Skip to content

This study gives hope to those with type 2 diabetes that it may be reversible - even if they've had it for up to 10 years. Researchers demonstrated that in 40% of the 30 study participants on a very low calorie diet (VLCD) of 600 to 700 calories daily for 8 weeks achieved remission of their diabetes for as long as 6 months (the length of the study). They returned to nondiabetic blood glucose levels, had improvement in acute insulin secretion, normalization of liver fat content and insulin sensitivity, and were off all diabetes medicine. The average weight loss was 31 pounds and they maintained this weight loss over the length of the study, even though most remained obese or overweight. The researchers mention that there is already evidence that diabetes reversal lasts for at least 3 years, as long as weight is not regained.

What they did: A) 3 diet shakes per day and 240 grams (1 cup or 1/2 pound) of non-starchy vegetables taking in between 600 and 700 calories per day for 8 weeks, B) volunteers then gradually returned to eating normal food over the next two weeks with very careful instruction on how much to eat, C) volunteers were seen once a month and supported with an individualized weight maintenance program over the next 6 months, D) to keep weight steady after the weight loss, they were eating around one third less than before the study.

Overall, 12 patients who had had diabetes for less than 10 years reversed their condition, and 6 months later they remained diabetes free. In fact, after 6 months a thirteenth patient had reversed their diabetes. The 30 people with diabetes in the study had it between 0.5 and 23 years. The best results were in those who had it for a shorter time. Thus, while 40% of study participants overall reversed their diabetes, 60% of those with short-duration of diabetes (under 10 years) reversed their diabetes. These are fantastic results!

The researchers say that the study results "...supports our theory of a Personal Fat Threshold. If a person gains more weight than they personally can tolerate, then diabetes is triggered, but if they then lose that amount of weight then they go back to normal. Individuals vary in how much weight they can carry without it seeming to affect their metabolism -- don't forget that 70% of severely obese people do not have diabetes." The researchers say type 2 diabetes can now be understood to be a metabolic syndrome that is potentially reversible by substantial weight loss, and that this is an important paradigm shift. They also comment that studies and population data indicate that type 2 diabetes is solely a response to overnutrition.

Excerpts from Diabetes Care:  Very Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiological Changes in Responders and Nonresponders.

Type 2 diabetes mellitus (T2DM) is generally regarded as an irreversible chronic condition. Because a very low-calorie diet (VLCD) can bring about acute return to normal glucose control in some people with T2DM, this study tested the potential durability of this normalization. The underlying mechanisms were defined.

People with a T2DM duration of 0.5-23 years (n = 30) followed a VLCD for 8 weeks. All oral agents or insulins were stopped at baseline.....Weight fell (98.0 ± 2.6 to 83.8 ± 2.4 kg) and remained stable over 6 months (84.7 ± 2.5 kg). Twelve of 30 participants achieved fasting plasma glucose <7 mmol/L after return to isocaloric diet (responders), and 13 of 30 after 6 months. Responders had a shorter duration of diabetes and a higher initial fasting plasma insulin level....A robust and sustainable weight loss program achieved continuing remission of diabetes for at least 6 months in the 40% who responded to a VLCD by achieving fasting plasma glucose of <7 mmol/L. T2DM is a potentially reversible condition.

However, restoration of normal glucose control is possible after weight loss in some individuals with T2DM . Although most commonly seen after bariatric surgery, reversal of diabetes can occur after any sharp decrease in calorie intake. In short-duration T2DM, fasting plasma glucose becomes normal within days on a very-low-calorie diet (VLCD) because of a rapid decrease in liver fat and return of normal hepatic insulin sensitivity, and normal b-cell function returns over 8 weeks.

This prospective, longitudinal, single center study comprised three phases: VLCD for 8 weeks; a stepped return to isocaloric intake of normal food over 2 weeks; and a structured, individualized weight maintenance program over 6 months. Assessments were carried out before the VLCD, after return to isocaloric eating, and at the end of the 6-month follow-up. The primary outcome measure was fasting blood glucose at 6 months in the group achieving nondiabetic levels after VLCD and return to normal eating, and the primary comparison was the change between post– weight loss and 6 months in responders.

We demonstrate that in 40% of study participants who responded to a VLCD by achieving fasting plasma glucose ,7 mmol/L, remission of T2DM lasts for at least 6 months. Return to nondiabetic blood glucose levels was characterized by improvement in acute insulin secretion, and this was sustained while off all hypoglycemic agents. Hepatic insulin sensitivity improved in both responders and nonresponders....Weight loss brought about normalization of liver fat content and insulin sensitivity in both responders and nonresponders. Of note, no redistribution of fat was seen to the liver from the subcutaneous or other deposits over 6 months of weight stability, even though the participants remained obese or overweight.

The present demonstration of ongoing reversal of T2DM (in 41% of the cohort overall or 60% of individuals with short-duration diabetes) is reflected in population data that indicate that T2DM is solely a response to overnutrition. Ready access to low-cost food is uniformly accompanied by high rates of T2DM, and when food supply becomes limited for any reason, the prevalence of T2DM falls.....The present data confirm reversal of T2DM for at least 6 months in those who achieve nondiabetic plasma glucose levels after VLCD. However, the critical question for health-care delivery is whether truly long-term reversal of T2DM can be achieved in primary care.

The likelihood of VLCD responders remaining free of diabetes indefinitely must be considered. After media coverage of our earlier study, many people with T2DM reversed their own diabetes (37). For such motivated individuals who avoid weight regain, maintenance of normoglycemia for up to 3 years has been reported.... Because progression of longterm complications of diabetes relates to ambient blood glucose control, durable reversal of diabetes would be expected to be associated with longterm health. T2DM can now be understood to be a metabolic syndrome potentially reversible by substantial weight loss, and this is an important paradigm shift. 

