From Chaos To Calm: A Life Changed By Ketamine


An anesthetic and sometimes-party drug, ketamine is helping some patients calm the symptoms of mental disorders.

For six years now, life has been really good for James. He has a great job as the creative director of an advertising firm in New York City. He enjoys spending time with his wife and kids.

And it has all been possible, he says, because for the past six years he has been taking a drug called ketamine.

Before ketamine, James was unable to work or focus his thoughts. His mind was filled with violent images. And his mood could go from ebullient to dark in a matter of minutes.

Ketamine “helped me get my life back,” says James, who asked that we not use his last name to protect his career.

Ketamine was developed as a human and animal anesthetic in the 1960s. And almost from the time it reached the market it has also been used as a mind-bending party drug.

But ketamine’s story took a surprising turn in 2006, when researchers at the National Institutes of Health showed that an intravenous dose could relieve severe depression in a matter of hours. Since then, doctors have prescribed ketamine “off label” to thousands of depressed patients who don’t respond to other drugs.

And pharmaceutical companies are testing several new ketamine-related drugs to treat depression. Johnson & Johnson expects to seek approval for its nasal spray esketamine later this year, though the approval would be limited to use in a clinical setting.

Meanwhile, doctors have begun trying ketamine on patients with a wide range of psychiatric disorders other than depression. And there is now growing evidence it can help people with anxiety, bipolar disorder, post-traumatic stress disorder, and perhaps even obsessive-compulsive disorder.

“I think it’s actually one of the biggest advances in psychiatry in a very long time,” says Dr. Martin Teicher, an associate professor of psychiatry at Harvard Medical School and director of the Developmental Biopsychiatry Research Program at McLean Hospital.

Ketamine may also offer new hope for people like James who have symptoms of several different psychiatric disorders.

James had a happy childhood, he says. But his thoughts were out of control. “I always felt like I was crossing a freeway and my thoughts were just racing past me,” he says.

He spent much of his childhood terrified of “an unknown, an ambiguous force out there.” The fear was “overwhelming,” he says. “I literally slept with the cover over my head with just room to breathe through my mouth until I went to college.”

And there was something else about James: his body temperature.

“I overheated constantly,” he says. “I would wear shorts all year long. In my 20s in my apartment I would sleep with the windows open in the middle of the winter.”

In his late 20s, James saw a doctor who told him he had attention deficit hyperactivity disorder. So he started taking stimulants.

At first, the pills helped him focus. Then they didn’t, no matter how many he took.

He’d done well as an idea guy in the advertising industry. But now James was trying to work at home, and it wasn’t going well.

“ADHD pills will make you interested in anything,” he says. “So I was putting the desk together and taking the desk apart. I was putting a laptop stand together and taking it apart. I was going in a massive downward spiral.”

James had always suffered from mood swings. But now they were rapid and extreme. And he couldn’t stop thinking about gruesome scenarios, like a murderer coming for his family.

“My wife took a summer off to be with me because she was scared of what was going to happen to me,” he says. “She would go to work for a few hours, then rush home. There would be times I’d call her just screaming, ‘Please come home. I can’t get through another minute.’ ”

Eventually, James found his way to Dr. Demitri Papolos, an associate professor of clinical psychiatry at Albert Einstein College of Medicine.

“He was like a whirling dervish when he came into my office,” Papolos says. “He was extremely fearful and scanning the environment all the time and he overheated at the drop of a hat.”

Papolos diagnosed James with a variant of bipolar disorder he calls the “fear of harm phenotype.” It typically appears in childhood and often doesn’t respond to traditional psychiatric drugs.

But Papolos has found that the condition does respond to ketamine. “It’s been transformational,” he says.

In January, Papolos published a study of 45 children with the problem. They inhaled a nasal mist containing ketamine about twice a week. Nearly all got dramatically better.

Scientists still aren’t sure why ketamine works, but there’s evidence that it encourages the brain to rewire, to alter the connections between cells. That process has been linked to recovery from depression. And it may also explain why ketamine helps people who have symptoms associated with several different psychiatric disorders.

“I think it’s having multiple effects, and that means it’s probably useful for multiple different disorders,” Teicher says.

One of those effects involves a part of the brain involved in temperature regulation. And that could explain why patients like James usually stop overheating once they are taking ketamine.

James started taking a ketamine nasal spray every other day. He says his response was dramatic.

“One day I turn to my wife and I’m like, ‘I feel calm today. I don’t know if it’s the sun coming in, I don’t know if it’s just the way we’re sitting here, but I feel like I could go and sit at the computer and work.’ ”

The next day, James did sit down at his computer. A month later, he was back at work.

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No more sweet tooth? Scientists switch off pleasure from food in brains of mice


Altering activity in brain’s emotion center can eliminate the natural craving for sweet; findings could inform treatments for eating disorders

New research in mice has revealed that the brain’s underlying desire for sweet, and its distaste for bitter, can be erased by manipulating neurons in the amygdala, the emotion center of the brain. The research points to new strategies for understanding and treating eating disorders including obesity and anorexia nervosa.

Brain illustration

New research in mice has revealed that the brain’s underlying desire for sweet, and its distaste for bitter, can be erased by manipulating neurons in the amygdala, the emotion center of the brain.

The study showed that removing an animal’s capacity to crave or despise a taste had no impact on its ability to identify it. The findings suggest that the brain’s complex taste system — which produces an array of thoughts, memories and emotions when tasting food — are actually discrete units that can be individually isolated, modified or removed all together. The research points to new strategies for understanding and treating eating disorders including obesity and anorexia nervosa.

The research was published today in Nature.

“When our brain senses a taste it not only identifies its quality, it choreographs a wonderful symphony of neuronal signals that link that experience to its context, hedonic value, memories, emotions and the other senses, to produce a coherent response,” said Charles S. Zuker, PhD, a principal investigator at Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute and the paper’s senior author.

Today’s study builds upon earlier work by Dr. Zuker and his team to map the brain’s taste system. Previously, the researchers revealed that when the tongue encounters one of the five tastes — sweet, bitter, salty, sour or umami — specialized cells on the tongue send signals to specialized regions of the brain so as to identify the taste, and trigger the appropriate actions and behaviors.

To shed light on that experience, the scientists focused on sweet and bitter taste and the amygdala, a brain region known to be important for making value judgments about sensory information. Previous research by Dr. Zuker, a professor of biochemistry and molecular biophysics and of neuroscience and a Howard Hughes Medical Institute Investigator at Columbia University Irving Medical Center, and others showed that the amygdala connects directly to the taste cortex.

