Amyotrophic Lateral Sclerosis (ALS), “Lou Gehrig’s Disease” and Glutathione

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Amyotrophic Lateral Sclerosis (ALS), commonly known as “Lou Gehrig’s Disease,” is a terminal, paralytic illness that affects nerve cells in the brain and spinal cord. Although ALS’s cause is currently unknown, recent studies implicate the affect of free radicals in the death and deterioration of motor neurons caused by this disease. The motor neuron’s death erodes the brain’s ability to initiate and control muscle movements. It is not uncommon to see advanced ALS patients completely paralyzed.

Studies further indicate that glutathione activity is greatly reduced in the parts of the brain that are affected by ALS. These findings suggest that glutathione levels and free radicals may be involved in the evolution and manifestation of the disease.

Research shows that raising the levels of glutathione in ALS patients may help prevent cellular damage by free radicals.

 

 

 

  • http://www.alsa.org/about-als/what-is-als.html
  • http://www.ncbi.nlm.nih.gov/pubmed/8967746

Acetaminophen Poisoning and Glutathione

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Tylenol (Acetaminophen) poisoning happens when someone takes more than the suggested dose. The recommended dose is 4000 mg daily. While considered safe in medicinal doses, at larger doses, acetaminophen can be fatal. Nearly half of all cases of acute liver failure in the United States and England can be attributed to acetaminophen poisoning.

Symptoms of acetaminophen poisoning may not present until 12 or more hours after the acetaminophen was ingested. Without early treatment, within the first 8 hours after the overdose, acetaminophen poisoning may lead to liver failure and death within 3 to 5 days.

Once the acetaminophen is ingested, a complex sequence of events begins which ultimately leads to liver failure. In the second step of this process the glutathione levels in the liver are completely depleted which allows for the formation of oxidative stress among other things.

Studies show that early treatment with GSH and its precursor N-acetylcysteine (NAC) can protect patients with acetaminophen poisoning against the overdose by raising the liver’s mitochondrial levels of GSH and providing support to the energy metabolism of the mitochondria.

 

 

 

http://www.nlm.nih.gov/medlineplus/ency/article/002598.html

http://www.ncbi.nlm.nih.gov/pubmed/19821517

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836803/

Type 2 Diabetes and Glutathione

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Diabetes is a disease that causes the body’s blood sugar (glucose) levels to rise. Sometimes this is also referred to as hyperglycemia. Type 2 diabetes is the most common form of this disease found in humans.

Type 2 diabetic’s bodies resist their own insulin; unlike type 1 diabetes in which the body does not produce insulin at all. The stress put on the glutathione (GSH) levels in the body of a person with type 2 diabetes seriously depletes its reserves and weakens the body’s natural detoxification mechanisms until not only many symptoms of the disease present but also the body is now susceptible to a whole host of other diseases.

Glutathione belongs to a group of detoxification enzymes that protect cells against toxins and oxidative stress. Oxidative stress produces cellular dysfunction that creates favorable conditions for the onset of multiple diseases including cancer and type 2 diabetes mellitus. Oxidative stress is a main feature of diabetes. It has been suggested that oxidative damage is the primary cause and aging and age associated diseases. Recent studies show that GSH deficiency is of great significance in the way the disease type 2 Diabetes Mellitus forms.

 

 

 

http://www.ncbi.nlm.nih.gov/pubmed/22058002

http://www.diabetes.org/diabetes-basics/type-2

Diabetic Retinopathy and Glutathione

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Diabetic retinopathy is a complication of diabetes that causes damage to the blood vessels of the retina. This complication may occur in anyone with types 1 or 2 diabetes. Factors contributing to the development of diabetic retinopathy include the length of time a patient has diabetes and the amount of control the patient has over their blood sugar. Commonly occurring in both eyes, it is not unusual to have early stages of the disease and not know it.

Studies show that glutathione (GSH) levels are significantly lower in patients and rats with diabetic retinopathy. Scientists believe that this GSH deficiency is significant in the manifestation of diabetes mellitus and, over time, the development of the complication diabetic retinopathy.

 

http://www.nature.com/eye/journal/v14/n5/abs/eye2000193a.html

Diabetic Neuropathy (DN) and Glutathione

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Diabetes and its compilations are caused by many factors. Antioxidant substances can be used to protect the body’s naturally occurring neurons. When used as an antioxidant enzyme, glutathione protects tissues from the oxidative damage experienced in Type 1 diabetes and it’s complications.

Diabetic Neuropathy (DN) is a secondary complication of diabetes that specifically attacks the nerves. Symptoms may include impaired senses and extreme pain.

Studies show that when diabetic patients were supplemented with glutathione neurological changes were prevented. Researchers conclude that glutathione supplementation provides a stronger neuroprotective affect that than glutamine and significantly reduces oxidative stress. Glutathione supplementation may prohibit the development of DN.

 

http://www.ncbi.nlm.nih.gov/pubmed/23021798

Diabetic Nephropathy and Glutathione

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Diabetic nephropathy is a complication of diabetes that causes kidney disease and damage. In diabetics, nephrons, the filtering structures that make up kidneys, slowly scar and thicken over time. This results in kidney leakage and albumin (a protein) to pass into the urine. Often, the damage happens 5 to 10 years before any symptoms present.

Patients with advanced nephropathy may experience the following symptoms:

  • Chronic feeling of illness and fatigue
  • Poor apatite
  • Swelling in the legs
  • Headaches
  • Nausea and Vomiting

Recent studies have looked at the role of oxidative stress in the progression of kidney impairment and diabetic nephropathy. Researchers found that glutathione (GSH) significantly suppressed one of the markers of oxidative stress in diabetic nephropathy patients. Scientists conclude that GSH supplementation treatment can potentially be used to reduce diabetic complications in nephropathy patients.

 

http://www.ncbi.nlm.nih.gov/pubmed/11983810

http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm