Dr. Stone speaking about TrueScience

Dr. Stone speaking about TrueScience

Is Washing Your Hands any More Natural than Defying Aging?

October 06, 2009

 

Dear Future Centenarian, About thirty years ago, I was hospitalized with a blood infection. In their infinite wisdom, the hospital staff gave me an intravenous injection of antibiotics which cleared up my infection... but it also damaged my hearing. My right ear is especially affected, and my doctor advised hearing aids don't seem to help this type of damage very much. I mention this because I often hear people object to age reversal pursuits as "not being natural". But these same people probably don't think wearing hearing aids or getting cochlear implants is 'unnatural'. But they are the same things in principal. Virtually everything we do in modern society can be considered unnatural. Every time you use tools created by human intelligence to enhance your life or to prevent damage which would undermine your health, you are defying nature. Since we understand what causes tooth decay, we brush our teeth. And since we know certain bacteria can make us sick, we wash our hands with soap. These seem like natural responses to your environment, don't they? And they are if you use your head. So don't you think it actually is natural to enhance your health and longevity with toothpaste, soap, antibiotics and pacemakers too? Isn't that what our intellect is designed to do? Reversing the aging process is way more complex, as are the tools we will need to develop to stop the damage aging heaps upon us, but the principle is the same. Reversing hearing loss and aging are simply extensions of basic medicine as we march into the 21st century. Here's an example of what science is doing to keep me from annoying you every time I ask you to repeat yourself.

An Israeli discovery on the function of tiny molecules called (miRNAs) in the inner ears of mice could lead to the cure of human deafness in adults caused by aging, disease, drugs and noise, or genetic disease in children.

The research carried out over three years by world-renowned geneticist Prof. Karen Avraham of Tel Aviv University's Sackler School of Medicine and Dr. Lilach Friedman and other post-doctoral researchers in her lab, gives hundreds of millions hope for a better life.

About one out of every two elderly people suffers from some degree of hearing disability, while one in 1,000 infants is born deaf due to mutant genes. Healthy babies are born with 15,000 sensory hair cells in each ear that allow them to hear. These hair cells are responsible for translating sounds to electrical pulses that the brain can interpret.

When these cells die off in a process called apoptosis, sometimes caused by stupid mistakes made by hospitals, it results in hearing disability. When the hair cells are all gone, profound deafness follows. Finding the mechanism in which apoptosis occurs might make it possible to prevent it.

The TAU team - working with cooperation from the Weizmann Institute of Science molecular genetics department and biologists at Indiana's Purdue University - has discovered for the first time that microRNAs are vital to the development and survival of hair cells in the inner ear and for normal hearing. This important discovery opens an entirely new window for possible treatments and a cure for all types of deafness, whether age-related, caused by trauma or genetic.

Today, it's reversing hearing loss. Tomorrow, aging!

David A. Kekich

Two Abstracts About Oxidative Stress & Alzheimer's Disease

Abstract:

Oxidative stress hypothesis in Alzheimer’s disease: a reappraisal

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Domenico Praticò
Department of Pharmacology, Temple University, School of Medicine, Philadelphia, PA 19140, USA

Available online

Alzheimer’s disease (AD) is the most common form of neurodegenerative disorder with dementia. In its sporadic form, AD results from the combination of genetic factors with different epigenetic events. Among them, oxidative metabolic reactions and their by-products have been consistently implicated in AD pathogenesis and represent the biological basis for the ‘oxidative stress hypothesis of AD. Numerous studies demonstrate that different biomarkers of oxidative-stress-mediated events are elevated in the AD brain. Studies in animal models of the disease with antioxidants report significant improvements of their AD-like phenotype. Although epidemiologic studies show that dietary intake of antioxidants reduces the risk of AD, clinical trials with antioxidants show only a marginal positive or no effect. These conflicting results have created a wave of criticism towards the oxidative stress hypothesis of AD. Here, I review the available data and discuss the necessary paths for a fair reappraisal of the hypothesis.

Abstract:

Serial review: causes and consequences of oxidative stress in Alzheimer’s disease

Antioxidant neuroprotection in Alzheimer’s disease as preventive and therapeutic approach

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Christian Behland Bernd Moosmann

Max Planck Institute of Psychiatry, Munich, Germany

Received 6 February 2002; 

accepted 18 April 2002. 

Available online

Abstract

Various neurodegenerative disorders and syndromes are associated with oxidative stress. The deleterious consequences of excessive oxidations and the pathophysiological role of reactive oxygen species (ROS) have been intensively studied in Alzheimer’s disease (AD). Neuronal cell dysfunction and oxidative cell death caused by the AD-associated amyloid β protein may causally contribute to the pathogenesis of AD. Antioxidants that prevent the detrimental consequences of ROS are consequently considered to be a promising approach to neuroprotection. While there is ample experimental evidence demonstrating neuroprotective activities of antioxidants in vitro, the clinical evidence that antioxidant compounds act as protective drugs is still relatively scarce. Nevertheless, antioxidants constitute a major part of the panel of clinical and experimental drugs that are currently considered for AD prevention and therapy. Here, focus is put mainly on phenolic antioxidant structures that belong to the class of direct antioxidants. Experimental and clinical evidence for the neuroprotective potential of α-tocopherol (vitamin E) and 17β-estradiol (estrogen) is shortly summarized and an outlook is given on possible novel antioxidant lead structures with improved pharmacological features.
Author Keywords: Alzheimer’s disease; Antioxidant; Estrogen; Free radical; Neuroprotection; Oxidative stress; Phenol; Tocopherol
Abbreviations: AD, Alzheimer’s disease; Aβ, amyloid β protein; ACh, acetylcholine; AGEs, advanced glycation endproducts; APP, Aβ precursor protein; ROS, reactive oxygen species; TMP, 2,4,6-trimethylphenol; THC, (−)Δ⁹-tetrahydrocannabinol

Montel Williams, Dr McCord, and  Dr Perlmutter

discuss anti aging, and oxidative stress.

Watch the video HERE

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David A Kekich

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4. Why following your mother’s advice may keep you from losing your memory
5. Why we can reverse aging in your lifetime in spite of the fact we have not even been able to cure cancer yet
6. The truth about sun exposure.
7. That the medical specialist you now see is almost certainly not the one you should have caring for you. 
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9. Why less may be more when it comes to exercise
10. What two low-tech adjustments could add 20 years to average lifespans                
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DEDICATED TO HELPING PEOPLE REACH THEIR WELLNESS GOALS THROUGH SCIENCE-BASED SOLUTIONS TO OXIDATIVE STRESS.

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