What happens to your brain when you stop exercising? The results of this Univ. of Maryland study should be a wake up call for those who are not quite convinced of exercise's health benefits to the brain. The researchers examined cerebral blood flow in athletes (ages 50-80 years, who were recruited from running clubs) before and after a 10-day period during which they stopped all exercise. Using MRI brain imaging techniques, they found a significant decrease in blood flow to several brain regions important for cognitive health, including the hippocampus, after they stopped their exercise routines.

As the researchers pointed out: "...the take home message is simple -- if you do stop exercising for 10 days, just as you will quickly lose your cardiovascular fitness, you will also experience a decrease in blood brain flow." The only good news was that there were no differences on cognitive measures both before and after stopping exercise for 10 days. From Science Daily:

Use it or lose it: Stopping exercise decreases brain blood flow

We all know that we can quickly lose cardiovascular endurance if we stop exercising for a few weeks, but what impact does the cessation of exercise have on our brains? New research led by University of Maryland School of Public Health researchers examined cerebral blood flow in healthy, physically fit older adults (ages 50-80 years) before and after a 10-day period during which they stopped all exercise. Using MRI brain imaging techniques, they found a significant decrease in blood flow to several brain regions, including the hippocampus, after they stopped their exercise routines.

"We know that the hippocampus plays an important role in learning and memory and is one of the first brain regions to shrink in people with Alzheimer's disease," says Dr. J. Carson Smith, associate professor of kinesiology and lead author of the study, which is published in Frontiers in Aging Neuroscience in August 2016. "In rodents, the hippocampus responds to exercise training by increasing the growth of new blood vessels and new neurons, and in older people, exercise can help protect the hippocampus from shrinking. So, it is significant that people who stopped exercising for only 10 days showed a decrease in brain blood flow in brain regions that are important for maintaining brain health."

The study participants were all "master athletes," defined as people between the ages of 50 and 80 (average age was 61) who have at least 15 years history of participating in endurance exercise and who have recently competed in an endurance event. Their exercise regimens must have entailed at least four hours of high intensity endurance training each week. On average, they were running 36 miles (59 km) each week or the equivalent of a 10K run a day! Not surprisingly, this group had a V02 max (maximum volume of oxygen) above 90% for their age. This is a measure of the maximal rate of oxygen consumption of an individual and reflects their aerobic physical fitness.

Dr. Smith and colleagues measured the velocity of blood flow in brain with an MRI scan while they were still following their regular training routine (at peak fitness) and again after 10 days of no exercise. They found that resting cerebral blood flow significantly decreased in eight brain regions, including the areas of the left and right hippocampus and several regions known to be part of the brain's "default mode network" -- a neural network known to deteriorate quickly with a diagnosis of Alzheimer's disease. This information adds to the growing scientific understanding of the impact of physical activity on cognitive health.

Image result for antibiotics Yes, of course this makes sense!.... Many rounds of antibiotics have an effect not just in one area of the body, but kill off both good and bad bacteria in many areas of the human body. The researchers in this study found that taking antibiotics for a reason OTHER THAN SINUSITIS was associated with an increased risk of developing chronic sinusitis (as compared to those people not receiving antibiotics). Use of antibiotics more than doubles the odds of developing chronic sinusitis without nasal polyps. And this effect lasted for at least 2 years. Other research has already associated antibiotic use with "decreased microbial diversity" in our microbiome  and with "opportunistic infections" such as Candida albicans and Clostridium difficile. Diseases such as Crohn's disease and diabetes are also linked to antibiotic use. In other words, when there is a disturbance in the microbiome (e.g.from antibiotics) and the community of microbes becomes "out of whack", then pathogenic bacteria are "enriched" (increase) and can dominate.