“Our earlier work revealed a clear divide between the sweet and bitter regions of the taste cortex,” said Li Wang, PhD, a postdoctoral research scientist in the Zuker lab and the paper’s first author. “This new study showed that same division continued all the way into the amygdala. This segregation between sweet and bitter regions in both the taste cortex and amygdala meant we could independently manipulate these brain regions and monitor any resulting changes in behavior.”

The scientists performed several experiments in which the sweet or bitter connections to the amygdala were artificially switched on, like flicking a series of light switches. When the sweet connections were turned on, the animals responded to water just as if it were sugar. And by manipulating the same types of connections, the researchers could even change the perceived quality of a taste, turning sweet into an aversive taste, or bitter into an attractive one.

In contrast, when the researchers instead turned off the amygdala connections but left the taste cortex untouched, the mice could still recognize and distinguish sweet from bitter, but now lacked the basic emotional reactions, like preference for sugar or aversion to bitter.

“It would be like taking a bite of your favorite chocolate cake but not deriving any enjoyment from doing so,” said Dr. Wang. “After a few bites, you may stop eating, whereas otherwise you would have scarfed it down.”

Usually, the identity of a food and the pleasure one feels when eating it are intertwined. But the researchers showed that these components can be isolated from each other, and then manipulated separately. This suggests that the amygdala could be a promising area of focus when looking for strategies to treat eating disorders.

In the immediate future, Drs. Zuker and Wang are investigating additional brain regions that serve critical roles in the taste system. For example, the taste cortex also links directly to regions involved in motor actions, learning and memory.

“Our goal is to piece together how those regions add meaning and context to taste,” said Dr. Wang. “We hope our investigations will help to decipher how the brain processes sensory information and brings richness to our sensory experiences.”

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Age related BP targets for chronic kidney disease patients work better


A cautious approach to lowering blood pressure (BP) in elderly patients with chronic kidney disease (CKD) is recommended, said US-based researchers. Treatment of hypertension in younger patients with CKD can follow current clinical guidelines, they added.

“Hypertension affects almost all patients with CKD, and is one of the few conditions that is treatable with a wide array of medications,” said lead author Professor Casaba P. Kovesdy, from the Division of Nephrology, Memphis Veterans Affairs Medical Center, Memphis, Tennessee, US.

Kovesdy and team examined systolic BP (SBP) and diastolic BP (DBP) with all-cause mortality, together with the incidence of chronic heart disease (CHD), ischaemic stroke, and end stage renal disease (ESRD) in 339,887 patients with CKD. [Clin J Am Soc Nephrol 2016;doi:10.2215/CJN.08660815]

During the 4.8 year median follow-up 100,763 patients died (95 percent confidence interval [CI], 62.6- 63.4). Mortality rates were high in older SBP patients. SBP ≥ 140mmHg and <120 mmHg was associated with higher mortality rates across all age groups. Lowest mortality was seen in SBP 120-139 mmHg for patients <80 years, and SBP 120-159 mmHg for patients ≥80 years.

Compared to SBP of 130-139 mmHg, SBP ≥170mmHg in patients aged <50, 50-59, 60-69, 70-79, and ≥80 years were adjusted hazard ratio [aHR], 1.95, 95 percent CI, 1.34-2.84; aHR, 2.01, 95 percent CI, 1.75-2.30; aHR, 1.68, 95 percent CI, 1.49-1.89; aHR, 1.39, 95 percent CI, 1.25-1.54; and aHR, 1.30, 95 percent CI, 1.17-1.44, respectively.

Lower DBP was associated with high mortality. DBP of 70-79 mmHg in patients <50 years and 80-89 mmHg in patients ≥50 years had the lowest mortality.

CHD was experienced in 9,450 patients during the study period (95 percent CI, 9.6-10.0). Higher SBP was associated with higher CHD rates in patients <80 years. However, lowest CHD rates were associated with SBP<110 mmHg in patients <70 years and SBP<140 mmHg in patients ≥70 years. DBP on the other hand had no association with CHD.

Ischaemic stroke was experienced by 14,557 patients (95 percent CI, 10.2-10.6). While higher SPB was associated with higher stroke rates across all age groups, DBP showed no association. Lowest stroke risk was seen in patients with SBP <100mmHg.

ESRD rates were found to be lower in older individuals compared to younger patients. ESRD was seen in 5,161 patients (95 percent CI, 3.2-3.3). DBP was found to have no association with ESRD, but high SBP was associated with high ESRD incidence. Patients <80 years with SBP ≥170mmHg had high ESRD risk, but SBP <170mmHg in this age group had no associated risk.

“Our results reinforce the significant association of elevated SBP with all the studied outcomes but suggest weak association in the elderly, especially in patients aged ≥80years,” said Kovesdy. “The best outcomes were seen with SBP of 120-130 mmHg in patients <80 years and of 120-159 mmHg in those ≥80years.”

In a separate editorial, Assistant Professor Jessica W. Weiss from the Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon, US said that the study by Kovesdy and team added to the collective understanding of the relationship between BP and a wide range of various clinical outcomes in older adults with CKD, a group rarely studied. This, she said, may be useful in guiding the design of future studies in this area. [Clin J Am Soc Nephrol 2016;doi:10.2215/CJN.03100316]

“These results may also add a note of caution to newfound enthusiasm for lower BP targets after the release of the SPRINT* via the suggestion that harm may persist at upper and lower extremes of BP among populations more comorbid and complex than those evaluated in the setting of a clinical trial,” said Weiss.

 

Evolocumab plus statin potentially reduces atherosclerosis progression in GLAGOV study


The addition of evolocumab to statin therapy in individuals with angiographic coronary disease appeared to encourage coronary atherosclerosis regression, as demonstrated in the GLAGOV* trial presented at the Scientific Sessions of the American Heart Association (AHA 2016) held in New Orleans, Louisiana, US.

