If glyphosate is indeed substituting for glycine during protein synthesis, the consequences are mindboggling

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A health freedom crisis of increasingly epic proportions has overrun the United States, with CA on the precipice of utter disparity and Florida now on the chopping block. But it’s not too late to act!

Florida is where I live. It’s where I have raised my family. And it’s where I have come to understand that all Americans must actively affirm and protect their health rights against governmental mandates, lest those rights be take away, and their bodies (and their children’s bodies), be the de facto property of the State. 

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Cannabidiol (CBD) oil is everywhere and seemingly in everything these days. It’s touted as a panacea for a massive range of illnesses and conditions and even recommended as a daily supplement to help one smooth out the rough edges of life. CBD is one of the many chemical compounds called cannabinoids that is isolated from cannabis (marijuana).

Cannabis contains over 400 chemicals including at least 120 cannabinoids, which are chemicals that stimulate cannabinoid receptors in the body. Yes, your body has cannabinoid receptors and you actually produce your own cannabinoids. The most well-studied cannabinoids that are isolated from cannabis are delta-9-tetrahydrocannabinol (THC) and CBD.

CBD is not psychoactive like THC, and there are hundreds if not thousands of producers and products now on the market, sold everywhere from country markets to pet stores to pharmacies. Like most panaceas, the hype outpaces the evidence.

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Credits:
Sources: https://sciencebasedmedicine.org

New Link: https://sciencebasedmedicine.org/cbd-oil-the-new-miracle-cure/

The post CBD Oil: The new miracle cure appeared first on AlternativeWellness.

PMID: 

Behav Brain Res. 2019 Jul 17 ;374:112105. Epub 2019 Jul 17. PMID: 31325514

Abstract Title: 

Protective effect of exercise training against the progression of Alzheimer's disease in 3xTg-AD mice.

Abstract: 

Mechanisms underlying the protective effect of exercise training against the progression of Alzheimer's disease (AD) are not fully understood. This study investigated the effects of treadmill running on Aβ plaque burden and hyper-phosphorylated tau protein, neuro-inflammation, mitochondrial dysfunction, and adult neurogenesis markers in conjunction with cognitive impairments in triple transgenic AD (3xTg-AD) mice. At age of three months, the 3xTg-AD mice were assigned to control (AD, n = 10) orexercise training (AD-EXE, n = 10). The AD-EXE mice were trained on a rodent motor-driven treadmill with a frequency of 5 days per week for 12 weeks. As a consequence, AD-EXE mice had lower levels of Aβ plaque burden and neuro-inflammation, positive changes in mitochondrial function toward a more robust phenotype, and increases in hippocampal adult neurogenesis markers in the hippocampus and cerebral cortex compared to AD mice. The alleviating effects of treadmill running against the progression of the disease were accompanied by enhanced AD-like cognitive performances based on Morris water maze. The current findings support and extend previous studies reporting the protective effect of physical exercise against the progression of the disease in AD animal models.

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PMID: 

Cells. 2019 Jul 9 ;8(7). Epub 2019 Jul 9. PMID: 31324021

Abstract Title: 

Physical Exercise Inhibits Inflammation and Microglial Activation.

Abstract: 

Accumulating evidence indicates that exercise can enhance brain function and attenuate neurodegeneration. Besides improving neuroplasticity by altering the synaptic structure and function in various brain regions, exercise also modulates multiple systems that are known to regulate neuroinflammation and glial activation. Activated microglia and several pro-inflammatory cytokines play active roles in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. The purpose of this review is to highlight the impacts of exercise on microglial activation. Possible mechanisms involved in exercise-modulated microglial activation are also discussed. Undoubtedly, more studies are needed in order to disclose the detailed mechanisms, but this approach offers therapeutic potential for improving the brain health of millions of aging people where pharmacological intervention has failed.

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PMID: 

Oxid Med Cell Longev. 2019 ;2019:2415243. Epub 2019 Jul 4. PMID: 31354903

Abstract Title: 

Aerobic Physical Exercise as a Neuroprotector Strategy for Ethanol Binge-Drinking Effects in the Hippocampus and Systemic Redox Status in Rats.

Abstract: 

The heavy and episodic EtOH drinking pattern, equivalent to weekend consumption, characterizes the binge-drinking pattern and promotes a misbalance of encephalic metabolic functions, concurring to neurodegeneration and cerebral dysfunction. And for being a legal drug, it has global public health and social relevance. In this way, we aimed to investigate the effects of physical training, in a treadmill, on the deleterious effects of EtOH on hippocampal functions, related to memory and learning. For this, we used 40 Wistar rats, divided into four groups: Control group, Trained group (trained animals with doses of distilled water), EtOH group (nontrained animals with doses of 3 g/kg/day of EtOH, 20%/), and Trained+EtOH group (trained animals exposed to EtOH). The physical exercise was performed by running on a treadmill for 5 days a week for 4 weeks, and all doses of EtOH were administered through intragastric gavage in four repeated cycles of EtOH in binge. After the experimental period, the animals were submitted to the object recognition task and Morris water maze test, and after being euthanized, the blood and hippocampus were collected for Trolox Equivalent Antioxidant Capacity (TEAC), Reduced Glutathione Content (GSH), and Nitrite and Lipid Peroxidation (LPO) level measurements. Our results showed that EtOH caused marked oxidative stress and mnemonic damage, and the physical exercise promoted neuroprotective effects, among them, the modulation of oxidative biochemistry in plasma (by restoring GSH levels) and in the hippocampus (by reducing LPO levels and increasing antioxidant parameters) and cognitive function improvement. Therefore, physical exercise can be an important prophylactic and therapeutic tool in order to ameliorate and even prevent the deleterious effects of EtOH on cognitive functions.