Newly published research found that children who are thumb-suckers or nail-biters are less likely to develop atopic sensitization or allergic sensitivities (as measured by positive skin-prick tests to common allergens). And, if they have both 'habits', they are even less likely to be allergic to such things as house dust mites, grass, cats, dogs, horses, wool, or airborne fungi. The finding emerges from a longitudinal study which followed the progress of 1,037 persons born in Dunedin, New Zealand in 1972-1973 from childhood into adulthood. However, the researchers found no relationship to these 2 habits to allergic asthma or "hay fever" - a contradictory finding that the researchers don't have an answer for.

"Our findings are consistent with the hygiene theory that early exposure to dirt or germs reduces the risk of developing allergies," said Professor Sears (one of the researchers).  The researchers were testing the idea that the common childhood habits of thumb-sucking and nail-biting would increase microbial exposures, affecting the immune system and reducing the development of allergic reactions also known as atopic sensitization. 31% of the children were frequent thumb suckers or nail biters.

Among all children at 13 years old, 45% showed atopic sensitization, but among those with no habits 49% had allergic sensitization; and those with one oral habit - 40% had allergic sensitization. Among those with both habits, only 31% had allergic sensitization. This trend continued into adulthood, and showed no difference depending on smoking in the household, ownership of cats or dogs; or exposure to house dust mites.

Excerpts of the study from Pediatrics: Thumb-Sucking, Nail-Biting, and Atopic Sensitization, Asthma, and Hay Fever

The hygiene hypothesis suggests that early-life exposure to microbial organisms reduces the risk of developing allergies. Thumb-sucking and nail-biting are common childhood habits that may increase microbial exposures. We tested the hypothesis that children who suck their thumbs or bite their nails have a lower risk of developing atopy, asthma, and hay fever in a population-based birth cohort followed to adulthood. Parents reported children’s thumb-sucking and nail-biting habits when their children were ages 5, 7, 9, and 11 years. Atopic sensitization was defined as a positive skin-prick test (≥2-mm weal) to ≥1 common allergen at 13 and 32 years. 

Thirty-one percent of children were frequent thumb-suckers or nail-biters at ≥1 of the ages. These children had a lower risk of atopic sensitization at age 13 years  and age 32 years. These associations persisted when adjusted for multiple confounding factors. Children who had both habits had a lower risk of atopic sensitization than those who had only 1. No associations were found for nail-biting, thumb-sucking, and asthma or hay fever at either age.

What This Study Adds: Children who sucked their thumbs or bit their nails between ages 5 and 11 years were less likely to have atopic sensitization at age 13. This reduced risk persisted until adulthood. There was no association with asthma or hay fever.

The “hygiene hypothesis” was suggested by Strachan1 to explain why children from larger families and those with older siblings are less likely to develop hay fever. Strahan hypothesized that this could be explained if “allergic diseases were prevented by infection in early childhood transmitted by unhygienic contact with older siblings, or acquired prenatally from a mother infected by contact with her older children.” The hypothesis is supported by evidence showing that children who grow up in large families are at greater risk of coming into contact with more infections....The hygiene hypothesis remains controversial, however, as it is unable to fully explain many associations, including the rise of allergies in “unhygienic” inner-city environments, and why probiotics are ineffective at preventing allergic diseases.3

Thumb-sucking and nail-biting are common oral habits among children, although the reported prevalence varies widely, from <1% to 25%.47 These habits have the potential to increase the exposure to environmental microorganisms, and have been associated with the oral carriage of Enterobacteriaceae, such as Escherichia coli and intestinal parasite infections.812 It seems likely that thumb-sucking and nail-biting would introduce a wide variety of microbes into the body, thus increasing the diversity of the child’s microbiome. If the hygiene hypothesis is correct, it is plausible that this would influence the risk for allergies.... 

Of 1013 children providing data, 317 (31%) had ≥1 oral habit: there was no significant sex difference in prevalence of these habits. Of the 724 children who had skin-prick tests at age 13 years, 328 (45%) showed atopic sensitization. The prevalence of sensitization was lower among children who had an oral habit (38%) compared with those who did not (49%) (P = .009). The lower risk of atopic sensitization was similar for thumb-sucking and nail-biting. Children with only 1 habit were less likely to be atopic (40%) than children with no habit at all (49%), but those with both habits had the lowest prevalence of sensitization (31%) .

An interesting study (published in September 2015) looked at how prevalent biofilms are in the sinuses of people with chronic sinusitis (with or without nasal polyps) as compared to healthy people (without chronic sinusitis). Biofilms are communities of bacteria sticking to one another and coated with a protective slime. The researchers found that the most biofilms were found in people with chronic sinusitis who also had nasal polyps (97.1%) , followed by those with chronic sinusitis without nasal polyps (81.5%), and the least in the control group of healthy patients (56%). They felt that the biofilms contributed to or had a role in chronic sinusitis. But note that the majority of people in all groups had biofilms.

Unfortunately nowhere in the study was there an analysis of the bacteria making up the biofilms. Are the bacteria in the biofilms different in the healthy people versus those with chronic sinusitis? The general assumption is that biofilms are formed from pathogenic (bad) bacteria such as Staphylococcus aureus, but it is known that beneficial bacteria such as Lactobaccillus plantarum and Lactobacillus reuteri can also form biofilms. One study concluded that: "L. reuteri biofilms secreted factors that confer specific health benefits such as immunomodulation and pathogen inhibition." So what was in the biofilms of healthy people (without chronic sinusitis)? Were the biofilms in healthy sinuses made up of protective beneficial bacteria or pathogenic bacteria that were kept in check by other "beneficial" microbes (which can be bacteria, fungi, viruses, etc) in the sinus microbiome?

Biofilms are very hard to eradicate, even with antibiotics. The researchers mentioned that "To date many different modalities have been tested, from Manuka honey to ultrasound and surfactant, but none have been shown to be very efficient." However, they did not mention other bacteria (probiotics) as a treatment possibilty in eradicating biofilms in the sinuses. There has been research looking at using probiotics against biofilms elsewhere in the body (such as dental plaque on teeth).

