Alzheimer's Disease May Be a Problem With the Brain's Waste System!

"In Alzheimer's disease, our brains accumulate molecular waste; excess buildup of proteins that could become toxic and disrupt communication between brain cells. A new study asks whether the endolysosomal system, which takes care of cellular waste, may be involved in the development of this condition." Read more...

Alzheimer's tied to brain's 'waste removal system'.  Maria Cohut. August 23,2018. https://www.medicalnewstoday.com/articles/322857.php?utm_source=

 

Air Pollution Shortens Your Lifespan!

"Air pollution shortens human lives by more than a year, according to a new study from a team of leading environmental engineers and public health researchers. Better air quality could lead to a significant extension of lifespans around the world."

Read more at: https://phys.org/news/2018-08-air-pollution-global-life-year.html#jCp





Air pollution reduces global life expectancy by more than one year, study finds. August 22, 2018, University of Texas at Austin

Exercise in Middle Age Can Lengthen Your Lifespan!

"A single blood pressure reading at age 50 won't say much about survival decades later, but one spin on a bicycle ergometer in middle age showing a good fitness level may predict extra years of life, a new analysis suggests." Read more...

Fitness Levels in Middle-Age May Predict Survival Decades Later . Steve Stiles . August 21, 2018

A Healthy Gut Biome via Probiotics Induces the Activities of the Natural Antioxidant System in the Body!

Over the past ten years, many studies have been published about how important it is to keep the gut healthy. Generally, that is because commensal bacteria that live in the intestines provide important functions for the benefit of the host, in our case, to us humans. Research has shown that the gut biome forms perinatally and that the most common way to upset the biome is through the ingestion of chemicals in food or the use of antibiotics.

So what does these commensal bacteria do for the host? One of the main function is communicate with the epithelium in the gut to provide upregulation of the Nrf2. As we have described before, the Nrf2 pathway upregulates hundreds of genes that regulate the antioxidant system for protection against xenobiotics. It also regulates functions like mitochondrial biogenesis for ARP or energy synthesis and adipogenesis for fat accumulation.  To understand just how the bacteria in the gut communicates to the Nrf2 system a researcher designed a study to show how probiotics do this in mice and flies. Through this study he found:

1. Lactobacillus plantarum induces cytoprotection against oxidative stress. Noting that germ-free animals are more susceptible to the effects of Paraquat toxicity. The induction of certain phase 2 genes was probiotic specific. 
2. Deletion of Nrf2 by inactivating pathway resulted in increased toxicity to Paraquat at levels similar to germ-free animals. 
3. Animals fed the probiotic, Lactobacillus rhamnosus had enhanced survival and less weight loss when exposed to radiation.  The cytoprotective influences were abolished in Nrf2 -/-  animals.
4. The stressor of reactive species from the activities of the microbes is an example of "hormesis" where the stressor is beneficial to the host, in this case, it activates the Nrf2 system. (1) 

1. Lactobacilli Modulate Epithelial Cytoprotection through the Nrf2 Pathway. Cell reports, Vol. 12, No. 8. (25 August 2015), pp. 1217-1225 by Rheinallt M. Jones, Chirayu Desai, Trevor M. Darby, et al.

Is There a Link Between Vitamin D, Gums and Diabetes. Seems Like There Is!

"A new paper draws interesting links between gum infections, a reduced level of vitamin D, and diabetes. This marks the first time that the joint effects of periodontitis and vitamin D deficiency on diabetes have been examined." Read more,,,,,

What's the link between vitamin D, gum health, and diabetes? Tim Newman. August 22, 2018. https://www.medicalnewstoday.com/articles/322830.php?utm_source=

Suppression of the Antioxidant System By Insecticide Chemicals Can Lead to Obesity and Diabetes!

The Nrf2 pathway controls the transcription of at least 200 genes necessary to carry out functions that include neutralizing oxidative stress. Oxidative stress is a process that occurs through the natural metabolism of the cell. It was only recently that other process for the Nrf2 pathway have been found and include activating processes that are important for mitochondrial biogenesis and dictating the metabolism in adipose tissue and regulating adipogenesis. As discussed previously, pyrethroids are insecticides used in agriculture. One of their effects is that they may depress the Nrf2 pathway in adipose tissues through methylation and negatively impact adipose metabolism and function that leads to inflammation, obesity and possibly diabetes.

So how does Nrf2 activity prevent obesity? Sahin writes, "obesity is induced by adipose size and number. and their differentiation is dependent on metabolic, hormonal, gene and cell morphology changes. Several transcription factors control fat homeostasis as they regulate gene necessary for fat accumulation, fatty acid transport and lipolysis. (1) Oxidative stress is an important cause of obesity- related diseases. To counteract this, the Nrf2-Ho-1 pathway neutralizes the free radicals that cause oxidative stress. Interestingly, Ho-1 metabolic role goes beyond oxidative stress. Therefore, the Nrf2-HO-1 pathway may be a link to preventing obesity and its related diseases.

To understand how Nrf2 pathway prevents obesity, Sahin used butein, a chalcone derived from natural plants as an Nrf2 activator. Butein had also been reported to inhibit adipocyte differentiation  and used to treat inflammation. The purpose of the study was to determine if Nrf2 is responsible for the activation of adipocyte transcription factors known to effect fat homeostasis. To determine this, preadipocytes were treated with butein. After 6 days, the researchers found that treatment with butein significantly decreased lipid accumulation than fully differentiated adipocytes. Next, they showed that butein greatly increases Nrf2 translocation to the nucleus and transcription of Ho-1 in a dose dependent manner. The results suggested that the butein-induced Ho-1 reduced  lipid accumulation through key adipogenic transcription factors such as PPARγ and C/EBPα. In summary this study showed that butein inhibits lipid accumulation through the inhibition of key adipogenic regulators and also upregulates the Nrf2/HO-1 antioxidant pathway. (1)



1. Inhibitory Effects of Butein on Adipogenesis through Upregulation of the Nrf2/HO-1 Pathway in 3T3-L1 Adipocytes. Preventive nutrition and food science, Vol. 22, No. 4. (December 2017), pp. 306-311 by Jinwoo Yang, Jeehye Sung, Younghwa Kim, Heon Sang S. Jeong, Junsoo Lee

Dehydration Causes Your Brain to Slow Its Function!

"When dehydration strikes, part of the brain can swell, neural signaling can intensify, and doing monotonous tasks can get harder. " Read more....

Dehydration alters human brain shape and activity, slackens task performance. August 21, 2018, Georgia Institute of Technology.