Category: Health News

Exposure to and accumulation of environmental toxins represents a major challenge to optimizing health in our current environment.

BPA – Bisphenol A is one of these environmental toxins which has received considerable coverage over the last several years.

The article I want to share with you today –from an article posted on the Science Daily website suggests that levels of accumulation in humans has been seriously underestimated.

This article was based upon a published study done at Washington State University and published in The Lancet Diabetes & Endocrinologythe citation is included at the end of this article.

Just before you read this information, here is an excerpt from an abstract on”Health Risk of Exposure to Bisphenol A” (abstract included at the end of this article) on some of the potential issues that exposure to BPA may cause:

” Due to its phenolic structure BPA has been shown to interact with estrogen receptors and to act as agonist or antagonist via estrogen receptor (ER) dependent signalling pathways. Therefore, BPA has been shown to play a role in the pathogenesis of several endocrine disorders including female and male infertility, precocious puberty, hormone dependent tumours such as breast and prostate cancer and several metabolic disorders including polycystic ovary syndrome (PCOS)”

Due to the prevalence of exposure to BPA in our environment – as well as other chemicals and heavy metals periodic monitoring and supervised detox programs to clear out this toxin load are serious considerations for optimizing health and potentially extending healthspan.

Summary:

  Researchers have developed a more accurate method of measuring bisphenol A (BPA) levels in humans and found that exposure to the endocrine-disrupting chemical is far higher than previously assumed. The study provides the first evidence that the measurements relied upon by regulatory agencies, including the US Food and Drug Administration, are flawed, underestimating exposure levels by as much as 44 times. Researchers have developed a more accurate method of measuring bisphenol A (BPA) levels in humans and found that exposure to the endocrine-disrupting chemical is far higher than previously assumed.

The study, published in the journal The Lancet Diabetes & Endocrinology on Dec. 5, provides the first evidence that the measurements relied upon by regulatory agencies, including the U.S. Food and Drug Administration, are flawed, underestimating exposure levels by as much as 44 times.

“This study raises serious concerns about whether we’ve been careful enough about the safety of this chemical,” said Patricia Hunt, Washington State University professor and corresponding author on the paper. “What it comes down to is that the conclusions federal agencies have come to about how to regulate BPA may have been based on inaccurate measurements.”

BPA can be found in a wide range of plastics, including food and drink containers, and animal studies have shown that it can interfere with the body’s hormones. In particular, fetal exposure to BPA has been linked to problems with growth, metabolism, behavior, fertility and even greater cancer risk.

Despite this experimental evidence, the FDA has evaluated data from studies measuring BPA in human urine and determined that human exposure to the chemical is at very low, and therefore, safe levels. This paper challenges that assumption and raises questions about other chemicals, including BPA replacements, that are also assessed using indirect methods.

Hunt’s colleague, Roy Gerona, assistant professor at University of California, San Francisco, developed a direct way of measuring BPA that more accurately accounts for BPA metabolites, the compounds that are created as the chemical passes through the human body.

Previously, most studies had to rely on an indirect process to measure BPA metabolites, using an enzyme solution made from a snail to transform the metabolites back into whole BPA, which could then be measured.

Gerona’s new method is able to directly measure the BPA metabolites themselves without using the enzyme solution.

In this study, a research team comprised of Gerona, Hunt and Fredrick vom Saal of University of Missouri compared the two methods, first with synthetic urine spiked with BPA and then with 39 human samples. They found much higher levels of BPA using the direct method, as much as 44 times the mean reported by the National Health and Nutrition Examination Survey (NHANES). The disparity between the two methods increased with more BPA exposure: the greater the exposure the more the previous method missed.

Gerona, the first author on the paper, said more replication is needed.

“I hope this study will bring attention to the methodology used to measure BPA, and that other experts and labs will take a closer look at and assess independently what is happening,” he said.

The research team is conducting further experiments into BPA measurement as well as other chemicals that may also have been measured in this manner, a category that includes environmental phenols such as parabens, benzophenone, triclosan found in some cosmetics and soaps, and phthalates found in many consumer products including toys, food packaging and personal care products.

“BPA is still being measured indirectly through NHANES, and it’s not the only endocrine-disrupting chemical being measured this way,” Gerona said. “Our hypothesis now is that if this is true for BPA, it could be true for all the other chemicals that are measured indirectly.”

This study was supported by grants from the National Institutes of Health.


Story Source:

Materials provided by Washington State University. Original written by Sara Zaske. Note: Content may be edited for style and length.


Journal Reference:

  1. Roy Gerona, Frederick S vom Saal, Patricia A Hunt. BPA: have flawed analytical techniques compromised risk assessments? The Lancet Diabetes & Endocrinology, 2019; DOI: 10.1016/S2213-8587(19)30381-X

Rocz Panstw Zakl Hig. 2015;66(1):5-11.

Health risk of exposure to Bisphenol A (BPA).

Konieczna A1, Rutkowska A1, Rachoń D1.  

Abstract

Bisphenol A (BPA) belongs to chemicals that are produced in large quantities worldwide. It is commonly used as monomer in polycarbonate synthesis, plasticizer in the production of epoxy resins, as well as an additive for the elimination of surfeit of hydrochloric acid during the polyvinyl chloride (PVC) production. BPA is not only used in the production of plastics intended to a direct contact with food, including plastic packaging and kitchenware, but also in inner coatings of cans and jar caps. There are various routes of human exposure to this substance such as oral, by inhalation and transdermal. The main sources of exposure to BPA include food packaging and dust, dental materials, healthcare equipment, thermal paper, toys and articles for children and infants. BPA is metabolized in the liver to form bisphenol A glucuronide and mostly in this form is excreted with urine. Due to its phenolic structure BPA has been shown to interact with estrogen receptors and to act as agonist or antagonist via estrogen receptor (ER) dependent signalling pathways. Therefore, BPA has been shown to play a role in the pathogenesis of several endocrine disorders including female and male infertility, precocious puberty, hormone dependent tumours such as breast and prostate cancer and several metabolic disorders including polycystic ovary syndrome (PCOS).

Because of the constant, daily exposure and its tendency to bio-accumulation, BPA seems to require special attention such as biomonitoring. This observation should include clinical tests of BPA concentration in the urine, which is not only one of the best methods of evaluation of the exposure to this compound, but also the dependence of the daily intake of BPA and the risk of some endocrine disorders. PMID: 25813067

From the Science Alert website:

People who live with depression have low blood levels of a specific molecule, new medical research has revealed. It’s called acetyl-L-carnitine, and those with particularly severe, treatment-resistant or childhood onset depression were found to have the lowest levels.

Naturally produced by the body, acetyl-L-carnitine plays a crucial role in metabolising fat and the production of energy. It’s also widely available as a dietary supplement – not some strange and esoteric thing.

Now researchers from multiple institutions have found a link to depression, noticing a clear correlation between the condition and noticeably low levels of acetyl-L-carnitine.

In recent years, more and more evidence has been building to suggest this link. Since at least 1991, medical researchers have been aware of acetyl-L-carnitine’s potential to treat depression, particularly in geriatric and comorbid patients, with the substance showing greater efficacy than a placebo.

More recently, Carla Nasca of the Rockefeller University led a study on rodents, which found that acetyl-L-carnitine had a fast-acting antidepressant effect on rats, kicking into effect in just a few days, rather than the weeks it takes for drugs like SSRIs.

Now Nasca and colleagues have conducted a study on human patients to see if there’s a basis for a similar trial in people.

“As a clinical psychiatrist, I have treated many people with this disorder in my practice,” said Stanford University School of Medicine psychiatrist Natalie Rasgon.

“It’s the number one reason for absenteeism at work, and one of the leading causes of suicide. Worse, current pharmacological treatments are effective for only about 50 percent of the people for whom they’re prescribed. And they have numerous side effects, often decreasing long term compliance.”

The research team recruited 71 patients with a diagnosis of depression. These were men and women, aged between 20 and 70. They also recruited 45 demographically matched healthy controls.

The patients had to fill out a detailed questionnaire, undergo a clinical assessment and medical history, and give a blood sample. Of the patients with depression, 28 had moderate depression and 43 had severe depression at the time of the study.

When compared to the age- and sex-matched healthy controls, the patients with depression had substantially lower levels of acetyl-L-carnitine.

Those with the most severe depression had the lowest levels. This included patients whose depression had resisted antidepressant drugs, those with early onset, and those who had experienced childhood abuse, neglect, poverty or violence.