In comparison with patients on statin alone who experienced a nonsignificant 0.05 percent increase in percent atheroma volume (PAV), those on combined therapy of statin and evolocumab had a 0.95 percent reduction in PAV (difference, -1.0 percent, 95 percent confidence interval [CI], -1.8 to -0.64 percent; p<0.001). Normalized total atheroma volume (TAV) decreased by 0.9 mm3 (nonsignificant) in those on statin alone compared with 5.8 mm3 in those on statin and evolocumab (difference, -4.9 mm3, 95 percent CI, -7.3 to -2.5; p<0.001). [AHA 2016, LBCT 03; JAMA 2016;doi:10.1001/jama.2016.16951]

Plaque regression occurred in a greater number of patients on evolocumab and statin compared with those on statin alone (64.3 percent vs 47.3 percent; difference, 17.0 percent, 95 percent CI, 10.4 to 23.6 percent; p<0.001 for PAV and 61.5 percent vs 48.9 percent; difference, 12.5 percent, 95 percent CI, 5.9 to 19.2 percent; p<0.001 for TAV).

“We are really reducing plaque burden in the coronaries if we can get [low-density lipoprotein cholesterol (LDL-C)] down to these very low levels,” said study chair Dr Steven Nissen from the Department of Cardiovascular Medicine at the Cleveland Clinic, Cleveland, Ohio, US, who presented the findings. “It turns out that a little bit of change in plaque volume translates into a very big change in plaque behaviour.”

“[These findings] suggest a new era in lipid management,” said discussant Dr Raul Santos from the University of São Paulo, Brazil.

Evolocumab appeared to be well tolerated with comparable incidences of injection site reactions (0.4 percent vs 0 percent), myalgia (7.0 percent vs 5.8 percent), neurocognitive events (1.4 percent vs 1.2 percent), and new onset diabetes (3.6 percent vs 3.7 percent) for evolocumab plus statin vs statin monotherapy, respectively.

In this double-blind, placebo-controlled, multicentre trial, participants (n=968, mean age 59.8 years; 72 percent male) with angiographic coronary disease, LDL-C levels ≥80 mg/dL or 60–80 mg/dL with additional high-risk features, and on stable statin therapy were randomized to receive monthly subcutaneous injections of the proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor, evolocumab (420 mg) or placebo for 76 weeks. After angiography, participants underwent intravascular ultrasound (IVUS) of the same artery at baseline and at week 78.

“Both the primary and secondary IVUS efficacy measures showed atherosclerosis regression … in patients treated with the combination of evolocumab and statins and absence of regression in patients treated with a statin alone,” said study lead investigator Dr Steven Nicholls, also from the Cleveland Clinic. “These findings provide evidence that PCSK9 inhibition produces incremental benefits on coronary disease progression in statin-treated patients.”

“Over the last 4 decades, evidence has accumulated suggesting that optimal LDL levels for patients with coronary disease may be much lower than commonly achieved. While we await large outcome trials for PCSK9 inhibitors, the GLAGOV trial provides intriguing evidence that clinical benefits may extend to LDL-C levels as low as 20 mg/dL,” said Nissen, who acknowledged the limitations of the trial such as the small number of patients and short treatment period. “IVUS is a useful measure of disease activity, but the critical determination of benefit and risk will require completion of large outcome trials currently underway,” he said.

Other factors that could potentially influence disease progression in the setting of very low LDL-C levels also need to be investigated, said Nicholls.

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Dapagliflozin drives HbA1c, SBP, and weight down in DERIVE


Dr Siew-Pheng Chan.

The use of the sodium/glucose cotransporter 2 (SGLT-2) inhibitor dapagliflozin in patients with type 2 diabetes (T2D) and moderate renal impairment provides benefits beyond glucose lowering, with no new safety signals, in the phase III DERIVE* study.

At 6 months, the primary endpoint of mean reduction in HbA1c level was greater by 0.34 percent in patients treated with dapagliflozin vs placebo (p< 0.001). There were also greater reductions in systolic blood pressure (SBP, 3.1 mm Hg; p<0.05) and mean body weight (1.25 percent, p< 0.001) with dapagliflozin. (APSC 2018, abstract S105-01)

“Dapagliflozin induces glycosuria and lowers blood glucose. However, the glycaemic efficacy of dapagliflozin is attenuated in patients with moderate renal impairment, for example in stage 3 CKD, because less glucose is cleared in the kidney in this group,” said Dr Siew-Pheng Chan, consultant endocrinologist at Subang Jaya Medical Centre in Subang Jaya, Malaysia, who is unaffiliated with the study.

Researchers led by Dr Paola Fioretto of the University of Padova in Padua, Italy conducted the DERIVE study to compare the efficacy and safety of dapagliflozin vs placebo in 321 patients with T2D (HbA1c of 7 –11 percent) and moderate renal impairment (stage 3A chronic kidney disease (CKD), estimated glomerular filtration rate (eGFR), 45 to <60 mL/min/1.73m2). Patients were randomized to either dapagliflozin 10 mg (n=160) or placebo (n=161) over 6 months. Randomization was stratified by background glucose-lowering medication. Both groups had similar baseline characteristics.

At 6 months, treatment with dapagliflozin resulted in a significant reduction in mean HbA1c (-0.37 percent vs -0.03 percent for placebo) and mean body weight (-3.17 vs -1.92 kg, respectively) from baseline. The mean fasting plasma glucose was also significantly reduced with dapagliflozin (-21.46 vs -4.87 mg/dL for placebo) as was mean SBP (-4.8 vs -1.7 mm Hg, respectively) from baseline to 6 months.

In terms of safety, mean eGFR was reduced with dapagliflozin (-3.23 mL/min/1.73m2) vs placebo (-0.63 mL/min/1.73m2). Urinary tract infection and genital infection were the most common adverse events of interest reported. Overall, the safety profile of dapagliflozin was consistent with previous reports seen for T2D. No bone fractures or amputations were reported.

Dapagliflozin is currently indicated as an adjunct to diet and exercise to improve glycaemic control in adults with T2D. Dapagliflozin remains contraindicated in patients with an eGFR <30 mL/min/1.73 m².

 

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Low ankle-brachial index tied to cognitive decline


Even in the absence of peripheral arterial disease, a lower ankle-brachial index (ABI) is significantly associated with larger declines in cognitive function, according to a poster presented at the 2018 Congress of the Asian Pacific Society of Cardiology (APSC 2018) in Taipei, Taiwan.

“The present study aimed to investigate whether a graded association between ABI and cognitive function exists, and whether this association is independent of artery stiffness, which is a recognized predictor of cognitive impairment,” said researchers.

