Multi-Strain Probiotic Improves Insulin Resistance in Patients with Diabetes

Multi-Strain Probiotic Improves Insulin Resistance in Patients 

with Diabetes

Targeted probiotic in personalized therapeutic plan for patients with diabetes shows promise

 Courtesy of metagenics Institute 

https://www.metagenicsinstitute.com/articles/probiotics-impact-diabetes-study/?_hsmi=270084925&_hsenc=p2ANqtz--12rgpeKxQk3oOUlQ3Qsa3SnjmN2H9hzOcemL-JVvNpOuQXu6cfFKwYJ0RYni6kOVxYkbcjvP3mi-8f_4VIVvjk7ni3Q

by Bianca Garilli, ND and Ashley Jordan Ferira, PhD, RDN

Type 2 diabetes (T2D) is no longer a Western world phenomena, but rather a global epidemic, with research revealing an association between higher T2D rates and a country’s wealth or economic growth.1 As a clear example, in a publication titled “Prevalence of type 2 diabetes in the Arab world: impact of GDP and energy consumption”, it was observed that the higher a country’s gross domestic product (GDP), the higher the T2D prevalence.1 T2D rates in these regions include Kingdom of Saudi Arabia- 31.6%, Oman- 29%, Kuwait- 25.4%, Bahrain- 25%, and United Arab Emirates- 25%.1

Recognizing the worldwide impact of T2D, it is critical to identify underlying causes and practical, implementable tools for prevention and treatment. It is well documented that T2D is a chronic, inflammatory condition. Higher levels of lipopolysaccharides (LPS) have been observed in diabetic vs. non-diabetic individuals.2 LPS are Gram-negative bacterial fragments that are considered endotoxins, and can, if left untreated, overgrow in the gastrointestinal tract leading to increased gut permeability.3 A “leaky gut” environment increases the opportunity for these endotoxins to migrate out of the gut and into the circulation, ultimately contributing to systemic inflammation.3

(click link above for full article)

Long term Impact of Childhood trauma...

 

Long-Term Impact of Childhood Trauma Explained

Pauline Anderson

May 02, 2023

https://www.medscape.com/viewarticle/991452?ecd=mkm_ret_230506_mscpmrk_psych_anxiety&uac=149193PV&impID=5403082#vp_1

Dysregulated stress systems may help explain why childhood trauma has such a dramatic and enduring psychiatric impact, new research suggests.

"We already knew childhood trauma is associated with the later development of depressive and anxiety disorders, but it's been unclear what makes sufferers of early trauma more likely to develop these psychiatric conditions," study investigator Erika Kuzminskaite, PhD candidate, Department of Psychiatry, Amsterdam University Medical Center (UMC), the Netherlands, told Medscape Medical News.

"The evidence now points to unbalanced stress systems as a possible cause of this vulnerability, and now the most important question is, how we can develop preventive interventions," she added.

The findings were presented at the Anxiety and Depression Association of America (ADAA) 2023.

Elevated Cortisol, Inflammation 

The study included 2,779 adults from the Netherlands Study of Depression and Anxiety (NESDA). Two thirds of participants were female.

Participants retrospectively reported childhood trauma, defined as emotional, physical, or sexual abuse or emotional or physical neglect, before the age of 18 years. Severe trauma was defined as multiple types or increased frequency of abuse.

Of the total cohort, 48% reported experiencing some childhood trauma ― 21% reported severe trauma, 27% reported mild trauma, and 42% reported no childhood trauma.

Among those with trauma, 89% had a current or remitted anxiety or depressive disorder, and 11% had no psychiatric sequelae. Among participants who reported no trauma, 68% had a current or remitted disorder, and 32% had no psychiatric disorders.

At baseline, researchers assessed markers of major bodily stress systems, including the hypothalamic-pituitary-adrenal (HPA) axis, the immune-inflammatory system, and the autonomic nervous system (ANS). They examined these markers separately and cumulatively.

In one model, investigators found that levels of cortisol and inflammation were significantly elevated in those with severe childhood trauma compared to those with no childhood trauma. The effects were largest for the cumulative markers for HPA-axis, inflammation, and all stress system markers (Cohen's d = 0.23, 0.12, and 0.25, respectively). There was no association with ANS markers.

