Skip to content

Monosodium glutamate is an additive used as a "flavor enhancer" that has long been used in foods (processed and packaged foods, as well as fast food and restaurant meals) - and it has also been controversial for decades. Even four decades ago some people complained of headaches after having foods with added monosodium glutamate, and since then health complaints have just increased. Since so much is still unknown about the health effects of additives commonly added to foods, then many people just want to avoid them. But it's tricky because manufacturers sneak monosodium glutamate into foods using various other name such as hydrolyzed vegetable protein, autolyzed yeast, glutamic acid, and yeast extract.

The FDA points out on its web-site that monosodium glutamate (MSG) is the "sodium salt of the common amino acid glutamic acid" - in other words, it is a form of glutamic acid. Glutamic acid is an amino acid naturally present in our bodies, and found naturally in many foods, such as tomatoes, cheeses, meat, seaweed, and mushrooms. The FDA views MSG as "generally recognized as safe". But even if a form of something may occur naturally in foods, that does NOT mean that we want to eat foods with added forms of it, or that we should be eating food with added additives, including MSG.

Sometimes the term "natural flavor" is used by the food industry for glutamic acid (which is chemically similar to MSG). So read ingredient lists carefully. And note that "natural flavor" can mean many things, that they are produced in a lab, and that the Food and Drug Administration (FDA) does not require disclosure of components and amounts of "natural flavor". From Tech Insider:

Here’s how food companies sneak MSG into foods

That savory, meaty, salty taste you get after taking a bite of Chinese beef and broccoli or after a crunch into a Doritos nacho cheese chip is unmistakable. It hits your tongue, makes it water, and leaves you craving more. MSG, which stands for monosodium glutamate — a naturally-occurring food additive — is largely responsible for that irresistible taste. Chemists have been infusing it into everything from broths, frozen pizzas, flavored potato chips, salad dressings, deli meats, and hot dogs, for more than a century to make them taste addictively delicious.

MSG is a naturally occurring amino acid that makes up proteins in our bodies. But the compound's safety has been debated for years. While it is generally recognized as safe by the Food and Drug Administration, some claim that it can cause adverse reactions in sensitive people, including chest pain, flushing, and sweating. It's also reportedly caused numbness or burning near the mouth and facial pressure or swelling. While there haven't been any studies to back up this claim, it would be helpful for sensitive or MSG-wary people to know which processed foods contain the ingredient. But because the additive can go by many different names, it can be difficult to tell which foods contain it.

Take this Doritos label, for instance. You can easily tell that there's MSG in it, because it's listed simply by its full name, "Monosodium Glutamate."....But check out this nutrition label for Nissin Chicken Garden Vegetable Flavor Soup. While it does reveal that it indeed contains monosodium glutamate, it also contains many other forms of glutamates that are often considered slight variations on MSG. Hydrolyzed protein, for example, is just proteins that are broken down into their animo acid components – one of which is glutamic acid, another name for MSG. Autolyzed yeast is a similar example, yeast cells are allowed to die and pop open, which releases their innards, which then break down into individual amino acids — including glutamic acid.

MSG can go by these and many other synonymous names as well, including monosodium salt, monohydrate, monosodium glutamate, monosodium glutamate monohydrate, monosodium L-glutamate monohydrate, MSG monohydrate, sodium glutamate monohydrate, UNII-W81N5U6R6U, L-Glutamic acid, monosodium salt, and monohydrate. Foods that contain these ingredients, of course, aren't necessarily bad for you. Glutamate is a naturally occuring chemical in cheeses, tomatoes, mushrooms, broccoli, peas, and walnuts. Japanese biochemist Kikunae Ikeda first isolated MSG from seaweed in 1908.

The spice turmeric is very popular these days, especially because studies link it to various health benefits. But is this true? Is it better to eat turmeric in foods or take it in pill form as a supplement? Today's post is about a study that was done by the BBC teaming up with researchers at Newcastle University (in the UK) where they looked at whether modest doses of turmeric had health benefits when ingested daily for 6 weeks. Specifically, they looked at what turmeric does to various blood markers thought to be associated with inflammation and changes that could eventually lead to the onset of cancer. It is currently thought that many or turmeric's supposed health benefits come from the compound curcumin found in it.

The researchers took blood samples of 100 volunteers, who were then split up into 3 groups (turmeric powder, a turmeric pill, or a placebo pill daily). Only the group that ingested turmeric in powder form (1 teaspoon mixed in food) showed changes after 6 weeks, and they were exciting beneficial changes in the methylation of DNA. This is because "methylation of the DNA can ‘go wrong’ and this can cause cells to become cancerous".

It's still early days in this research, and more has to be done, but it is exciting. In the meantime, don't take turmeric in pill form, but eat it in foods. It seems that more of the turmeric gets absorbed when eaten with foods, especially foods with fat, and also with a little black pepper. Excerpts from the article written by Michael Mosley, one of the presenters of the broadcast show "Trust Me, I'm A Doctor", from the BBC News:

Could turmeric really boost your health?

Turmeric is a spice which in its raw form looks a bit like ginger root, but when it's ground down you get a distinctive yellowy orange powder that's very popular in South Asian cuisine.....So we tracked down leading researchers from across the country and with their help recruited nearly 100 volunteers from the North East to do a novel experiment. Few of our volunteers ate foods containing turmeric on a regular basis.

Then we divided them into three groups. We asked one group to consume a teaspoon of turmeric every day for six weeks, ideally mixed in with their food. Another group were asked to swallow a supplement containing the same amount of turmeric, and a third group were given a placebo, or dummy pill. The volunteers who were asked to consume a teaspoon of turmeric a day were ingenious about what they added it to, mixing it with warm milk or adding it to yoghurt. Not everyone was enthusiastic about the taste, with comments ranging from "awful" to "very strong and lingering".

But what effect was eating turmeric having on them? We decided to try and find out using a novel test developed at University College, London, by Prof Martin Widschwendter and his team....There are at least 200 different compounds in turmeric, but there's one that scientists are particularly interested in. It gives this spice its colour. It's called curcumin. Thousands of scientific papers have been published looking at turmeric and curcumin in the laboratory - some with promising results. But they've mainly been done in mice, using unrealistically high doses. There have been few experiments done in the real world, on humans.

Prof Widschwendter is not particularly interested in turmeric but he is interested in how cancers start. His team have been comparing tissue samples taken from women with breast cancer and from women without it and they've found a change that happens to the DNA of cells well before they become cancerous. The change is in the "packaging" of the genes. It's called DNA methylation. It's a bit like a dimmer switch that can turn the activity of the gene up or down. The exciting thing is that if it is detected in time this change can, potentially, be reversed, before the cell turns cancerous.

So we asked Prof Widschwendter whether testing the DNA methylation patterns of our volunteers' blood cells at the start and end of the experiment would reveal any change in their risk of cancer and other diseases, like allergies. It was something that had not been done before. Fortunately he was very enthusiastic. "We were delighted," he said, "to be involved in this study, because it is a proof of principle study that opens entirely new windows of opportunity to really look into how we can predict preventive measures, particularly for cancer."

So what, if anything, happened? When I asked him that, he pulled out his laptop and slowly began to speak."We didn't find any changes in the group taking the placebo," he told me. That was not surprising. "The supplement group also didn't also show any difference," he went on. That was surprising and somewhat disappointing.

"But the group who mixed turmeric powder into their food," he continued, "there we saw quite substantial changes. It was really exciting, to be honest. We found one particular gene which showed the biggest difference. And what's interesting is that we know this particular gene is involved in three specific diseases: depression, asthma and eczema, and cancer. This is a really striking finding."

It certainly is. But why did we see changes only in those eating turmeric, not in those taking the same amount as a supplement? Dr Kirsten Brandt, who is a senior lecturer at Newcastle University and who helped run the experiment, thinks it may have something to do with the way the turmeric was consumed. "It could be," she told me, "that adding fat or heating it up makes the active ingredients more soluble, which would make it easier for us to absorb the turmeric.....She also told me, because our volunteers all tried consuming their turmeric in different ways, that we can be confident it was the turmeric that was making the difference and not some other ingredient used to make, say, chicken tikka masala. There is a lot more research that needs to be done, including repeating the experiment to see if these findings can be confirmed.

More information about the study and results from BBC News: Does turmeric really help protect us from cancer?

A new study conducted in China found an association between low vitamin D levels and future cognitive decline in older adults. The lower the vitamin D levels at the initial screening (the baseline), the more people with cognitive decline at a 2 year follow-up. There were were no gender differences. (Another study with similar results.) Vitamin D is produced naturally in the skin when exposed to sunlight, and also found in smaller amounts in food such as fish (e.g. salmon) and eggs. Vitamin D helps maintain healthy bones and muscles, but it also plays a key part in brain function and is viewed as neuroprotective. Low levels are associated with greater risk of cardiovascular and neurodegenerative diseases.

