lifestyle, diabetes, dyslipidemia, cigarette smoking and hypertension contribute to most of the population-attributable risk in the large, international INTERHEART study of acute myocardial infarction (heart attacks). The identification of single gene disorders may pave the way to a better understanding of complex metabolic pathways. Understanding the genes that regulate high density lipoprotein (HDL) metabolism may lead to novel therapeutic approaches. This has been emphasized by two therapeutic approaches for the treatment of CAD:

     

  • The infusion of apo AI containing proteoliposomes, using wild-type or a mutant form of apo AI, apo AIMilano, in patients with acute coronary syndromes;

     

     

  • The long-term treatment of subjects with low HDL-C with the cholesteryl ester transfer protein (CETP) inhibitor Torcertapib. While Torcetrapib proved to have off-target toxic effects, two other CETP inhibitors (Anacetrapib and Delcetrapib) are being tested clinically. Experimentally, however, CETP inhibitors may not reduce atherosclerosis

     

Novel therapeutic approaches using agonists of the LxR/RxR pathway to up-regulate the ABCA1 transporter, or the transcriptional regulation of apo AI, are being explored.

 

Plasma (or serum) level of HDL-C is a continuous and graded negative cardiovascular risk factor. Most international CAD prevention guidelines define HDL-C as a categorical risk factor and the absolute level of HDL-C is used in a multivariate model to predict cardiovascular risk and determine the need and intensity of preventive therapies. A low HDL-C is considered a diagnostic criterion for the metabolic syndrome.

To underlie the importance of plasma lipoproteins in the pathogenesis of CAD and acute myocardial infarction, the largest case-control study of myocardial infarction (INTERHEART) has shown that the apo B/apo AI ratio (respectively an index of atherogenic lipoproteins and protective lipoproteins) accounts for approximately half (49%) of the population-attributable risk of acute myocardial infarction. The prevalence of a low HDL-C in patients with CAD has been examined in several case-control and prospective studies. It is estimated that approximately 40% of patients with premature CAD have a low HDL-C and this represents the most common lipoprotein disorder in patients with CAD. Most patients with a low HDL-C have multiple cardiovascular risk factors and features of the metabolic syndrome, with obesity (predominantly abdominal), elevated plasma triglyceride levels, high blood pressure and hyperglycemia, insulin resistance or diabetes. Despite the strong association between metabolic disorders and HDL-C, plasma levels of HDL-C are strongly genetically determined. Experimental evidence shows that the atheroprotective effects of HDL are pleiotropic and extend beyond removing cholesterol from lipid-laden macrophages in the atherosclerotic plaque. HDL are known to have anti-inflammatory effects, to prevent oxidation of low-density lipoproteins (LDL), possess anti-thrombotic properties, modulate vasomotor tone and may improve endothelial cell survival (by preventing apoptosis), migration and proliferation. Nonetheless, the major cardio-protective effect of HDL has been attributed to its key role in reverse cholesterol transport, a process in which cholesterol from peripheral tissues such as foam cells is selectively returned to the liver for excretion in the bile. Mutations in any of the proteins regulating this complex metabolic pathway may potentially decrease HDL-C levels and accelerate CAD.

 

Mutations or polymorphisms in several genes have been associated with altered plasma HDL-C levels. Mutations in the cholesteryl ester transfer protein (CETP) gene are associated with increases in HDL-C whereas mutations in the apolipoprotein (apo) AI gene (the major apolipoprotein of HDL particles), or the lecithin:cholesterol acyl transferase (LCAT) gene cause a low HDL-C. Of the approximately 46 mutations affecting the structure of apo AI, not all are associated with CAD. Mutations in the lipoprotein lipase (LPL) and hepatic lipase (HL) genes also affect HDL-C levels. The identification of the ATP binding cassette A1 gene (ABCA1) as the cause of Tangier disease and familial HDL deficiency has led to a better understanding of the role of cellular cholesterol and phospholipid transport in the metabolism of nascent HDL particles. Based upon the analysis of a selected group of subjects, we estimate that approximately 10-20% of subjects with severe HDL deficiency have mutations of the ABCA1 gene. Other genes have been found in animal models to have a profound impact on HDL-C levels, although no human counterpart disorders have yet been identified.

