Glutathione - Redox To Detox

Glutathione has been hailed the mother of all antioxidants. 

The more we learn about this powerhouse the more we realize how life sustaining it is. Glutathione is a simple tripeptide made from the amino acids glycine, glutamate and cysteine. Glutathione is the most abundant and important intracellular antioxidant that helps support health aging by supporting crucial detoxifying process. Glutathione’s major ‘duty’ is to help cells rid themselves of toxins and other intracellular debris that are associated with chronic disease such as cancer, heart disease, Alzheimer’s disease and Autism. Glutathione is sticky and grabs on to toxins and helps escort them out of the body.

Glutathione: What Does It Do

Under optimal conditions, glutathione recycles antioxidants (chemicals that block the activity of other chemicals known as free radicals that may seriously damage cells). Glutathione also helps support tissue building and repair and plays a huge role in supporting and maintaining a functional immune system. Healthy levels of glutathione help us sustain optimal physical and mental function by controlling dangerous inflammatory processes that lead to chronic disease. Of note, research has shown that glutathione may be helpful in reducing the side effects of several chemotherapeutic medications.

Glutathione: Where Is It Made

In healthy tissue, glutathione is produced in every single cell and is concentrated in the liver. It is found in abundance in the retina and other ocular tissues.

Glutathione: Redox to Detox

Every living cell participates in the metabolic process known as “redox” (reduction-oxidation). Redox reactions are chemical reactions where atoms oxidative states change due to a transfer of electrons (redox = gaining electrons; oxidation = loss of electrons) between species (atoms and other molecules). Species in this context may sound like the next “Cosmic Thriller” and in one way it is because this transfer of energy makes life as we know it possible! A good example of redox signaling involves glutathione peroxidase, which plays a crucial role in oxidative signaling, protecting the cell against the threatening effects of extreme oxidation.

Glutathione: When Levels Drop

Low levels of glutathione are associated with cardiovascular disease, autoimmune disorders, arthritis, cancer and autism. Research has shown that depleted levels of glutathione correlate with reduced levels of dopamine, the neurotransmitter which may contribute to the neurodegenerative and  cognitive changes observed in Alzheimer's disease and Parkinson's.

Glutathione: Why Levels Drop

A poor diet, chronic illness, certain medications, stress, infections and radiation can deplete glutathione stores. Repeated exposure to toxic elements (mercury, lead, arsenic, cadmium, manganese, iron) can also deplete glutathione levels because the body cannot keep up with the toxic overload. Remember, glutathione grabs onto toxins and escorts them out of the body. When glutathione levels are depleted, the body becomes overwhelmed with toxins and the immune system loses a healthy grip on our health. So begins a dangerous cycle spinning out of control towards a myriad of chronic diseases.

Glutathione: What's Your Level

Want to learn more about how to live clean in a toxic world? Join us in a Virtual Detox Summit

Resources

High Blood Glutathione Levels Accompany Excellent Physical and Mental Health in Women Ages 60 to 103 Years.
http://www.ncbi.nlm.nih.gov/pubmed/12486409


Effect of Zinc Deficiency on Blood Glutathione Levels
http://jn.nutrition.org/content/111/6/1098.full.pdf


Glutathione Redox State Regulates Mitochondrial Reactive Oxygen Production
http://m.jbc.org/content/280/27/25305.long


Mitochondrial Redox Signalling at a Glance
http://jcs.biologists.org/content/125/4/801.full


The Effects of Redox Controls Mediated by Glutathione Peroxidases on Root Architecture in Arabidopsis thaliana
http://jxb.oxfordjournals.org/content/early/2014/01/24/jxb.ert486.full


Glutathione, Oxidative Stress and Neurodegeneration
http://www.ncbi.nlm.nih.gov/pubmed/10931172


Statistical Evaluation of Preventive Use of Glutathione Against Side-Effects of Surgical Adjuvant Chemotherapy in Gastric Cancer Patients
http://jjco.oxfordjournals.org/content/5/1/19.extract


