Dr. Bray Links

Thursday, March 30, 2017

Metformin Linked to Dementia, Parkinson's in Patients With T2DM

VIENNA, Austria — Long-term use of the diabetes medication metformin may increase the risk for neurodegenerative disease in patients with type 2 diabetes mellitus (T2DM), new research suggests.

In a cohort study that followed about 9300 patients with T2DM in Taiwan for up to 12 years, the risk for Parkinson's disease (PD) or Alzheimer's dementia was more than double during a 12-year period for those who took metformin vs those who did not — even after adjusting for multiple confounders.

In addition, outcome risks increased progressively with higher dosage and longer duration of treatment.


Many EHR Vendors, Providers Block Information Exchange: Study


Half of electronic health record (EHR) vendors and a quarter of hospitals and health systems routinely engage in information blocking that restricts data flow between providers with different EHRs, according to officials of public health information exchanges (HIEs) surveyed by researchers at the University of Michigan.

The top motivation for EHR developers was revenue maximization, whereas the hospital systems were mainly motivated by a desire to maintain or enhance their competitive position, the authors state. The study was published online March 7 in the Milbank Quarterly.


Wednesday, March 29, 2017

Justice Department Joins Lawsuit Alleging Massive Medicare Fraud By UnitedHealth | Kaiser Health News

The Justice Department has joined a California whistleblower's lawsuit that accuses insurance giant UnitedHealth Group of fraud in its popular Medicare Advantage health plans.

Justice officials filed legal papers to intervene in the suit, first brought by whistleblower James Swoben in 2009, on Friday in federal court in Los Angeles. On Monday, they sought a court order to combine Swoben's case with that of another whistleblower.

Swoben has accused the insurer of "gaming" the Medicare Advantage payment system by "making patients look sicker than they are," said his attorney, William K. Hanagami. Hanagami said the combined cases could prove to be among the "larger frauds" ever against Medicare, with damages that he speculates could top $1 billion.


Monday, March 27, 2017

Mycotoxins - Leaky Gut, Hormone Disruption, Immune Suppression?

Fusarium Head Blight — Small Grains — Penn State Extension

Fusarium graminearum is known to produce two important mycotoxins, deoxynivalenol (DON) and zearalenone, which can contaminate the diseased grain. The mycotoxin DON can cause reduced feed intake and lower weight gain in animals at levels as low as 1–3 ppm, especially in swine. Vomiting and feed refusal can occur when levels of DON exceed 10 ppm. Humans are also sensitive to DON, and the FDA has recommended that DON levels not exceed 1 ppm in human food. Ruminant animals, including dairy cows and beef cattle, are less sensitive to the toxin. The fungal toxin zearalenone has estrogenic properties and produces many reproductive disorders in animals. Swine are the most sensitive to the toxin, but cattle and sheep may also be affected. Zearalenone concentrations of 1–5 ppm can result in negative effects in animals and humans. Producers concerned about these mycotoxins should have grain tested prior to feeding to animals. Contact the state or local extension office for more information about testing for mycotoxins.


Sunday, March 26, 2017

Reversing Alzheimer’s Disease - Dr. Dale Bredesen, MD

"Reversing Alzheimer’s Disease" is a presentation by Dr. Dale Bredesen, MD that took place at Silicon Valley Health Institute on November 17, 2016.

Alzheimer’s disease affects 5 million people in the U.S. and about 30 million worldwide. Until now, the prognosis seemed poor for this population Dale Bredesen MD, the founding president of the Buck Institute for Research on Aging, has developed a program which has had success in reversing the symptoms of Alzheimer’s Disease. His research model addresses several possible disease components at once (diet, exercise, etc.) rather than testing one drug at a time to rule out the effects from other drugs or interventions. Bredesen says that studying one drug at a time is like patching one hole in a roof that has dozens of holes.

Dr. Bredesen sees Alzheimer’s disease,- as an imbalance rather than a toxicity resulting in amyloid beta plaques which block nerve cell signaling and lead to memory loss. Amyloid beta, he and others say, also has a normal function in the brain, performing important roles, such as helping the brain’s plasticity – how nerve cells signal to make and store memories and delete unneeded ones.
After intense testing of a patient, Dr. Bredesen determines which factors have gone awry, and personalizes a program to correct the issues.

Among the measures he recommends:

  • A diet that eliminates processed foods and other unhealthy ingredients, and boosts fruits, vegetables and healthy fish
  • Stress reduction with meditation, yoga, music or other means
  • Eight hours of sleep a night
  • At least 30 minutes of exercise four to six times a week
  • Very good oral hygiene
  • Improvement of gut health with probiotics and prebiotics
  • Fasting for 12 hours between dinner and breakfast, and three hours or more between dinner and bedtime, to keep insulin levels low

Published in the September Journal Aging, he did a study on ten patients. Nine of the 10 patients improved. Six who had been on leave from work or were struggling with work due to memory loss and other Alzheimer’s-related issues returned or improved their work performance. The one patient who did not improve was in the late stages of Alzheimer’s Disease. One 67 year old patient is still doing well after three years. She had a demanding job when her memory issues surfaced. She couldn’t finish work reports properly and would even forget her longtime pets’ names. Within months of beginning the program, she was doing well at work. “Four times she went off the program and each time she got worse. When she went back on, she went back to normal.”

Dr. Bredesen hopes to start a clinical trial this year. He also hopes to launch a program where interested patients could learn how to follow it during a one-week intensive stay, returning periodically for progress checks and program tweaks. The Alzheimer’s Association cautions against Alzheimer’s patients trying to self-start Bredesen’s program. That’s despite the fact that the Association recommends some of the program features for better brain health.







Lyme disease: time for a new approach?

Our common understanding of Lyme disease is that a tick bite is followed by the development of a classic rash pattern (erythema migrans). When treated early with a relatively short course of antibiotics, most patients have good outcomes.6 But the standard two tier testing for Lyme disease is inaccurate in the early stages, and many patients and doctors fail to recognise the rash.7 Patients who present with the later stages of the disease can also be easily dismissed because the two tier testing lacks sensitivity and cannot distinguish between current and past infection. At the same time, the evidence remains limited on the reasons for treatment failure and unresolved systemic symptoms in patients with or without serological evidence of the disease. Most patients will present to family physicians, who often have few subsequent resources when the initial treatment proves unsuccessful.

Recently, the medical community has been collectively forced out of its comfort zone on Lyme disease by increasing evidence of the complexity of this multisystem disease.8 To further complicate matters, some patients develop long term symptoms. The complexities are essentially related to either a lack of understanding of the disease or conflicting evidence. Many questions await full answers (box).9 Evidence that answers these questions, and especially that highlights the inter-relatedness of the different components, could underpin the necessary rethinking around this condition.
Tick box: research agenda

    Range of clinical presentations, including between sexes

    Diagnostic criteria and tools

    Treatments and their efficacy

    Transmission modes and vectors

    Role of coinfections

    Uncertainty over clinical definition of chronic Lyme disease and whether detection of active infection is essential

    Whether and for how long the pathogen can persist

    Role of psychoneuroimmunology, host-pathogen interactions, and autoimmunity to residual or persisting antigens

    Role of toxins or other bacterial products in symptoms and signs

    Contribution of environmental factors

Recent evidence shedding light on how spirochaetes of the Borrelia genus evade host immune defences and survive antibiotic challenge10 11 12 13 14 15 threaten current beliefs about the persistence of infection, one of the largest points of contention in the medical community. The possibility of persistent infection has important implications for diagnosis, treatment, and doctor-patient interactions.16


Saturday, March 25, 2017

New flicker-free lighting to replace fluorescent bulbs

Researchers have created a new technology which provides flicker-free, shatterproof lighting which is easy on the eyes and may soon replace the buzzing overhead fluorescent light bulbs in your office. The lighting, based on field-induced polymer electroluminescent (FIPEL) technology, also gives off soft, white light - not the yellowish glint from fluorescents or bluish tinge from LEDs, claim scientists at Wake Forest University.