The 1,202 participants (60 years or older) in China had their baseline vitamin D levels measured at the start of the study, and their cognitive abilities assessed over two years. What I found interesting in this study was that the vitamin D levels in the people was in general pretty low - this was without any supplementation, thus from sunlight. The researchers specified vitamin D levels (25-Cholecalciferol) in nmol/l, but in the United States values are generally specified in ng/ml. In the study the median level of vitamin D levels in the lowest quartile converted to ng/ml was 10.0 ng/ml, and in the highest quartile the median level was 26.4 ng/ml. With those low numbers, all 4 groups in the United States would be advised to supplement daily with vitamin D (specifically vitamin D3). From Journals of Gerontology: Medical Sciences:

Vitamin D Levels and the Risk of Cognitive Decline in Chinese Elderly People: the Chinese Longitudinal Healthy Longevity Survey

Vitamin D has a neuroprotective function, potentially important for the prevention of cognitive decline. Prospective studies from Western countries support an association between lower vitamin D level and future cognitive decline in elderly people.

This community-based cohort study of elderly people in China follows 1,202 cognitively intact adults aged ≥60 years for a mean duration of 2 years. Plasma vitamin D level was measured at the baseline. Cognitive state of participants was assessed using the Mini-Mental State Examination (MMSE). Cognitive impairment was defined as an MMSE score <18. Cognitive decline was defined as ≥3 points decline from baseline....Participants with low vitamin D level had an increased risk of cognitive decline. This first follow-up study of elderly people, including the oldest-old, in Asia shows that low vitamin D levels were associated with increased risk of subsequent cognitive decline and impairment.

Vitamin D is a secosteroid hormone necessary for maintaining good musculoskeletal health; its deficiency is associated with increased risks of cardiovascular and neurodegenerative diseases. Vitamin D is primarily synthesized in the skin upon exposure to sunlight; smaller amounts are obtained through dietary intake. More recently, enzymes responsible for the synthesis of its active form have been found to be distributed throughout the human brain.... This growing body of evidence suggests that vitamin D has a neuroprotective function that is potentially important for the prevention of cognitive decline. Although the importance of vitamin D cannot be disregarded, there is still no consensus on its optimal level. This is especially pertinent in the elderly people, the oldest-old in particular, as cutaneous synthesis of vitamin D decreases with age. Moreover, their impaired mobility and limited outdoor activities can further exacerbate vitamin D deficiency.

Cross-sectional studies have generally found a positive association between vitamin D status and cognitive performance in older adults. Recent prospective studies from United States and Europe support an association between diminished vitamin D status and future cognitive decline. Since cutaneous synthesis is the main source of vitamin D, there exists great variability in vitamin D levels across populations due to differences in latitude, seasons, and race/ethnicity, such as level of skin pigmentation.

Our findings were consistent with previous cohort studies showing that vitamin D status predicts cognitive decline....A notable observation in the present study is that the association of vitamin D status and cognitive decline were similar in both oldest-old and less elderly people. In this study, there was a clear association between lower 25(OH)D3 level and cognitive impairment in subjects aged ≥80....An additional difference from previous studies is that the current study indicates that the association between vitamin D and cognitive impairment is not gender specific.

The observation of temporal association between 25(OH)D3 levels and subsequent cognitive function supports the notion that vitamin D has a clinically important neuroprotective effect. A wide variety of mechanisms for this effect has been proposed and is supported by animal studies. Vitamin D has been found to modulate neuronal calcium homeostasis, cerebral process of detoxification, immunomodulation, and beta-amyloid clearance.....Further, it was unlikely that vitamin D supplementation would explain the association in this study, as 87% of the participants reported no use of vitamin supplements....In conclusion, our longitudinal study indicates that low 25(OH) D3 levels are associated with subsequent cognitive decline and cognitive impairment

Image result for meat, fish, eggs It is important to eat a varied diet for health, one that focuses on the food groups (and no - cookies and cake are not necessary foods). The first study looks at liver cancer risk and selenium - which is found in fish, shellfish, meat, milk, eggs, and certain South American nuts, such as Brazil nuts. The second article focuses on colorectal cancer and retinoic acid, a compound derived in the body from vitamin A. Vitamin A rich foods can provide you with retinoic acid, such as the lungs, kidneys, and liver of beef, lamb, pork. Also poultry giblets, eggs, cod liver oil, shrimp, fish, fortified milk, butter, cheddar cheese and Swiss cheese. Red and orange vegetables and fruits such as sweet potatoes, squash, carrots, pumpkins, cantaloupes, apricots, peaches and mangoes all contain significant amounts of beta-carotene, thus retinoids. Note that research generally has found health benefits from real foods, not from supplements.