If biofilms from pathogenic bacteria are so pervasive in chronic sinusitis (81.5% to 97.1%), then it appears that some bacteria such as Lactobacillus sakei somehow predominate over them. I am saying this based on the majority of people writing to me saying that L. sakei treated their chronic sinusitis, as well as the experiences of my own 4 family members (at least 3, perhaps all 4 of us probably had biofilms in our sinuses based on the 81.5% to 97.1% numbers in this research). Something to contemplate. From the journal Acta Oto-Laryngologica:

Bacterial biofilms in chronic rhinosinusitis; distribution and prevalence.

Biofilms were more prevalent in patients with CRSwNP [chronic rhinosinusitis with nasal polyps] compared to both CRSsNP [chronic rhinosinusitis without nasal polyps] and controls [healthy people], and also on the ethmoid bulla compared to the middle turbinate, supporting a biofilm-related pathogenesis of CRSwNP....This study comprised 27 patients with CRSsNP, 34 patients with CRSwNP, and 25 controls.

Chronic rhinosinusitis (CRS) is today understood as a multifaceted group of diseases. The most established differentiation is between CRS with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP)....Patients with CRSwNP have the worst quality-of-life scores, and they have frequent recurrences of their symptoms after surgery.

The pathophysiology of nasal polyps is poorly understood. Bacterial infection, in the form of biofilms, is proposed as a major drive behind the inflammation in CRS. Bacterial biofilms is identified as the agent behind an ever increasing number of chronic infectious diseases, ranging from endocarditis to dental caries. Bacterial biofilms are communities of bacteria in their sessile form, and can be extremely difficult to eradicate with conventional antibiotic therapy.

The total number of patients in the CRS group was 61, 23 females and 38 males, and median age was 40 years....Bacterial biofilms were detected in 97.1% of patients with CRSwNP, 81.5% of patients with CRSsNP, and 56% of controls. Patients with CRSwNP had highly significantly increased prevalence of biofilms compared to controls....The prevalence of biofilms in different anatomical locations within the nasal cavity differed....Biofilms were detected in 79.6% of the samples from the ethmoid bulla, 70.9% of the samples from the uncinated process, and 62.0% of the samples from the middle turbinate.

In this study a significantly increased prevalence of biofilms were found in patients with CRSwNP compared to controls, but also compared to CRSsNP. Indeed only one of the patients with CRSwNP was biofilm negative. This indicates a role for biofilms in the pathogenesis of CRS, but specifically in CRSwNP.

The pathophysiological mechanisms underlying nasal polyps are still poorly understood. Biofilms are shown to be heterogeneous and can be composed of both bacteria and fungi. Staphylococcus Aureus feature prominently in most biofilms found in the sinonasal cavity, being isolated in 50% of the samples. and can possibly facilitate co-colonization with fungi....Bacteria in a biofilm are shown to have up to a 1000-fold increased resistance to antibiotics compared to planktonic bacteria. These features of biofilms make them notoriously hard to eradicate.... In the setting of CRS we have the opportunity of direct local treatment which gives us a greater range of potential treatment options. To date many different modalities have been tested, from Manuka honey to ultrasound and surfactant, but none have been shown to be very efficient....In regards to nasal polyps, further studies are needed to investigate why some patients with biofilms develop nasal polyps while others do not.

Biofilms thrive in moist areas without too much turbulence, conditions found deep in the middle meatus. This may also explain why there were a higher number of biofilm positive CRSwNP patients, as regular nasal polyps originate in the ethmoid....In the opinion of the authors the findings in this article suggest a role for biofilms in CRSwNP.

Bacterial biofilm in a person with chronic sinusitis Credit: Thiago Freire Pinto Bezerra et al,  Braz. j. otorhinolaryngol. (Impr.) vol.75 no.6 São Paulo Nov./Dec. 2009

Of course eating meals prepared at home is healthier! The study results - that people who often consume meals prepared at home are less likely to suffer from type 2 diabetes than those who consume such meals less frequently shouldn't be surprising. The researchers attributed the higher incidence of type 2 diabetes to weight gain in those eating fewer meals prepared at home, but there are other things going on also.

Restaurant and fast food meals tend to have very large portions, frequently with rich sauces, and the meal choices tend to be heavy on fat and salt. The meals can be high in calories, contain many artificial ingredients, and may be low in nutritional quality (and so also not nourishing the beneficial gut microbes that are linked to health). At home you can limit portions, control the food ingredients, and eat only healthy foods (see earlier post on this). From Science Daily:

Enjoying meals prepared at home: Short-cut to avoiding diabetes?

People who often consume meals prepared at home are less likely to suffer from type 2 diabetes than those who consume such meals less frequently, according to  new epidemiological research reported by Qi Sun, of the Harvard T.H. Chan School of Public Heath, Boston, USA and colleagues as part of PLOS Medicine's special issue on Preventing Diabetes.

Internationally, there is an increasing tendency for people to eat out, and this could involve consumption of fast food, for example. Concerns have been raised that such people have a diet that is rich in energy but relatively poor in nutrients -- this could lead to weight gain which is, in turn, associated with an increased risk of type 2 diabetes.

Sun and colleagues employed large prospective data sets in which US health professionals -- both men and women--were followed-up for long periods, with rigorous collection of data on health indicators, including self-reported information on eating habits and occurrence of diabetes. The results were corrected for various known factors that could affect dining habits, including marital status. All in all, the study analyzed 2.1 million years of follow-up data.

The findings indicate that people who reported consuming 5-7 evening meals prepared at home during a week had a 15% lower risk of type 2 diabetes than those who consumed 2 such meals or fewer in a week. A smaller, but still statistically significant, reduction was apparent for those who reported consuming more midday meals prepared at home. Other analyses suggest that less weight gain could partially explain the reported reduction in occurrence of type 2 diabetes in those often eating meals prepared at home.