These patients constitute around 25-30 percent of all people suffering depression, and are the most in need of help, the researchers said.

But there are a few steps to be done before acetyl-L-carnitine supplements can be approved as a treatment. In particular, clinical trials on human patients with depression, since, as we know, results from rodent models can’t always be replicated in humans.

The researchers also don’t know the reason for the correlation, or the effect it has. The rat research suggests that acetyl-L-carnitine plays a role in the brain, preventing the excessive firing of excitatory neurons, but this will need to be explored further as well.

“We’ve identified an important new biomarker of major depression disorder,” Rasgon said.

“We didn’t test whether supplementing with that substance could actually improve patients’ symptoms. What’s the appropriate dose, frequency, duration? We need to answer many questions before proceeding with recommendations, yet. This is the first step toward developing that knowledge, which will require large-scale, carefully controlled clinical trials.”

And we’ll be eagerly awaiting the results of those trials.

Meanwhile, the team’s research can be found in the journal PNAS.

Here in Canada, the government agency which is responsible for licensing natural health products is the NNHPD – Natural and Non-Prescription Health Products Directorate.

The regulatory approval process to get natural health products approved can be challenging, frustrating and take a long time: some of our formulations have taken over 2 years before they were finally approved!

Nevertheless, we feel that this regulatory framework ultimately makes for a better regulated market which ultimately helps consumers.

Our company, Robert Lamberton Consulting and our various brands: Cutting Edge Naturals, SmartBrain Formulations and OPN – Optimum Performance Nutrition follow these guidelines.

‘Silken’ bags for premium teas are made of PET or nylon, but it’s not known if that poses health risk

From the CBC website:

You may be swallowing billions of tiny plastic particles while sipping a cup of freshly brewed gourmet tea, a new study from McGill University in Montreal suggests.

Many fancier teas now come in “silken” bags instead of paper. Some of them are pyramid-shaped, which is billed as a way to make room for the large leaves in premium teas to expand. 

Nathalie Tufenkji, a professor of chemical engineering at the Montreal university, was surprised to find one such bag in the tea she ordered from a coffee shop one morning.

It looked like plastic, she recalled. “I said, ‘Oh God, I’m sure if it’s plastic it’s, like, breaking down into the tea.'”

So when she got into the lab, she asked her graduate student, Laura Hernandez, to go out and buy a bunch from different brands.

Sure enough, Hernandez’s lab tests showed that when steeped in hot water, the tea bags released microplastic and even smaller nanoplastic particles — and not just the hundreds or thousands Tufenkji had been expecting.

“We were shocked when we saw billions of particles in a single cup of tea,” she said.

One cup from a single tea bag could contain 11.6 billion microplastic and 3.1 billion nanoplastic particles, the researchers estimated from their results, published Wednesday in the journal Environmental Science & Technology.

The bits are so tiny — on average, the size of grains of dust or pollen — that the amount in one cup is about 16 micrograms or one-sixtieth of a milligram of plastic. 

But that’s still much more than has been found in other foods and beverages, including tap and bottled water, beer, honey, fish and shellfish, chicken and salt. Tufekji said that’s partly because her study included and counted smaller particles than most other studies. But it’s also because, for most foods and beverages, the plastic is an accidental contaminant. With tea “you’re literally adding plastic into the beverage.”

That may sound unappetizing, but is it a health risk?

The Tea and Herbal Association of Canada told CBC News in a statement that the materials used in the tea bags in the study, PET (polyethylene terephthalate, found in plastic drink bottles) and nylon (used in many food bags and pouches), have been deemed safe for use in contact with hot food and beverages. It added there is no evidence the microparticles pose a risk to human health.

The World Health Organization has said the risk from microplastics in drinking water is low, especially if the particles are relatively large.

But in general, there isn’t much known on the impact of microplastics on human health.

“There’s really no research. But this really points to the need to do those studies,” Tufenkji said. “Think of people who drink one or two or three cups of tea a day, every day.”

Collectively, Canadians drink about 10 billion cups of tea a year.

Tufenkji says the potential health risk isn’t the only reason to stick to paper tea bags and loose leaf tea.

“Personally, I would say avoid the plastic tea bags because it’s just another single-use plastic” — something many governments, including Canada’s, are trying to reduce due to the impact on oceans and the challenges of recycling it.

