Alzheimer’s disease is a neurodegenerative, progressive form of dementia, and although commonly thought of as an “old person’s disease”, early onset can begin as early as the 4th or 5th decade of life.
According to the Alzheimer’s Association, Alzheimer’s Disease is the only leading cause of death which cannot be prevented, cured or slowed. While we recognize that there are no current FDA-approved drugs which can prevent, cure or slow this horrific disease, we respectfully disagree that there are not viable, safe, non-competitive, therapeutic options to do just that.
Let’s examine the undisputed and medically recognized biochemical and physiological causes of Alzheimer’s.
Fact #1: The hallmarks of Alzheimer’s Disease are an accumulation of amyloid-β(Aβ) plaques, hyperphosphylated tau proteins, and increased oxidative stress due to the abundance of free radicals.
“The existence of amyloid-β (Aβ) plaques and hyper-phosphorylated tau proteins trigger the neuro-degeneration associated with Alzheimer’s Disease (AD), resulting in cognitive deterioration with impaired speech, vision, behavior, and eventually death. One possible vehicle for deposition and accumulation of Aβ in AD is oxidative stress (OS), caused by the production of reactive oxygen species. In the process of aging and neurodegenerative diseases,” there is a normal decline in antioxidants which increases the brain’s vulnerability to free radicals. This violent combination leads to massive cellular damage. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620382/
Fact #2: These altered cellular behaviors cause brain deterioration and cumulative loss of normal, daily functions, cognition, and behavior.
“Alzheimer’s Disease (AD), unfortunately, is relentlessly progressive, marked with insidious memory impairment , disorientation, personality and judgment dysfunction, speech abnormalities, and a decrease in the ability to take care of one’s self. AD patients often live out their final months and sometimes years in a vegetative state and bed bound, as this tragic illness robs the patient of their individuality and dignity.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941917/
Fact #3: If you have a brain, you are at risk for Alzheimer’s.
None of us is immune to the risk of neurodegeneration and Alzheimer’s Disease. In fact, our risk has increased exponentially due to our lifestyles, diets and environmental exposures.
So, is there hope? Are there therapies you can put in place to PREVENT
this devestating disease?
We believe the answer is YES!* We do not engage in false hope or marketing hype. We rely on science and research to drive our product development, and the words of scientists, physicians and researchers to state our case.
Let’s examine the scientific research that virtually proves there are legitimate options to PREVENT this scarring, incurable disease.*
Melatonin and Oxidative Stress
- Although “Reactive Oxygen Species (ROS, or free radical) molecules are natural byproducts of normal cellular biochemistry”, as we age our antioxidant capacity diminishes rapidly and leaves our brain especially susceptible to the damage and cellular dysfunction that these free radicals cause.
- Unfortunately, most antioxidants, including our body’s own powerful antioxidants, can undergo a process called “redox” and can themselves be transformed into free radicals.
- “The level of melatonin decreases dramatically during Alzheimer’s disease (AD)” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260/
- “Melatonin is known to retard aging. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100547/
Melatonin and Amyloid Plaques
- “The Amyloid cascade hypothesis states that excessive production of Aβ is the primary cause of the disease.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001214/
- “Amyloid-beta (Aβ) pathology is related to mitochondrial dysfunction accompanied by energy reduction and an elevated production of reactive oxygen species (ROS).” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359765/
- “Melatonin efficiently protects neuronal cells from Aβ-mediated toxicity via antioxidant and anti-amyloid properties.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260/ However, the highest level of protection and benefit was shown when adequate levels of melatonin was present in the brain prior to Aβ accumulation.
Melatonin and Tau Hyperphosphorylation
- “Inhibition of tau hyperphosphorylation is one target in Alzheimer’s Disease (AD) treatment and the results from our studies provide evidence for the strong efficacy of melatonin in inhibiting tau hyperphosphorylation.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260
Melatonin and Inflammation
- “A common factor in AD pathogeny is the over expression of pro-inflammatory cytokines, and although non-steroidal anti-inflammatory drug (NSAID) use decreases the incidence of AD,” these are drugs and not without side effects. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260/
- “Melatonin reduced the pro-inflammatory response and the Aβ-induced levels of pro-inflammatory cytokines by nearly 50%.”http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260/
So, what’s the next step?
The next step is to understand the pharmacology of melatonin. Melatonin has low absolute oral bioavailabilty due to poor oral absorption and large first-pass metabolism. Melatonin is, on average, only about 15% absorbable. That means if you take a 5mg melatonin capsule you are actually only absorbing about 0.75mg of melatonin. In no way does that represent the therapeutic dosage required to exert a protective, anti-neurodegnerative effect. One recent study carried out their work with 20 mg/kg/day, ABSORBED.