  Interesting study that supports music instruction for children - that it appears to accelerate brain development in young children, particularly in the areas necessary for general auditory processes such as language, speech and social interaction. Unfortunately music instruction is being cut in many schools, either for budget reasons or because it is perceived as unnecessary. From Developmental Cognitive Neuroscience:

Researchers find that children's brains develop faster with music training

Music instruction appears to accelerate brain development in young children, particularly in the areas of the brain responsible for processing sound, language development, speech perception and reading skills, according to initial results of a five-year study by USC neuroscientists.

These initial study results, published in the journal Developmental Cognitive Neuroscience, provide evidence of the benefits of music education at a time when many schools around the nation have either eliminated or reduced music and arts programs. The study shows music instruction speeds up the maturation of the auditory pathway in the brain and increases its efficiency.

For this longitudinal study, the neuroscientists are monitoring brain development and behavior in a group of 37 children from underprivileged neighborhoods of Los Angeles. Thirteen of the children, at 6 or 7 years old, began to receive music instruction through the Youth Orchestra Los Angeles program at HOLA....The children learn to play instruments, such as the violin, in ensembles and groups, and they practice up to seven hours a week.

The scientists are comparing the budding musicians with peers in two other groups: 11 children in a community soccer program, and 13 children who are not involved in any specific after-school programs. The neuroscientists are using several tools to monitor changes in them as they grow: MRI to monitor changes through brain scans, EEG to track electrical activity in the brains, behavioral testing and other such techniques.

Within two years of the study, the neuroscientists found the auditory systems of children in the music program were maturing faster than in the other children. The fine-tuning of their auditory pathway could accelerate their development of language and reading, as well as other abilities—a potential effect which the scientists are continuing to study. The enhanced maturity reflects an increase in neuroplasticity, a physiological change in the brain in response to its environment—in this case, exposure to music and music instruction.

"The auditory system is stimulated by music," Habibi said. "This system is also engaged in general sound processing that is fundamental to language development, reading skills and successful communication." The auditory system connects our ear to our brain to process sound. When we hear something, our ears receive it in the form of vibrations that it converts into a neural signal. That signal is then sent to the brainstem, up to the thalamus at the center of the brain, and outward to its final destination, the primary auditory cortex, located near the sides of the brain.

A new report authored by dozens of scientists, health practitioners and children's health advocates is highlighting the (growing annually) evidence that many common and widely available chemicals endanger neurological development in fetuses and children of all ages. The chemicals contribute to such health problems as ADHD, autism spectrum disorders, lowered IQ, behavior disorders, and many other problems. Many of the chemicals have hormonal effects (endocrine disruptors) and interfere with normal hormonal activity. The chemicals of highest concern are all around us and are found in most pregnant women, their fetuses, and in growing children. In fact, in all of us.

Especially worrisome chemicals are:  leadmercury; organophosphate pesticides (used in agriculture and home gardens), phthalates (in medicines, plastics, and personal care products), flame retardants known as polybrominated diphenyl ethers (found in upholstered furniture, car seats), air pollutants produced by the combustion of wood and fossil fuels), and polychlorinated biphenyls (once used as coolants and lubricants in electrical equipment, but still pervasive). It is important to note that out of the thousands of chemicals that people are exposed to, that the great majority of chemicals are untested for neurodevelopmental effects.

Especially alarming is that the U.S. Centers for Disease Control found that 90% of pregnant women in the United States have detectable levels of 62 chemicals in their bodies, out of 163 chemicals for which the women were screened. This shows that we are exposed to mixtures of chemicals - not just to one chemical at a time.  Unfortunately the substitutes for problematic chemicals are NO better than the originals, because they tend to be similar chemically. For example, the substitutes for BPA are just as bad, if not worse, than BPA (bisphenol A). And remember, we are exposed to mixtures of chemicals - not just to one chemical at a time.

The report criticizes current regulatory lapses that allow chemicals to be introduced into people's lives with little or no review of their effects on fetal and child health. "For most chemicals, we have no idea what they're doing to children's neurodevelopment," Professor Schantz (one of the signers of the report) said. "They just haven't been studied." So why aren't policymakers doing something? Why is industry dictating what we're exposed to? Why are chemicals innocent until proven guilty, and even then they're allowed to be used? Who is looking out for the ordinary person, and especially developing children?

From the journal Environmental Health Perspectives: Project TENDR: Targeting Environmental Neuro-Developmental Risks. The TENDR Consensus Statement

Children in America today are at an unacceptably high risk of developing neurodevelopmental disorders that affect the brain and nervous system including autism, attention deficit hyperactivity disorder, intellectual disabilities, and other learning and behavioral disabilities. These are complex disorders with multiple causes—genetic, social, and environmental. The contribution of toxic chemicals to these disorders can be prevented. 

Leading scientific and medical experts, along with children’s health advocates, came together in 2015 under the auspices of Project TENDR: Targeting Environmental Neuro-Developmental Risks to issue a call to action to reduce widespread exposures to chemicals that interfere with fetal and children’s brain development. Based on the available scientific evidence, the TENDR authors have identified prime examples of toxic chemicals and pollutants that increase children’s risks for neurodevelopmental disorders. These include chemicals that are used extensively in consumer products and that have become widespread in the environment. Some are chemicals to which children and pregnant women are regularly exposed, and they are detected in the bodies of virtually all Americans in national surveys conducted by the U.S. Centers for Disease Control and Prevention. The vast majority of chemicals in industrial and consumer products undergo almost no testing for developmental neurotoxicity or other health effects.

Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. 

The TENDR Consensus Statement is a call to action to reduce exposures to toxic chemicals that can contribute to the prevalence of neurodevelopmental disabilities in America’s children. The TENDR authors agree that widespread exposures to toxic chemicals in our air, water, food, soil, and consumer products can increase the risks for cognitive, behavioral, or social impairment, as well as specific neurodevelopmental disorders such as autism and attention deficit hyperactivity disorder (ADHD) (Di Renzo et al. 2015; Gore et al. 2015; Lanphear 2015; Council on Environmental Health 2011). This preventable threat results from a failure of our industrial and consumer markets and regulatory systems to protect the developing brain from toxic chemicals. To lower children’s risks for developing neurodevelopmental disorders, policies and actions are urgently needed to eliminate or significantly reduce exposures to these chemicals.