 

To examine the genetic contribution to the determination of HDL-C levels, there have been at least nine published studies in twins and 14 family studies. Estimates for the heritability of plasma HDL-C levels varies between 0.24 to 0.83 and is most often quoted as approximately 0.5.

 

The inverse epidemiological association between serum levels of HDL-C and risk of CAD is graded and has been validated in multiple studies. However, there is remaining controversy whether a low HDL-C should not predominantly be considered a marker of poor lifestyle (obesity, lack of exercise, hypertriglyceridemia, diet, etc.), rather than a primary causal agent for atherosclerosis in the majority of the population. Specific mutations in genes affecting HDL-C levels have had considerable discordant effects on CAD risk. For instance, mutations in the apo AI gene affecting HDL-C levels can be strongly associated with premature CAD, but apo AIMilano and apo AIParis are notable exceptions. Mutations in the LCAT gene cause a marked decreased level of HDL-C but are not considered to be associated with CAD. While loss-of-function mutations in the CETP gene cause an elevated HDL-C, cardiovascular risk does not seem decreased and may in fact be increased. Mutations in ABCA1 are associated with very low HDL-C and increase cardiovascular risk 3.5 fold in one study, but more recent data from the Copenhagen Heart Study suggests that ABCA1 mutations are not associated with increase cardiovascular risk, despite being associated with a low HDL-C. Important questions therefore remain which genetic forms of HDL deficiency confer cardiovascular risk. This has implications for the identification and treatment of patients with HDL deficiency. It remains to be determined whether a genetic form of HDL deficiency confers cardiovascular risk.

Source: European Society of Cardiology

 

Genetics of HDL and risk of cardiovascular disease

Heritability of HDL-C

Genes that affect HDL-C levels

Epidemiology of HDL and risk of coronary artery disease CAD risk

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Heavy breathing — an obscure link in asthma and obesity

May 15th, 2009 BMI

There is a strong link between obesity and asthma and as the prevalence of both conditions has been increasing steadily, epidemiologists have speculated that there is an underlying condition that connects the two. But one long-suspected link, the systemic inflammation associated with obesity, has been ruled out by a recent New Zealand study that found no evidence of its involvement.

“We were disappointed not to find a ‘smoking gun’ that would explain the common association between obesity and asthma,” said lead researcher, D. Robin Taylor, M.D., of the University of Otago in New Zealand. “However, this research points us to other possibilities that future research should examine.”

The results were reported in the first issue for September of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

“We hypothesized that the low-grade systemic inflammation present in obesity would augment the inflammation of asthma (a synergistic effect),” wrote Dr. Taylor. “Or alternatively, that the inflammation of obesity might affect the airways independently (an additive effect), perhaps resulting in mixed airway inflammation.”

In order to determine if there was indeed an interaction between systemic and local inflammation, the researchers recruited 79 women—20 who were obese with asthma, 19 who were of a normal weight with asthma, 20 who were obese but who did not have asthma and 20 controls.

Asthmatics were told to stop using their anti-inflammatory inhaler treatment to avoid confounding effects until “loss of control.” After the withdrawal period of four weeks, subjects underwent blood tests and tests for biomarkers of systemic and airway inflammation, such as C-reactive protein (CRP) and cytokines in blood and inflammatory cells and cytokines in sputum. Those that are known to be relevant in both obesity and asthma were chosen. The researchers then analyzed for interactions between systemic and airway-specific markers of inflammation.

“What we found was that although inflammatory cells and other biomarkers of inflammation were increased, there was no significant interaction demonstrated between obesity and asthma,” said Dr. Taylor.

Although their inflammation hypothesis was not supported by their results, Dr. Taylor points out that it does provide valuable direction for future research. “This does not change the fact that there is a well-established link between asthma and obesity. Sometimes a negative result is important, and the results add to our body of knowledge regarding the obesity-asthma link. Now we need to look in other directions for the answers.”

Animal studies suggest that changes in innate immunity may occur with obesity. “We did not look at this in our patients. Given that asthma is immunologically driven, this is a potential avenue for further research,” said Dr. Taylor. “Alternatively, it may be that dynamic changes in lung function that occur with episodes of asthma are different with excess body weight.”