"People often complain that fluorescent lights bother their eyes, and the hum from the fluorescent tubes irritates anyone sitting at a desk underneath them," said David Carroll, the scientist leading the development of this technology at Wake Forest. "The new lights we have created can cure both of those problems and more," Carroll said in a statement. The team uses a nano-engineered polymer matrix to convert the charge into light. This allows the researchers to create an entirely new light bulb - overcoming one of the major barriers in using plastic lights in commercial buildings and homes. The device is made of three layers of moldable white-emitting polymer blended with a small amount of nanomaterials that glow when stimulated to create bright and perfectly white light similar to the sunlight human eyes prefer.


Characterizing and Minimizing LED Flicker in Lighting Applications

The effect of flicker

According to studies about 1 in 4,000 people are highly susceptible to flashing lights cycling in the 3 to 70 Hz range. Such obvious flickering can trigger ailments as serious as epileptic seizures. Less well known is the fact that long-term exposure to higher frequency (unintentional) flickering (in the 70 to 160 Hz range) can also cause malaise, headaches, and visual impairment.

Unfortunately, unless a person is in natural daylight, they are likely to be exposed to this higher frequency flickering, because all mains-powered light sources, whether incandescent, halogen, fluorescent or LED, are subject to flickering. The source is the AC component of the power supply and the frequency of the flickering is typically either equal to the mains frequency (usually 50 or 60 Hz) or double the mains frequency.

Tests show that humans find it difficult to directly sense light flickering at these higher frequencies, but that seems to hardly matter. Scientists have conducted research that indicates the human retina is able to resolve light flickering at 100 to 150 Hz, even if the subject is not aware of it, leading to the conclusion that the brain may well be reacting.

The insidious effects of this so-called imperceptible flickering in the 100 to 150 Hz range are not just a function of frequency; physical and physiological factors also play a big part. For example, bright light is worse than dim, and the difference between "bright" and "dark" parts of the lighting pattern are important (a light that goes completely dark during the "off" part of the cycle is worse than one which only partially dims). Red light and alternating red and blue can be particularly troublesome, and the position of the light source on the retina is important, as light sensed by the center is worse than that falling on the periphery.

Some researchers even claim the retina can sense flickering up to 200 Hz, but tests have shown that above 160 Hz the health effects of flickering are negligible.¹ 


Friday, March 24, 2017

Iris - Save your eyes

Why I created Iris?

When I was young my vision was perfect, but as a programmer I was sitting for more than 10 hours per day in front of computer. Not short after that I started to experience huge eye pain and strain. I even got glasses for the first time in my life. It was time for a change. I started to search the internet for programs for eye protection and started to read every single article for eye and vision health. After I didn't find anything good enough out there I decided to create my own software for eye protection, health and productivity. Iris is the product of this decision.


Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging



    A modified FOXO4-p53 interfering peptide causes p53 nuclear exclusion in senescent cells

    This FOXO4 peptide induces targeted apoptosis of senescent cells (TASC)

    TASC neutralizes murine liver chemotoxicity from doxorubicin treatment

    TASC restores fitness, hair density, and renal function in fast and naturally aged mice


The accumulation of irreparable cellular damage restricts healthspan after acute stress or natural aging. Senescent cells are thought to impair tissue function, and their genetic clearance can delay features of aging. Identifying how senescent cells avoid apoptosis allows for the prospective design of anti-senescence compounds to address whether homeostasis can also be restored. Here, we identify FOXO4 as a pivot in senescent cell viability. We designed a FOXO4 peptide that perturbs the FOXO4 interaction with p53. In senescent cells, this selectively causes p53 nuclear exclusion and cell-intrinsic apoptosis. Under conditions where it was well tolerated in vivo, this FOXO4 peptide neutralized doxorubicin-induced chemotoxicity. Moreover, it restored fitness, fur density, and renal function in both fast aging XpdTTD/TTD and naturally aged mice. Thus, therapeutic targeting of senescent cells is feasible under conditions where loss of health has already occurred, and in doing so tissue homeostasis can effectively be restored.


Is the Mediterranean Diet the New Ambiguous Diet?

Along these lines, there is less snacking and longer periods between meals, and many have pointed out that this may be a large part of the benefit seen in the initial studies assessing the Greek population. The constituents of the original Mediterranean diet study fasted for up to 103 days per year. This was astutely pointed out by Katerina Sarri and her group in Crete. Fasting provides a plethora of health benefits, including cardiovascular benefits,5–7 improved brain health,9 and potential anticancer effects.8

Her group found significant consumption differences between the fasting versus non-fasting Greek Orthodox Christians living in Crete for over a year. Greek Orthodox Christians often fast multiple times over the year: 40 days during Christmas, 48 days during Lent, and 15 days during the Assumption.10 The initial study published the year before made no assessment of the effect of fasting, nor did they even mention fasting.11


Is the Mediterranean Diet the New Ambiguous Diet?

The "calorie is a calorie" crowd has strongly pushed the "eat less, exercise more" message to millions of Americans over the last 30 years. Not surprisingly, intangible psychological and physical failure followed, often coupled with angst and even self-loathing. Perhaps summed up best by Dr. Richard Feinman in The World Turned Upside Down, this same crowd often also preaches against fat. If all calories are the same and we need to eat less, why should we care if it is fat? Such inconsistencies define these groups as they love pushing intangible and esoteric messages that few can follow. More recently, the dietary world and media have been praising the merits of the Mediterranean Diet.

Thursday, March 23, 2017

'Suggestion' of Brain Changes on Statins by fMRI in STOMP

New research is weighing in on the "do statins impair cognition?" debate with a report of transient brain-activation changes on functional magnetic resonance imaging (fMRI) scans[1].

A substudy of the Effect of Statins on Muscle Performance (STOMP) study showed similar scores on several neuropsychological tests for statin-naïve patients (mean age 48 years) taking 80 mg/day of atorvastatin for 6 months and those taking matching placebo—echoing findings just released from the EBBINGHAUS trial of patients on the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor evolocumab (Repatha, Amgen) plus statins vs placebo.

However, the STOMP analysis did find "small but significant" between-group differences in activation patterns in two brain areas. While on study treatment, the placebo group had greater activation in the right putamen/dorsal striatum during a verbal memory task than did the atorvastatin group. However, after the drug "washed out," the atorvastatin group had greater activation in that area.

While "on drug," the atorvastatin group had greater activation in the bilateral precuneus during a figural memory task vs the placebo group—but this pattern also reversed after the washout phase.

So what does this mean? "We aren't sure," admitted Dr Beth Taylor (University of Connecticut and Hartford Hospital) to heartwire from Medscape. "There was no convincing evidence of measurable verbal or nonverbal memory dysfunction due to statins."


Association between fatty acid metabolism in the brain and Alzheimer disease neuropathology and cognitive performance: A nontargeted metabolomic study

We performed metabolic profiling on brain tissue samples from 43 individuals ranging in age from 57 to 95 y old who were stratified into three groups: AD (N = 14), controls (N = 14) and "asymptomatic Alzheimer's disease" (ASYMAD), i.e., individuals with significant AD neuropathology at death but without evidence for cognitive impairment during life (N = 15) from the autopsy sample of the Baltimore Longitudinal Study of Aging (BLSA). We measured 4,897 metabolite features in regions both vulnerable in the middle frontal and inferior temporal gyri (MFG and ITG) and resistant (cerebellum) to classical AD pathology. The levels of six unsaturated fatty acids (UFAs) in whole brain were compared in controls versus AD, and the differences were as follows: linoleic acid (p = 8.8 x 10−8, FC = 0.52, q = 1.03 x 10−6), linolenic acid (p = 2.5 x 10−4, FC = 0.84, q = 4.03 x 10−4), docosahexaenoic acid (p = 1.7 x 10−7, FC = 1.45, q = 1.24 x 10−6), eicosapentaenoic acid (p = 4.4 x 10−4, FC = 0.16, q = 6.48 x 10−4), oleic acid (p = 3.3 x 10−7, FC = 0.34, q = 1.46 x 10−6), and arachidonic acid (p = 2.98 x 10−5, FC = 0.75, q = 7.95 x 10−5). These fatty acids were strongly associated with AD when comparing the groups in the MFG and ITG, respectively: linoleic acid (p < 0.0001, p = 0.0006), linolenic acid (p < 0.0001, p = 0.002), docosahexaenoic acid (p < 0.0001, p = 0.0024), eicosapentaenoic acid (p = 0.0002, p = 0.0008), oleic acid (p < 0.0001, p = 0.0003), and arachidonic acid (p = 0.0001, p = 0.001). Significant associations were also observed between the abundance of these UFAs with neuritic plaque and neurofibrillary tangle burden as well as domain-specific cognitive performance assessed during life. Based on the regional pattern of differences in brain tissue levels of these metabolites, we propose that alterations in UFA metabolism represent both global metabolic perturbations in AD as well as those related to specific features of AD pathology. Within the middle frontal gyrus, decrements in linoleic acid, linolenic acid, and arachidonic acid (control>ASYMAD>AD) and increases in docosahexanoic acid (AD>ASYMAD>control) may represent regionally specific threshold levels of these metabolites beyond which the accumulation of AD pathology triggers the expression of clinical symptoms. The main limitation of this study is the relatively small sample size. There are few cohorts with extensive longitudinal cognitive assessments during life and detailed neuropathological assessments at death, such as the BLSA