The results were partially explained by lifestyle, said Kuzminskaite, who noted that people with severe childhood trauma tend to have a higher body mass index, smoke more, and to have other unhealthy habits that may represent a "coping" mechanism for trauma.

Those who experienced childhood trauma also have higher rates of other disorders, including asthma, diabetes, and cardiovascular disease. Kuzminskaite also noted that people with childhood trauma have at least double the risk of cancer in later life.

When researchers adjusted for lifestyle factors and chronic conditions, the association for cortisol was reduced and that for inflammation disappeared. However, the cumulative inflammatory markers remained significant.

Another model examined lipopolysaccharide-stimulated (LPS) immune-inflammatory markers by childhood trauma severity. This provides a more "dynamic" measure of stress systems than looking only at static circulating levels in the blood, as was done in the first model, said Kuzminskaite.

"These levels should theoretically be more affected by experiences such as childhood trauma and they are also less sensitive to lifestyle."

Here, researchers found significant positive associations with childhood trauma, especially severe trauma, after adjusting for lifestyle and health-related covariates (cumulative index d = 0.19).

"Almost all people with childhood trauma, especially severe trauma, had LPS-stimulated cytokines upregulated," said Kuzminskaite. "So again, there is this dysregulation of immune system functioning in these subjects."

And again, the strongest effect was for the cumulative index of all cytokines, she said.

Personalized Interventions 

Kuzminskaite noted the importance of learning the impact of early trauma on stress responses. "The goal is to eventually have personalized interventions for people with depression or anxiety related to childhood trauma, or even preventative interventions. If we know, for example, something is going wrong with a patient's stress systems, we can suggest some therapeutic targets."

Investigators in Amsterdam are examining the efficacy of mifepristone, which blocks progesterone and is used along with misoprostol for medication abortions and to treat high blood sugar. "The drug is supposed to reset the stress system functioning," said Kuzminskaite.

It's still important to target unhealthy lifestyle habits "that are really impacting the functioning of the stress systems," she said. Lifestyle interventions could improve the efficacy of treatments for depression, for example, she added.

Commenting for Medscape Medical News, Luana Marques, PhD, associate professor, Department of Psychiatry, Harvard Medical School, said such research is important.

"It reveals the potentially extensive and long-lasting impact of childhood trauma on functioning. The findings underscore the importance of equipping at-risk and trauma-exposed youth with evidence-based skills for managing stress," she said.

No conflicts of interest were reported.

Anxiety and Depression Association of America (ADAA) Conference 2022: Abstract 78. Presented April 14, 2022.

Regulate the GUT microbiome with Long-term deep meditation

I love this article from News-Medical life sciences by Emily Henderson B.Sc

It is so wonderful that there is so much research going into meditation and that It is becoming more mainstream. I have loved meditation for years and practice it daily. It helps calm the mind and body and now we have regulation of the gut microbiome that supports immunity and better health.

Long-term deep meditation may help to regulate the gut microbiome for better health

 Regular deep meditation, practiced for several years, may help to regulate the gut microbiome and potentially lower the risks of physical and mental ill health, finds a small comparative study published in the open access journal General Psychiatry.

The gut microbes found in a group of Tibetan Buddhist monks differed substantially from those of their secular neighbors, and have been linked to a lower risk of anxiety, depression, and cardiovascular disease.

Research shows that the gut microbiome can affect mood and behavior through the gut–brain axis. This includes the body's immune response, hormonal signaling, stress response and the vagus nerve-;the main component of the parasympathetic nervous system, which oversees an array of crucial bodily functions.

The significance of the group and specimen design is that these deep-thinking Tibetan monks can serve as representatives of some deeper meditations. Although the number of samples is small, they are rare because of their geographical location.

Meditation is increasingly being used to help treat mental health disorders, such as depression, anxiety, substance abuse, traumatic stress, and eating disorders as well as chronic pain. But it's not clear if it might also be able to alter the composition of the gut microbiome, say the researchers.

In a bid to find out, the researchers analyzed the stool and blood samples of 37 Tibetan Buddhist monks from three temples and 19 secular residents in the neighboring areas.