Whatever the link is, uncovering it will have important clinical implications. “Obese patients with asthma are more difficult to treat because their response to bronchoconstriction is exaggerated and gives the impression that the asthma is worse,” said Dr. Taylor. “They may well have worse symptoms, but not as a result of underlying airway inflammation. Still, the typical response is often to increase their inhaled anti-inflammatory therapy. This is unlikely to provide the answer and may even do harm. The answer lies in dealing with the obesity itself.”

Source: American Thoracic Society

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Low levels of brain chemical may lead to obesity, NIH study of rare disorder shows

May 15th, 2009 BMI

A brain chemical that plays a role in long term memory also appears to be involved in regulating how much people eat and their likelihood of becoming obese, according to a National Institutes of Health study of a rare genetic condition.

Brain derived neurotrophic factor (BDNF) is, as its name implies, produced in the brain. Studies of laboratory animals have suggested it also helps control appetite and weight. The NIH study, appearing in the August 28 New England Journal of Medicine, provides the first strong evidence that BDNF is important for body weight in human beings as well.

The NIH researchers studied children and adults with WAGR syndrome, a rare genetic condition. The researchers found that some of the people with this syndrome lack a gene for BDNF and have correspondingly low blood levels of the substance. The people in this subgroup also have unusually large appetites and a strong tendency towards obesity.

“This is a promising new lead in the search for biological pathways that contribute to obesity,” said Duane Alexander, M.D., director of the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development. “This finding may eventually lead to the development of new drugs to regulate appetite in people who have not had success with other treatments.”

The study’s first author was Joan C. Han, M.D. and the senior author was Jack A. Yanovski, M.D., Ph.D., both of NICHD’s Unit on Growth and Obesity. Other authors of the study were from the National Human Genome Research Institute and the National Institute on Drug Abuse, also part of the NIH. Funding for the study was provided by the NICHD and the NIH Office of Rare Diseases.

WAGR syndrome is an acronym for the complex of symptoms seen in people who have the condition. These include Wilms tumor, a tumor of the kidneys; aniridia, absence of the iris, in the eye; genital and urinary tract abnormalities; and mental retardation. WAGR syndrome occurs in one out of every 500,000 to 1 million persons.

People with WAGR syndrome lack genes that are grouped on chromosome 11. All people with WAGR syndrome lack two specific genes, called WT1 and PAX6, but each person can also be missing other nearby genes. For the most part, human chromosomes are arranged in pairs, and the genetic deletions found in WAGR syndrome occur on only one of the two copies of chromosome 11.

WT1 and PAX6 are located in the region of the chromosome that’s near the gene for BDNF. For this reason, the NIH researchers examined chromosome 11 from WAGR syndrome patients to learn if the gene for BDNF was affected, explained Dr. Yanovski.

Studies of mice had determined that animals missing a working copy of the BDNF gene were prone to excessive eating and obesity. Studies in human beings, however, hadn’t proved that BDNF was important in people.

In the current study, the NIH researchers conducted analyses of chromosome 11 in 33 patients with WAGR syndrome. A total of 19 patients (58 percent) had deletions of all or a major proportion of one copy of the gene for BDNF. By age 10, all of the 19 were obese and were reported to have a strong tendency to overeat. Moreover, all of the 19 had blood levels of BDNF that were roughly 50 percent lower than those of patients who had two working copies of the BDNF gene. The patients who had two working copies of the BDNF gene were no more likely to develop childhood onset obesity than the general population, and did not report unusually high levels of overeating.

Dr. Yanovski explained that BDNF is believed to work in combination with a variety of other substances that regulate appetite and body weight. Chief among these is leptin, a hormone found to be involved in signaling hunger. Dr. Yanovski added that release of BDNF in the hypothalamus, a part of the brain involved in controlling eating, is believed to be indirectly triggered by leptin. Studies of the relationship between the two, and of BDNF’s action on tissues, may lead to the development of new drugs to treat obesity in some individuals.

Source: NIH/National Institute of Child Health and Human Development

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Not all fat is created equal

May 15th, 2009 BMI

A Temple University study finds fat in obese patients is “sick” when compared to fat in lean patients.