Categorizing 708 participants according to quartiles of ABI, researchers found that there was a significant and inverse correlation between ABI values and global cognitive function, represented as scores in the Mini-Mental Short Examination (MMSE; p=0.0011 for trend). [APSC 2018, abstract P006]

Specifically, mean MMSE scores were lowest in the first ABI quartile (27.4±3.1) and increased in the second (27.8±2.8), third (28.2±2.3) and fourth (28.4±2.0) quartiles.

The significant relationship between ABI and global cognitive function was confirmed in general linear (β, –0.137; p=0.0007) and fully adjusted multivariable logistic regression models (Q4 vs Q1: adjusted odds ratio [OR], 3.623; 95 percent CI, 1.096–11.972).

Researchers likewise found a significant and positive relationship between MMSE scores and carotid-femoral pulse wave velocity (CF-PWV; β, 0.114; p=0.0044).

Notably, using patients with both high ABI and low PWV as reference, the odds of cognitive function decline was elevated in those with high PWV only (OR, 2.34) and low ABI only (OR, 2.28). The effect was substantially more pronounced in those with both low ABI and high PWV (OR, 8.19).

ABI also showed a significant and inverse association with mean brachial pulse pressure (Q1: 58.3±11.8; Q2: 56.6±13.2; Q3: 54.7±10.6; Q4: 54.9±10.6 mm Hg; p=0.0094 for trend). There was a significantly higher proportion of male patients in the third (58.52 percent) and fourth (57.30 percent) ABI quartiles than in the first (35.16 percent) and second (42.42 percent; p<0.0001 for trend).

The findings of the present study show that a lower ABI value is significantly associated with a greater decline in global cognitive function, said researchers. In addition, the relationship was independent of and additive to the effect of arterial stiffness.

For the study, researchers recruited 708 adults without peripheral arterial disease (ABI >0.9; mean age 69.0±7.0 years; 48.35 percent male). Volume-plethysmographic apparatus was used to measure ABI, while CF-PWV was used as a measure of arterial stiffness.

Of the participants, 182 had ABI from 0.9–1.10 and were placed in the lowest quartile (mean age 69.3±7.1 years) while 165 had ABI from 1.10–1.14 and fell within the second quartile (mean age 69.1±6.9 years). The third (ABI 1.14–1.19; mean age 68.8±7.3 years) and fourth (ABI ≥1.19; mean age 68.9±6.6 years) quartiles included 176 and 185 participants, respectively.

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Fasting boosts stem cells’ regenerative capacity .


A drug treatment that mimics fasting can also provide the same benefit, study finds
Age-related declines in stem cell function can be reversed by a 24-hour fast, according to a new study. Biologists found fasting dramatically improves stem cells’ ability to regenerate, in both aged and young mice.

Intestinal stem cells from mice that fasted for 24 hours, at right, produced much more substantial intestinal organoids than stem cells from mice that did not fast, at left.
 

As people age, their intestinal stem cells begin to lose their ability to regenerate. These stem cells are the source for all new intestinal cells, so this decline can make it more difficult to recover from gastrointestinal infections or other conditions that affect the intestine.

This age-related loss of stem cell function can be reversed by a 24-hour fast, according to a new study from MIT biologists. The researchers found that fasting dramatically improves stem cells’ ability to regenerate, in both aged and young mice.

In fasting mice, cells begin breaking down fatty acids instead of glucose, a change that stimulates the stem cells to become more regenerative. The researchers found that they could also boost regeneration with a molecule that activates the same metabolic switch. Such an intervention could potentially help older people recovering from GI infections or cancer patients undergoing chemotherapy, the researchers say.

“Fasting has many effects in the intestine, which include boosting regeneration as well as potential uses in any type of ailment that impinges on the intestine, such as infections or cancers,” says Omer Yilmaz, an MIT assistant professor of biology, a member of the Koch Institute for Integrative Cancer Research, and one of the senior authors of the study. “Understanding how fasting improves overall health, including the role of adult stem cells in intestinal regeneration, in repair, and in aging, is a fundamental interest of my laboratory.”

David Sabatini, an MIT professor of biology and member of the Whitehead Institute for Biomedical Research, is also a senior author of the paper, which appears in the May 3 issue of Cell Stem Cell.

“This study provided evidence that fasting induces a metabolic switch in the intestinal stem cells, from utilizing carbohydrates to burning fat,” Sabatini says. “Interestingly, switching these cells to fatty acid oxidation enhanced their function significantly. Pharmacological targeting of this pathway may provide a therapeutic opportunity to improve tissue homeostasis in age-associated pathologies.”

The paper’s lead authors are Whitehead Institute postdoc Maria Mihaylova and Koch Institute postdoc Chia-Wei Cheng.

Boosting regeneration

For many decades, scientists have known that low caloric intake is linked with enhanced longevity in humans and other organisms. Yilmaz and his colleagues were interested in exploring how fasting exerts its effects at the molecular level, specifically in the intestine.

Intestinal stem cells are responsible for maintaining the lining of the intestine, which typically renews itself every five days. When an injury or infection occurs, stem cells are key to repairing any damage. As people age, the regenerative abilities of these intestinal stem cells decline, so it takes longer for the intestine to recover.

“Intestinal stem cells are the workhorses of the intestine that give rise to more stem cells and to all of the various differentiated cell types of the intestine. Notably, during aging, intestinal stem function declines, which impairs the ability of the intestine to repair itself after damage,” Yilmaz says. “In this line of investigation, we focused on understanding how a 24-hour fast enhances the function of young and old intestinal stem cells.”

After mice fasted for 24 hours, the researchers removed intestinal stem cells and grew them in a culture dish, allowing them to determine whether the cells can give rise to “mini-intestines” known as organoids.

The researchers found that stem cells from the fasting mice doubled their regenerative capacity.

“It was very obvious that fasting had this really immense effect on the ability of intestinal crypts to form more organoids, which is stem-cell-driven,” Mihaylova says. “This was something that we saw in both the young mice and the aged mice, and we really wanted to understand the molecular mechanisms driving this.”

Metabolic switch

Further studies, including sequencing the messenger RNA of stem cells from the mice that fasted, revealed that fasting induces cells to switch from their usual metabolism, which burns carbohydrates such as sugars, to metabolizing fatty acids. This switch occurs through the activation of transcription factors called PPARs, which turn on many genes that are involved in metabolizing fatty acids.

The researchers found that if they turned off this pathway, fasting could no longer boost regeneration. They now plan to study how this metabolic switch provokes stem cells to enhance their regenerative abilities.