Wednesday, March 22, 2017

Breast Implants Linked to Cancer: How Does It Happen?

On Wednesday (March 22), the FDA said that, in light of new data, the agency now recognizes that a rare type of cancer called anaplastic large cell lymphoma (ALCL) can develop after a person receives breast implants. ALCL is not breast cancer; rather, it is a type of lymphoma, which is a cancer of immune system cells, the FDA said in a statement. In the cases that were reported to the FDA, the cancer typically occurred in the scar tissue around the implant, the agency said. So the cancer occurs in the immune system cells around the breast implant, but not in the breast tissue cells themselves.


AGA Clinical Practice Update: PPIs should be prescribed sparingly, carefully

PPIs should be used on a short-term basis for individuals with gastroesophageal reflux disease (GERD) or conditions such as erosive esophagitis. These patients can also use PPIs for maintenance and occasional symptom management, but those with uncomplicated GERD should be weaned off PPIs if they respond favorably to them.

If a patient is unable to be weaned off PPIs, then ambulatory esophageal pH and impedance monitoring should be done, as this will allow clinicians to determine if the patient has a functional syndrome or GERD. Lifelong PPI treatment should not be considered until this step is taken, according to the new best practice statements.

"Short-term PPIs are highly effective for uncomplicated GERD [but] because patients who cannot reduce PPIs face lifelong therapy, we would consider testing for an acid-related disorder in this situation," the authors explained. "However, there is no high-quality evidence on which to base this recommendation."

Patients who have symptomatic GERD or Barrett's esophagus, either symptomatic or asymptomatic, should be on long-term PPI treatment. Patients who are at a higher risk for NSAID-induced ulcer bleeding should be taking PPIs if they continue to take NSAIDs.

When recommending long-term PPI treatment for a patient, the patient need not use probiotics on a regular basis; there appears to be no need to routinely check the patient's bone mineral density, serum creatinine, magnesium, or vitamin B12 level on a regular basis. In addition, they need not consume more than the Recommended Dietary Allowance of calcium, magnesium, or vitamin B12.


Tuesday, March 21, 2017

Pop a Pill for Heartburn? Try Diet and Exercise Instead - NYTimes.com

Many Americans would rather take a drug than change their habits to control a persistent ailment. Yet, every medication has side effects, some of which can be worse than the disease they are meant to treat. Drugs considered safe when first marketed can turn out to have hazards, both bothersome and severe, that become apparent only after millions of people take them for a long enough time.

Such is the case with a popular class of drugs called proton pump inhibitors, or P.P.I.s, now used by more than 15 million Americans and many more people worldwide to counter an increasingly common ailment: acid reflux, which many people refer to as heartburn or indigestion.

These medications are now linked to a growing number of complications, ranging in seriousness from nutrient deficiencies, joint pain and infections to bone fractures, heart attacks and dementia. While definitive evidence for most of the risks identified thus far is lacking, consumers plagued by acid reflux would be wise to consider an alternative approach, namely diet and lifestyle changes that can minimize symptoms and even heal damage already done.

Acid reflux is more than just a nuisance. It involves the backward flow of stomach acid into the tissues above it. It results when the lower esophageal sphincter, a ring of muscle between the esophagus and the stomach, fails to close tightly enough to prevent the contents of the stomach from moving up instead of down. Sometimes the upper sphincter, between the esophagus and the throat, malfunctions as well.

Acid reflux is a serious disorder that can and must be treated to prevent symptoms and stave off potentially life-threatening consequences. Known medically and commercially as GERD, the acronym for gastroesophageal reflux disease, repeated bathing of the soft tissues of the esophagus with corrosive stomach acid can seriously damage them and even cause esophageal cancer, which is often fatal.

Contrary to what many believe, heartburn is but one of the many symptoms of GERD, and failure to recognize the others when heartburn is not among them can result in harmful untreated reflux. In addition to indigestion, GERD can cause a persistent dry cough, sore throat, frequent throat clearing, hoarseness, burping or hiccups, bloating, difficulty swallowing and a sensation of a lump in the throat.

If, when faced with such an otherwise unexplainable symptom, your doctor fails to think of GERD as a possible reason, you might suggest it yourself. An examination of the esophagus may be the only way to find out if someone without obvious heartburn has acid reflux but doesn't know it.

Dr. Jonathan Aviv, an ear, nose and throat specialist affiliated with Mount Sinai Icahn School of Medicine in New York, was in his mid-30s when he developed a frightening symptom that turned out to be caused by acid reflux. He was suddenly awakened one night gasping for air and feeling like he was being choked. Because he'd never complained of heartburn, his own doctor had trouble believing that acid reflux could be the explanation. Yet treating this ailment brought relief and set Dr. Aviv on a yearslong journey to learn how best to manage it.

He has now written a book, "The Acid Watcher Diet," that both explains how the varied symptoms of acid reflux arise, and details a program for healing and prevention that can help many, if not most, people avoid the medications commonly prescribed to treat it.

One characteristic often associated with acid reflux — being overweight, especially with abdominal obesity — largely explains why the condition has become so common in Western countries. Someone with a body mass index in the overweight range is almost twice as likely to have GERD as a person of normal weight. Losing weight is one of the best ways to find relief without having to rely on medication.

Quitting smoking, limiting alcohol and avoiding carbonated drinks are also important protective measures. Smoking and alcohol can loosen tension of the upper esophageal sphincter and cause symptoms of reflux like hoarseness, postnasal drip and shortness of breath by irritating the mouth, larynx and trachea, Dr. Aviv reports.

Eating big meals, lying down before a meal is digested, and exercising too soon after eating can also trigger symptoms. Reflux sufferers are often advised to eat five or six small meals a day rather than one or two big ones, and to avoid eating within three hours of bedtime. For further protection, the head of the bed can be raised by six inches or more.


Monday, March 20, 2017

Inflammation Stimulates the Expression of PCSK9

Inflammation induces marked changes in lipid and lipoprotein metabolism. Proprotein convertase subtilisin kexin 9 (PCSK9) plays an important role in regulating LDL receptor degradation. Here, we demonstrate that LPS decreases hepatic LDL receptor protein but at the same time hepatic LDL receptor mRNA levels are not decreased. We therefore explored the effect of LPS on PCSK9 expression. LPS results in a marked increase in hepatic PCSK9 mRNA levels (4h 2.5-fold increase; 38h 12.5-fold increase). The increase in PCSK9 is a sensitive response with 1microg LPS inducing a (1/2) maximal response. LPS also increased PCSK9 expression in the kidney. Finally, zymosan and turpentine, other treatments that induce inflammation, also stimulated hepatic expression of PCSK9. Thus, inflammation stimulates PCSK9 expression leading to increased LDL receptor degradation and decreasing LDL receptors thereby increasing serum LDL, which could have beneficial effects on host defense.