When our bodies don’t work properly, we say we’re sick. A study published in the September issue of Diabetes finds that the same could be said for fat tissue found in obese patients. The cells in their fat tissue aren’t working properly and as a result, are sicker than cells found in lean patients’ fat tissue.

Lead author Guenther Boden, M.D. theorizes that “sick fat” could more fully explain the link between obesity and higher risk of diabetes, heart disease and stroke.

Researchers from the departments of endocrinology, biochemistry and surgery at the Temple University School of Medicine took fat biopsies from the upper thighs of six lean and six obese patients and found significant differences at the cellular level.

“The fat cells we found in our obese patients were deficient in several areas,” said Boden, Laura H. Carnell Professor of Medicine and chief of endocrinology. “They showed significant stress on the endoplasmic reticulum, and the tissue itself was more inflamed than in our lean patients.”

Endoplasmic reticulum (ER) is found in every cell and helps synthesize proteins and monitor how they’re folded. The stress that Boden describes causes the ER in fat cells to produce several proteins that ultimately lead to insulin resistance, which has been found to play a major role in the development and progression of obesity-related conditions.

The National Institutes of Health recently reported that each time a body mass index (BMI) over 25 is raised by one point, the risk for diabetes increases 25 percent and the risk for heart disease increases 10 percent.

Reducing weight can help reduce stress on the ER, which can lower the risk of insulin resistance and the resulting conditions. Currently Boden and his team are looking at whether free fatty acids are a potential cause for this ER stress.

Source: Temple University

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Early trigger for type 1 diabetes found in mice, Stanford scientists report

May 15th, 2009 BMI

STANFORD, Calif. – Scientists at the Stanford University School of Medicine are shedding light on how type-1 diabetes begins.

Doctors have known the disease is caused by an autoimmune attack on the pancreas, but the exact trigger of the attack has been unclear. Now, a new study in mice implicates the immune signal interferon-alpha as an early culprit in a chain of events that upend sugar metabolism and make patients dependent on lifelong insulin injections.

“We never considered that interferon-alpha could be a major player in early type-1 diabetes,” said Qing Li, MD, PhD, a postdoctoral scholar in microbiology and immunology who was the primary author of a paper describing the new result. The study is published in today’s issue of Proceedings of the National Academy of Sciences. “This was a pretty surprising finding.”

Interferon-alpha normally helps the body fight viruses. Synthetic interferon-alpha is injected as a drug for treating hepatitis C and some forms of cancer, Li noted.

“Everybody’s been wondering what process initiates type-1 diabetes,” said Hugh McDevitt, MD, professor of microbiology and immunology and the study’s senior author.

Type-1 diabetes is caused by complete deficiency of insulin, a hormone that helps the body store and burn sugar. About 1 million Americans have the disease, also known as juvenile diabetes because it tends to be diagnosed in children and young adults, for which there is no effective prevention or cure. Diabetes is a leading cause of heart disease, blindness, limb amputations and kidney failure.

The early pathology of type-1 diabetes is hard to study in humans, McDevitt said, because it’s almost impossible to predict who will get the disease and when it will develop. Scientists have relied on animal models, such as diabetic mice, because they predictably develop high blood sugar and other features of the human disease.

To pinpoint interferon-alpha, Li and McDevitt worked backwards from what they knew about how type-1 diabetes starts. Prior studies in diabetic mice showed a pathogenic role for immune cells called CD4+ T cells. These cells are an early player in the immune attack on the body’s insulin factories, pancreatic beta cells. The scientists used silicon gene-chip technology to measure which genes are revved up in the CD4+ T cells just before they assault the pancreas. The measurements fell into a pattern: many of the upregulated genes were known to be controlled by interferon-alpha.

To confirm the signal’s nefarious role, the researchers gave mice an antibody that blocks interferon-alpha activity several weeks before the animals were expected to develop diabetes. Thwarting interferon-alpha delayed the start of the disease by an average of four weeks, and, in 60 percent of treated mice, it prevented diabetes entirely.

The finding confirmed the importance of interferon-alpha and helped the scientists connect the dots between normal mouse physiology and early diabetes. Mice are born with more pancreatic beta cells than they need, Li noted. The extras soon undergo programmed cell death, leaving plenty of working beta cells to pump out insulin. However, in mice that develop diabetes, debris left behind by the dying cells triggers an inappropriate immune response, with lots of interferon-alpha. The interferon-alpha cues immune destruction of more and more beta cells, causing insulin deficiency and diabetes.