They also found that they could reproduce the beneficial effects of fasting by treating mice with a molecule that mimics the effects of PPARs. “That was also very surprising,” Cheng says. “Just activating one metabolic pathway is sufficient to reverse certain age phenotypes.”

The findings suggest that drug treatment could stimulate regeneration without requiring patients to fast, which is difficult for most people. One group that could benefit from such treatment is cancer patients who are receiving chemotherapy, which often harms intestinal cells. It could also benefit older people who experience intestinal infections or other gastrointestinal disorders that can damage the lining of the intestine.

The researchers plan to explore the potential effectiveness of such treatments, and they also hope to study whether fasting affects regenerative abilities in stem cells in other types of tissue.


Journal Reference:

  1. Maria M. Mihaylova, Chia-Wei Cheng, Amanda Q. Cao, Surya Tripathi, Miyeko D. Mana, Khristian E. Bauer-Rowe, Monther Abu-Remaileh, Laura Clavain, Aysegul Erdemir, Caroline A. Lewis, Elizaveta Freinkman, Audrey S. Dickey, Albert R. La Spada, Yanmei Huang, George W. Bell, Vikram Deshpande, Peter Carmeliet, Pekka Katajisto, David M. Sabatini, Ömer H. Yilmaz. Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging. Cell Stem Cell, 2018; 22 (5): 769 DOI: 10.1016/j.stem.2018.04.001

First 3D-printed human corneas


The first human corneas have been 3D-printed by scientists. It means the technique could be used in the future to ensure an unlimited supply of corneas.


Dr. Steve Swioklo and Professor Che Connon with a dyed cornea.
 

The first human corneas have been 3D printed by scientists at Newcastle University, UK.

It means the technique could be used in the future to ensure an unlimited supply of corneas.

As the outermost layer of the human eye, the cornea has an important role in focusing vision.

Yet there is a significant shortage of corneas available to transplant, with 10 million people worldwide requiring surgery to prevent corneal blindness as a result of diseases such as trachoma, an infectious eye disorder.

In addition, almost 5 million people suffer total blindness due to corneal scarring caused by burns, lacerations, abrasion or disease.

The proof-of-concept research, published today in Experimental Eye Research, reports how stem cells (human corneal stromal cells) from a healthy donor cornea were mixed together with alginate and collagen to create a solution that could be printed, a ‘bio-ink’.

Using a simple low-cost 3D bio-printer, the bio-ink was successfully extruded in concentric circles to form the shape of a human cornea. It took less than 10 minutes to print.

The stem cells were then shown to culture — or grow.

Che Connon, Professor of Tissue Engineering at Newcastle University, who led the work, said: “Many teams across the world have been chasing the ideal bio-ink to make this process feasible.

“Our unique gel — a combination of alginate and collagen — keeps the stem cells alive whilst producing a material which is stiff enough to hold its shape but soft enough to be squeezed out the nozzle of a 3D printer.

“This builds upon our previous work in which we kept cells alive for weeks at room temperature within a similar hydrogel. Now we have a ready to use bio-ink containing stem cells allowing users to start printing tissues without having to worry about growing the cells separately.”

The scientists, including first author and PhD student Ms Abigail Isaacson from the Institute of Genetic Medicine, Newcastle University, also demonstrated that they could build a cornea to match a patient’s unique specifications.

The dimensions of the printed tissue were originally taken from an actual cornea. By scanning a patient’s eye, they could use the data to rapidly print a cornea which matched the size and shape.

Professor Connon added: “Our 3D printed corneas will now have to undergo further testing and it will be several years before we could be in the position where we are using them for transplants.

“However, what we have shown is that it is feasible to print corneas using coordinates taken from a patient eye and that this approach has potential to combat the world-wide shortage.”

How Walking Benefits Your Health and Longevity


Story at-a-glance

  • Inactivity is the fourth biggest killer of adults worldwide, responsible for 9 percent of premature deaths. Walking more, ideally daily, can go a long way toward reducing this risk
  • Walking for 20 to 25 minutes per day has been found to add anywhere from three to seven years to your life span. Smokers may also increase their life span by nearly four years by walking regularly
  • Walking can be tremendously beneficial for those struggling with chronic diseases such as obstructive pulmonary disease and cardiovascular disease
  • Walking has also been shown to lower your risk of Type 2 diabetes, depression, dementia, hormonal imbalances, arthritis, PMS, thyroid disorders, fatigue, varicose veins and constipation
  • British research suggests that when it comes to weight management, regular walking can be just as beneficial, or more, than working out in a gym

By Dr. Mercola

While a regimented fitness routine is certainly part of a healthy lifestyle, what you do outside the gym is equally important. Most adults spend 10 hours or more each day sitting, and research1,2 shows this level of inactivity cannot be counteracted with a workout at the end of the day. To maintain health, you really need mild but near-continuous movement throughout your waking hours.

One strategy that has been shown to have a positive impact is simply to stand up more. Increasing your daily walking is another key strategy that pays significant dividends, both short term and long term. According to the World Health Organization, inactivity is the fourth biggest killer of adults worldwide, responsible for 9 percent of premature deaths,3 and walking more could go a long way toward reducing this risk.

Walking Produces Beneficial Biochemical Changes in Your Body

The short video above reviews what happens in your body while walking. For starters, when you take your first few steps, your body releases chemicals that give your body a quick boost of energy. Once you get going, your heart rate will increase, from about 70 to about 100 beats per minute. This boost in blood flow will warm up your muscles. As you move, your body will also increase production of fluid in your joints, thereby reducing stiffness.

Walking for six to 10 minutes can raise your heartbeat to about 140 beats per minute and trigger your body to start burning up to six calories per minute. While your blood pressure will rise from the exertion, this increase is counteracted by chemicals that help expand your blood vessels, such as nitric oxide. This expansion in turn allows greater amounts of oxygen-rich blood to reach your muscles and organs, including your heart and brain. Over time, taking regular walks will help lower your blood pressure if it tends to be high.

Walking for 11 to 20 minutes results in an increase in body temperature and sweating as blood vessels closer to the surface of your skin expand to release heat. At this point, you start burning about seven calories per minute. The increase in heart rate also causes you to breathe deeper. Epinephrine (adrenaline) and glucagon also begin to rise at this point to boost muscle activity. Epinephrine helps relieve asthma and allergies, which helps explain why walking and other exercises tend to have a beneficial impact on these ailments.