We are witnessing an alarming increase in learning and behavioral problems in children. Parents report that 1 in 6 children in the United States, 17% more than a decade ago, have a developmental disability, including learning disabilities, ADHD, autism, and other developmental delays (Boyle et al. 2011). As of 2012, 1 in 10 (> 5.9 million) children in the United States are estimated to have ADHD (Bloom et al. 2013). As of 2014, 1 in 68 children in the United States has an autism spectrum disorder (based on 2010 reporting data) (CDC 2014).

Many toxic chemicals can interfere with healthy brain development, some at extremely low levels of exposure. Research in the neurosciences has identified “critical windows of vulnerability” during embryonic and fetal development, infancy, early childhood and adolescence (Lanphear 2015; Lyall et al. 2014; Rice and Barone 2000). During these windows of development, toxic chemical exposures may cause lasting harm to the brain that interferes with a child’s ability to reach his or her full potential.

The developing fetus is continuously exposed to a mixture of environmental chemicals (Mitro et al. 2015). A 2011 analysis of the U.S. Centers for Disease Control and Prevention’s (CDC) biomonitoring data found that 90% of pregnant women in the United States have detectable levels of 62 chemicals in their bodies, out of 163 chemicals for which the women were screened (Woodruff et al. 2011). Among the chemicals found in the vast majority of pregnant women are PBDEs, polycyclic aromatic hydrocarbons (PAHS), phthalates, perfluorinated compounds, polychlorinated biphenyls (PCBs), perchlorate, lead and mercury (Woodruff et al. 2011). Many of these chemicals can cross the placenta during pregnancy and are routinely detected in cord blood or other fetal tissues.

The following list provides prime examples of toxic chemicals that can contribute to learning, behavioral, or intellectual impairment, as well as specific neurodevelopmental disorders such as ADHD or autism spectrum disorder: Organophosphate (OP) pesticides, PBDE flame retardants, combustion-related air pollutants, which generally include PAHs, nitrogen dioxide and particulate matter, and other air pollutants for which nitrogen dioxide and particulate matter are markers, lead, mercuryPCBs .

The United States has restricted some of the production, use and environmental releases of these particular chemicals, but those measures have tended to be too little and too late. We face a crisis from both legacy and ongoing exposures to toxic chemicals.....The examples of developmental neurotoxic chemicals that we list here likely represent the tip of the iceberg....Only a minority of chemicals has been evaluated for neurotoxic effects in adults. Even fewer have been evaluated for potential effects on brain development in children (Grandjean and Landrigan 2006, 2014). Further, toxicological studies and regulatory evaluation seldom address combined effects of chemical mixtures, despite evidence that all people are exposed to dozens of chemicals at any given time.

Some chemicals, like those that disrupt the endocrine system, present a concern because they interfere with the activity of endogenous hormones that are essential for healthy brain development. Endocrine-disrupting chemicals (EDCs) include many pesticides, flame retardants, fuels, and plasticizers. One class of EDCs that is ubiquitous in consumer products are the phthalates. These are an emerging concern for interference with brain development and therefore demand attention.

Under our current system, when a toxic chemical or category of chemicals is finally removed from the market, chemical manufacturers often substitute similar chemicals that may pose similar concerns or be virtually untested for toxicity. This practice can result in “regrettable substitution” whereby the cycle of exposures and adverse effects starts all over again. The following list provides examples of this cycle: When the federal government banned some uses of OP pesticides, manufacturers responded by expanding the use of neonicotinoid and pyrethroid pesticides. Evidence is emerging that these widely used classes of pesticides pose a threat to the developing brain (Kara et al. 2015; Richardson et al. 2015; Shelton et al. 2014). 

When the U.S. Government reached a voluntary agreement with flame retardant manufacturers to stop making PBDEs, the manufacturers substituted other halogenated and organophosphate flame retardant chemicals. Many of these replacement flame retardants are similar in structure to other neurotoxic chemicals but have not undergone adequate assessment of their effects on developing brains. When the federal government banned some phthalates in children’s products, the chemical industry responded by replacing the banned chemicals with structurally similar new phthalates. These replacements are now under investigation for disrupting the endocrine system.

4

A wonderful journal article from March 17, 2015 by E.K. Cope and S.V. Lynch (one of the original L. sakei - sinusitis researchers) in which they discuss various probiotic (beneficial bacteria) species that might have some benefit in treating chronic sinusitis, which they refer to as chronic rhinosinusitis (CRS). They discuss bacteria that have have been (somewhat) studied in humans or mice and could have potential in sinusitis treatment: Lactobacillus sakei, Lactobacillus rhamnosus, Lactobacillus casei, Lactobacillus plantarum, Lactobacillus johnsonii, and Staphylococcus epidermidis. [NOTE: So few studies (almost none) have been done with probiotics in CRS  that the odds are really good that other species of bacteria, or combinations of bacteria, will also prove to be beneficial.]

It seems that a nasal spray with a mixture of beneficial bacteria may ultimately work the best because the bacterial diversity of the sinus microbiome is depleted in persons with chronic sinusitis, and there is "enrichment of sinus pathogens" (bacteria that can cause disease). As I've mentioned in other posts, S.V. Lynch is involved in developing a nasal probiotic spray containing L. sakei and other Lactobacillus species to treat sinusitis, but it is unknown when that will be available.

The authors also made the point that probiotics (beneficial bacteria) may work several ways in the sinus microbiome (a community of microbes living in the sinuses). This "niche" with its own ecosystem or community of species can be altered, with some bacteria species wiped out, perhaps by illness and/or repeated courses of antibiotics. Therefore, think of the different microbial species in the sinus microbiome as having different functions: as a keystone (a species that has a very large effect on the community), pioneer (species that are the first to colonize the niche after a disruption), or dominant species found in a healthy state (species with a relatively high abundance in a niche).