Bile – not Acid – is Bad Guy in Triggering Precancerous Condition Associated with Reflux Disease

Acid-reducing drugs called proton pump inhibitors or PPIs are some of the most popular and best-selling drugs in America according to IMS Health, an organization that tracks pharmacy data. While the drugs do a great job of masking GERD symptoms by neutralizing stomach acid, Peters' research suggests they may not be the answer when it comes to blocking Barrett's esophagus. Other research even indicates that such drugs may actually make patients more prone to developing Barrett's.


The Damage of Reflux (Bile, Not Acid) - NYTimes.com

Symptoms and Causes

Both acid reflux and bile reflux may afflict the same person, which can make diagnosis a challenge. But the stomach inflammation that results from bile reflux often causes a burning or gnawing pain in the upper abdomen that is not felt with acid reflux, according to experts at the Mayo Clinic. Other symptoms of bile reflux may include frequent heartburn (the main symptom of acid reflux), nausea, vomiting bile, sometimes a cough or hoarseness and unintended weight loss.

A brief anatomy lesson makes the problem easier to understand. The main organs of the digestive tract are separated by valvelike tissues that, when functioning properly, allow food and digestive fluids to pass in only one direction: down. Thus, as food and liquids pass through the digestive process, they normally travel from the mouth to the throat, then down the esophagus into the stomach, and finally into the small intestine. The opening between the esophagus and stomach, a muscular ring called the lower esophageal sphincter, is meant to keep stomach acid from backing up. When it malfunctions, acid reflux — chronic heartburn — is the usual result.

Likewise, the pyloric valve, the muscular ring between the stomach and small intestine, is supposed to open just enough to permit a fraction of an ounce of liquefied food to pass into the small intestine, but not enough to allow bile to back up into the stomach. When this valve fails to close properly, refluxed bile can cause gastritis, an irritation and inflammation of the stomach lining. Untreated, that can result in a bleeding ulcer or even stomach cancer.

If the esophageal sphincter malfunctions at the same time, or there is a build-up of pressure in the stomach, bile and acid can reach the lower portion of the esophagus, inflaming the delicate lining of this organ. If the problem persists, it can cause scarring that narrows the esophagus, which may result in choking, or the cellular abnormality called Barrett's esophagus, which can become precancerous and eventually develop into cancer that is nearly always fatal.

Gastroenterologists have recently demonstrated that Barrett's esophagus can often be effectively treated with radiofrequency therapy, which might help patients like Mrs. Kozma.

Bile reflux can occur as a complication of certain surgeries, like the gallbladder surgery Mrs. Kozma underwent. More often, though, damage to the pyloric valve results from gastric surgery — total removal of the stomach or the gastric bypass operation used to treat morbid obesity.

Occasionally, the pyloric valve is obstructed by a peptic ulcer, for example, or scar tissue, which prevents the valve from opening enough to permit quick transport of stomach contents into the intestine. That causes pressure to build up in the stomach, pushing both acid and bile into the esophagus.


Chronic Bile Reflux

The most common forms of treatments for bile reflux gastritis are with medications such as ursodeoxycholic acid or proton pump inhibitors, as well as with surgery in the most severe of cases.

However, there are also natural treatments that are finally beginning to be used in the United States.

All of these natural treatments will involve herbs, and there are four that can be very effective; chamomile, licorice, slippery elm, as well as marshmallow.

Chamomile has long been associated with helping with most all types of sleeping problems, but it also has one other very important quality; it helps to fight inflammation.

It is a very strong anti-inflammatory agent and has been used for hundreds of years in Europe to fight the inflammation that is caused by this condition.

By far and away the most effective way to use this natural treatment is with a Chamomile tea as it can slow inflammation very quickly and has virtually no side effects.

The herb licorice is next of the list of natural treatments for chronic bile reflux, and this has been used to not only treat acid reflux disease, but also to treat gastritis.

It has also been used for ulcers and several other digestive problems for hundreds if not thousands of years.

Slippery elm approaches chronic bile reflux in a different manner as it is very effective at building up your mucous linings to their full strength.

This is critical with this condition simply because they can very easily become weakened by the repeated attacks.

However if you can maintain the strength of these critical linings, you can reduce the intensity of the symptoms. 

The most effective method of taking this herb is in a powder form mixed with water as soon as you have eaten.

The final herb that can help is marshmallow.

It has also been used for hundreds of years to treat GERD as it can also have a huge impact on the symptoms because of its anti-inflammatory attributes. 


Sunday, March 19, 2017

Prescribing a Diet to Treat Depression

The first-ever randomized controlled clinical trial[1] to test a dietary intervention as a treatment for clinical depression has just been published. I am Dr Drew Ramsey. I am assistant clinical professor of psychiatry at Columbia University in New York City, and I am reporting for Medscape Psychiatry. I am excited to share the results of this very interesting study with you.

Two researchers, Felice Jacka and Michael Berk, led a consortium of Australian Institutions based at the Food & Mood Centre at Deakin University in Victoria, Australia. Over 3 years, they recruited several hundred patients with moderate to severe depression and entered 67 into a 12-week parallel group trial. The treatment group received seven 60-minute sessions of dietary counselling. The parallel control group received a matching social support protocol. All but nine of the 67 participants were receiving another active treatment—either psychotherapy, medications, or both.

In the dietary counseling sessions, participants were implored to increase consumption of foods in 12 food categories. The food categories, as you may guess, included whole grains, fruits, vegetables, nuts and legumes, and lean meats, chicken, and seafood, and to decrease consumption of foods that are correlated with a higher risk for depression: empty carbohydrates, refined starches, and highly processed foods. During the past decade, a mountain of evidence has been building that dietary patterns are strongly correlated with risk for depression. We have not had a randomized controlled trial like this to direct our clinical care, however.

The outcome was quite robust. The researchers found a statistically significant 7.1-point difference on the Montgomery-Asberg Depression Rating Scale (MADRS) in favor of the treatment group, which was their primary outcome. The researchers extrapolated that there was a 2.2-point reduction in the MADRS for every 10% adherence to the healthier dietary pattern.

They developed that pattern, which they called the Modified Mediterranean Diet, or the Modi-Medi Diet, by combining recommendations from the Australian government and the Greek government, and data from an earlier analysis by Felice Jacka and her colleagues[2] that determined which dietary factors played the largest role in fighting depression with diet.

In this latest study, the number needed to treat was 4.1. That compares favorably with data from two pooled analyses of adjunctive aripiprazole[3,4] in which the number needed to treat was 10. The augmentation effect was quite robust for an adjunctive treatment. In the treatment group, about 32% of patients achieved remission, compared with 8% in the control group. In terms of risk-benefit profiles, a dietary intervention is emerging as a very safe and effective way for us to engage our patients.


Top Food Sources of Saturated Fat Among U.S. Population, 2005-2006 NHANES

Pizza and cheese are the biggest food sources of saturated fat in the U.S. diet, and other dairy products and meat products are also are also major contributors. Keep in mind that all foods contain a mix of fats. Even “healthy” foods like chicken, fish, nuts, and oils do contribute some saturated fat to the diet, though they are much lower in saturated fat than beef, cheese, and ice cream. And it would be a mistake to cut back on nuts, oils, and fish to minimize saturated fat.

As a general rule, it’s a good idea to keep your intake of saturated fats as low as possible. We can’t eliminate saturated fat from our diets completely, because foods that are good sources of healthy fats—olive oil, peanuts, salmon—also contain a little bit of saturated fat. Since red meat and full-fat dairy products are among the main sources of saturated fat in our diets, keeping these foods low is the best way to reduce intake of saturated fat. And when you cut back on red meat and dairy products, replace them with foods that contain healthy fats—fatty fish like salmon, nuts and seeds, plant oils, avocadoes—not with foods that are high in refined carbohydrates. Here is a table showing the top food sources of saturated fat in the American diet.



Is chicken recommended by your doctor?

Left: industrial chicken; Right: free-range chicken

Switching from beef to chicken, doesn't lower cholesterol.
K C Maki, M E Van Elswyk, T M Rains, E L Sohn, S McNeill. A meta-analysis of randomized controlled trials that compare the lipid effects of beef versus poultry and/or fish consumption. J Clin Lipidol. 2012 Jul-Aug;6(4):352-61.