At 21 to 45 minutes, you’ll start burning more fat, courtesy of a drop in insulin. This is also when you’ll start experiencing greater physical and mental relaxation as your brain starts to release “feel good” endorphins. Walking has also been shown to boost memory and creative problem-solving,4 so taking a walk when you’re puzzling over a problem may allow you to come up with better solutions. One Stanford University study found walking increased creative output by an average of 60 percent, compared to sitting still.5

After 30 to 45 minutes, you’re really oxygenating your whole body, burning more fat, strengthening your heart and cardiovascular system, and boosting your immune function. Provided you’re walking outdoors and the weather complies, an hour of sunshine will also help boost your mood and provide a number of beneficial health effects associated with vitamin D production.

Those struggling with depression would do well to get out of the concrete jungle and into nature, as nature walks have been found to be particularly beneficial for your mood by decreasing rumination — the obsessive mulling over negative experiences.

Walking Boosts Health and Longevity

Several studies have confirmed that walking boosts health and longevity. For example:

In one, walking for 20 to 25 minutes per day (140 to 175 minutes per week) was found to add anywhere from three to seven years to a person’s life span.6

Research7 published last year found that as little as two hours (120 minutes) of walking per week may reduce mortality risk in older adults, compared to inactivity. Meeting or exceeding the activity guidelines of 2.5 hours (150 minutes) of moderate activity per week in the form of walking lowered all-cause mortality by 20 percent.

Research published in 2012 found brisk walking improved life expectancy even in those who are overweight.8

Smokers may also increase their life span by nearly four years by engaging in physical activity9 such as walking. Former smokers who kept up their physical activity increased their life expectancy by 5.6 years on average, reducing their all-cause mortality risk by 43 percent.

Smokers who were physically active were also 55 percent more likely to quit smoking than those who remained inactive, and 43 percent less likely to relapse once they quit. A Norwegian study10 also showed that regular exercise is as important as quitting smoking if you want to reduce your mortality risk.

About 5,700 older men were followed for about 12 years in this study, and those who got 30 minutes of exercise — even if all they did was light walking — six days a week, reduced their risk of death by about 40 percent. Getting less than one hour of light activity per week had no effect on mortality in this study, highlighting the importance of getting the “dosage” right if you want to live longer.

Walking Is Good for Whatever Ails You

Other studies have shown walking can be tremendously beneficial for people struggling with chronic diseases such as obstructive pulmonary disease (COPD) and cardiovascular disease. In one, COPD patients who walked 2 miles a day or more cut their chances of hospitalization from a severe episode by about half.11,12

Another study13 found that daily walking reduced the risk of stroke in men over the age of 60. Walking for an hour or two each day cut a man’s stroke risk by as much as one-third, and it didn’t matter how fast or slow the pace was. Taking a three-hour long walk each day slashed the risk by two-thirds. Walking has also been shown to lower your risk of:14,15

Type 2 diabetes Depression and anxiety
Dementia and Alzheimer’s Arthritis
Hormonal imbalances PMS symptoms
Thyroid disorders Fatigue
Varicose veins Constipation

So, while walking might not seem like it would be “enough” to make a significant difference in your health, science disagrees. It makes sense that walking would be an important health aspect considering humans are designed for walking. And, in our historical past, before conveniences such as automobiles and even the horse and buggy, humans walked a lot. Every day.

Walkers Generally Weigh Less Than Other Exercisers

Research16 from the London School of Economics and Political Science suggests that when it comes to weight management, regular walking can be just as beneficial, or more, than working out in a gym. To reach this conclusion, the researchers assessed the effects of a number of different workouts, comparing health markers in more than 50,000 adults who were followed for 13 years. Activities were divided into:

  • Brisk walking
  • Moderate-intensity sports (examples: swimming, cycling, gym workouts, dancing, running, football, rugby, badminton, tennis and squash)
  • Heavy housework and/or walking with heavy shopping bags
  • Heavy manual work (examples: digging, felling trees, chopping wood, moving heavy loads)

The big surprise? People who regularly walked briskly for more than 30 minutes generally weighed less than those who hit the gym on a regular basis and/or exclusively did high-intensity workouts. According to the press release, these results were “particularly pronounced in women, people over 50 and those on low incomes.”17 According to the authors:

“Given the obesity epidemic and the fact that a large proportion of people … are inactive, recommending that people walk briskly more often is a cheap and easy policy option. Additionally, there is no monetary cost to walking so it is very likely that the benefits will outweigh the costs.

It has also been shown by the same authors that walking is associated with better physical and mental health. So, a simple policy that ‘every step counts’ may be a step toward curbing the upward trend in obesity rates and beneficial for other health conditions.”

Indeed, walking has been a longstanding recommendation to meet fitness guidelines, and the U.S. Centers for Disease Control, the American College of Sports Medicine and the American Heart Association have all recommended getting 30 minutes of brisk walking several days a week for general health and disease prevention.18,19

Walking Can Also Be a High-Intensity Exercise

While taking daily walks forms a great foundation upon which to build your health, research also shows that to really maximize health and longevity, higher intensity exercise is called for. Based on two large-scale studies20,21 the ideal amount of exercise to promote longevity is between 150 and 450 minutes of moderate exercise per week. During the 14-year follow up period, those who exercised for 150 minutes per week reduced their risk of death by 31 percent, compared to non-exercisers.

Those who exercised for 450 minutes lowered their risk of premature death by 39 percent. Above that, the benefit actually began to diminish. In terms of intensity, those who added bouts of strenuous activity each week also gained an extra boost in longevity. Those who spent 30 percent of their exercise time doing more strenuous activities gained an extra 13 percent reduction in early mortality, compared to those who exercised moderately all the time.

Besides doing high-intensity exercises on an elliptical, bike or treadmill, super-slow strength training is another excellent high-intensity exercise worth considering. That said, if you’re out of shape and/or overweight, the idea of high intensity interval training can seem too daunting to even attempt. The elderly may also shy away from high intensity exercises for fear of injury. My recommendation? Don’t allow such concerns to overwhelm you and prevent you from getting started.

Once you’re walking on a regular basis, you can easily turn this activity into a high-intensity exercise simply by intermittently picking up the pace. Japanese researchers, who developed a walking program designed specifically for the elderly, have shown that a combination of gentle strolling and fast walking provide greater fitness benefits than walking at a steady pace.22,23

The program they developed consists of repeated intervals of three minutes of fast walking followed by three minutes of slow strolling. Completing five sets of these intervals, totaling 30 minutes of walking, at least three times a week, led to significant improvements in aerobic fitness, leg strength and blood pressure.