The researchers counted the plastic particles by cutting open bags of tea, removing the tea, rinsing off any pieces that might have come off during cutting, and then steeping the bags in distilled water at 95 C. They then took a sample, let the water evaporate, and counted the plastic particles under an electron microscope, then extrapolated to get the amount in one cup. They also used other instruments to identify the type of plastic in each bag.

The researchers also repeated the experiment with uncut bags that still contained tea to make sure the cutting didn’t cause the bags to shed, and with loose tea leaves, confirming that uncut bags shed microplastics too (although they were harder to count) and the plastic didn’t originate from the tea itself.

Finally, they did a preliminary study where they exposed water fleas — tiny freshwater animals distantly related to shrimp — to the microplastics from the tea bags, which are similar in size to their food.

The water fleas didn’t die, but swam “crazily,” Tufenkji said. “It really stresses them out.”

They also changed shape, revealed CT scans performed by McGill researcher Hans Larsson. The study described the exposed water fleas as having a “ballooned” carapace.

Tufenkji said the results point to the need for more studies with other animals.

It also motivates her research group to see if other plastic packaging might be releasing particles into food and beverages.

The study was funded by the Canada Research Chairs program, the Canada Foundation for Innovation, the Natural Science and Engineering Research Council of Canada, and McGill University.

Here are the takeaways

Matthew Hoffman, a researcher who studies freshwater plastic pollution at the Rochester Institute of Technology but wasn’t involved in the new study, said the experiments seemed well designed and robust.

“One of the big takeaways,” he wrote in an email, “is that the humans would be exposed to orders of magnitude more plastic particles than has been reported from previous food and drink studies.”

His colleague, Christy Tyler, an aquatic ecologist who was also not involved in the newly released research, noted the small size of the particles in the study.

“We’re getting a clearer understanding that nanoscale plastics (like other nano-scale particles) can cross into cells,” she wrote.

While it wasn’t clear exactly how the microplastics were causing changes in the water fleas, and we don’t know the effects on humans, she added, “it’s still cause for caution in how we approach widespread use of these materials in our everyday products.”

We all know that when necessary taking antibiotics can be very beneficial – and in fact it can even save peoples’ lives.

There are of course negative side effects associated with the consumption of antibiotics, one of the key ones being disruption of the microbiome.

Following is an article from Science Daily on some research coming out of the University of British Columbia in Canada suggesting that common antibiotics may cause heart problems.

Following is the story.

Source: University of British Columbia

Summary: Scientists have shown for the first time a link between two types of heart problems and one of the most commonly prescribed classes of antibiotics. Share:


Scientists have shown for the first time a link between two types of heart problems and one of the most commonly prescribed classes of antibiotics.

In a study published today in the Journal of the American College of Cardiology, researchers at the University of British Columbia (UBC) in partnership with the Provincial Health Services Authority’s (PHSA) Therapeutic Evaluation Unit found that current users of fluoroquinolone antibiotics, such as Ciprofloxacin or Cipro, face a 2.4 times greater risk of developing aortic and mitral regurgitation, where the blood backflows into the heart, compared to patients who take amoxicillin, a different type of antibiotic. The greatest risk is within 30 days of use.

Recent studies have also linked the same class of antibiotics to other heart problems.

Some physicians favour fluoroquinolones over other antibiotics for their broad spectrum of antibacterial activity and high oral absorption, which is as effective as intravenous, or IV, treatment.

“You can send patients home with a once-a-day pill,” said Mahyar Etminan, lead author and associate professor of ophthalmology and visual sciences in the faculty of medicine at UBC. “This class of antibiotics is very convenient, but for the majority of cases, especially community-related infections, they’re not really needed. The inappropriate prescribing may cause both antibiotic resistance as well as serious heart problems.”

The researchers hope their study helps inform the public and physicians that if patients present with cardiac issues, where no other cause has been discovered, fluoroquinolone antibiotics could potentially be a cause.

“One of the key objectives of the Therapeutic Evaluation Unit is to evaluate different drugs and health technologies to determine whether they enhance the quality of care delivered by our programs or improve patient outcomes,” said Dr. Bruce Carleton, director of the unit and research investigator at BC Children’s Hospital, a program of PHSA. “This study highlights the need to be thoughtful when prescribing antibiotics, which can sometimes cause harm. As a result of this work, we will continue working with the BC Antimicrobial Stewardship Committee to ensure the appropriate prescribing of this class of antibiotics to patients across British Columbia, and reduce inappropriate prescribing.”