E Ashton, M Ball. Effects of soy as tofu vs meat on lipoprotein concentrations. Eur J Clin Nutr. 2000 Jan;54(1):14-9.

E L Ashton, F S Dalais, M J Ball. Effect of meat replacement by tofu on CHD risk factors including copper induced LDL oxidation. J Am Coll Nutr. 2000 Nov-Dec;19(6):761-7.

K K Carroll, P M Giovannetti, M W Huff, O Moase, D C Roberts, B M Wolfe. Hypocholesterolemic effect of substituting soybean protein for animal protein in the diet of healthy young women. Am J Clin Nutr. 1978 Aug;31(8):1312-21.

R L Shorey, B Bazan, G S Lo, F H Steinke. Determinants of hypocholesterolemic response to soy and animal protein-based diets. Am J Clin Nutr. 1981 Sep;34(9):1769-78.

S L Wiebe, V M Bruce, B E McDonald. A comparison of the effect of diets containing beef protein and plant proteins on blood lipids of healthy young men. Am J Clin Nutr. 1984 Nov;40(5):982-9.

P M Clifton. Protein and coronary heart disease: the role of different protein sources. Curr Atheroscler Rep. 2011 Dec;13(6):493-8.

H R Ferdowsian, N D Barnard. Effects of plant-based diets on plasma lipids. Am J Cardiol. 2009 Oct 1;104(7):947-56.

D J Jenkins, C W Kendall, A Marchie, D Faulkner, E Vidgen, K G Lapsley, E A Trautwein, T L Parker, R G Josse, L A Leiter, P W Connelly. The effect of combining plant sterols, soy protein, viscous fibers, and almonds in treating hypercholesterolemia. Metabolism. 2003 Nov;52(11):1478-83.

Y Wang, C Lehane, K Ghebremeskel, M A Crawford. Modern organic and broiler chickens sold for human consumption provide more energy from fat than protein. Public Health Nutr. 2010 Mar;13(3):400-8.

Virus found in chicken can cause obesity.
Mitra AK, Clarke K. Viral obesity: fact or fiction? Obes Rev. 2010 Apr;11(4):289-96. Epub 2009 Oct 27.

Dhurandhar NV, Kulkarni P, Ajinkya SM, Sherikar A. Effect of adenovirus infection on adiposity in chicken. Vet Microbiol. 1992 Jun 1;31(2-3):101-7.

Dhurandhar NV, Kulkarni PR, Ajinkya SM, Sherikar AA, Atkinson RL. Association of adenovirus infection with human obesity. Obes Res. 1997 Sep;5(5):464-9.

Pasarica M, Dhurandhar NV. Infectobesity: obesity of infectious origin. Adv Food Nutr Res. 2007;52:61-102.

Halkjaer J, Tjønneland A, Overvad K, Sørensen TI. Dietary predictors of 5-year changes in waist circumference. J Am Diet Assoc. 2009 Aug;109(8):1356-66.

Chicken comsumption associated with a higher risk of lymphoma.
Key TJ, Appleby PN, Spencer EA, Travis RC, Allen NE, Thorogood M, Mann JI. Cancer incidence in British vegetarians. Br J Cancer. 2009 Jul 7;101(1):192-7.

Rohrmann S, Linseisen J, Jakobsen MU, Overvad K, Raaschou-Nielsen O, Tjonneland A, Boutron-Ruault MC, Kaaks R, Becker N, Bergmann M, Boeing H, Khaw KT, Wareham NJ, Key TJ, Travis R, Benetou V, Naska A, Trichopoulou A, Pala V, Tumino R, Masala G, Mattiello A, Brustad M, Lund E, Skeie G, Bueno-de-Mesquita HB, Peeters PH, Vermeulen RC, Jakszyn P, Dorronsoro M, Barricarte A, Tormo MJ, Molina E, Argüelles M, Melin B, Ericson U, Manjer J, Rinaldi S, Slimani N, Boffetta P, Vergnaud AC, Khan A, Norat T, Vineis P. Consumption of meat and dairy and lymphoma risk in the European Prospective Investigation into Cancer and Nutrition. Int J Cancer. 2011 Feb 1;128(3):623-34.

Fernandes A, Mortimer D, Rose M, Gem M. Dioxins (PCDD/Fs) and PCBs in offal: occurrence and dietary exposure. Chemosphere. 2010 Sep;81(4):536-40.

Chicken intake associated with increased rates of breast cancer and higher saturated fat intake.
Beasley JM, Newcomb PA, Trentham-Dietz A, Hampton JM, Bersch AJ, Passarelli MN, Holick CN, Titus-Ernstoff L, Egan KM, Holmes MD, Willett WC. Post-diagnosis dietary factors and survival after invasive breast cancer. Breast Cancer Res Treat. 2011 Jul;128(1):229-36.

American Cancer Society. Breast Cancer Facts & Figures 2011-2012.

National Cancer Institute. 2010. Top Food Sources of Saturated Fat among US Population.

Sugimura T, Wakabayashi K, Nakagama H, Nagao M. Heterocyclic amines: Mutagens/carcinogens produced during cooking of meat and fish. Cancer Sci. 2004 Apr;95(4):290-9.

Cho E, Spiegelman D, Hunter DJ, Chen WY, Stampfer MJ, Colditz GA, Willett WC. Premenopausal fat intake and risk of breast cancer. J Natl Cancer Inst. 2003 Jul 16;95(14):1079-85.

Chicken bacteria is associate with urinary tract infections in women, simply from handling.
X. Xia, J. Meng, P.F. McDermott, S. Ayers, K. Blickenstaff, T.T. Tran, J. Abbott, J. Zheng, & S. Zhao. Presence and characterization of shiga toxin-producing Escherichia coli and other potentially diarrheagenic E. coli strains in retail meats. Appl Environ Microbiol, 76(6):1709-1717, 2010.

T.A. Russo & J.R. Johnson. Medical and economic impact of extraintestinal infections due to Escherichia coli: focus on an increasingly important endemic problem. Microbes Infect, 5(5):449-456, 2003.

C. Vincent, P. Boerlin, D. Daignault, C.M. Dozois, L. Dutil, C. Galanakis, R.J. Reid-Smith, P.P. Tellier, P.A. Tellis, K. Ziebell, A.R. Manges. Food reservoir for Escherichia coli causing urinary tract infections. Emerg Infect Dis, 16(1):88-95, 2010.

J.R. Johnson, M.A. Kuskowski, K. Smith, T.T. O’Bryan, S. Tatini. Antimicrobial-resistant and extraintestinal pathogenic Escherichia coli in retail foods. J Infect Dis, 191(7):1040-1049, 2005.

D. Vandekerchove, P. De Herdt, H. Laevens, F. Pasmans. Risk factors associated with colibacillosis outbreaks in caged layer flocks. Avian Pathol, 33(3):337-342, 2004.

Cancer caused by arsenic-laced chicken.
G. X. Sun, P. N. Williams, A. M. Carey, Y. G. Zhu, C. Deacon, A. Raab, J. Feldmann, R. M. Islam, and A. A. Meharg. Inorganic arsenic in rice bran and its products are an order of magnitude higher than in bulk grain. Environmental science & technology, 42(19):7542{7546, 2008.

C. F. Jelinek and P. E. Corneliussen. Levels of arsenic in the united states food supply. Environ. Health Perspect., 19:83{87, 1977.

E. K. Silbergeld and K. Nachman. The environmental and public health risks associated with arsenical use in animal feeds. Ann. N.Y. Acad. Sci., 1140:346{357, 2008.


Saturday, March 18, 2017

Amgen Cholesterol Drug Repatha Prevents Heart Attacks, Stroke

The trial tested an Amgen drug called Repatha against a placebo in a 27,500-patient (there's one of our numbers) multi-nation, Phase 3, randomized, double-blind trial to see how effective it was in reducing the risk of nasty cardiovascular events. And the results were impressive. Repatha, a monoclonal antibody that substantially lowers LDL cholesterol in the blood, was shown to reduce the risk of heart attacks in patients (who already had evidence of atherosclerosis) by 27%. (There's number No. 2.) The drug reduced the risk of "hard major adverse cardiovascular events" by 20%—but didn't appear to affect overall mortality from cardiovascular disease (which wasn't expected anyway.)