From Science Daily:  Selenium status influence cancer risk

As a nutritional trace element, selenium forms an essential part of our diet. Researchers have been able to show that high blood selenium levels are associated with a decreased risk of developing liver cancer. Selenium (Se) is found in foods like fish, shellfish, meat, milk and eggs; certain South American nuts, such as Brazil nuts, are also good sources of selenium. It is a trace element that occurs naturally in soil and plants, and enters the bodies of humans and animals via the food they ingest. European soil has a rather low selenium concentration, in comparison with other areas of the world, especially in comparison to North America. Deficiencies of varying degrees of severity are common among the general population, and are the reason why German livestock receive selenium supplements in their feed.

While in Europe, neither a selenium-rich diet nor adequate selenium supplementation is associated with adverse effects, selenium deficiency is identified as a risk factor for a range of diseases. "We have been able to show that selenium deficiency is a major risk factor for liver cancer," says Prof. Dr. Lutz Schomburg of the Institute of Experimental Endocrinology, adding: "According to our data, the third of the population with lowest selenium status have a five- to ten-fold increased risk of developing hepatocellular carcinoma -- also known as liver cancer."....Previous studies had suggested a similar relationship between a person's selenium status and their risk of developing colon cancer, as well as their risk of developing autoimmune thyroid disease. (Original study)

From Science Daily: Retinoic acid suppresses colorectal cancer development, study finds

Retinoic acid, a compound derived in the body from vitamin A, plays a critical role in suppressing colorectal cancer in mice and humans, according to researchers at the Stanford University School of Medicine. Mice with the cancer have lower-than-normal levels of the metabolite in their gut, the researchers found. Furthermore, colorectal cancer patients whose intestinal tissues express high levels of a protein that degrades retinoic acid tend to fare more poorly than their peers.

"The intestine is constantly bombarded by foreign organisms," said Edgar Engleman, MD, professor of pathology and of medicine. "As a result, its immune system is very complex. There's a clear link in humans between inflammatory bowel disease, including ulcerative colitis, and the eventual development of colorectal cancer. Retinoic acid has been known for years to be involved in suppressing inflammation in the intestine. We wanted to connect the dots and learn whether and how retinoic acid levels directly affect cancer development."

"We found that bacteria, or molecules produced by bacteria, can cause a massive inflammatory reaction in the gut that directly affects retinoic acid metabolism," said Engleman. "Normally retinoic acid levels are regulated extremely tightly. This discovery could have important implications for the treatment of human colorectal cancer."

Further investigation showed that retinoic acid blocks or slows cancer development by activating a type of immune cell called a CD8 T cell. These T cells then kill off the cancer cells. In mice, lower levels of retinoic acid led to reduced numbers and activation of CD8 T cells in the intestinal tissue and increased the animals' tumor burden, the researchers found. "It's become very clear through many studies that chronic, smoldering inflammation is a very important risk factor for many types of cancer," said Engleman.

Can eating a vegetarian diet lower blood pressure? Both this review and other reviews of studies say YES, that those following vegetarian diets have a lower prevalence of hypertension. Overall, the mean prevalence of hypertension was 21% in those consuming a vegetarian diet and 29% in those consuming a nonvegetarian diet (the differences varied between studies).Those following a vegetarian diet also tended to have a healthier lifestyle. As the researchers point out: blood pressure medicine lowers blood pressure for one day, while lifestyle changes (diet, exercise, not smoking, limiting or avoiding alcohol) can lower blood pressure for life. From Medscape:

Vegetarian Diet: A Prescription for High Blood Pressure?

Hypertension is one of the most costly and poorly treated medical conditions in the United States and around the world. Consequences of hypertension include morbidity and mortality related to its long-term effects, which include stroke, myocardial infarction, renal failure, limb loss, aortic aneurysm, and atrial fibrillation, among many others. Although there is an armamentarium of medications to treat hypertension, we do little for prevention. In this review we examine the relationship between vegetarian and nonvegetarian diets and the prevalence of hypertension. 

