2016

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Lafora disease (LD) is one of the progressive and fatal forms of a neurodegenerative disorder and is characterized by teenage-onset myoclonic seizures. Neuropathological changes in LD include the formation of abnormal glycogen as Lafora bodies, gliosis, and neuroinflammation. LD is caused by defects in the gene coding for phosphatase (laforin) or ubiquitin ligase (malin). Mouse models of LD, developed by targeted disruption of these two genes, develop most symptoms of LD and show increased susceptibility to induced seizures. Studies on mouse models also suggest that defective autophagy might contribute to LD etiology. In an attempt to understand the specific role of autophagy in LD pathogenesis, in this study, we fed LD animals with trehalose, an inducer of autophagy, for 3 months and looked at its effect on the neuropathology and seizure susceptibility. We demonstrate here that trehalose ameliorates gliosis, neuroinflammation, and endoplasmic reticulum stress and reduces susceptibility to induced seizures in LD animals. However, trehalose did not affect the formation of Lafora bodies, suggesting the epileptic phenotype in LD could be either secondary to or independent of Lafora bodies. Taken together, our results suggest that autophagy inducers can be considered as potential therapeutic molecules for Lafora disease.

It is well established that trehalose (TRH) affects the physical properties of lipid bilayers and stabilizes biological membranes. We present molecular dynamics (MD) computer simulations to investigate the interactions between lipid membranes formed by 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and TRH. Both atomistic and coarse-grained (CG) interaction models were employed, and the coarse graining of DMPC leads to a reduction in the acyl chain length corresponding to a 1,2-dilauroyl-sn-glycero-3-phosphocholine lipid (DLPC). Several modifications of the Martini interaction model, used for CG simulations, were implemented, resulting in different potentials of mean force (PMFs) for DMPC bilayer–TRH interactions. These PMFs were subsequently used in a simple two-site analytical model for the description of sugar binding at the membrane interface. In contrast to that in atomistic MD simulations, the binding in the CG model was not in agreement with the two-site model. Our interpretation is that the interaction balance, involving water, TRH, and lipids, in the CG systems needs further tuning of the force-field parameters. The area per lipid is only weakly affected by TRH concentration, whereas the compressibility modulus related to the fluctuations of the membrane increases with an increase in TRH content. In agreement with experimental findings, the bending modulus is not affected by the inclusion of TRH. The important aspects of lipid bilayer interactions with biomolecules are membrane curvature generation and sensing. In the present investigation, membrane curvature is generated by artificial buckling of the bilayer in one dimension. It turns out that TRH prefers the regions with the highest curvature, which enables the most favorable situation for lipid–sugar interactions.

Does Coffee Cause Autoimmune Disease? The simple answer is, it depends. Research studies have linked coffee consumption to a number of different autoimmune conditions. Type I Diabetes, Hashimoto's Thyroiditis, rheumatoid arthritis, GERD (reflux), and celiac disease are all on the list of diseases that coffee can contribute to. If you have been diagnosed with these conditions, show your doctor this research and ask if coffee is right for you ;) To connect with Dr. Osborne visit: Facebook: https://www.facebook.com/DoctorPeterO... Pinterest: https://www.pinterest.com/docosborne/ Instagram: https://www.instagram.com/drosborne Twitter: https://twitter.com/glutenology *These statements have not been evaluated by the Food and Drug Administration. This video is not intended to diagnose, treat, cure or prevent any disease. It is strictly intended for educational purposes only. Additionally, this information is not intended to replace the advice of your physician. Dr. Osborne is not a medical doctor. He does not treat or diagnose disease. He offers nutritional support to people seeking an alternative from traditional medicine. Dr. Osborne is licensed with the Pastoral Medical Association.

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Reality Check with Ben Swann - http://truthinmedia.com/reality-check-fdas-disinformation-campaign-kratom/ The opioid crisis is killing tens of thousands of Americans each year. So why would the FDA crack down on a substance that may be helping millions of addicts get off drugs like heroin and Oxycontin? This is a Reality Check you won't get anywhere else. Did you remember to subscribe to my YouTube channel? Also follow me here: Facebook - https://www.facebook.com/BenSwannRealityCheck Twitter - https://twitter.com/BenSwann_ Instagram - https://www.instagram.com/BenSwann_/ Newsletter signup - http://truthinmedia.com/newsletter-signup

A groundbreaking new study published in Advances in Mind Body Medicine validates the role of holistic approaches in helping patients successfully withdraw from psychotropic drugs