Repatha, which has to be injected, is also priced at $14,000 a year. (Number No. 3.)

So what happened? Naturally, Amgen stock tanked in early morning trading (My colleague Sy Mukherjee has a write-up in today's Fortune Brainstorm Health Daily newsletter). Why, you ask? Because many were expecting even more dramatic results—especially for a medicine with a $14,000-a-year price tag.


'Healthiest hearts in the world' found

The scientists looked for coronary artery calcium or "CAC" - which is a sign of clogged up blood vessels and risk of a heart attack.

The scientists scanned 705 people's hearts in a CT scanner after teaming up with a research group scanning mummified bodies.

At the age of 45, almost no Tsimane had CAC in their arteries while 25% of Americans do.

By the time they reach age 75, two-thirds of Tsimane are CAC-free compared with the overwhelming majority of Americans (80%) having signs of CAC.

The researchers have been studying this group for a long time so it is not simply a case of the unhealthy Tsimane dying young.

Michael Gurven, a professor of anthropology at University of California, Santa Barbara, told the BBC: "It is much lower than in every other population where data exists.

"The closest were Japanese women, but it's still a different ballpark altogether."



Water Quality in Gainesville Florida

I recently tested our water quality with NTL (http://www.ntllabs.com/products.html). This was tested with water just prior to entering my house and was unfiltered. Below are the results from the report. Please note, this testing does not include pharmaceutical drugs. Our water comes from GRU. In general, the water quality is good. It would be nice to see less of the chlorine byproducts, but that can easily be filtered with carbon or RO. GRU does their own testing, but I always found the reported numbers of little value to me since the reported values for many contaminants were from testing done years ago (https://www.gru.com/OurCommunity/Content/WaterQuality.aspx).

Enormous PCBs increase in oysters from the coast of Guangdong, China

Polychlorinated biphenyls (PCBs) were added into many industrial products (e.g. as dielectric fluids in capacitors and transformers, additives in printing inks) to optimize performance (Jiang et al., 1997 ;  Li, 2006). Concerns about the environmental persistence, bioaccumulation capacity and ecosystem toxicity of chlorinated hydrocarbons have lead to the phasing out of PCBs globally (Ross, 2004). PCBs were listed as a serious threat to public health by the Stockholm Convention (Xing et al., 2005).

Due to their wide distribution and the available information for comparisons of chemical pollution over the long term, bivalve shellfish including oysters and mussels serve worldwide as sentinel organisms to assess the pollution status of the marine environment (Farrington et al., 1982). There have been many “Mussel and/or Oyster Watch” programs, such as the reports by Tripp et al., 1992; Stephenson and Martin, 1995; O’Connor, 2002 ;  Monirith et al., 2003, as well as Tanabe and Subramanian (2006).

Spatial monitoring of PCBs in marine bivalves has been reported in several bays and estuaries from the coast of China (e.g. Chen et al., 2002 ;  Fang et al., 2004) but there have been few surveys involving temporal monitoring (Jia et al., 2004). The Jinjiang oyster, Crassostrea rivularis Gould, common along the South China coast, was used in a Mussel Watch of the South China Sea during the period 1989–1993 and in the China Marine Mussel Watch Program during 2003–2007. Here we present a recent PCBs data set from the Guangdong coast, and compare it with the early results published by Jia et al. (2004).


Persistent organic pollutants enter humans primarily through the food chain, and PCB intake in people living in coastal areas can be mainly attributed to the consumption of seafood (Nakata et al., 2002). Oysters are popular seafood, and in addition to local consumption, Jinjiang oysters from the Guangdong coastline are often sold in the markets of Hong Kong, Macao and other provinces of China. The permissible PCBs limits (w.w.) in Australian seafood (NFA, 1992) were 0.5, and in China and the USA, 2 mg kg−1 (Kannan et al., 1997, Henry et al., 1998 and Health Ministry of China, 2005). PCB residuals in our 45 oyster samples ranged from 0.0043 to 0.253 mg kg−1 (w.w.), and were lower than these criteria.


Friday, March 17, 2017

Human exposure assessment of fluoride from tea (Camellia sinensis L.)

Fluoride concentrations in UK tea, including the leading supermarket economy labelled products, were determined. Fluoride ranged from 93 to 820 mg/kg in the products and 0.43 to 8.85 mg/L in the infusions. The UK supermarket economy teas contained elevated fluoride, ranging from 3.60 to 7.96 mg/L in a 2 minute brewing infusion, comparable to Chinese brick tea, indicating the use of mature leaves in their manufacture. Considering the dietary reference intake (DRI) of 4 mg/day of fluoride for an adult consuming 1 L of tea, prepared from an economy tea, containing 6.0 mg/L fluoride, 75–120% of the DRI fluoride is available for absorption by the human system in the presence of food, increasing to 150% when fasting. Excess fluoride in the diet can lead to detrimental health effects such as fluorosis of the teeth and skeletal fluorosis and consuming economy branded tea will lead to exposure.


Overall, for the tea products as a whole data set, increasing fluoride is released into a tea infusion with time. For the individual tea groups, the 2 minute infusion contained significantly lower fluoride compared to the longer infusion times of 10 and 30 min. Most of the fluoride was released into the tea infusion after 10 min with no significant differences between 10 and 30 min (p ≥ 0.09). This fluoride is available for absorption by the human system and can partly or completely fulfil the recommended DRI of 4 mg/day for an adult. Detrimental health effects such as fluorisis of the teeth or in the extreme calcification and osteoporosis, indicative of skeletal fluorosis could occur when an adult consumes 1 L of tea daily, especially when prepared using a UK supermarket Economy brand. However, if consuming other tea varieties, such as Oolong/Pu'er, Assam, Ceylon or Darjeeling, then exposure to fluoride is significantly lower.

Tea is a globally popular beverage, for which there are studies suggesting many beneficial health effects from some components in tea, such as anti-oxidants. Benefits should be contrasted with potential detrimental health effects from fluoride extracted from tea. However all tea products should be considered as a main source of fluoride in the diet. Supermarkets and manufacturers of tea should consider stating fluoride concentration as part of the nutritional information found on food packaging.


Wednesday, March 15, 2017

Iodine in autism spectrum disorders

Autism spectrum disorders (ASD) and iodine deficiency disorders (IDDs) are both global health problems. Autism spectrum disorder has no single known cause [1]. The major challenge facing progress in research into the etiology of autism is the complex interplay between many factors (environmental, genetic, social) and their poorly understood effect on the function and development of the autistic brain. ASD are developmental disorders that become evident during early childhood. Usually they are evidenced by problems forming relationships, difficulty communicating with other people and certain abnormal behavioral patterns. ASD is an umbrella term that was outlined by diagnosis criteria presented in the Diagnostic and Statistical Manual of Mental Disorders (DSM), currently in its 5th edition [2] and encompasses what were previously recognized as distinct subtypes including autistic disorder, Asperger syndrome, childhood disintegrative disorder and pervasive developmental disorder-not otherwise specified. The exact number of children affected by ASD in Poland is hard to quantify. Up until 2010 the healthcare & disability coding system did not distinguish between persons affected by autism disorders and other psychiatric or neurological problems. However, we do know that the global trend of increasing ASD diagnosis is consistent with the increasing incidence here in Poland [3] ;  [4]. The best estimates indicate that around 30,000–50,000 children in Poland are affected by ASD [5].

Although the exact etiology of ASD is unknown, the subject is one of much recent inquiry. Numerous studies have documented statistically significant nutritional and metabolic aberrations in persons affected by ASD when compared to normal populations [6] ;  [7]. Abundant effort has been devoted to determining the content of elements that may contribute to the development of ASD, even if their exact mechanism or roles in the disorder remain unclear.