This study lumped together chronic sinusitis without nasal polyps (CRSsNP) and chronic sinusitis with nasal polyps (CRSwNP), but when the 2 groups are separated out, then antibiotic use was mainly associated with later chronic sinusitis without polyps. It appeared that antibiotic exposure did not significantly impact the odds of developing chronic sinusitis with nasal polyps. The researchers write: "This effect was primarily driven by the CRSsNP subgroup, which also supports the evolving concept of CRSwNP (chronic sinusitis with nasal polyps) as a disease of primary inflammation rather than infection. Despite this, we elected to analyze the CRS (chronic rhinosinusitis) group as a whole because the precise relationship between CRS with and without nasal polyps remains incompletely understood, and it is possible that a proportion of the CRSsNP patients could go on to develop nasal polyps over time."

Which makes me wonder, will giving beneficial bacteria (such as Lactobacillus sakei) to those who have chronic sinusitis with nasal polyps show the same improvement in symptoms as those people without nasal polyps? Or do 2 treatments have to occur at once: something to lower the inflammation (which may be the reason for the nasal polyps) and also beneficial microbes to treat the bacterial imbalance of sinusitis? We just don't know yet. Note that CRS = chronic rhinosinusitis (commonly called chronic sinusitis). From The Laryngoscope :

General antibiotic exposure is associated with increased risk of developing chronic rhinosinusitis 

Antibiotic use and chronic rhinosinusitis (CRS) have been independently associated with microbiome diversity depletion and opportunistic infections. This study was undertaken to investigate whether antibiotic use may be an unrecognized risk factor for developing CRS. Case-control study of 1,162 patients referred to a tertiary sinus center for a range of sinonasal disorders.

Patients diagnosed with CRS according to established consensus criteria (n = 410) were assigned to the case group (273 without nasal polyps [CRSsNP], 137 with nasal polyps [CRSwNP]). Patients with all other diagnoses (n = 752) were assigned to the control group. Chronic rhinosinusitis disease severity was determined using a validated quality of life (QOL) instrument. The class, diagnosis, and timing of previous nonsinusitis-related antibiotic exposures were recorded. Results were validated using a randomized administrative data review of 452 (38.9%) of patient charts. The odds ratio of developing CRS following antibiotic exposure were calculated, as well as the impact of antibiotic use on the subsequent QOL.

Antibiotic use significantly increased the odds of developing CRSsNP  as compared to nonusers. Antibiotic exposure was significantly associated with worse CRS QOL {Quality of Life} scores over at least the subsequent 2 years. These findings were confirmed by the administrative data review. Use of antibiotics more than doubles the odds of developing CRSsNP and is associated with a worse QOL for at least 2 years following exposure. These findings expose an unrecognized and concerning consequence of general antibiotic use.

Antibiotic use and chronic rhinosinusitis (CRS) have been independently associated with microbiome diversity depletion and opportunistic infections. This study was undertaken to investigate whether antibiotic use may be an unrecognized risk factor for developing CRS.....Antibiotics have also been associated with significant adverse side effects. It has long been recognized that antibiotic use may lead to increased susceptibility to secondary mucosal infections from pathogens including Candida albicans and Clostridium difficile.  Recent studies on the concept of mucosal microbial dysbiosis have suggested that these infections arise as a result of antibiotic induced depletion of the diverse commensal microbial assemblage, which enables the proliferation of pathogenic species.

Chronic rhinosinusitis (CRS) impacts more than 30 million Americans....Chronic rhinosinusitis is defined....as having greater than 12 weeks of sinonasal symptoms, along with at least one objective measure of infection or inflammation by nasal endoscopy or radiographic imaging. Studies on the pathogenesis of CRS have proposed multiple etiologic agents, including bacteria, fungus, and biofilms, resulting in chronic infection with associated mucosal inflammation. However the distinct lack of long-term disease resolution following antimicrobial therapy and in some cases surgery, suggests that additional factors are likely involved. Through these studies, CRS with nasal polyps (CRSwNP) has been recognized as an inflammatory subtype characterized by eosinophilic inflammation and a T-helper cell type 2 immunologic profile. Although CRSwNP lacks the features of a classic infectious process, the precise role of bacteria and their byproducts in the promotion of nasal polyp-related inflammation remains unclear.