They also discuss what are the main pathogens found in chronic sinusitis, but they also mention that bacteria that we think of as pathogenic (the bad bacteria) are also present in healthy persons - just at a lower level than in chronic sinusitis sufferers. Also, these diverse microbial communities can vary between healthy individuals - that is, the healthy microbial communities are a little different among people. Common pathogenic bacteria found in CRS are: Staphylococcus aureus, Pseudomonas aeruginosa, Corynebacterium tuberculostearicum (normally a harmless skin bacteria), and Streptococcus species. Remember, healthy sinuses have greater bacterial diversity than sinusitis sufferers, and CRS patients have "substantial microbiome dysbiosis" (microbial communities out-of-whack), with "microbiome community collapse" and "enrichment of specific sinus pathogens". In other words, the microbial sinus communities in CRS are in bad shape and need to get good bacteria in there.

For information on how some people are already successfully using probiotics such as L. sakei for sinusitis treatment, read The One Probiotic That Treats Sinusitis (products, brands, and methods).

When reading the following, remember that dysbiosis means "the microbial community is out of whack". Some excerpts from the Cope and Lynch article from Current Allergy and Asthma Reports:

Novel Microbiome-Based Therapeutics for Chronic Rhinosinusitis

The human microbiome, i.e. the collection of microbes that live on, in and interact with the human body, is extraordinarily diverse; microbiota have been detected in every tissue of the human body interrogated to date. Resident microbiota interact extensively with immune cells and epithelia at mucosal surfaces including the airways, and chronic inflammatory and allergic respiratory disorders are associated with dysbiosis of the airway microbiome. Chronic rhinosinusitis (CRS) is a heterogeneous disease with a large socioeconomic impact, and recent studies have shown that sinus inflammation is associated with decreased sinus bacterial diversity and the concomitant enrichment of specific sinus pathogens.

Similar to other chronic inflammatory diseases, including inflammatory bowel disease and asthma, evidence is emerging for the role of the sinus microbiome in defining upper airway health.....two trends in the literature are evident. First, all three studies that have examined the microbiota of healthy subjects demonstrate the presence of a diverse microbiome that includes bacterial groups classically considered as causative agents of respiratory disease, including Pseudomonas, Staphylococcus, and Streptococcus. Second, substantial sinonasal microbiome dysbiosis is associated with CRS. In one example, Abreu and colleagues demonstrated microbiome community collapse in the maxillary sinuses of CRS patients compared to healthy controls characterized by the outgrowth of Corynebacterium tuberculostearicum. In another study, nasal lavage specimens from CRS patients revealed microbiome collapse coincident with Staphylococcus enrichment.

Immune responses in individuals with CRS vary considerably across patients.... While the underlying processes contributing to a patient’s immune response are not well understood, there is evidence for microbial stimulation. Staphylococcus aureus exotoxins are associated with a Th2 inflammatory response characterized by eosinophilia and enterotoxin-specific IgE , and the Th2 cytokines IL-4 and IL-13 have been associated with S. aureus outgrowth in other inflammatory diseases. Another common sinus pathogen, Pseudomonas aeruginosa, can induce antimicrobial nitric oxide production by host recognition of bacterial quorum sensing molecules through stimulation of the bitter taste receptor T2R38. There is clearly heterogeneity across patients with CRS; thus, future therapeutic microbiome manipulation strategies must be targeted to the specific microbiome perturbation and immune dysfunction of the patient.

Since CRS is immunologically and microbiologically diverse, it is not surprising that current treatment strategies using corticosteroids alone or in combination with antibiotics are variably successful. Some patients recover completely without recurrence, although 10–25 % of patients require repeated treatment....Patients who do not respond to medical management are candidates for functional endoscopic sinus surgery (FESS). The goal of FESS is to remove polypoid tissue and open ostia to facilitate sinus drainage. While some patients rebuild their native, healthy microbial communities and epithelium following FESS, many patients require revision sinus surgeries. Importantly, these therapies only manage chronic airway diseases and, in many cases, do not address the underlying source of disease, e.g., dysregulated microbiota. Since it is clear that the microbiome plays a fundamental role in respiratory health, it is essential to begin to define the interaction between pathogens or pathobionts in the context of the healthy host microbiota.

As discussed above, the most common route of probiotic delivery (oral) takes advantage of the GI-respiratory axis. In the only clinical trial of probiotic use in chronic rhinosinusitis, Mukerji and colleagues reported that oral administration of L. rhamnosus R0011 improved patient-reported symptoms of rhinosinusitis in the short term (<4 weeks), but not the long term (8 weeks). These results suggest a potential role for GI microbiome manipulation to affect the sinus immune response; however, there has not been a follow-up study to further elucidate this role. Repeated dosing or inoculation with mixed species could improve these results.

Several variables should be considered when designing probiotics for potential treatment of sinus disease. The first consideration, the route of administration, will determine the mechanism of action of the probiotic. Oral probiotic supplements primarily affect the respiratory tract through translocation of microbial metabolites, cytokines, or immune cells to the airways via systemic circulation, while local delivery via sprays or nasal lavage will affect the sinonasal microbiota and local immune responses...This first variable, route of administration, will determine which probiotic species are used. A second consideration for probiotic development is whether to supplement with a single species or a mixed-species consortium. Single species or species mixtures can be selected based on how best to leverage the healthy microbiome. From an ecological perspective, the potential role of the probiotic(s) should be considered. For example, the specie(s) may function as keystone (a species that has a disproportionately large effect on the community), pioneer (species that are the first to colonize the niche after a disruption), or dominant species found in a healthy state (species with a relatively high abundance in a niche).

