Friday, August 3, 2018

Type 2 Diabetes Resolved After Weight Loss!




A clinical trial recently showed that nearly half of individuals with type 2 diabetes achieved remission to a non-diabetic state after a weight-loss intervention delivered within six years of diagnosis. Now a new study eveals that this successful response to weight loss is associated with the early and sustained. Read more... 


Cell Press. "Why weight loss produces remission of type 2 diabetes in some patients." ScienceDaily. ScienceDaily, 2 August 2018. <www.sciencedaily.com/releases/2018/08/180802141722.htm>.

Vitamin D May Help Treat Mold Illness!





"Research conducted by Dr. Jay Kolls, Professor and Chair of Genetics at LSU Health Sciences Center New Orleans, and colleagues, has found that vitamin D may be an effective therapeutic agent to treat or prevent allergy to a common mold that can complicate asthma and frequently affects patients with Cystic Fibrosis." Read more. 


Louisiana State University Health Sciences Center. "Vitamin D may treat or prevent allergy to common mold." ScienceDaily. ScienceDaily, 18 August 2010. <www.sciencedaily.com/releases/2010/08/100816122122.htm>.

Thursday, August 2, 2018

Degradation of Plastic Causes Greenhouse Gases!








"A new study, published today in PLOS ONE, reports the unexpected discovery of the universal production of greenhouse gases methane and ethylene by the most common plastics when exposed to sunlight. The science team tested polycarbonate, acrylic, polypropylene, polyethylene terephthalate, polystyrene, high-density polyethylene and low-density polyethylene (LDPE) -- materials used to make food storage, textiles, construction materials, and various plastic goods. Polyethylene, used in shopping bags, is the most produced and discarded synthetic polymer globally and was found to be the most prolific emitter of both gases." 


Sarah-Jeanne Royer, Sara Ferrón, Samuel T. Wilson, David M. Karl. Production of methane and ethylene from plastic in the environment. PLOS ONE, 2018; 13 (8): e0200574 DOI: 10.1371/journal.pone.0200574

Broccoli May Have Health Benefits in People with Chronic Fatigue Syndrome!








In past blogs, we have discussed the many benefits of eating broccoli which contains the isothiocyanate sulforaphane. Past discussions have focused on how it may reduce inflammation that leads to cancer and depression and be beneficial in the treatment of other diseases.  It has now been shown that it acts directly on the inflammasome NLRP3 by inhibiting the maturation of Il-1b. Interestingly, this discovery represents a new pathway for sulfurophane's action because in this case, its action is independent of Nrf2. (2)  

A recent study has demonstrated that in a mouse model of chronic fatigue syndrome, fatigue was caused by activation of the inflammasome NLRP3. Inflammasomes are sensing protein complexes that are part of the immune response. that eventually produces Il-1 and Il-6. In the model, mice were exposed to an LPS challenge and a swim test. After the experiment, test mice showed an increase of both Il-1 and Il-6 in the brain and behaviorally, slower motor responses. The author wrote, "LPS-induced fatigue is an Il-1-dependent process and the NLRP3/caspase-1 pathway is involved in the mechanism of LPS-induced fatigue behaviors. NLRP3/caspase-1 inhibition may be a promising therapy for fatigue treatment. " (1)


Related Posts: 
*Depression in Environmental Illness May Be Relieved by Eating Broccoli! 

What's Next:
* Nrf2 and inflammasomes.
1. Activation of the NLRP3 inflammasome in lipopolysaccharide-induced mouse fatigue and its relevance to chronic fatigue syndrome. Journal of neuroinflammation, Vol. 13, No. 1. (05 April 2016) by Zi-Teng T. Zhang, Xiu-Ming M. Du, Xiu-Juan J. Ma, et al. http://www.citeulike.org/user/kimberlykramer2015/article/14620278

2. Sulforaphane inhibits multiple inflammasomes through an Nrf2-independent mechanism. Journal of leukocyte biology, Vol. 99, No. 1. (January 2016), pp. 189-199 by Allison J. Greaney, Nolan K. Maier, Stephen H. Leppla, Mahtab Moayeri. 

Wednesday, August 1, 2018

Mold Toxin Causes Oxidative Stress, Inhibits Nrf2 and Regulates Autism Genes!