Recent findings from culture independent investigations of the sinonasal microbiome have offered new insights into the pathogenesis of CRS. These studies have suggested that a decreased microbial diversity exists in CRS patients as compared to healthy controls with a selective enrichment of pathogenic species. Furthermore, some studies have shown that antibiotic exposure may be a risk factor associated with this loss of biodiversity,  echoing the findings seen in postantibiotic C. difficile infections.  Although systemic antibiotics have long been a mainstay of therapy for CRS, these findings lead inexorably to the paradoxical hypothesis that antibiotic exposure may, in fact, promote its onset.

We performed a....case control study of 1,574 patients referred to the Massachusetts Eye and Ear Infirmary Sinus Center in 2014 with symptoms of presumed sinonasal disease.... Inclusion criteria included all antibotic naive patients, and all antibiotic exposed patients for whom antibiotic use was for nonsinonasal-related infections. Among the antibiotic exposed group, only patients who used antibiotics for nonsinonasal-related infections prior to the onset of symptoms of CRS (within the case group) were enrolled in the study.....The case group was further substratified into CRS patients without nasal polyps (CRSsNP, n =273) and with nasal polyps (CRSwNP, n =137) based on the presence of nasal polyps on sinonasal endoscopy.

Among the case patients, 56.34% reported a previous nonsinus-related antibiotic exposure as compared to 42.02% of control patients. Antibiotic use significantly increased the odds of developing both CRSsNP and any form of CRS as compared to nonusers. This odds ratio was similar even when excluding patients who were treated for upper aerodigestive infections. In contrast, antibiotic exposure did not significantly impact the odds of developing CRSwNP. The percent of patients with any form of CRS and CRSsNP only, which was attributable to a previous exposure to antibiotics, was 24.69%  and 33.70%, respectively. In both the case and control groups, the most common class of antibiotic patients received was a penicillin (52.63% vs. 45.77%), and the most common reported reason for antibiotic prescription was the diagnosis of pharyngitis(18.06% vs. 16.67%).

Among the CRS patients (i.e., case group), the use of antibiotics was significantly associated with worse QOL scores as compared to antibiotic-naıve CRS patients. The effect on QOL was enduring because patients who used antibiotics at least 2 years prior to the development of CRS (36.81%) had similar disease severity scores as compared to those with more recent exposures. There was no significant difference in QOL score among patients using different antibiotic classes and among patients with different underlying reasons for antibiotic use.

The human microbiome project has provided new insights into the distribution and abundance of bacterial species in both health and disease. Opportunistic pathogens, as defined by the pathosystems resource integration center, were found nearly ubiquitously in the nares of healthy subjects, albeit at relatively low abundance. Additional studies of the normal nasal cavity found an inverse correlation between the prevalence of Firmicutes such as S. aureus and benign commensal organisms, suggesting a homestatic anatagonism between potential pathogens and the remainder of the healthy microbial assemblage. Extrapolation of this concept would therefore predict that events resulting in a perturbation or loss of the commensal microbial community would enable proliferation of pathogenic species,resulting in the disease phenotype. This prediction has borne out in several studies of the sinonasal microbiome in patients with CRS. Feazel et al. found a decreased number of bacterial types and an overabundance of S. aureus among CRS patients as compared to controls. Antibiotic exposure was one of the most significant clinical factors driving this effect. Similar findings were published by Choi et al. and Abreu et al.... Although literature regarding the sinonasal microbiome in health and disease remains nascent, it has provided some limited clues that antibiotics may lead to a reduction of sinonasal microbial biodiversity, which in turn may be a significant feature of CRS.