The mechanism may be more complex in humans, the scientists cautioned, explaining that while their new finding goes a long way toward explaining the beginnings of diabetes in the mice, additional genetic and environmental factors influence the human disease. But the basic principle of disease is likely the same in diabetic mice and humans, they said.

“A normal process – programmed cell death – causes a normal response,” McDevitt said. “But it does this in such a way that, in a small subset of the population, it starts them on the road to type-1 diabetes.”

Source: Stanford University Medical Center

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High cholesterol levels drop naturally in children on high-fat anti-seizure diet, Hopkins study show

May 15th, 2009 BMI

Elevated cholesterol levels return to normal or near normal levels over time in four out of 10 children with uncontrollable epilepsy treated with the high-fat ketogenic diet, according to results of a Johns Hopkins Children’s Center study reported in the Journal of Child Neurology. The study appears online ahead of print at http://jcn.sagepub.com/cgi/reprint/23/7/758.

In the four-year study, the Hopkins Children’s team followed 121 epileptic children with intractable seizures on the high-fat, low-carbohydrate ketogenic diet designed to control such seizures. While most children developed high cholesterol after starting the diet, cholesterol gradually improved in nearly half of them, returning to normal or near-normal levels, with or without modifications to their diet to reduce fat intake.

In fact, researchers point out, diet modifications-including reducing total fat content or certain types of fats called saturated fats and adding nutritional supplements-reduced high cholesterol just as much as doing nothing. High cholesterol is defined as total cholesterol greater than 200 mg per deciliter of blood, bad or LDL (low-density lipoprotein) cholesterol greater than 130, triglycerides greater than 130, and good or HDL (high-density lipoprotein) lower than 35.

Researchers prescribed dietary modifications to increase “good,” polyunsaturated fats in the diets of 15 children with elevated cholesterol. Dietary modifications decreased cholesterol by 20 percent in 9 out of the 15 (60 percent) children whose diets were modified. Surprisingly, cholesterol also dropped by at least 20 percent in 41 percent of the 37 children whose diets remained unchanged. The findings, while encouraging overall, also mean that relying on diet changes alone may not do much for those children in whom cholesterol remains persistently elevated, and that new approaches for these patients are needed, researchers say.

The findings should come as comforting news to pediatric neurologists, general pediatricians and parents of children treated with the ketogenic diet, and reassure them that, in most patients, increases in cholesterol may be short-lived, researchers say. Previous long-term studies by the Hopkins group of children who were on the diet between six and 12 years echoed these findings. The ketogenic diet, believed to work by triggering biochemical changes that eliminate seizure-provoking short-circuits in the brain’s signaling system, is used in many children with hard-to-control epilepsy and in those whose seizures do not respond to traditional anticonvulsant medications.

“We are greatly encouraged by our findings because the nearly half of the children on the diet were either able to maintain healthy cholesterol or gradually metabolized the extra fat and returned to somewhat normal cholesterol levels,” says senior investigator Eric Kossoff, M.D., a pediatric neurologist at Hopkins Children’s. “This means the benefits of the diet-a diet that is lifesaving in many children and therapeutic in most of them-continue to outweigh the risks.”

Noting that 40 percent of children maintained normal cholesterol even after starting the diet, researchers found that children fed a formula-based, liquid-only ketogenic diet were nearly three times less likely to develop high cholesterol. Researches attribute this finding to the nearly zero fat content in commonly used ketogenic diet formulas.

In the group with normal cholesterol, 78 percent of children (31 out of 40) were fed formula-based ketogenic diet. This finding, while requiring further study, points to another possible treatment for high cholesterol, Kossoff says, by switching children with persistently elevated cholesterol to formula-based ketogenic diets at least some of the time. The formula-based ketogenic diet contains only one-third the amount of saturated fats-the worst kind in terms of cholesterol-of the solid food version of the ketogenic diet. Because doctors can tweak the ratio of fat vs. carbohydrates depending on each child’s severity of seizures, the investigators examined whether higher-fat versions of the ketogenic diet raised cholesterol additionally, but found that higher-fat ratio did not make cholesterol worse than a lower-fat ratio.