Tibetan Buddhist meditation originates from the ancient Indian medical system known as Ayurveda, and is a form of psychological training, say the researchers. The monks in this study had been practicing it for at least 2 hours a day for between 3 and 30 years.

None of the participants had used agents that can alter the volume and diversity of gut microbes: antibiotics; probiotics; prebiotics; or antifungal drugs in the preceding 3 months.

Both groups were matched for age, blood pressure, heart rate, and diet.

Stool sample analysis revealed significant differences in the diversity and volume of microbes between the monks and their neighbors.

Bacteroidetes and Firmicutes species were dominant in both groups, as would be expected. But Bacteroidetes were significantly enriched in the monks' stool samples (29% vs 4%), which also contained abundant Prevotella (42% vs 6%) and a high volume of Megamonas and Faecalibacterium.

"Collectively, several bacteria enriched in the meditation group [have been] associated with the alleviation of mental illness, suggesting that meditation can influence certain bacteria that may have a role in mental health," write the researchers.

These include Prevotella, Bacteroidetes, Megamonas and Faecalibacterium species, the previously published research suggests.

The researchers then applied an advanced analytical technique to predict which chemical processes the microbes might be influencing. This indicated that several protective anti-inflammatory pathways, in addition to metabolism-;the conversion of food into energy-;were enhanced in the meditation people.

Finally, blood sample analysis showed that levels of agents associated with a heightened risk of cardiovascular disease, including total cholesterol and apolipoprotein B, were significantly lower in the monks than in their secular neighbors by their functional analysis with the gut microbes.

Although a comparative study, it is observational and the numbers of participants were small, all male, and lived at high altitude, making it difficult to draw any firm or generalizable conclusions. And the potential health implications could only be inferred from previously published research.

But based on their findings, the researchers suggest that the role of meditation in helping to prevent or treat psychosomatic illness definitely merits further research.

And they conclude: "These results suggest that long-term deep meditation may have a beneficial effect on gut microbiota, enabling the body to maintain an optimal state of health."

Brain Aging and Magnesium L-Threonate

 