Current nonpharmacologic treatments include: physical activity (≥ 30 minutes of moderate-intensity activity on most days of the week); smoking cessation; dietary modification (lower sodium, increased potassium; mainly plant-based foods; low-fat foods; reduced-fat dairy products; moderate amounts of lean unprocessed meats, poultry, and fish; and moderate amounts of polyunsaturated and monounsaturated fats, such as olive oil); weight reduction; management of stress; and limited alcohol consumption.

It is well known that hypertension is modulated by dietary influences. In this review we examine vegetarian, vegan, and nonvegetarian (omnivore) diets and prevalence of hypertension among these dietary populations. A vegetarian diet (ie, lacto/ovo-vegetarian) includes plant foods, dairy products, and eggs (excludes all meat, such as turkey, beef, poultry, seafood, bacon, etc.). A vegan diet is similar to vegetarian, except it further excludes dairy products and eggs (no animal or animal products). On the other hand, an omnivore diet (referred to as nonvegetarians throughout this study) includes both plant and animal foods and products.....The majority of studies included in this review addressed vegetarians and vegans as a single group (vegetarians), whereas others differentiated them. Vegetarian diets are known to be low in saturated fat and cholesterol, high in fiber, low in sodium, and high in potassium. These key elements have been shown to correlate with lower incidence of cancer, heart disease, and other chronic diseases, such as diabetes type II, hypertension, and hyperlipidemia.

The exact percentage of those following a vegetarian or vegan diet in the US is unknown; however, a 2014 study found that 221 of 11,399 adult respondents, from a group generally representing the demographics of the US, identified as vegan (0.5%), vegetarians (1.5%), or meat-eaters (98%). The prevalence of hypertension in the US in 2011 was roughly 33.8%.

The mean prevalence of hypertension in those consuming a vegetarian diet was 21% and 29% in those consuming a nonvegetarian diet. The overall prevalence of hypertension among vegetarians was 33% lower than nonvegetarian diets. These data support the hypothesis of a decreased prevalence of hypertension in those maintaining a vegan or vegetarian diet versus a nonvegetarian diet, in cross-sectional, cohort, and case-control studies, and in those consuming a vegan or vegetarian diet according to an experimental dietary change. The blood pressure benefit is noted to disappear in those reverting back to a nonvegetarian diet. 

Overall, these findings support previous reviews and meta-analyses of vegetarian and nonvegetarian diets and blood pressure. A recent meta-analysis that identified 39 studies with 21,915 participants concluded vegetarian diets were associated with a drop in mean systolic (-5.9 mm Hg) and diastolic (-3.5 mm Hg) blood pressures when compared with nonvegetarians. Other reviews had similar conclusions, showing that vegetarians have a lower blood pressure compared with nonvegetarians. Of the studies that included a vegan diet separate from other vegetarians (eg, lacto/ovo), the data show a significantly lower prevalence of hypertension when compared with nonvegetarians and other vegetarians. However, limited research has been conducted on strict, consistent vegan diets.

There are possible rationalizations for the observed associations between diet and hypertension. First, vegetarians have a lower rate of smoking tobacco. Smoking can increase blood pressure acutely and chronically over time.....Second, vegetarians tend to drink less alcohol compared with nonvegetarians. Alcohol, specifically ≥ 2 drinks/day, increases blood pressure by causing vasodilation, followed by a compensatory increase in blood pressure.....Further, vegetarians have a lower mean BMI when compared with nonvegetarians, which means a lower overall weight....Fourth, vegetarians tend to exercise more than nonvegetarians. Vegetarians reported a greater incidence of physical activity of ≥ 30 minutes of moderate to vigorous activity per day.

A limitation of this study is that it remains unclear whether vegetarians are more health conscious and therefore live healthier lives, or whether a predominant diet of fruits and vegetables is a basis for lower blood pressure.