Everyone Can Benefit From Walking More Each Day

As mentioned, walking can be an excellent entry into higher intensity training, regardless of your age and fitness level. Personally, I typically take an hourlong walk on the beach every day that I’m home. As you’ve probably heard by now, chronic sitting is the new smoking — it actually has a mortality rate similar to this toxic habit.24 It even raises your risk of lung cancer by over 50 percent. What’s worse, it raises your risk of disease and early death independently of your fitness and other healthy lifestyle habits.

According to Dr. James Levine, codirector of Obesity Solutions at Mayo Clinic in Phoenix and Arizona State University, you need at least 10 minutes of movement for every hour you sit down. I recommend limiting your sitting to less than three hours a day, and to make it a point to walk more every day. I suggest aiming for about 10,000 steps per day, over and above any other fitness routine you may have.

A fitness tracker can be a very helpful tool to monitor your progress and ensure you’re hitting your mark. Just be sure that you are using one that does not have Bluetooth enabled (the Oura ring and Apple Watch are the two that I know of that allow you to turn off the Bluetooth). Tracking your steps can also show you how simple and seemingly minor changes to the way you move around at work can add up. For example, you can:

  • Walk across the hall to talk to a co-worker instead of sending an email
  • Take the stairs instead of the elevator
  • Park your car further away from the entrance
  • Take a longer, roundabout way to your desk
  • Take a walk during your lunch hour (importantly, this habit has been shown to reduce work-related stress25).

Watch the video. URL:https://youtu.be/A7vk13pOn4s

Toxic Weed Killer Found in Most Foods Sold in the US


Story at-a-glance

  • Between 1974 — the year glyphosate entered the U.S. market — and 2014, glyphosate use in the U.S. increased more than 250fold
  • Few people had detectable levels of glyphosate in their urine in 1993, but by 2016, 70 percent had detectable levels. Between 1993 and 2016, the glyphosate levels in people’s bodies increased by 1,208 percent
  • While both the U.S. Department of Agriculture’s Pesticide Data Program and the U.S. Food and Drug Administration (FDA) measure pesticide residues in foods, neither include glyphosate in their official testing
  • Internal FDA emails reveal Roundup has been found in virtually all foods tested, including granola, oatmeal products, crackers and honey
  • Independent testing has found significant amounts of glyphosate in a wide range of foods as well, including grains (especially oats), legumes, beans, orange juice, wine and ice cream.

 

By Dr. Mercola

Earlier this year, researchers from University of California San Diego School of Medicine reported there’s been a dramatic increase in glyphosate exposure in recent decades and, subsequently, the level found in people’s bodies.1 As one would expect, the introduction of so-called “Roundup Ready” genetically engineered (GE) crops led to a massive increase in the use of Roundup, the active ingredient of which is glyphosate.

Glyphosate has also become a popular tool for desiccating non-GE grains, legumes and beans, which has further spurred the use of the chemical. Between 1974 — the year glyphosate entered the U.S. market — and 2014, glyphosate use in the U.S. increased more than 250fold.2,3 Globally, glyphosate use has risen nearly fifteenfold since 1996, two years after the first GE crops hit the market.

Farmers now apply nearly 5 billion pounds (over 2 billion kilograms) of glyphosate to farm crops each year, worldwide.4 Approximately 300 million pounds are applied on U.S. farmland. According to the researchers, few people had detectable levels of glyphosate in their urine in 1993 when the study began.5 By 2016, 70 percent had detectable levels.6 Overall, between 1993 and 2016, the glyphosate levels in people’s bodies increased by 1,208 percent.

Food Testing Reveals Widespread Glyphosate Contamination

While Monsanto still argues that Roundup (and glyphosate in general) is perfectly safe, mounting research tells a very different story, which is why it’s becoming increasingly crucial to assess just how much glyphosate is in our food. Unfortunately, while both the U.S. Department of Agriculture (USDA) Pesticide Data Program and the U.S. Food and Drug Administration (FDA) measure pesticide residues in foods, neither of them includes glyphosate in their official testing.

The USDA promised to begin glyphosate testing in 2017, yet mere days before the testing was scheduled to begin, the plan was called off. The reason has never been disclosed. The only time the USDA tested for glyphosate was in 2011, when 300 soybean samples were tested and all were found to be contaminated.

Meanwhile, the FDA began a limited testing program for glyphosate in 2016, in which high levels of glyphosate was found in oatmeal products and honey, but the agency did not release the results publicly. Now, internal FDA emails obtained by investigative journalist Carey Gillam7 through Freedom of Information Act (FOIA) requests reveal Roundup has been found in virtually all foods tested, including granola and crackers. Gillam writes:

“[T]he internal documents obtained by the Guardian show the FDA has had trouble finding any food that does not carry traces of the pesticide. ‘I have brought wheat crackers, granola cereal and corn meal from home and there’s a fair amount in all of them,’ FDA chemist Richard Thompson wrote to colleagues in an email last year regarding glyphosate … broccoli was the only food he had ‘on hand’ that he found to be glyphosate-free …

Separately, FDA chemist Narong Chamkasem found ‘over-the-tolerance’ levels of glyphosate in corn, detected at 6.5 parts per million [ppm], an FDA email states. The legal limit is 5.0 ppm. An illegal level would normally be reported to the Environmental Protection Agency (EPA), but an FDA supervisor wrote to an EPA official that the corn was not considered an ‘official sample.’”

Independent Testing Also Highlights Massive Glyphosate Problem

The Health Research Institute Labs (HRI Labs) is an independent laboratory that tests both micronutrients and toxins found in food, and is often hired to test foods claiming to be non-GMO, “all natural” and/or organic. One of the toxins HRI Labs is currently focusing on is glyphosate, and the public testing being offered (see below) allows them to compile data on the pervasiveness of this chemical in the food supply.

HRI was recently tasked with testing Ben & Jerry’s ice cream, which was also found to contain glyphosate. The samples were provided by the Organic Consumers Association (OCA) and Regeneration Vermont, which are concerned about the environmental impact Ben & Jerry’s dairy producers are having in Vermont. Using sensitive state-of-the-art testing equipment to look at the quality of the ingredients, 10 of the 11 ice cream samples were found to contain substantial levels of glyphosate.