Magnesium L-Threonate and Brain Aging Massachusetts Institute of Technology (MIT) researchers discovered and patented magnesium L-threonate based on its unique ability to boost brain levels of magnesium. Rapid absorption and the ability to enter the brain enables this magnesium to structurally reverse certain aspects of brain aging.(1-4)  A 2016 human study published in the J Alzheimers Dis. 2016;49(4):971-90, demonstrated the benefits of magnesium L-threonate in adults with cognitive dysfunction, sleep disorders, and anxiety.(1) The most startling finding is a reversal of more than nine years in clinical measures of brain aging in people who supplemented with magnesium L-threonate.  Magnesium L-threonate is special because of the way it boosts brain magnesium levels when taken orally. This effect is due to its unique ability to cross the blood-brain barrier.(2) Research has shown that once magnesium L-threonate gets into the brain, it increases the density of synapses, which are the communication connections between brain cells.(1) This is critical because loss of synaptic density is associated with brain shrinkage and cognitive decline.(5,6) Published Human Data: Scientists at three independent institutions carried out a randomized, double-blind, placebo-controlled clinical trial of magnesium L-threonate in older adults with cognitive impairment.(1) To participate in the study, candidates had to be between the ages of 50 and 70, and have self-reported complaints of memory problems, sleep disorders, and anxiety.(1) This study was based on the premise that sleep and anxiety disorders correlate with perceived memory loss.(7) Those who report mild cognitive impairment and who also have sleep and anxiety disorders are more likely to develop Alzheimer’s.(1,8-11) In this multi-center study, participants were randomly assigned to receive placebo or magnesium L-threonate in the dose of 1,500-2,000 mg. each day (depending on body weight) for 12 weeks. Baseline cognitive testing commenced before people started taking magnesium L-threonate or placebo. These cognitive tests were then repeated at six-week and 12-week points.(1) The following four separate tests were used to evaluate cognitive function: Executive function Working memory Attention Episodic memory (ability to recall fleeting events) Findings from this study revealed: Magnesium L-threonate improved body magnesium status. After 12 weeks researchers found significant increases in red blood-cell concentration and in urinary excretion of magnesium in the treated group.(1) Increased urinary excretion indicates that large amounts of magnesium have been absorbed, while increased levels in red blood cells show high circulating levels of magnesium in the body. Magnesium L-threonate improved cognitive abilities. Using a test of visual attention and task switching, researchers saw significant increases in performance speed for executive function and cognitive processing. These benefits appeared as early as week six on some of the tests.(1) Most tellingly, the overall composite scores for all tests of the magnesium L-threonate-supplemented group increased significantly compared with baseline scores and with those of placebo recipients at weeks six and 12. Magnesium L-threonate reduced fluctuation in cognitive ability. When cognitive functions are worse on some days than others, it is a warning sign of developing mild cognitive impairment.(12,13) In the present study, while placebo recipients showed considerable fluctuation in their cognitive scores, those in the magnesium L-threonate group had primarily positive changes.(1) Magnesium L-threonate reversed clinical measures of brain aging. This is a significant finding, which which is explained in more detail in the next section. Understanding Your Brain Age Brains do not functionally age at the same rate as whole-body chronological age. For example, a 60-year-old person can have a brain age of 70, meaning they are functioning at an “older” level.(1) This variance of brain aging is based on measurable performance and physiological parameters.(14-17) In the magnesium L-threonate study, the average chronological age of all subjects in the study was 57.8 years. Their average baseline “functional” brain age, however, was estimated to be 68.3 years. In other words, the study subjects were about 10 years older in terms of their cognitive function.(1) What the researchers found next was remarkable. The average functional brain age of subjects receiving magnesium L-threonate supplements decreased from an older 69.6 years at the start of the study, to 60.6 after just six weeks of treatment. That’s a nine-year reduction in brain age in a matter of weeks.(1) This improvement continued until week 12 with total reduction in brain age of 9.4 years. By the end of the study, cognitive abilities were brought almost back to normal for their younger chronological age in subjects who took magnesium L-threonate. In other words, magnesium L-threonate treatment was found to reverse these measured aspects of brain aging until it was nearly identical to their cognitively healthy peers.