 Eating several servings of seafood (especially fish) weekly has beneficial health effects throughout life, and now research finds another benefit in older adults. Seafood contains both EPA and DHA, which are two types of omega-3 fatty acids. DHA or docosahexanoic acid has "neuroprotective qualities" and is found in both the gray and white matter of the brain. Higher DHA levels (measured in the blood) was associated with better memory, less brain atrophy (better brain volume), and fewer amyloid plaques (which are associated with Alzheimer's) in cognitively healthy older adults. From Medscape:

Higher Serum DHA Linked to Less Amyloid, Better Memory

New research supports neuroprotectant effects of docosahexaenoic acid (DHA) in the aging brain. In a small cross-sectional study of cognitively healthy older adults, higher serum DHA levels were associated with less cerebral amyloidosis, better memory scores, and less regional brain atrophy.

"The interesting finding was the association of low serum DHA levels with cerebral amyloidosis (amyloid plaques) in older adults without evidence of dementia," Hussein N. Yassine, MD, Department of Medicine, University of Southern California, Los Angeles, told Medscape Medical News. "This association was predominantly driven by persons at the lowest quartile of serum DHA levels who likely have limited intake of seafood." "This study adds to the existing evidence on the benefit of seafood consumption on [Alzheimer's disease] AD risk factors," Dr Yassine added.

The study was published online August 8 in JAMA Neurology. In a linked editorial, Joseph F. Quinn, MD, Department of Neurology, Oregon Health and Science University, Portland, notes that DHA is "the most abundant polyunsaturated fatty acid in the brain, playing an important structural role in synapses while also modulating a number of signaling pathways. "Brain DHA levels are also modulated by dietary intake, so it is plausible for dietary DHA to alter brain concentrations and affect downstream targets including brain pathology and function."

Dr Yassine and colleagues assessed serum DHA levels, measures of amyloid burden based on positron emission tomography with Pittsburgh compound B, brain volume, and neuropsychological test scores in 61 adults without dementia in the Aging Brain Study.

They found that serum DHA levels (percentage of total fatty acids) were 23% lower in those with cerebral amyloidosis relative to those without. Serum DHA levels were inversely correlated with brain amyloid load, independent of age, sex, years of education, and apolipoprotein E genotype. They also noted a positive correlation between serum DHA levels and brain volume in several subregions affected by AD, in particular the left subiculum and the left entorhinal volumes.

Clinically, there was a significant association between serum DHA levels and nonverbal memory. This association persisted after adjustment for age but not after adjustment for apolipoprotein E genotype. Serum DHA levels were not associated with measures of global cognition, executive function, or verbal memory scores.

Yes! Treating young children who have peanut allergies with doses of peanut protein (oral immunotherapy or OIT) for one month works in treating the peanut allergies in the overwhelming majority of young children in an important study. Several studies have now shown that early exposure to nuts is important for prevention of nut allergies, and in this study the researchers showed that both lower and higher dose oral immunotherapy works in treating nut allergies in young children (9 to 36 months of age). Note that this is a paradigm change - before this the thinking was avoid, avoid, avoid for the child to not get or to not worsen the allergy (whether nuts or animals), but now it's early exposure is good in preventing and treating allergies. From Futurity:

Can therapy before 3 wipe out a peanut allergy?

Preschool children with a peanut allergy were able to start eating peanuts after taking part in oral immunotherapy, a new study shows. The findings confirm and extend previous results that show oral immunotherapy (OIT) can protect children from potentially life-threatening anaphylaxis caused by peanut exposure.

The phase two clinical trial results, published online in the Journal of Allergy and Clinical Immunology, show that one month after completing the OIT protocol, almost 80 percent of trial participants achieved “sustained unresponsiveness,” the highest rate yet reported.

“These findings, if confirmed in larger studies, could transform the care of peanut-allergic children early in life,” says Brian P. Vickery, lead investigator of the trial and assistant professor of pediatrics at the University of North Carolina at Chapel Hill. Approximately three million people in the United States report having allergies to peanuts and tree nuts. According to a study released in 2013 by the Centers for Disease Control and Prevention, food allergies among children increased approximately 50 percent between 1997 and 2011.

The initial allergic reaction to peanuts commonly occurs within the first year or two of life, and the condition persists in 80 percent of affected patients, placing them at life-long risk of anaphylaxis. Based on other studies suggesting that peanut allergies strengthen over time, researchers enrolled 40 peanut-allergic children aged 9 to 36 months in the trial, the first study to specifically target children under the age of three.

Children were randomly assigned to high-dose peanut OIT with a target daily dose of 3,000 milligrams of peanut protein or a low-dose regimen with a target dose of 300 milligrams. The trial was double-blinded. Participants took 3,000 mg of study protein, but for the low-dose group, 2,700 mg of placebo was added to the OIT medication. As in previous studies, nearly all participants experienced some side effects, most of which were mild and required little or no treatment.