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PMID: 

Redox Biol. 2019 Jul 26 ;26:101285. Epub 2019 Jul 26. PMID: 31374361

Abstract Title: 

Exercise training prevents the perivascular adipose tissue-induced aortic dysfunction with metabolic syndrome.

Abstract: 

: The aim of the study was to determine the effects of exercise training on improving the thoracic perivascular adipose tissue (tPVAT) phenotype (inflammation, oxidative stress, and proteasome function) in metabolic syndrome and its subsequent actions on aortic function.METHODS: Lean and obese (model of metabolic syndrome) Zucker rats (n=8/group) underwent 8-weeks of control conditions or treadmill exercise (70% of max speed, 1 h/day, 5 days/week). At the end of the intervention, the tPVAT was removed and conditioned media was made. The cleaned aorta was attached to a force transducer to assess endothelium-dependent and independent dilation in the presence or absence of tPVAT-conditioned media. tPVAT gene expression, inflammatory /oxidative phenotype, and proteasome function were assessed.RESULTS: The main findings were that Ex induced: (1) a beige-like, anti-inflammatory tPVAT phenotype; (2) a greater abundance ofNO in tPVAT; (3) a reduction in tPVAT oxidant production; and (4) an improved tPVAT proteasome function. Regarding aortic function, endothelium-dependent dilation was greater in exercised lean and obese groups vs. controls (p 

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PMID: 

Rev Diabet Stud. 2019 ;15:35-48. Epub 2019 Aug 4. PMID: 31380886

Abstract Title: 

Impact of Physical Exercise on Gut Microbiome, Inflammation, and the Pathobiology of Metabolic Disorders.

Abstract: 

BACKGROUND: The gastrointestinal tract (GIT) harbors a complex and diverse microbial composition that outnumbers our own body cells and their gene contents. These microbes play a significant role in host metabolism and energy homeostasis. Emerging evidence suggests that the GIT microbiome significantly contributes to host health and that impairments in the microbiome may cause the development of metabolic diseases. The microbiome architecture is shaped by several genetic and environmental factors, including nutrition and physical activity. Physical exercise has preventive or therapeutic effects in respiratory, cardiovascular, neuroendocrine, and muscular diseases. Yet, we still have little information of the beneficial effects of physical exercise on GIT health and microbial composition. Furthermore, we are not aware whether exercise-derived benefits on microbiome diversity can beneficially influence other tissues and body organs.OBJECTIVES: The aim of this article is to review the available literature on exercise-induced microbiome changes and to explain how these changes may induce inflammatory, immune, and oxidative responses that may contribute to the improvement of metabolic disorders.METHODS: A systemic and comprehensive search of the relevant literature using MEDLINE and Google Scholar databases was conducted during fall 2018 and spring 2019. The search identified sixty-two research and review articles that discussed exercise-induced microbiome changes.RESULTS: The review of the relevant literature suggests that exercise-induced microbial changes affect the host's immune pathways and improve energy homeostasis. Microbes release certain neuroendocrine and immune-modulatory factors that may lower inflammatory and oxidative stress and relieve patients suffering from metabolic disorders.CONCLUSIONS: Exercise-induced changes in microbial diversity are able to improve tissue metabolism, cardiorespiratory fitness, and insulin resistance.

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PMID: 

Cells. 2019 Aug 11 ;8(8). Epub 2019 Aug 11. PMID: 31405230

Abstract Title: 

Physical Exercise Affects Adipose Tissue Profile and Prevents Arterial Thrombosis inVal66Met Mice.

Abstract: 

Adipose tissue accumulation is an independent and modifiable risk factor for cardiovascular disease (CVD). The recent CVD European Guidelines strongly recommend regular physical exercise (PE) as a management strategy for prevention and treatment of CVD associated with metabolic disorders and obesity. Although mutations as well as common genetic variants, including theVal66Met polymorphism, are associated with increased body weight, eating and neuropsychiatric disorders, and myocardial infarction, the effect of this polymorphism on adipose tissue accumulation and regulation as well as its relation to obesity/thrombosis remains to be elucidated. Here, we showed that white adipose tissue (WAT) of humanized knock-in BDNFVal66Met (BDNF) mice is characterized by an altered morphology and an enhanced inflammatory profile compared to wild-type BDNF. Four weeks of voluntary PE restored the adipocyte size distribution, counteracted the inflammatory profile of adipose tissue, and prevented the prothrombotic phenotype displayed, per se, by BDNFmice. C3H10T1/2 cells treated with the Pro-BDNFMet peptide well recapitulated the gene alterations observed in BDNFWAT mice. In conclusion, these data indicate the strong impact of lifestyle, in particular of the beneficial effect of PE, on the management of arterial thrombosis and inflammation associated with obesity in relation to the specific BDNF Val66Met mutation.

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