(1) Overall, the results of this clinical trial are potentially game-changing for the aging population. The study found that magnesium L-threonate significantly improved cognitive performance on several standardized tests, while reducing the fluctuations in performance that are a warning of developing cognitive impairment in the future. It also showed a reversal of the brain age of magnesium L-threonate-supplemented subjects by nearly a decade. How Magnesium L-Threonate Regenerates Aging Brains The study detailed above shows that magnesium L-threonate improved cognitive function in aging adults, and helped “rejuvenate” their brains towards normal function for their age. The key takeaway of this study is that achieving higher brain levels of magnesium results in a younger brain. References Liu G, Weinger JG, Lu ZL, et al. Efficacy and Safety of MMFS-01, a Synapse Density Enhancer, for Treating Cognitive Impairment in Older Adults: A Randomized, Double-Blind, Placebo-Controlled Trial. J Alzheimers Dis. 2016;49(4):971-90. Slutsky I, Abumaria N, Wu LJ, et al. Enhancement of learning and memory by elevating brain magnesium. Neuron. 2010;65(2):165-77. Abumaria N, Yin B, Zhang L, et al. Effects of elevation of brain magnesium on fear conditioning, fear extinction, and synaptic plasticity in the infralimbic prefrontal cortex and lateral amygdala. J Neurosci. 2011;31(42):14871-81. Li W, Yu J, Liu Y, et al. Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer’s disease mouse model. Mol Brain. 2014;7:65. Fox NC, Scahill RI, Crum WR, et al. Correlation between rates of brain atrophy and cognitive decline in AD. Neurology. 1999;52(8):1687-9. Terry RD, Masliah E, Salmon DP, et al. Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol. 1991;30(4):572-80. Mitchell AJ. The clinical significance of subjective memory complaints in the diagnosis of mild cognitive impairment and dementia: a meta-analysis. Int J Geriatr Psychiatry. 2008;23(11):1191-202. Ju YE, McLeland JS, Toedebusch CD, et al. Sleep quality and preclinical Alzheimer disease. JAMA Neurol. 2013;70(5):587-93. Palmer K, Berger AK, Monastero R, et al. Predictors of progression from mild cognitive impairment to Alzheimer disease. Neurology.2007;68(19):1596-602. Mander BA, Rao V, Lu B, et al. Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging. Nat Neurosci. 2013;16(3):357-64. Apostolova LG, Di LJ, Duffy EL, et al. Risk factors for behavioral abnormalities in mild cognitive impairment and mild Alzheimer’s disease. Dement Geriatr Cogn Disord. 2014;37(5-6):315-26. Kaduszkiewicz H, Eisele M, Wiese B, et al. Prognosis of mild cognitive impairment in general practice: results of the German AgeCoDe study. Ann Fam Med. 2014;12(2):158-65. Palop JJ, Chin J, Mucke L. A network dysfunction perspective on neurodegenerative diseases. Nature. 2006;443(7113):768-73. Cole JH, Leech R, Sharp DJ. Prediction of brain age suggests accelerated atrophy after traumatic brain injury. Ann Neurol.2015;77(4):571-81. Liem F, Varoquaux G, Kynast J, et al. Predicting brain-age from multimodal imaging data captures cognitive impairment. Neuroimage. 2017;148:179-88. Lin L, Jin C, Fu Z, et al. Predicting healthy older adult’s brain age based on structural connectivity networks using artificial neural networks. Comput Methods Programs Biomed. 2016;125:8-17. Luders E, Cherbuin N, Gaser C. Estimating brain age using high-resolution pattern recognition: Younger brains in long-term meditation practitioners. Neuroimage. 2016;134:508-13. Slutsky I, Sadeghpour S, Li B, et al. Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity. Neuron. 2004;44(5):835-49. Zhou H, Liu G. Regulation of density of functional presynaptic terminals by local energy supply. Mol Brain. 2015;8:42. Scheff SW, Price DA. Alzheimer’s disease-related alterations in synaptic density: neocortex and hippocampus. J Alzheimers Dis. 2006;9(3 Suppl):101-15. Anaya-Martinez V, Gutierrez-Valdez AL, Ordonez-Librado JL, et al. The presence of perforated synapses in the striatum after dopamine depletion, is this a sign of maladaptive brain plasticity? Microscopy (Oxf). 2014;63(6):427-35. Bhatt DH, Zhang S, Gan WB. Dendritic spine dynamics. Annu Rev Physiol. 2009;71:261-82. Lovden M, Wenger E, Martensson J, et al. Structural brain plasticity in adult learning and development. Neurosci Biobehav Rev.2013;37(9 Pt B):2296-310. Sale A, Berardi N, Maffei L. Environment and brain plasticity: towards an endogenous pharmacotherapy. Physiol Rev. 2014;94(1):189-234. Kim YJ, McFarlane C, Warner DS, et al. The effects of plasma and brain magnesium concentrations on lidocaine-induced seizures in the rat. Anesth Analg. 1996;83(6):1223-8. McKee JA, Brewer RP, Macy GE, et al. Analysis of the brain bioavailability of peripherally administered magnesium sulfate: A study in humans with acute brain injury undergoing prolonged induced hypermagnesemia. Crit Care Med. 2005;33(3):661-6. Abumaria N, Luo L, Ahn M, et al. Magnesium supplement enhances spatial-context pattern separation and prevents fear overgeneralization. Behav Pharmacol. 2013;24(4):255-63. Schiller D, Delgado MR. Overlapping neural systems mediating extinction, reversal and regulation of fear. Trends Cogn Sci.2010;14(6):268-76.   Magtein® Magnesium L-Threonate | Support for Cognitive Health and Brain Function* Magtein® (magnesium L-threonate) is a unique, patented form of magnesium resulting from 10 years of research at MIT. It is the only form of magnesium shown to cross the blood-brain barrier, effectively increasing magnesium concentration in the brain.*     Clinical applications of Magtein®: Supports healthy synaptic density and function* Supports a healthy stress response, and a healthy mood* Supports cognitive health, focus, and attention* Unlike other brain boosting supplements, which often overstimulate the brain, Magtein® works by nourishing the synapses with magnesium, which helps keep them healthy without overstimulation. The nourishing effects of Magtein® can help your brain think clearly and maintain resiliency.*