Some of the other findings:

 

  • One-fourth of 121 children had elevated total cholesterol before starting the diet, which increased to 60 percent (59 out of 99 children at follow-up) after the initiation of the diet.
  • 18 percent (22 out of 119) had triglycerides over 130 before the diet, which increased to 51 percent (49 out of 96) after starting the diet.
  • 19 percent (21 out 110) had bad cholesterol over 130 before the diet, which increased to 53 percent (48 out of 93) after starting the diet.

Source: Johns Hopkins Medical Institutions

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Olive leaf extract can help tackle high blood pressure and cholesterol

May 15th, 2009 BMI

Taking 1000mg of a specific olive leaf extract (EFLA®943) can lower cholesterol and lower blood pressure in patients with mild hypertension (high blood pressure). These findings came from a ‘Twins’ trial, in which different treatments were given to identical twins. By doing this, researchers could increase the power of their data by eliminating some of the uncertainties caused by genetic variations between individual people.

The research is published in the latest edition of Phytotherapy Research.

Hypertension is one of the most common and important disease risk factors imposed by the modern lifestyle. Many people would therefore benefit from finding ways of reducing blood pressure. Experiments in rats had previously indicated that olive leaf extract could be one way of achieving this goal.

To test this in humans, researchers from Switzerland and Germany conducted a pilot trial with 20 identical (monozygotic) twin pairs who had an increased blood pressure. Individuals were either given placebo capsules or capsules containing doses of 500mg or 1000mg of olive leaf extract EFLA®943. Pairs of twins were assigned to different treatments. After the subjects had taken the extract for eight weeks researchers measured blood pressures as well as collecting data about aspects of life-style.

“The study confirmed that olive leaf extract EFLA®943 has antihypertensive properties in humans,” says one of the co-authors, Cem Aydogan, General Manager, Frutarom Health.

“This works showed that taking a 1000mg dose has substantial effects in people with borderline hypertension,” says Aydogan.

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New study shows health benefits of probiotic could extend to the entire body

May 15th, 2009 BMI

Cork, Ireland – August 25, 2008 – Data from a recent study demonstrate the anti-inflammatory and pathogen protection benefits of Bifidobacterium infantis 35624 a probiotic bacterial strain of human origin. Gastrointestinal benefits of probiotics have been well-documented, but more and more research is revealing that probiotic benefits extend to the entire body. The report was published in the August issue of the Public Library of Science (PLoS) Pathogens.

The inflammatory response is a key part of the immune system’s battle against invaders. The normal response to infection is rapid and effective, however, the immune response may occasionally cause inflammation and damage to healthy tissue.

“Inflammation is a major factor in a number of chronic diseases affecting millions of people and can cause an unwanted impact on healthy tissue,” said Dr. Liam O’Mahony, lead investigator. “Past research has shown that the probiotic Bifidobacterium infantis 35624 can positively impact the body’s immune defense3, and this most recent data suggests that its benefits are not restricted to the gastrointestinal tract.”

Inflammation is associated with a wide range of conditions, such as inflammatory bowel disease, arthritis, bacterial-induced colitis, type I diabetes and organ transplantation. Bifidobacterium infantis 35624 has previously shown ability to modulate the inflammatory response in a clinical trial of patients with irritable bowel syndrome.2 The new data suggests additional health benefits of this particular probiotic strain.

The published study examined the effect of Bifidobacterium infantis 35624 administration on immunity to Salmonella (Salmonella typhimurium), harmful bacteria that can cause intestinal infections and trigger the body’s inflammatory response. Bifidobacterium infantis 35624, a probiotic strain isolated from healthy human gastrointestinal tissue, was administered to mice in freeze-dried powder at least three weeks prior to salmonella infection. Animals that received Bifidobacterium infantis 35624 showed dramatically increased numbers of certain immune cells that control the immune system response to harmful pathogens, in this case Salmonella.

Additionally, data show increased numbers of T-regulatory (Treg) cells, or cells that suppress inflammatory disease in a wide range of autoimmune diseases. Administration of Bifidobacterium infantis 35624 resulted in the induction of these Treg cells, which protected the host from excessive inflammation during the course of infection. Researchers concluded that the introduction of Bifidobacterium infantis 35624 results in enhanced protection from infection, while limiting pro-inflammatory damage caused by superfluous activation of the innate immune system.