After receiving OIT for 29 months on average, participants abstained from peanut exposure for four weeks before undergoing a final peanut challenge—where participants ingest a small amount of peanut in a controlled setting. If the challenge is successful, then doctors reintroduce normal amounts of peanuts—such as in a peanut butter and jelly sandwich—into the diets of participants. After the four-week period, nearly 80 percent of children in both the high- and low-dose groups consumed peanut with no allergic response and achieved sustained unresponsiveness.

The OIT-treated children were compared with a matched control group of 154 peanut-allergic children who avoided peanut. The OIT-treated children experienced beneficial changes in their immune responses to peanut and were 19 times more likely to successfully incorporate peanut into their diets. 

  Again, another study showing the importance of lifestyle factors in the development of protein buildups in the brain that are associated with the onset of Alzheimer's disease. Specifically, the study found that each one of several lifestyle factors—a healthy body mass index, physical activity and a Mediterranean diet, were linked to lower levels of plaques and tangles on brain scans in people who already had mild memory changes, (but not dementia). Other posts discussing Mediterranean diet and brain health (brain volume, etc.) are here, here, and here. Activity levels and brain health posts are here, here, and here. From Medical Xpress:

Diet and exercise can reduce protein build-ups linked to Alzheimer's

A study by researchers at UCLA's Semel Institute for Neuroscience and Human Behavior has found that a healthy diet, regular physical activity and a normal body mass index can reduce the incidence of protein build-ups that are associated with the onset of Alzheimer's disease.

In the study, 44 adults ranging in age from 40 to 85 (mean age: 62.6) with mild memory changes but no dementia underwent an experimental type of PET scan to measure the level of plaque and tangles in the brain. Researchers also collected information on participants' body mass index, levels of physical activity, diet and other lifestyle factors. Plaque, deposits of a toxic protein called beta-amyloid in the spaces between nerve cells in the brain; and tangles, knotted threads of the tau protein found within brain cells, are considered the key indicators of Alzheimer's.

The study found that each one of several lifestyle factors—a healthy body mass index, physical activity and a Mediterranean diet—were linked to lower levels of plaques and tangles on the brain scans. (The Mediterranean diet is rich in fruits, vegetables, legumes, cereals and fish and low in meat and dairy, and characterized by a high ratio of monounsaturated to saturated fats, and mild to moderate alcohol consumption.)

"The fact that we could detect this influence of lifestyle at a molecular level before the beginning of serious memory problems surprised us," said Dr. David Merrill, the lead author of the study, which appears in the September issue of the American Journal of Geriatric Psychiatry.

Earlier studies have linked a healthy lifestyle to delays in the onset of Alzheimer's. However, the new study is the first to demonstrate how lifestyle factors directly influence abnormal proteins in people with subtle memory loss who have not yet been diagnosed with dementia, Merrill said. Healthy lifestyle factors also have been shown to be related to reduced shrinking of the brain and lower rates of atrophy in people with Alzheimer's."The study reinforces the importance of living a healthy life to prevent Alzheimer's, even before the development of clinically significant dementia," Merrill said. 

Image result for cherries wikipedia Another study reporting health benefits of drinking tart cherry juice, specifically in speeding recovery following prolonged, repeat sprint activity (think soccer and rugby). The researchers found that after a prolonged, intermittent sprint activity, the cherry juice significantly lowered levels of Interleukin-6, a marker for inflammation and that there was a decrease in muscle soreness.  The study participants drank the cherry juice (1 oz cherry juice concentrate mixed with 100 ml water) for several days before and several days after the sprint activity. Montmorency tart cherry juice is a polyphenol rich food that is already used by many professional sports teams to aid recovery. From Medical Xpress:

New study: Montmorency tart cherry juice found to aid recovery of soccer players

Montmorency tart cherry juice may be a promising new recovery aid for soccer players following a game or intense practice. A new study published in Nutrients found Montmorency tart cherry juice concentrate aided recovery among eight semi-professional male soccer players following a test that simulated the physical and metabolic demands of a soccer game .The U.K. research team, led by Glyn Howatson at Northumbria University, conducted this double-blind, placebo-controlled study to identify the effects of Montmorency tart cherry juice on recovery among a new population of athletes following prolonged, intermittent exercise..... many teams in professional and international soccer and rugby already use Montmorency tart cherry juice to aid recovery."