Our results demonstrate that exposure to antibiotics is a significant risk factor for the development of CRS and accounts for approximately 25% of the disease burden in our study population. These findings harmonize with the predictions of the nascent literature on the sinonasal microbiome. This effect was primarily driven by the CRSsNP subgroup, which also supports the evolving concept of CRSwNP as a disease of primary inflammation rather than infection. Despite this, we elected to analyze the CRS group as a whole because the precise relationship between CRS with and without nasal polyps remains incompletely understood, and it is possible that a proportion of the CRSsNP patients could go on to develop nasal polyps over time.....

One unexpected outcome of our study was that a large percentage of exposures preceeded the onset of the diagnosis of sinusitis by more than 2 years. This indicates that, regardless of the mechanism, the sequelae of antibiotic use may endure much longer then previously thought. The fact that we could not isolate this effect to any single agent or underlying premorbid infection suggests that this risk must be taken into consideration when prescribing any class of antibiotic, regardless of the type of infection.

The impact of antibiotics on promoting bacterial resistance, and the development of mucosal infections from pathogens such as C. difficile and C. albicans, has been well established. This study demonstrates that antibiotics also significantly increase the risk of developing CRS, an effect that is driven primarily by CRS patients who do not have nasal polyps. Furthermore, premorbid antibiotic use could account for approximately 25% of our patients who developed CRS, and exposure conferred a worse disease-specific quality of life.

 Studies are accumulating evidence that the hormone disrupting effects of compounds BPA (bisphenol A) and BPS (the common substitute for BPA) have numerous negative health effects in humans, including reproductive disorders. But now a second BPA substitute - BPSIP - is also being found in humans, and may be even more persistent than BPA and BPS. This is because they're all chemically similar, and all three are endocrine disruptors. This article points out that they have slightly different effects, and when we are exposed to more than one of them (which we are), then the health effects will be even more worrisome.

Unfortunately these plasticizers are in products all around us, and so detected within almost all of us. They're in food packaging containers (and therefore in food), water bottles, can linings, toys, personal care products, thermal paper products such as cash receipts, etc. Canned foods are considered one of the most significant routes of human exposure to bisphenol A (BPA). Other endocrine disruptors include phthalates - so read personal care product labels to avoid these. Another way to lower exposure to endocrine disruptors is to buy and store food not in plastic containers, but in glass containers or stainless steel. Don't microwave food in any sort of plastic containers. Avoid products with fragrances in them, including air fresheners. Avoid flexible vinyl (e.g. shower curtains). (For all posts on endocrine disruptors, and an article from National Institutes of Health.) From PLOS Biology:

Wreaking Reproductive Havoc One Chemical at a Time

Bisphenol A (BPA), unlike DES, remained obscure until the 1950s, when chemists tapped it to make polycarbonate plastics and epoxy resins. BPA now tops the list of high-volume chemicals, and is found in numerous consumer products, including water bottles, food packaging containers and can linings, and thermal paper products like cash receipts and boarding passes (Fig 1). And because it can leach out of products, it’s been detected in the urine of nearly every person tested. It’s also been found in breast milk, follicular and amniotic fluid, cord blood, placental tissue, fetal livers, and the blood of pregnant women.

Hundreds of studies have associated the BPA levels found in most of us with reproductive disorders, cancers, obesity, and other adverse effects in both animals and humans. Although chemical manufacturers with a stake in the $16 billion BPA market continue to question this evidence, they’ve responded to safety concerns by offering BPA-free alternatives. But as a recent study in PLOS Genetics [1] shows, the new versions seem an awful lot like the original. When one chemical comes under scrutiny, manufacturers often substitute compounds with similar structures to save time and money. But similar structures often cause similar problems. And that’s exactly what the PLOS Genetics authors found.