Source: Manning Selvage & Lee

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Low cholesterol associated with cancer in diabetics

May 15th, 2009 BMI

Low levels of LDL cholesterol as well as high levels are associated with cancer in patients with type 2 diabetes, found a prospective cohort study http://www.cmaj.ca/press/pg427.pdf published in CMAJ.

Researchers from the Hong Kong Institute of Diabetes and Obesity, the Li Ka Shing Institute of Health Sciences and The Chinese University of Hong Kong conducted a study of 6107 Chinese patients with type 2 diabetes and found a V-shaped risk relation between LDL cholesterol and cancer in patients not receiving statin therapy.

“LDL cholesterol levels below 2.80 mmol/L and levels of at least 3.90 mmol/L were both associated with markedly elevated risk of cancer among patients who did not use statins,” state Dr. Juliana Chan and coauthors.

The study excluded people on statins as statins obscured the association between LDL cholesterol and all-site cancer.

Increasing data suggests an association between type 2 diabetes and an elevated risk of cancer, including breast, colorectal, pancreatic and liver cancers. An elevated risk of cancer in patients with low LDL was linked to cancers of digestive organs and peritoneum, genital and urinary organs, lymphatic and blood tissues as well as other areas. Patients with an LDL cholesterol level above 3.80 mmol/L had heightened risks of oral, digestive, bone, skin, connective tissue, breast and other cancers.

Regarding clinical implications, the authors suggest “the use of these levels as risk markers may help clinicians to assess their patients more fully and thus to prevent premature deaths in patients who have high risk.”

They call for re-analysis of data from clinical trials to confirm or refute these findings.

In a related commentary, Drs. Frank Hu and Eric Ding of Harvard School of Public Health (Todd Datz, Public Relations, Harvard School of Public Health, 617-432-3952 for Dr. Frank Hu) say confounding factors such as indication for the use of statins, lifestyle and socioeconomic status must be considered when looking at the association of high levels of LDL cholesterol and the risk of cancer.

“Low serum cholesterol is commonly observed in individuals with ill health (e.g. cancer patients) and those with unhealthy lifestyle characteristics such as smoking and heavy drinking,” states Hu.

Source: Canadian Medical Association Journal

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M&Ms as diet food? 100-calorie pack misconceptions

May 15th, 2009 BMI

Beware of mini-packs and mini-foods, especially if you’re a dieter.

Chronic dieters tend to consume more calories when foods and packages are smaller, according to a new study in the Journal of Consumer Research. Authors Maura L. Scott, Stephen M. Nowlis, Naomi Mandel, and Andrea C. Morales (all Arizona State University) examined consumer behavior regarding “mini-packs,” 100-calorie food packages that are marketed to help people control calorie intake.

“Interestingly, one group that over-consumes the mini-packs is chronic dieters—individuals constantly trying to manage their weight and food intake,” write the authors.

The researchers believe their research shows that the ubiquitous small packages may actually undermine dieters’ attempts to limit calories. “On the one hand, consumers perceive the mini-packs to be a generous portion of food (numerous small food morsels in each pack and multiple mini-packs in each box); on the other hand, consumers perceive the mini-packs to be diet food. For chronic dieters, this perceptual dilemma causes a tendency to overeat, due to their emotion-laden relationship with food.”

In a series of studies, the researchers assessed peoples’ perceptions of M&Ms in mini-packs versus regular-sized packages. They found that participants tended to have conflicting thoughts about the mini-packs: They thought of them as “diet food,” yet they overestimated how many calories the packages contained. In subsequent studies, the researchers assessed participants’ relationship with food, dividing them into “restrained” and “unrestrained” eaters. The “restrained” eaters tended to consume more calories from mini-packs than “unrestrained” participants.

The authors conclude that dieters should keep an eye on small packages: “While restrained eaters may be attracted to smaller foods in smaller packages initially, presumably because these products are thought to help consumers with their diets, our research shows that restrained eaters actually tend to consume more of these foods than they would of regular foods.”

Source: University of Chicago Press Journals

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