For the study, scientists analyzed data from the U.S. Food and Drug Administration’s adverse reporting system. They also analyzed a massive private insurance health claims database in the U.S. that captures demographics, drug identification, dose prescribed and treatment duration. Researchers identified 12,505 cases of valvular regurgitation with 125,020 case-control subjects in a random sample of more than nine million patients. They defined current fluoroquinolone exposure as an active prescription or 30 days prior to the adverse event, recent exposure as within days 31 to 60, and past exposure as within 61 to 365 days prior to an incident. Scientists compared fluoroquinolone use with amoxicillin and azithromycin.

The results showed that the risk of aortic and mitral regurgitation, blood backflow into the heart, is highest with current use, followed by recent use. They saw no increased risk aortic and mitral regurgitation with past use.

Etminan hopes that if other studies confirm these findings, regulatory agencies would add the risk of aortic and mitral regurgitation to their alerts as potential side effects and that the results would prompt physicians to use other classes of antibiotics as the first line of defense for uncomplicated infections.

This study was funded and conducted by the department of ophthalmology and the Therapeutic Evaluation Unit at the Provincial Health Services Authority.

Dietary intervention restores protective protein and decreases death rate in mice

Source: Society for Neuroscience

The incidence of dementia and Alzheimer’s continues to escalate in the general population.

LCHF/Keto diets have proven to be beneficial to individuals dealing with these health issues.

It has been suggested that these conditions may partly be due to impaired glucose metabolism in the brain, hence the increasing use of the term “Type 3 Diabetes”.

Enabling the brain to use ketones for its energy source therefore can provide some benefit with regards to brain function.

A major challenge with this is that a radical dietary shift in the geriatric population can be quite challenging – if not impossible.

Usage of exogenous ketone compounds is one potential option in this situation.

Following is an article from Science Daily which talks about published research which suggests that increasing ketone levels in the diet can help to protect neurons from death during the progression of Alzheimer’s disease.

Summary: A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.

Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease.


Story Source:

Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.


Journal Reference:

  1. Aiwu Cheng, Jing Wang, Nathaniel Ghena, Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019

Abstract

SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model

Impaired mitochondrial function and aberrant neuronal network activity are believed to be early events in the pathogenesis of Alzheimer’s disease (AD), but how mitochondrial alterations contribute to aberrant activity in neuronal circuits is unknown. In this study, we examined the function of mitochondrial protein deacetylase sirtuin 3 (SIRT3) in the pathogenesis of AD. Compared to AppPs1 mice, Sirt3-haploinsufficient AppPs1 mice (Sirt3+/-AppPs1) exhibit early epileptiform EEG activity and Seizure. Both male and female Sirt3+/-AppPs1 mice were observed to die prematurely before five months of age.

When comparing male mice among different genotypes, Sirt3 haploinsufficiency renders GABAergic interneurons in the cerebral cortex vulnerable to degeneration and associated neuronal network hyperexcitability. Feeding Sirt3+/-AppPs1 AD mice with a ketone ester-rich diet increases SIRT3 expression and prevents seizure-related death and the degeneration of GABAergic neurons, indicating that the aggravated GABAergic neuron loss and neuronal network hyperexcitability in Sirt3+/-AppPs1 mice are caused by SIRT3 reduction and can be rescued by increase of SIRT3 expression. Consistent with a protective role in AD, SIRT3 levels are reduced in association with cerebral cortical Aβ pathology in AD patients. In summary, SIRT3 preserves GABAergic interneurons and protects cerebral circuits against hyperexcitability, and this neuroprotective mechanism can be bolstered by dietary ketone esters.

SIGNIFICANCE STATEMENT

GABAergic neurons provide the main inhibitory control of neuronal activity in the brain. By preserving mitochondrial function, SIRT3 protects parvalbumin and calretinin interneurons against Aβ-associated dysfunction and degeneration in AppPs1 AD mice, thus restraining neuronal network hyperactivity. The neuronal network dysfunction that occurs in AD can be partially reversed by physiological, dietary, and pharmacological interventions to increase SIRT3 expression and enhance the functionality of GABAergic interneurons.