Iodine is a particularly important microelement in human physiology—it plays a crucial role as a component of thyroid hormones and deficiency at any stage of life can cause significant clinical manifestations [8]; [9]; [10]; [11]; [12] ;  [13]. The most critical time for proper iodine status, however, is early in life—hypothyroidism due to iodine deficiency which can lead to impaired neurodevelopment. Adequate levels of thyroid hormones are especially important for myelination, cell migration, differentiation and maturation of the fetal brain [14]; [15] ;  [16]. IDD are caused primarily by insufficient dietary iodine intake and/or inadequate iodine utilization due to, for example, the presence of goitrogens [17] ;  [18].

In one study performed in Egypt, 54% of tested autistic children were found to be iodine deficient [19]. Another study performed in USA found 45% lower iodine content in hair of children with autism when compared with healthy controls [7]. Up until now, such studies have not yet been performed in Poland. There is also a lack of current data assessing the effectiveness of iodine prophylaxis in Polish children between the ages of 2 and 17 years and whether iodine consumption is at a satisfactory level. Although significant steps have been taken in Poland to eliminate iodine deficiency and the resulting disorders [20], the situation still requires constant monitoring. Measurements of thyroid hormone levels and thyroid stimulating hormone levels are important in the assessment of thyroid function. The majority of dietary iodine, however, ends up in the urine, so although it is not a direct measurement of function, urinary iodine (UI) level is a great indicator of recent iodine intake and low values demonstrate a population is at risk for deficiency [14]; [21] ;  [22].

The primary aims of our study were to compare iodine excretion in ASD children with those of their normally developing peers and to correlate iodine status with fifteen common diagnostic criteria for ASD from the Childhood Autism Rating Scale (CARS) in order to check which items on the scale are mostly affected by iodine status. The data were also interpreted to identify whether or not there were any relationships between age, BMI, the severity of individual symptoms of ASD, thyroid hormones and urinary iodine. To the best of our knowledge, studies of iodine status in relation to specific items from the scale measuring the severity of autism are lacking not only in Poland but are also very rare in the entire world.


The severity of certain symptoms in autism is associated with iodine status in maturing boys. Thyroid hormones were within normal reference ranges in both groups while urinary iodine was significantly lower in autistic boys suggesting that further studies into the nonhormonal role of iodine in autism are required.


Toxicological Status of Children with Autism vs. Neurotypical Children and the Association with Autism Severity

This study investigates both the level of toxic metals in children with autism and the possible association of those toxic metals with autism severity. This study involved 55 children with autism ages 5–16 years compared to 44 controls with similar age and gender. The study included measurements of toxic metals in whole blood, red blood cells (RBC), and urine. The autism group had higher levels of lead in RBC (+41 %, p = 0.002) and higher urinary levels of lead (+74 %, p = 0.02), thallium (+77 %, p = 0.0001), tin (+115 %, p = 0.01), and tungsten (+44 %, p = 0.00005). However, the autism group had slightly lower levels of cadmium in whole blood (−19 %, p = 0.003). A stepwise, multiple linear regression analysis found a strong association of levels of toxic metals with variation in the degree of severity of autism for all the severity scales (adjusted R2 of 0.38–0.47, p < 0.0003). Cadmium (whole blood) and mercury (whole blood and RBC) were the most consistently significant variables. Overall, children with autism have higher average levels of several toxic metals, and levels of several toxic metals are strongly associated with variations in the severity of autism for all three of the autism severity scales investigated.


NRDC Sues EPA Over Withdrawal of Mercury Protection Rule

The Natural Resources Defense Council today sued the Environmental Protection Agency for illegally rescinding a rule that would protect the public from more than five tons of mercury discharges each year.

In a lawsuit filed in U.S. District Court here, NRDC said EPA broke the law by withdrawing the mercury protection rule without public notice or an opportunity for comment.  The White House ordered agencies to withdraw a broad array of rules issued by the Obama Administration to protect public health and the environment.

In its complaint, NRDC contends EPA cannot withdraw the mercury protection rule based on the Trump Administration’s fiat because the rule is final. EPA issued the rule in December to limit substantially the amount of mercury dental offices across the nation discharge regularly.

The following is a statement by Aaron Colangelo, litigation director at NRDC:

“The Trump White House ordered the EPA and other agencies to violate the law. That puts Americans at greater risk of exposure to this dangerous neurotoxin, which can do harm even in tiny amounts. EPA’s withdrawal of the mercury rule is not just illegal, but senseless. The rule imposes minimal burden, drew widespread praise from dental providers and benefits public health and the environment.”


Mercury can disrupt brain function and harm the nervous system.  It is especially harmful to pregnant women, babies and young children, even at tiny levels of exposure.

One way mercury gets into air and water is through amalgam cavity fillings washed down the drain at dental offices.  Most of the 130,000 dental offices in the US still use or remove amalgam fillings.  Fewer than half of those would need to install equipment to reduce mercury discharges under the rule into wastewater treatment plants, as many have already complied under mandatory state programs.  Installing that equipment would cost about $800 per office.

EPA issued the Mercury Effluent Rule on December 15, 2016 and withdrew it after January 20, 2017 in response to a White House memo.


Tuesday, March 14, 2017

The Bredesen Protocol™ Announces Progress in Reversal of Cognitive Decline in Alzheimer’s Disease | Business Wire

TIBURON, Calif.--(BUSINESS WIRE)--The inventor and developer of the original MEND protocol (metabolic enhancement for neurodegeneration), Dr. Dale Bredesen, has developed a more advanced and effective protocol, dubbed ReCODE™ for Reversal of Cognitive Decline. The MEND protocol was the first to result in the reversal of cognitive decline in patients with pre-Alzheimer's conditions and early Alzheimer's disease, as published in the journal Aging in 2014 by Dr. Bredesen.

    "These new features greatly enhance our ability to determine the underlying causes of cognitive decline, and improve the accuracy of information, which helps our trained physicians reverse cognitive decline"
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Since this initial publication, several new discoveries have been made, including the recognition of specific subtypes of Alzheimer's disease—published in 2015—and the recognition of specific toxic exposures contributing to Alzheimer's disease—published in 2015 and 2016. These discoveries and others led to the development of ReCODE™, an improved version of The Bredesen Protocol™. "These new features greatly enhance our ability to determine the underlying causes of cognitive decline, and improve the accuracy of information, which helps our trained physicians reverse cognitive decline," said Dr. Bredesen.

This enhanced ReCODE™ protocol will be the centerpiece of the upcoming Alzheimer's Immersion Program, the kickoff for an intensive one-year therapeutic program, which is limited to 100 qualifying pre-Alzheimer's, early stage, and mid-stage Alzheimer's participants, held in Indian Wells, California, on March 24 through 27, 2017.


How to Boost Brain Performance and Prevent Dementia

Perlmutter is chairman of the Institute for Functional Medicine's 2017 Annual International Conference, "The Dynamic Brain," held in Los Angeles June 1 through June 3. The meeting will focus on neurogenesis and neuroplasticity allowing recovery from neural degenerative conditions.

Speakers include Bredesen, Michael Merzenich, the leading pioneer in brain plasticity research at the Buck Institute, Rudolph Tanzi, professor of neurology at Harvard, who will speak about how activity and lifestyle changes affect BDNF, Dr. Terry Wahls, who will speak about strategies to upregulate mitochondrial function and the PGC-1α pathway through diet and other lifestyle choices, and Dr. Joe Pizzorno, a naturopathic physician who will speak about toxicity and detoxification. 


Friday, March 10, 2017

Folate status of gut microbiome affects lifespan

The first genes extending lifespan were identified in the nematode Caenorhabditis elegans [1], and several of the metabolic pathways they are involved in are conserved in other species, including flies, mice and humans. Some of the pioneering studies on aging in C. elegans made use of RNA interference (RNAi) to manipulate gene expression, a strategy that is easily applied in C. elegans by feeding the worms on Escherichia coli strains expressing the relevant RNA sequence.