Thinking BPA’s replacement, bisphenol S (BPS), might target the same pathways, Patrick Allard and his colleagues at the University of California at Los Angeles compared the effects of both substances....But, surprisingly, the authors say, the two bisphenols gummed up the works through somewhat different molecular steps. That means simultaneous exposure to BPA and BPS could potentially cause even more reproductive harm. Future studies will need to confirm this possibility, but it’s an unsettling prospect given the ubiquity of BPA and increasing use of BPS, which has already been found in food, shampoo, face cream and other personal care products, soil, and thermal paper products.

And now there’s another “safer” alternative to worry about, researchers reported in Environmental Health Perspectives [2]. Suspecting that cashiers would face higher exposures on the job, the authors screened their urine, blood, and receipts (as well as people who didn’t handle receipts) for BPA, BPS, and another analog called BPSIP. Cashiers’ BPA levels after work were highly variable, likely resulting from its widespread use, but levels of BPS and BPSIP were higher in most cases. Both BPS and BPSIP were also detected in people who weren’t cashiers....The authors were also surprised to see BPSIP in cashiers’ blood more often than the other compounds, suggesting it may be more persistent and our exposure more widespread than previously assumed. BPSIP’s health effects are unknown.

Much more is known about BPA’s estrogenic powers. Earlier this year Pat Hunt, who was among the first to report BPA’s ability to scramble mouse eggs [3], reported similar problems in mouse sperm in PLOS Genetics [4]. Low sperm counts, undescended testicles, malformed penises, and other reproductive anomalies have risen in recent decades, suggesting environmental estrogens may play a role. Hunt’s team investigated this possibility by exposing newborn male mice to BPA or a stronger synthetic estrogen, ethinyl estradiol, just when sperm differentiation begins. BPA exposure disrupts meiosis in males as it does in female mice, the authors discovered, but in different ways....

Health researchers are especially concerned about environmental contaminants that reach the womb during critical windows when even the slightest disturbance can rewire developmental programs to produce profound, irreversible changes that can take years to appear. These changes can cause a plethora of chronic health problems, including diabetes, cardiovascular disorders, birth defects, and cancer.

  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.

  Yikes! A good reason to lose weight now rather than years from now, and the importance of not ignoring a weight gain (you know, over the years as the pounds slowly creep up). The researchers found that for every 10 years of being overweight as an adult, there was an associated 7% increase in the risk for all obesity-related cancers. The degree of overweight (dose-response) during adulthood was important in the risk of developing cancer, especially for endometrial cancer. This study just looked at postmenopausal women, so it is unknown if it applies to men. From Medscape:

Longer Duration of Overweight Increases Cancer Risk in Women

A longer duration of being overweight during adulthood significantly increased the incidence of all cancers that are associated with obesity, a new study in postmenopausal women has concluded. The large population-based study was published August 16 in PLoS Medicine.

Dr Arnold and colleagues found that for every 10 years of being overweight as an adult, there was an associated 7% increase in the risk for all obesity-related cancers. The risk was highest for endometrial cancer (17%) and kidney cancer (16%). For breast cancer, the increased risk was 5%, but no significant associations were found for rectal, liver, gallbladder, pancreatic, ovarian, and thyroid cancer.

When the authors took into account the degree of excess weight over time, the risks were further increased, and there were "clear dose-response relationships," they note. Again, the risk was highest for endometrial cancer. For each additional decade spent with a body mass index (BMI) that was 10 units above normal weight, there was a 37% increase in the risk for endometrial cancer.

Study Details: The researchers used data from the huge American Women's Health Initiative (WHI) trial of postmenopausal women (aged 50 to 79 years at time of study enrollment). For this analysis, the team focused on a cohort of 73,913 postmenopausal women. During a mean follow-up of 12.6 years, 6301 obesity-related cancers were diagnosed. About 40% (n = 29,770) of women in the cohort were never overweight during their adult life....Women who were ever overweight were on average overweight for about 30 years, while those who were ever obese had been so for an average of 20 years. The authors found that the risk of being diagnosed with an obesity-related cancer rose for every 10 years of being overweight.