Animal models are powerful tools for exploring the relationship of the host-microbiome to health and disease.... In malnourished mice, nasal instillation of Lactobacillus casei can confer protection against pathogens by enhancing host innate immune response....Live L. casei had additional benefits of temporarily colonizing the respiratory mucosa to competitively exclude S. pneumonia. Intranasal administration of Lactobacillus plantarum DK119 protected mice from lethal loads of influenza A virus through modulating host immunity of alveolar dendritic cells and macrophages. Similarly, intranasal administration of L. rhamnosus GG protected mice from H1N1 influenza infection by activating lung natural killer cells..... They also show that this protection can be achieved through feeding a single species L. johnsonii, which was enriched in the cecum of mice fed house dust.... In a sinusitis model, Abreu and colleagues demonstrated that intranasal administration of Lactobacillus sakei, identified using 16S rRNA phylogenetic microarray analysis of healthy human sinuses, protects against C. tuberculostearicum-induced sinusitis. A similar murine study showed that Staphylococcus epidermidis can protect against S. aureus-induced sinusitis. Together, these studies show promise for microbiome based therapeutics in sinusitis. However, we must think critically about the species or community used for sinus protection, administration methods, as well as the timing for microbial intervention

Probiotic administration can influence the host-microbiome composition and function directly through production of antimicrobials, changing the pH, or through competitive colonization within a niche. Bacteriocins are antimicrobial peptides produced by bacteria with a wide range of activity, either narrow spectrum (active against similar species) or broad spectrum (active across genera). Lactic acid bacteria are well-established producers of bacteriocins. The protective species identified by Abreu and colleagues, L. sakei, is known to produce several bacteriocins with a wide range of characteristics and putative modes of action, although the best characterized bacteriocin from this species is sakacin. Sakacin has antimicrobial activity against Gram positive taxa, including Listeria spp. and Enterococcus spp., but not Gram-negative bacteria.

Other Lactobacillus species that are potential probiotics for the airways act through the production of alternative antimicrobial compounds. Lactobacillus reuteri produces the protein reuterin, which acts as an antimicrobial compound by inducing oxidative stress in competing bacteria. Reuterin production is increased in the presence of E. coli, suggesting that the effects of this protein are aimed at eliminating competing microbes, giving L. reuteri an advantage in adherence and colonization of host mucosa. Lactobacillus spp. also commonly produce acetic acid and lactic acid, thereby lowering the pH of their niche and inhibiting the growth of acid-intolerant taxa. Finally, probiotic species can compete for growth substrates or receptor binding sites. L. johnsonii competes with several known pathogens for adhesion receptors, which are either glycoproteins or glycolipids. One such receptor is gangliotetraosylceramide (asialo-GM1), a glycolipid that is abundant in pulmonary tissue.

Probiotic intervention for respiratory diseases is an area of active investigation, particularly in light of recent microbiome findings. While the field is still relatively nascent, the potential for probiotic manipulation of the sinus microbiome to treat or prevent CRS is great. However, our current understanding of the healthy sinus microbiome and, thus, how best to manipulate it in a disease state are not well defined. Whether to use mixed versus single species and strain inocula, specific species used, mode of delivery, inoculum concentration, and determining the frequency of supplementation are some of the factors that need to be addressed in optimizing probiotic effects. Most of the studies discussed in this article have focused on the gut microbiome and effects at distal sites because these interactions have formed the focus of the majority of stduies to date. However, the murine [mouse] studies discussed here suggest that local administration of probiotics to the sinuses can affect the dynamics of the sinus microbiome.

Lactobacillus sakei Credit: BacMap Genome Atlas

Previous research on the health benefits of eating fish, fish oil supplements, and other sources of omega-3 fatty acids has shown mixed results, with some studies revealing cardiac health benefits and others finding no benefit. However, when looking at recent studies separating eating foods rich in omega-3 fatty acids versus taking supplements, it appears that eating foods has various beneficial health effects, while taking a supplement may not find health benefits (here and here).

The latest research (reported in the journal JAMA Internal Medicine) looked at heart disease events (heart attack, cardiac related death) and actually measured the actual levels of omega-3 fatty acids in the participants' blood, as opposed to relying on questionnaires in which people report what they eat. The new study could not assess the usefulness of taking fish oil supplements, as opposed to eating fish, because so few people in the study took supplements. Thus the findings were generally from eating a diet rich in omega-3s from either fish or plant-based sources. (Note: By far the best source is fish. Some plant-based sources are: flaxseed, walnuts, edamame, black beans, kidney beans).

The new study — which combined 19 studies from 16 countries with more than 45,000 participants — found that higher circulating blood levels of omega-3 fatty acids were associated with a nearly 10 percent lower risk of a fatal heart attack, on average, compared with lower levels. The participants with the highest level of omega-3s in their blood had the greatest risk reduction — a more than 25 percent lower risk of having a fatal heart attack, the study found.

From Science Daily: Consumption of omega-3s linked to lower risk of fatal heart disease

A global consortium of researchers banded together to conduct an epidemiological study analyzing specific omega-3 fatty acid biomarkers and heart disease. They found that blood levels of omega-3 fatty acids from seafood and plant-based foods are associated with a lower risk of fatal heart attack.

A total of 19 studies were involved from 16 countries and including 45,637 participants. Of these, 7,973 people developed a first heart attack over time, including 2,781 deaths and 7,157 nonfatal heart attacks.

Overall, both plant-based and seafood-based omega-3s were associated with about a 10 percent lower risk of fatal heart attacks. In contrast, these fatty acids biomarkers were generally not associated with a risk of nonfatal heart attacks, suggesting a more specific mechanism for benefits of omega-3s related to death."At a time when some but not other trials of fish oil supplementation have shown benefits, there is uncertainty about cardiovascular effects of omega-3s," said Mozaffarian. "Our results lend support to the importance of fish and omega-3 consumption as part of a healthy diet."

Fish is the major food source of omega-3 fatty acids, including eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). According to the U.S. Department of Agriculture's National Nutrient Database, fatty fish such as salmon, trout, anchovies, sardines, and herring contain the highest amounts of omega-3 fatty acids, although all fish contain some levels. In addition to omega-3 fatty acids, fish provide specific proteins, vitamin D, selenium, and other minerals and elements. Alpha-linolenic acid (ALA) is the plant-based omega-3 fatty acid found in walnuts, flaxseed oil, and canola oil and some other seed and nuts and their oils.