However, it is becoming increasingly clear that the E. coli diet itself can have profound affects on C. elegans lifespan, and the degree of bacterial colonization within the worm gut has been shown to correlate inversely with worm lifespan [2]. In a recent paper in BMC Biology, Virk et al. [3] capitalize on a serendipitous finding - they show that a C. elegans lifespan extension phenotype originally attributed to an RNAi clone targeting the ugt-27 gene is actually due to a spontaneous mutation present in the host E. coli strain. The authors then use classic nutritional selection experiments and identify the mutation as an IS1 insertion element within the E. coli aroD gene. AroD is a dehydratase required for the production of shikimate (SHK; Figure 1), which is in turn a precursor of chorismate, a precursor of a wide variety of aromatic compounds in E. coli. Thus, the aroD mutation affects production of Phe, Tyr, and Trp (essential aromatic amino acids), menaquinol (vitamin K2), enterobactin (involved in E. coli iron uptake), coenzyme Q (an essential lipid component of the respiratory chain) and folates (vitamin B9). Virk et al. convincingly demonstrate that the lifespan extension in C. elegans can be returned to normal when the diet of E. coli aroD- is supplemented with either SHK or the folate precursor, pABA (Figure 1), but not when it is supplemented with the other aromatic products of this pathway. Because pABA supplementation abrogates the lifespan extension of C. elegans fed the aroD- E. coli diet, Virk et al. focus their attention on folate metabolism.

Folate supplementation, sulfa drugs, and human aging

Like C. elegans, mammals are unable to synthesize folate and acquire the metabolite through diet and gut microflora production. Since 1998, the US Food and Drug Administration has required folate supplementation in all cereal grains, which has resulted in higher blood folate content of the adult, non-supplement using population [9]. Recently, a study on the gut microflora of 531 human subjects across a wide range of ages, ethnicities, and geography showed that microbes residing in babies are enriched in genes involved in de novo folate biosynthesis, whereas the microbes residing in adult subjects were enriched in genes that metabolize dietary folate and THF [10]. However, because folate supplementation regulations and diet differ in the sampling population, there is insufficient data to assess whether the changes in microbial folate biosynthesis gene expression are linked to dietary folate. Interestingly, Virk et al. note that sulfa drugs have been reported to inhibit microbiome folate synthesis and extend lifespan in rats [1]. While the mechanism remains to be determined regarding how genetic or pharmacological knockdown of folate in E. coli can enhance C. elegans lifespan, Virk et al. have raised the intriguing possibility that manipulation of the folate status of gut microflora may impact lifespan in other species.


The use of folate-producing strains can be regarded as a new perspective on the specific uses of probiotics. Within the genus Lactobacillus, the strains belonging to the species L. plantarum are expected to produce folate in the presence of preformed pABA, while the other species cannot be regarded as folate producers. Therefore, the application of lactobacilli as folate-producing probiotics seems to be precluded, even though selected strains of L. plantarum deserve to be used in animal trials to provide evidence of their ability to produce folate in vivo. Unlike lactobacilli, several folate‑producing Bifidobacterium strains have been selected, but the release of high amounts of vitamin does not seem to be widespread within the genus. Animal trials confirmed that the administration of folate-producing bifidobacteria positively affected the plasmatic folate level, indicating that the vitamin is produced in vivo by the probiotic strains, and absorbed. In a human trial, the administration of the same strains resulted in a significant increase of folate concentration in feces. Even though the effect on plasmatic levels has not been investigated so far, folate-producing bifidobacteria may provide a complementary endogenous source of the vitamin and may contribute to prevent folate deficiency, which is often associated with premalignant changes in the colonic epithelia.


Thursday, March 9, 2017

Zinc in Gut-Brain Interaction in Autism and Neurological Disorders

Research from the last decades clearly shows that zinc has a vital role in neonatal development. Zinc is an essential trace element in humans and animals and is involved in countless metabolic and signaling pathways within the body. However, a particular role of zinc in the immune system and brain has been reported [1]. Zinc is one of the most prevalent metal ions in the brain and participates in the regulation of neurogenesis, neuronal migration, and differentiation, thereby shaping cognitive development and maintaining healthy brain function. Zinc deficiency during pregnancy results in specific impairments in the offspring, which have been observed in animal models but might also be present in humans [2]. Intriguingly, among individuals with Autism Spectrum Disorders (ASD), the incidence rate of zinc deficiency has been reported to be significantly increased compared to age matched healthy control subjects [3]. The occurrence of zinc deficiencies in ASD is particularly pronounced in very young age [4, 5], where a rate of almost 50% was reported in the age group of 0–3 years [5]. These low levels of zinc often occur along with copper overload and the Cu/Zn ratio was reported to correlate with the severity of symptoms associated with autism [6–8]. This early occurrence of zinc deficiency with decline later in life and the manifestation of some of the core features of ASD, such as impaired social behavior and language and communication problems in prenatal zinc deficient mice [9], have recently put maternal zinc status in the focus as a possible environmental factor in the etiology of ASD. Thus, maintaining adequate zinc status during pregnancy might be a promising approach to prevent cognitive and neurobehavioral deficits later in life. However, meeting the zinc requirement of the mother can be challenging.

Two major pools of zinc can be found within the body: a slowly zinc exchanging pool that contains about 90% of the body's zinc and a pool that rapidly exchanges zinc with the plasma. The latter, which contains the other 10% of zinc, is the one that is especially reactive to the amount of absorbed zinc and is the first to be depleted under conditions of zinc deficiency. Plasma zinc is also the source of the embryo's zinc supply. In order to maintain proper zinc levels during pregnancy, both endogenous losses and the increased demand resulting, for example, from synthesis of novel tissue must be covered by absorption of zinc from dietary sources. Thus, while the metabolic zinc requirement of 2.5 mg/d for an adult woman is generally met when consuming daily 10 to 15 mg zinc, due to the additional need for zinc during pregnancy, an additional 5–10 mg zinc per day must be consumed to meet the increasing demand of 0.08, 0.24, 0.53, and 0.73 mg of metabolic zinc per day for the four quarters of pregnancy [10]. Similarly, during lactation, the metabolic daily requirement increases by another 2.5 mg per day. Meeting these requirements is challenged by several factors. First, it is not uncommon for women of childbearing age to consume low zinc diets. Second, zinc status of women may be compromised due to increased intake of dietary constituents that reduce the availability of zinc.

Impact of low zinc status of the mother can be magnified depending on time and severity of the deficiency, ranging from teratogenic effects with severe deficiency to functional impairments acting, for example, on brain development with mild deficiency. In particular, teratogenic effects have been reported in rodent models [11, 12] as well as in humans, where women with Acrodermatitis enteropathica, a genetic disorder resulting in impaired zinc absorption, show a high incidence of birth defects [13]. In general, although the brain seems most vulnerable, all organ systems are affected by systemic zinc deficiency in times of active proliferation and differentiation. Thus, although mild zinc deficiency does not lead to gross morphological malformations in the offspring, the reported behavioral impairments might result from a combination of alterations in brain development and other organ systems. This novel vista on the role of zinc deficiency in ASD broadens the focus from the action of zinc within the brain to other organs such as the GI system.

Proper zinc status is necessary for healthy gut development and both pre- and perinatal zinc deficiency might affect the neonate and potentially trigger downstream events that contribute to pathological processes [14]. These processes may, among others, include inflammation due to increased intestinal epithelium permeability and immune system abnormalities including the generation of autoantibodies. Another consequence of impaired or delayed gut development will be lowered trace metal absorbance, which might contribute to the slow normalization of biometals in children with ASD after birth [5]. GI discomfort, changes in gut microbiome, food aversion, and an increased intestinal permeability have been shown to correlate with the severity of behavioral symptoms in individuals with ASD [15–21].

Given that inflammatory cytokines and other immune signaling molecules originating from the GI tract interact with the hypothalamic-pituitary-adrenal gland (HPA) stress axis, prenatal stress itself can be integrated in this pathomechanism, targeting the same structures [22]. Thus, some of the major environmental risk factors for the development of ASD are linked in this model.

Taken together, maternal zinc deficiency might impair the gut development of the offspring and thereby increase the risk for GI problems, inflammatory events, abnormal immune signaling, trace metal imbalances, and ultimately altered brain function. Data supporting this hypothesis will be discussed further in more detail.