 The problem of overdiagnosis and overtreatment has been discussed in a number of posts on this site. And back in April 15, 2016 I posted that a type of noninvasive thyroid cancer had just been reclassified as a noncancer. Now a study in the prestigious New England Journal of Medicine finds that looking at 12 countries (including the USA): "Overall, we estimate that more than 470,000 women and 90,000 men may have been overdiagnosed with thyroid cancer over two decades in these 12 countries..."

The researchers further state that the "vast majority" of these patients received a diagnosis of small, low-risk papillary carcinomas, and they underwent surgery and other treatments, but these interventions have not shown "benefits in terms of improved survival". In fact, studies show that watchful waiting is just as effective. From Medscape:

Thyroid Cancer Overdiagnosis in Half a Million Patients

A large fraction of thyroid cancer cases represent overdiagnoses, and at least half a million patients, most of them women, may have received unnecessary surgery and other cancer treatments, say researchers from the the International Agency for Research on Cancer (IARC), in Lyons, France.

Their warning about an epidemic of thyroid cancer overdiagnosis comes from an analysis of cancer registry data from 12 countries published August 17 in the New England Journal of Medicine . Salvatore Vaccarella, PhD, and colleagues at the IARC estimate that more than 470,000 women and 90,000 men may have been overdiagnosed withthyroid cancer in 12 "high-income" countries (Australia, Denmark, England, Finland, France, Italy, Japan, Norway, Republic of Korea, Scotland, Sweden, and the United States) from 1987 to 2007.

Most of these thyroid cancers were small, low-risk papillary carcinomas, they note. The "vast majority" of these patients underwent total thyroidectomy, and a "high proportion" also received neck lymph-node dissection and radiotherapy, but these interventions do not have "proven benefits in terms of improved survival," the researchers point out...."However, if we take the most recent available period, 2003 - 2007, as typical of current practice, we estimate that overdiagnosis in women accounts for 90% of thyroid-cancer cases in South Korea; 70 to 80% in the United States, Italy, France, and Australia; and 50% in Japan, the Nordic countries, and England and Scotland."

The overdiagnosis is blamed on increasing medical surveillance and the introduction of new diagnostic techniques, such as neck ultrasonography (since the 1980s) and, more recently, CTscanning and MRI. This new technology has led to the detection of a large number of indolent, nonlethal diseases that exist in abundance in the thyroid gland of healthy people of any age, the researchers comment, adding that most of these tumors are very unlikely to cause symptoms or death....."It is fair to say that the large number of thyroid cancers being diagnosed represent an epidemic of diagnosis, or an epidemic of medical testing, rather than an epidemic of true disease."

These results also mean that most patients are receiving treatment that does not benefit them and that subjects them to risks of injury to the voice, permanent hypoparathyroidism, as well as the attendant risks of radioactive iodine treatment, he pointed out.  

The researchers caution against systematic screening for thyroid cancer and overtreatment of nodules <1 cm. "Watchful-waiting approaches should be considered a research priority and a preferable option for patients with low-risk papillary thyroid cancers," they say. Studies from Japan suggest that immediate surgery and watchful waiting are equally effective in preventing mortality, Dr Vaccarella said. One study showed that of 1235 patients with papillary microcarcinomas, only 3.5% experienced clinical progression of disease during a 75-month follow-up, and there were no deaths.

At Memorial Sloan Kettering Cancer Center, active surveillance has been offered to patients with low-risk, small, intrathyroidal cancers for several years, Dr Morris said. "Our results have mirrored the Japanese results, and fewer than 5% of patients end up showing any signs of tumor growth under close observation," he said.

 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. 

 Two recent articles about BPA (bisphenol A), BPS (bisphenol B), and the "BPA-free" label  - one a study, and one a review article. The "BPA-free" label unfortunately means the product contains a product similar to BPA (typically BPS) and with the same problems as BPA. Both articles discuss the accumulating health reasons to try to avoid these endocrine disruptors. Which is really , really tough to do given that plastics are all around us and used by us every day.