The study involved 16 semi-professional male soccer players aged 21 to 29 who were randomly assigned to either a Montmorency tart cherry concentrate group or a placebo control group. Montmorency group participants consumed about 1 ounce (30 ml) of a commercially available Montmorency tart cherry juice concentrate mixed with 100 ml of water twice per day (8 a.m. and 6 p.m.) for seven consecutive days—for four days prior to the simulated trial and for three days after the trial. Following the same schedule, placebo group participants consumed a calorie-matched fruit cordial with less than 5 percent fruit mixed with water and maltodextrin. The 30 ml dosage of Montmorency tart cherry juice concentrate contained a total anthocyanin content of 73.5 mg, or the equivalent of about 90 whole Montmorency tart cherries.

Montmorency tart cherry juice, compared to a placebo, was found to maintain greater functional performance, impact a key marker of inflammation and decrease self-reported muscle soreness among study participants following prolonged activity that mirrors the demands of field-based sports. While additional research is needed, the authors suggest the dampening of the post-exercise inflammatory processes may be responsible.

Across every performance measure, including maximal voluntary isometric contraction, countermovement jump height, 20 m sprint time, knee extensors, 5-0-5 agility, the Montmorency group showed better performance than the placebo group. Additionally, the Montmorency group showed significantly lower levels of Interleukin-6, a marker for inflammation, particularly immediately post-trial. Ratings for muscle soreness (DOMS) were significantly lower in the Montmorency group across the 72-hour post-trial period. No significant effects in muscle damage or oxidative stress were observed in either the Montmorency group or the placebo group. These data support previous research showing similar results for athletes performing marathon running, high-intensity strength training, cycling, and metabolic exercise. 

Another interesting study looking at whether being overweight is linked to premature death, heart attacks, and diabetes. This study looked at sets of twins, in which one is heavier than the other, and followed them long-term (average 12.4 years) and found that NO - being overweight or obese (as measured by Body Mass Index or BMI) is NOT associated with premature death or heart attack (myocardial infarction), but it is associated with higher rates of type 2 diabetes. These results are in contrast with what a large study recently found. From Science Daily:

Higher BMI not associated with increased risk of heart attack or early death, twin study shows

A study of 4,046 genetically identical twin pairs with different amounts of body fat shows that twin siblings with a higher Body Mass Index, as a measure of obesity, do not have an increased risk of heart attack or mortality. The study, conducted by researchers at Umeå University in Sweden, also shows that a higher BMI is associated with an increased risk of type 2 diabetes...."The results suggest that lifestyle changes that reduce levels of obesity do not have an effect on the risk of death and heart attack, which contradicts conventional understandings of obesity-related health risks," says Peter Nordström, researcher at the Department of Community Medicine and Rehabilitation at Umeå University.

In the cohort study, Peter Nordström and research colleagues at Umeå University compared health data from 4,046 monozygotic twin pairs. All twins in the study had different levels of body fat, as measured in BMI....During a follow-up period of on average 12.4 years, differences between the twins were compared when it comes to incidents of mortality, heart attack and type 2 diabetes. The results clearly showed that twin siblings with a higher BMI did not have an increased risk of mortality or heart attack compared to their thinner counterparts. However, twins with a higher BMI did have an increased risk of developing type 2 diabetes.

The results showed that: - Among twin siblings with a higher BMI (mean value 25.1), there were 203 heart attacks (5 %) and 550 deaths (13.6 %) during the follow-up period. - Among twin siblings with a lower BMI (mean value 23.9), there were 209 heart attacks (5.2 %) and 633 deaths (15.6 %) during the same period. - Among the 65 twin pairs in the study who had a BMI difference of 7 or higher, and where the larger twin siblings had a BMI of 30 or higher, there were still no noticeably increased risk of mortality or heart attack associated with a higher BMI.

The study, described in the article Risks of Myocardinal Infarction, Death, and Diabetes in Identical Twin Pairs With Different Body Mass Index, is based on the Swedish Twin Registry, the largest of its kind in the world. The median age of the twins in the study was 57.5 and participants' ages ranged from 42-92. The cohort study was conducted between 1998 and 2003, with follow-ups regarding incident of mortality, heart attack and diabetes during a 10 year period until 2013. One study limitation was that weight and length (used to calculate BMI) was self-reported.