Amazing!  Researchers found that the bacteria found in breast cancer patients and healthy patients are different. (See post on their earlier work on breast microbiome.) And not only that, but the types of bacteria (Lactobacillus and Streptococcus) that are more prevalent in the breasts of healthy women are considered "beneficial" and may actually protect them from breast cancer. Meanwhile, elevated levels of the bacteria Escherichia coli and Staphylococcus epidermidis found in the breast tissue adjacent to tumors are the kind that do harm (e.g., known to induce double-stranded breaks in DNA) . This research raises the question: could probiotics (beneficial bacteria) protect breasts from cancer? From Science Daily:

Beneficial bacteria may protect breasts from cancer

Bacteria that have the potential to abet breast cancer are present in the breasts of cancer patients, while beneficial bacteria are more abundant in healthy breasts, where they may actually be protecting women from cancer, according to Gregor Reid, PhD, and his collaborators. These findings may lead ultimately to the use of probiotics to protect women against breast cancer. The research is published in the ahead of print June 24 in Applied and Environmental Microbiology, a journal of the American Society for Microbiology.

In the study, Reid's PhD student Camilla Urbaniak obtained breast tissues from 58 women who were undergoing lumpectomies or mastectomies for either benign (13 women) or cancerous (45 women) tumors, as well as from 23 healthy women who had undergone breast reductions or enhancements. They used DNA sequencing to identify bacteria from the tissues, and culturing to confirm that the organisms were alive. 

Women with breast cancer had elevated levels of Escherichia coli and Staphylococcus epidermidis, are known to induce double-stranded breaks in DNA in HeLa cells, which are cultured human cells. "Double-strand breaks are the most detrimental type of DNA damage and are caused by genotoxins, reactive oxygen species, and ionizing radiation," the investigators write. The repair mechanism for double-stranded breaks is highly error prone, and such errors can lead to cancer's development.

Conversely, Lactobacillus and Streptococcus, considered to be health-promoting bacteria, were more prevalent in healthy breasts than in cancerous ones. Both groups have anticarcinogenic properties. For example, natural killer cells are critical to controlling growth of tumors, and a low level of these immune cells is associated with increased incidence of breast cancer. Streptococcus thermophilus produces anti-oxidants that neutralize reactive oxygen species, which can cause DNA damage, and thus, cancer.

The motivation for the research was the knowledge that breast cancer decreases with breast feeding, said Reid. "Since human milk contains beneficial bacteria, we wondered if they might be playing a role in lowering the risk of cancer. Or, could other bacterial types influence cancer formation in the mammary gland in women who had never lactated? To even explore the question, we needed first to show that bacteria are indeed present in breast tissue." (They had showed that in earlier research.)

But lactation might not even be necessary to improve the bacterial flora of breasts. "Colleagues in Spain have shown that probiotic lactobacilli ingested by women can reach the mammary gland," said Reid. "Combined with our work, this raises the question, should women, especially those at risk for breast cancer, take probiotic lactobacilli to increase the proportion of beneficial bacteria in the breast? To date, researchers have not even considered such questions, and indeed some have balked at there being any link between bacteria and breast cancer or health."

Besides fighting cancer directly, it might be possible to increase the abundance of beneficial bacteria at the expense of harmful ones, through probiotics, said Reid. Antibiotics targeting bacteria that abet cancer might be another option for improving breast cancer management, said Reid. In any case, something keeps bacteria in check on and in the breasts, as it does throughout the rest of the body, said Reid. "What if that something was other bacteria--in conjunction with the host immune system?

A study found that a combination of cranberry supplement (120 mg cranberries, with a minimum proanthocyanidin content of 32mg), the probiotic Lactobacillus rhamnosus, and vitamin C (750 mg) three times a day was enough to prevent the recurrence of urinary tract infections (UTIs) for the majority of women in this small (36 patient) study. At 6 months there was a 61% success rate. No side effects were reported.

These are wonderful results, but why aren't more studies also being done on the effective product D-Mannose? The one study (see post) that I found looking at D-Mannose found an 85% success rate at 6 months. It is especially effective against E.coli, which is the cause of the majority of UTIs. But the great news is that finally women have some effective and safe treatments to try, and the wonderful possibility of getting off the vicious cycle of repeated courses of antibiotics. The article abstract from Pubmed.gov (National Library of Medicine):

Effectiveness of a Combination of Cranberries, Lactobacillus rhamnosus, and Vitamin C for the Management of Recurrent Urinary Tract Infections in Women: Results of a Pilot Study.

Urinary tract infections (UTIs) are common in women and many patients with recurrent UTIs do not eradicate the condition albeit being treated with multiple courses of antibiotics. The use of nutritional supplements might reduce the risk of recurrent UTIs. However, the role of supplements taken as single agents appears to be limited. We hypothesized that a combination of cranberries, Lactobacillus rhamnosus, and vitamin C might produce a clinical benefit due to their additive or synergistic effects. We prospectively enrolled 42 consecutive women with recurrent UTIs treated with 120mg cranberries (minimum proanthocyanidin content: 32mg), 1 billion heat-killed L. rhamnosus SGL06, and 750mg vitamin C thrice daily for 20 consecutive days. Patients were advised to stop taking these supplements for 10 d and then to repeat the whole cycle three times. Patients were contacted three mo and six mo following the end of the administration of these supplements and evaluated with a semistructured interview and urinalysis. Responders were defined as the absence of symptoms and negative urinalysis or urine culture. Follow-up data were available for 36 patients. Overall, 26 (72.2%) and 22 patients (61.1%) were responders at the 3-mo and 6-month follow-up. No major side effects were recorded. The administration of cranberries, L. rhamnosus, and vitamin C might represent a safe and effective option in women with recurrent UTIs.

PATIENT SUMMARY: We evaluated the effectiveness of cranberries, Lactobacillus rhamnosus, and vitamin C thrice daily for 20 consecutive d monthly for 3 mo for the management of recurrent urinary tract infections in women. Our results show that this approach might represent a safe and effective option.