Ochratoxin A is a mycotoxin produced from Aspergillus and Penicillium species. It is commonly found in contaminated food products, water damaged buildings and heating ducts. Currently, it is one of 20 mycotoxins that is monitored in food. Ochratoxin A is known to be nephrotoxic, immunotoxic, and carcinogenic. Therefore, it is a health concern in both humans and animals. 
Generally, Ochratoxin A has been found to induce oxidative stress, inflammation and psychiatric conditions. In males, it is especially neurotoxic. Genes that it upregulates have an effect on autism-regulated genes that decrease Nrf2 and cause high levels of reactive species and oxidative damage.  Research has shown that males are more commonly effected because the genes are found on the x chromosome. 

Mezzelani A. (2017) Ochratoxin A and Epigenetics. In: Patel V., Preedy V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham

Nrf2 deficiency exacerbates ochratoxin A-induced toxicity in vitro and in vivo. Toxicology, Vol. 389 (15 August 2017), pp. 42-52 by Agnieszka Loboda, Anna Stachurska, Mateusz Sobczak, et al. www.citeulike.org/user/kimberlykramer2015/article/14620230

Detection of mycotoxins in patients with chronic fatigue syndrome. Toxins, Vol. 5, No. 4. (11 April 2013), pp. 605-617 by Joseph H. Brewer, Jack D. Thrasher, David C. Straus, Roberta A. Madison, Dennis Hooper

A review of the diagnosis and treatment of Ochratoxin A inhalational exposure associated with human illness and kidney disease including focal segmental glomerulosclerosis. Journal of environmental and public health, Vol. 2012 (2012), doi:10.1155/2012/835059 by Janette H. Hope, Bradley E. Hope

Methylation Patterns are Different in Patients With Chronic Fatigue Syndrome!




Methylation is a biochemical process that changes or modifies gene expression without changing the DNA sequences. A recent study has demonstrated that patients with CFS had different methylation patterns than those study participants without CFS. The results seem to confirm past studies that also showed methylation may be a factor in CFS. More research is warranted to find out whether changes in methylation, especially in those genes related to immune response, is caused by CFS or CFS causes changes in methylation patterns. In addition, the author points out that "epigenetic mediation of the connection between genotype and phenotype has recently been proposed and these relationships may be worth investigating in assessments of disease and disease risk."(1) In a subsequent study, they found that "dysregulation in ME/CFS varied depending on the location relative to CpG islands. " (3) 


1. DNA methylation modifications associated with chronic fatigue syndrome. PloS one, Vol. 9, No. 8. (2014) by Wilfred C. de Vega, Suzanne D. Vernon, Patrick O. McGowan. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128721/


2. Identification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-associated DNA methylation patterns. PloS one, Vol. 13, No. 7. (2018) by Malav S. Trivedi, Elisa Oltra, Leonor Sarria, et al.http://journals.plos.org/plosone/article?
id=10.1371/journal.pone.0201066

3. Epigenetic modifications and glucocorticoid sensitivity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). BMC medical genomics, Vol. 10, No. 1. (23 February 2017) by Wilfred C. de Vega, Santiago Herrera, Suzanne D. Vernon, Patrick O. McGowan https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324230/

Oxidative Stress and Environmental Illnesses!




downloadlengkap.com

"The origin of oxidative stress is partly endogenous, as mentioned earlier. It is now, however, commonly admitted that environment and lifestyle may increase levels of oxidative stress. Smoking, pollution from pesticides, weed killers and endocrine disruptors (bisphenols and other plastic additives, parabens and phthalates) are the most common inducers of oxidative stress. All these compounds have some structural analogies with oestrogens and bind to oestrogen receptors, peroxisome proliferator-activated receptors, or both. Nutritional imbalance, food excesses, energy deprivation and excessive exercise also affect oxidative stress. Age increases basic oxidative stress, irrespective of gender."
 Oxidative stress and alterations in DNA methylation: two sides of the same coin in reproduction. Reproductive biomedicine online, Vol. 33, No. 6. (December 2016), pp. 668-683 by Yves J. Menezo, Erica Silvestris, Brian Dale, Kay Elder https://www.rbmojournal.com/article/S1472-6483(16)30514-4/fulltext