From Science Daily: Prenatal BPA exposure linked to anxiety and depression in boys

Boys exposed prenatally to a common chemical used in plastics may be morelikely to develop symptoms of anxiety and depression at age 10-12. The new study by researchers at the Columbia Center for Children's Environmental Health (CCCEH) within the Mailman School of Public Health examined early life exposure to the chemical Bisphenol A (BPA). Results are published in the journal Environmental Research.

BPA is a component of some plastics and is found in food containers, plastic water bottles, dental sealants, and thermal receipt paper. In the body, BPA is a synthetic estrogen, one of the class of chemicals known as "endocrine disruptors." The Columbia researchers, led by Frederica Perera, PhD, DrPH, director of CCCEH, previously reported that prenatal exposure to BPA was associated with emotionally reactive and aggressive behavior, and more symptoms of anxiety and depression in boys at age 7-9.

Perera and her co-investigators followed 241 nonsmoking pregnant women and their children, a subset of CCCEH's longstanding urban birth cohort study in New York City, from pregnancy through childhood....Researchers controlled for factors that have been previously associated with BPA exposure levels, including socioeconomic factors. After separating the data by sex, they found that boys with the highest levels of prenatal exposure to BPA had more symptoms of depression and anxiety than boys with lower levels of prenatal exposure to BPA; no such associations were found in girls.

From Endocrine News: Warning Signs: How Safe Is “BPA Free?”

While stickers are showing up declaring certain products “BPA Free,” that doesn’t mean they’re necessarily safe. Could bisphenol S be even worse than the compound it is supposed to be replacing? 

Human exposure to BPA is as ubiquitous as the stickers showing up now that proclaim products BPA free. The chemical used to make plastic has been linked to all kinds of reproductive issues, and even thought to play a role in the development of obesity and cardiovascular events, so industry is taking some steps to correct the problem (after much wailing and gnashing of teeth on their part). These stickers read “BPA FREE” and “NON-TOXIC PLASTIC” in bold letters and usually feature leaves and a green motif, the implication being that these products are safe and healthy. 

But “BPA free” does not mean “EDC free” [endocrine disruptor free] and many products now contain bisphenol S as a substitute for BPA. BPS is a similar chemical and has been found in everything from canned soft drinks to receipt paper to baby bottles. (The FDA banned BPA in baby bottles.) It’s been found in indoor dust samples and is beginning to show up in human urine, and it has been reported to be less biodegradable than BPA. Animal studies have implicated BPS in impaired offspring development. And the production of BPS is increasing annually.

“Recent studies testing BPS and comparing it to BPA show that BPS is as bad, if not worse, than BPA as an EDC,” says Andrea Gore, PhD, professor and Vacek Chair of Pharmacology at the University of Texas in Austin, and editor-in-chief of Endocrinology. “’BPA free’ can give consumers a false sense of security about the product.”

According to Kimberly H. Cox, a postdoctoral fellow studying reproductive endocrinology at Massachusetts General Hospital in Boston, the effects of BPA and BPS are subtler than say, PCBs or pesticides, where exposures came at high levels, with devastating effects. The effects of BPA and BPS depend on the timing, length, and dose of exposure, and numerous studies have shown that there are effects on the reproductive system, for example, at doses of BPA much lower than what has been determined as a “safe” exposure by the EPA. And now there also seem to be effects of BPS on the development of the reproductive system, as well as the brain regions that control reproduction.

“When endocrinologists talk about BPA, they frequently describe it as estrogenic – and do not point out the other endocrine systems that are being altered, such as thyroid hormone,” Wayne says. “Our paper emphasizes that BPA and BPS are activating both estrogenic and thyroid hormone pathways. This suggests that EDCs are having much broader effects on health and disease than just mimicking estrogens (which is bad enough).”