The misinformation and ignoring of scientific facts MUST END. The media and nutritional companies tout the benefits of compounds and ignore the absorption realities. They are giving false hope, robbing your financial resources, and taking away your “therapeutic window” of having a chance to influence your outcome.
“It must be emphasized that the failure of antioxidant clinical trials does not nullify the hypothesis” of the benefits of antioxidants for Alzheimer’s disease. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097013/
Rather it highlights the misguided use of inferior antioxidants (vitamins C and E), or clinically sub-therapeutic dosages of viable antioxidants which may very well have preventative properties against Alzheimer’s disease. Studies employing these methods are inherently flawed and erroneously “throwing the baby out with the bath water”.
We strongly encourage you to take some time to read the information regarding Zetpil™’s solution to preventing neurodegenerative diseases. We believe the research is clear that melatonin is a safe (no toxicity even at high dosages), non-competitive (melatonin does not cross-react with any known natural or pharmaceutical compounds), viable option for preventing dementia and Alzheimer’s Disease.*
Ask yourself these questions:
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If I can achieve therapeutic dosages of melatonin in a teaspoon of cream or one suppository a day, is that worth it to protect myself from losing all my memories, my mind, daily functions, and burdening my family? *
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Does the financial investment upfront far outweigh the cost of being progressively incapable of taking care of myself and the cost of round-the-clock care to my family?
http://www.zetpilnutrition.com/products/anti-aging/
http://www.zetpilnutrition.com/product/zetpil-melatonin-200mg-cream/
http://www.zetpilnutrition.com/product/zetpil-melatonin-400mg-sr-suppository/
http://www.zetpilnutrition.com/product/zetpil-melatonin-200mg-sr-suppository/
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
Research to Substantiate Claims
Alzheimer Disease
Rudy J. Castellani, et al
Dis Mon 2010 Sep; 56(9): 484–546
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941917/
Melatonin in Alzheimer’s Disease
Li Lin, et al
Int J Mol Sci. 2013
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742260/
The anti-apoptotic activity of melatonin in neurodegenerative diseases
Xin Wang
CNS Neurosci Ther. 2009 Winter; 15(4): 345–357
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846661/
Neurobiology, Pathophysiology, and Treatment of Melatonin Deficiency and Dysfunction
Rüdiger Hardeland
ScientificWorldJournal. 2012; 2012: 640389
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354573/
Neuronal Failure in Alzheimer Disease: A View through the Oxidative Stress Looking-Glass
David J. Bonda, B.S, et al
Neurosci Bull 2014 Apr; 30(2): 243–252
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097013/
Anti-Amyloidogenic and Anti-Apoptotic Role of Melatonin in Alzheimer Disease
Hongwen He, Weiguo Dong, Fang Huang
Curr Neuropharmacol. 2010 September; 8(3): 211–217
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001214/
Accumulation of Exogenous Amyloid-Beta Peptide in Hippocampal Mitochondria Causes Their Dysfunction: A Protective Role for Melatonin
Sergio Rosales-Corral, et al
Oxid Med Cell Longev 2012
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359765/
Melatonin: An Underappreciated Player in Retinal Physiology and Pathophysiology
Gianluca Tosini, et al
Exp Eye Res. 2012 October; 103: 82–89
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462291/
Therapeutic applications of melatonin
Ifigenia Kostoglou-Athanassiou
Ther Adv Endocrinol Metab. 2013 February; 4(1): 13–24
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593297/
Melatonin regulates aging and neurodegeneration through energy metabolism, epigenetics, autophagy and circadian rhythm pathways
Jenwitheesuk A, et al
Int J Mol Sci. 2014 Sep 22; 15(9):16848-84
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200827/
Melatonin combats molecular terrorism at the mitochondrial level
Russel J. Reiter, et al
Interdiscip Toxicol 2008 Sep; 1(2): 137–149
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993480/
Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans
Reiter RJ, et al
Acta Biochim Pol 2003; 50(4):1129-46
http://www.ncbi.nlm.nih.gov/pubmed/14740000
Melatonin in Mitochondrial Dysfunction and Related Disorders
Venkatramanujam Srinivasan, et al
Int J Alzheimers Dis. 2011; 2011: 326320
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100547/
Does melatonin play a role in aging processes?
Karasek M
J Physiol Pharmacol 2007 Dec; 58 Suppl 6:105-13
http://www.ncbi.nlm.nih.gov/pubmed/18212404
Potency of Melatonin in Living Beings
Donchan Choi
Balsaenggwa Saengsig. 2013 September; 17(3): 149–177
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4282293/