In part I of this series on pain medication side effects, I discuss the common pitfalls of using pain medication for chronic pain problems, including weight gain, nutritional deficiencies, muscle loss, leaky gut problems, and much much more. Make sure you watch part II as well. Subscribe to Dr. Osborne for more natural remedies and functional medicine solutions: Facebook: https://www.facebook.com/DoctorPeterO... Pinterest: https://www.pinterest.com/docosborne/ Instagram: https://www.instagram.com/drosborne Twitter: https://twitter.com/glutenology *These statements have not been evaluated by the Food and Drug Administration. This video is not intended to diagnose, treat, cure or prevent any disease. Additionally, this information is not intended to replace the advice of your physician. Dr. Osborne is not a medical doctor. He does not treat disease. He offers nutritional support to people seeking an alternative from traditional

Preexisting maternal diabetes increases the risk of neural tube defects (NTDs). The mechanism underlying maternal diabetes-induced NTDs is not totally defined, and its prevention remains a challenge. Autophagy, an intracellular process to degrade dysfunction ...

(2017). Trehalose pathway as an antifungal target. Virulence: Vol. 8, New Antifungal Compounds, pp. 143-149.

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(2017). Trehalose metabolism: A sweet spot for Burkholderia pseudomallei virulence. Virulence: Vol. 8, No. 1, pp. 5-7.

Remarkably high anti-tumor activities of DMTreC14 for the subcutaneous and orthotopic graft-bearing mice of lung carcinoma accompanied with apoptosis were revealed for the first time in vivo.

The inhibitory effects of trehalose liposomes (TL) comprising l-α-dimyristoylphosphatidylcholine (DMPC) and α-D-glucopyranosyl-α-D-glucopyranoside monomyritate (TreC14) were investigated on breast cancer MDA-MB-453 cells in vitro and in vivo. The IC50 values of TL for MDA-MB-453 cells wer …

Trehalose increases blood glucose levels slowly and induces a slight insulin response. The present study aimed to study the effect of trehalose on prolonged exercise performance. The participants were 12 healthy men (age: 21.3 ± 0.9 y). After an overnight fast (12 h), they first exercised with a constant load (intensity: 40% V˙O2peak) for 60 min using a bicycle ergometer. They continued to exercise with a constant load (40% V˙O2peak) for 30 min between four sets of the 30-s Wingate test. After the 1st set, each participant ingested 500 mL water (control), 8% glucose, or 8% trehalose in three trials. These three trials were at least one week apart and were conducted in a double-blind and randomized crossover manner. Blood was collected for seven biochemical parameters at 12 time points during the experiment. The area under the curve of adrenaline after ingestion of trehalose was significantly lower than that for water and tended to be lower than that for glucose in the later stage of the exercise. Lower secretion of adrenaline after a single dose of 8% trehalose during prolonged exercise reflected the preservation of carbohydrates in the body in the later stage of the exercise. In conclusion, a single ingestion of trehalose helped to maintain prolonged exercise performance.

The inhibitory effects of trehalose liposomes (TL) comprising l-α-dimyristoylphosphatidylcholine (DMPC) and α-D-glucopyranosyl-α-D-glucopyranoside mon…

Background Trehalose is a functional disaccharide that has anti-metabolic activities such as suppression of adipocyte hypertrophy in mice and alleviation of impaired glucose tolerance in humans. Trehalase hydrolyzes trehalose in the small intestine into two glucose molecules. In this study, we investigated whether trehalose can suppress adipocyte hypertrophy in mice in the presence or absence of trehalase. Methods Trehalase knockout (KO) mice and wild-type (WT) mice were fed a high fat diet (HFD) and administered water with 0.3% (w/v) or without trehalose for 8 weeks. At the end of the experimental period, mesenteric adipose tissues and the small intestine were collected and the adipocyte size and proportion of cytoplasmic lipid droplets (CLDs, %) in jejunum epithelium were measured by image analysis. Results Trehalose treatment was associated with suppressed adipocyte hypertrophy in both trehalase KO and WT mice. The rate of CLDs in the jejunal epithelium was increased in both trehalase KO and WT mice given water containing trehalose relative to untreated control mice. There was a negative correlation between jejunal epithelial lipid droplet volume and mesenteric adipocyte size. Chylomicron-TG tended to be decreased in both trehalose-treated trehalase KO and WT mice. Addition of trehalose to differentiated Caco-2 cells in vitro increased intracytoplasmic lipid droplets and decreased secretion of the chylomicron marker ApoB-48. Moreover, the jejunal epithelium containing lipid droplets falled into the intestinal lumen, and triglyceride (TG) levels in feces tended to be higher in the KO/HFD/Tre group than in the KO/HFD/Water group. Since then, the accumulation of CLDs has been reported to suppress CM secretion, and along with our results, the effect of trehalose to increase jejunum CLDs may induce suppression of adipocyte hypertrophy. Conclusions The suppression of adipocyte hypertrophy in the presence and absence of trehalase indicates that trehalose mediates effects prior to being hydrolyzed into glucose. In both trehalase KO and WT mice, trehalose treatment increased the rate of CLDs in jejunal epithelium, reduced chylomicron migration from the intestinal epithelium to the periphery, and suppressed adipocyte hypertrophy. Thus, trehalose ingestion could prevent metabolic syndrome by trapping fat droplets in the intestinal epithelium and suppressing rapid increases in chylomicrons.