HRI Labs has investigated a number of other foods as well, including grains, legumes and beans. Most if not all of these types of crops need to dry in the field before being harvested, and to speed that process, the fields are doused with glyphosate a couple of weeks before harvest. As a result of this practice, called desiccation, grain-based products, legumes and beans contain rather substantial amounts of glyphosate. Quaker Oats, for example, was found to contain very high levels.

Orange juice also contains surprising amounts of glyphosate. As it turns out, weeds in orange groves are managed by spraying glyphosate, which ends up in the oranges as the roots of the orange trees pick it up through the soil. A similar situation is occurring in vineyards, which is why many wines are contaminated.

HRI Labs has also analyzed more than 1,200 urine samples from U.S. residents. This testing is being done as part of a research project that will provide valuable information about the presence of glyphosate in the diet and how lifestyle and location affects people’s exposure to agrochemicals. Here are some of their findings to date:

  • 76 percent of people tested have some level of glyphosate in their system
  • Men typically have higher levels than women
  • People who eat oats on a regular basis have twice as much glyphosate in their system as people who don’t (likely because oats are desiccated with glyphosate before harvest)
  • People who eat organic food on a regular basis have an 80 percent lower level of glyphosate than those who rarely eat organic. This indicates organic products are a safer choice
  • People who eat five or more servings of vegetables per day have glyphosate levels that are 50 percent lower than those who eat fewer vegetables

How Is Glyphosate Affecting Human Health?

Glyphosate mimics glycine (hence the “gly” in glyphosate), a very common amino acid your body uses to make proteins. As a result, your body can substitute glyphosate for glycine, which results in damaged proteins being produced. According to research published in the journal Entropy in 2013, the main toxic effects of glyphosate are related to the fact that it:8,9

  • Inhibits the shikimate pathway, found in gut bacteria in both humans and animals
  • Interferes with the function of cytochrome P450 enzymes, required for activation of vitamin D in the liver, and the creation of both nitric oxide and cholesterol sulfate, the latter of which is needed for red blood cell integrity
  • Chelates important minerals, including iron, cobalt and manganese. Manganese deficiency, in turn, impairs mitochondrial function and can lead to glutamate toxicity in the brain
  • Interferes with the synthesis of aromatic amino acids and methionine, which results in shortages in critical neurotransmitters and folate
  • Disrupts sulfate synthesis and sulfate transport

Glyphosate also disrupts, destroys, impairs or inhibits:10

  • The microbiome, thanks to its antibiotic activity
  • Sulfur metabolism
  • Methylation pathways
  • Pituitary release of thyroid stimulating hormone, which can lead to hypothyroidism

The chemical has also been linked to certain cancers. In March 2015, the International Agency for Research on Cancer (IARC), a research arm of the World Health Organization, reclassified glyphosate as a Class 2A probable carcinogen11 based on “limited evidence” showing the weed killer can cause Non-Hodgkin lymphoma and lung cancer in humans, along with “convincing evidence” linking it to cancer in animals.

Since then, more than 3,500 individuals have filed lawsuits against Monsanto, claiming the weed killer caused their Non-Hodgkin lymphoma. Many of the cases in this multidistrict litigation are being handled in federal court in San Francisco under one judge. Internal documents obtained during discovery have been released by plaintiff attorneys, and have become known as “The Monsanto Papers.”

Disturbingly, some of this evidence reveals the EPA has protected the company’s interests by manipulating and preventing key investigations into glyphosate’s cancer-causing potential.

According to toxicologist Linda Birnbaum, director of the U.S. National Institute of Environmental Health Services, even minor exposure could have a detrimental effect on human health. “Even with low levels of pesticides, we’re exposed to so many, and we don’t count the fact that we have cumulative exposures,” she told Gillam.

Monsanto Sued for Misleading Consumers

In addition to the lawsuits against Monsanto over Roundup’s cancer-causing effects, the company is also being sued for false and misleading labeling.12 The lawsuit, which accuses Monsanto of falsely claiming glyphosate “targets an enzyme found in plants but not in people or pets” on the Roundup label was filed in April 2017 by the OCA and Beyond Pesticides.

As noted above, glyphosate affects the shikimate pathway, which is involved in the synthesis of the essential aromatic amino acids phenylalanine, tyrosine and tryptophan. While the shikimate pathway is absent in human and animal cells, this pathway is present in the gut bacteria of mammals, including humans.

So, by way of your gut bacteria, it still wields a significant influence on human health. Aside from a probable cancer link, Roundup’s effect on gut bacteria also suggests the chemical may play a significant role in digestive issues, obesity, autism, Alzheimer’s disease, depression, Parkinson’s disease, liver diseases and many other chronic health problems.

Monsanto filed a motion to have the case dismissed, saying the label is accurate because “the enzyme targeted is not produced by the human body or found in human cells,” but U.S. District Judge Timothy Kelly rejected the motion.

In his May 1 ruling, Kelly stated “The court concludes that Plaintiffs have adequately pleaded a claim that the statement at issue was false or misleading,” and that “defendants cannot dispute that the label’s statement that the enzyme at issue is ‘found in plants, but not in people’ is, at least on one reading, literally false.”

How Much Glyphosate Do You Have in Your Body?

According to Gillam, the FDA should publish its glyphosate test results sometime toward the end of this year, or early 2019. Time will tell whether this actually happens or not. The good news is you no longer need to rely on the government when it comes to glyphosate testing. You can test your own levels, thereby assessing your own individual exposure. As mentioned earlier, HRI Labs has developed home test kits for both water and urine.

If your levels are high, you would be wise to address your diet and consider buying more organic foods. You may also want to consider some form of detoxification protocol, and take steps to repair the damage to your gut caused by glyphosate and other agrochemicals. Chances are, if your glyphosate levels are high, you probably have a number of other pesticides in your system as well.

Fermented foods, particularly kimchi, are potent chelators of these kinds of chemicals. Taking activated charcoal after a questionable meal can help bind and excrete chemicals as well. Remember to stay well-hydrated to facilitate the removal of toxins through your liver, kidneys and skin.

Using a sauna on a regular basis is also recommended to help eliminate both pesticides and heavy metals you may have accumulated. For guidelines on how to improve your gut health and repair damage done, see “Go With Your Gut,” and “The Case Against Lectins.”

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