Antioxidants and Cancer Prevention (National Institutes of Health)
http://www.cancer.gov/cancertopics/factsheet/prevention/antioxidants


Glutathione: In Sickness and in Health
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)78428-2/fulltext#article_upsell

MTHFR & Homocysteine - Where's The Fire

MTHFR & Homocysteine – Methylation Malfunction 

Inflammation & Methylation 

As discussed in a previous post, MethylenetetrahydrofolateReductase (MTHFR) is an inherited genetic variant that researchers call a polymorphism (SNP). Growing research demonstrates that up to half of all Americans may carry at least one genetic variation (C677T & A1298C) known as MTHFR. This variation prevents the body, including the brain, from being able to properly use folic acid, which disrupts a process known as Methylation.

Methylation is a critical biologic process that requires adequate amounts of folic acid, Vitamin B6 and Vitamin B12 which act as cofactors in key enzymes that produce and balance neurotransmitters such as serotonin. Methylation is also extremely important for other bodily functions such as detoxifying homocysteine.

Homocysteine is a byproduct of cellular metabolism and is generated when methionine (amino acid found in fish, meats and dairy) is metabolized to help make proteins and to maintain tissues. When adequate levels of B Vitamins are available, they recycle left over homocysteine into methionine and the cycle repeats itself. If the Methylation process in not working correctly (MTHFR +/+), elevated levels of homocysteine may occur and become a risk factor for many chronic diseases such as heart disease, Alzheimer’s disease, Parkinson’s disease, stroke and debilitating migraines. So what’s in common with all of these health challenges?

                                                      INFLAMMATION   

Simply put, elevated levels of homocysteine accelerate inflammatory disease processes.

Increased inflammation translates to an accelerated aging process!

Research has demonstrated that an elevated homocysteine levels have been linked to telomere damage. (Telomeres are protective caps at the end of the chromosome that shorten with age). Research has also shown a direct link to elevated homocysteine levels and damage to the hippocampus, the area of the brain that plays a crucial role in memory formation. It is well documented that elevated levels of homocysteine may be related to a deficiency of three necessary B Complex Vitamins B6, Folic Acid & B12. This deficiency inhibits the body's ability to process dietary protein. The typical American diet is filled with nutrient deficient foods. Taking B vitamins may not lower homocysteine levels, however they play a critical role in balancing homocysteine levels.

What You Can Do: Right Now

• Lifestyle habits such as smoking and alcohol consumption may also affect homocysteine levels. Changes in these life style factors may reduce homocysteine levels and hopefully reduce the threat to cardiovascular health.

• Test Your Self: If you are interested in testing without a doctors visit or would simply like to learn more, click here: www.mylabsforlife.com

RESOURCES

Homocysteine levels and leukocyte telomere length

http://twinsuk.ac.uk/wp-content/uploads/2012/03/RichardsJB.Atherosclerosis.2008.pdf

Effect of lifestyle factors on plasma total homocysteine concentrations in relation to MTHFR (C677T) genotype.

http://www.ncbi.nlm.nih.gov/pubmed/15054427

Changes in lifestyle, biological risk factors and total homocysteine in relation to MTHFR C677T genotype: a 5-year follow-up study.

http://www.ncbi.nlm.nih.gov/pubmed/19654594

Plasma Homocysteine Concentration, C677T MTHFR Genotype, and 844ins68bp CBS Genotype in You Adults With Spontaneous Cervical Artery Dissection and Atherothrombotic Stroke.

http://stroke.ahajournals.org/content/33/3/664.full.pdf+html

Migraine Mediates the Influence of C677T MTHFR Genotypes on Ischemic Stroke Risk With a Stroke-Subtype Effect.

http://stroke.ahajournals.org/content/38/12/3145.full?sid=0a66a49d-26a8-484c-9ed2-4a1d1bdbdd1c

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