Background: Thyroid cancer has been growing rapidly during the last decades. Radioiodine-131 (I-131) as an appropriate therapy modality is currently using in the treatment of cancer and hyperthyroidism diseases. This radiotracer is considered as a cause of oxidative DNA damage in nontarget cells and tissues. The aim of this study was to investigate the effects of curcumin and trehalose on the level of DNA double-strand breaks (DSBs) caused by I-131 in human lymphocytes. Materials and Methods: First, 6-mL blood samples were taken from each of the five volunteers. After 1 h of preincubation with the antioxidants, a total of 20 μCi I-131/2 mL (blood + NaCl) was added to each sample, and then, the samples were reincubated for 1 h. Lymphocytes were separated and the mean DSB levels were measured for each sample through γ-H2AX assay to evaluate the effects of antioxidants. Results: After 1-h incubation with I-131, the DSBs increased by 102.9% compared to the control group (0.343 vs. 0.169 DSB/cell; P = 0.00). Furthermore, compared to the control + I-131 group, curcumin and trehalose reduced the DSBs by 42% and 38%, respectively. There was a significant decrement (P = 0.00) in the levels of DSBs of the curcumin + I-131 and trehalose + I-131 subgroups compared to the control + I-131 subgroup. Furthermore, there was no significant relationship between the radioprotective effect of curcumin and trehalose (P = 0.95). Conclusion: The use of curcumin and trehalose as antioxidant can reduce the numbers of DSBs caused by I-131. Meanwhile, the radioprotective effect of curcumin was more than trehalose.

Many neurodegenerative diseases, including Huntington's, Alzheimer's and Parkinson's diseases, are characterized by protein misfolding and aggregation. The capability of trehalose to interfere with protein misfolding and aggregation has been recently evaluated by several research groups. In the pres …

The accumulation of mis-folded and/or abnormally modified proteins is a major characteristic of many neurodegenerative diseases. In Lewy body disease (LBD), which includes Parkinson's disease and dementia with Lewy bodies, insoluble α-synuclein is widely deposited in the presynaptic terminals as wel …

Type 1 diabetes (T1DM) affects approximately 1 in 500 children. Diabetic peripheral neuropathy (DPN) is the most common form of peripheral neuropathy in diabetes and is a significant risk factor for serious pathological change. It is difficult and costly to treat DPN and although there have been sev …

Click here to subscribe - https://www.glutenfreesociety.org/wxrn What are The Best Natural & Non Toxic Sweeteners? Some of the best natural sweeteners to use instead of sugar, aspartame (Nutrasweet), sucralose (Splenda), etc are listed below, but be careful not to overdo these either. Remember that too much natural sugar can also be detrimental. 1. Eat real fruit when it is in season 2. Honey - make sure it is naturally sourced and organic. Many brands of honey are laced with corn syrup. 3. Maple - pure organic 4. Organic Dates 5. Stevia 6. Monk Fruit 7. Sugar Alcohol (xylitol derived from birch) If you want a more in depth look on the topic of natural sweeteners, toxic sweeteners, and alternatives, check out this video: https://www.youtube.com/watch?v=v4BWY-4ptzg To connect with Dr. Osborne visit: On the web: https://drpeterosborne.com/ Facebook: https://www.facebook.com/DoctorPeterO... Pinterest: https://www.pinterest.com/docosborne/ Instagram: https://www.instagram.com/drosborne Twitter: https://twitter.com/glutenology *These statements have not been evaluated by the Food and Drug Administration. This video is not intended to diagnose, treat, cure or prevent any disease. It is strictly intended for educational purposes only. Additionally, this information is not intended to replace the advice of your physician. Dr. Osborne is not a medical doctor. He does not treat or diagnose disease. He offers nutritional support to people seeking an alternative from traditional medicine. Dr. Osborne is licensed with the Pastoral Medical Association.