Healthy Life Extension

How to Kill a Cold Overnight

posted on June 21, 2011

Dear Future Centenarian,

Long life sucks if you’re sick.

I used to get at least a couple of colds a year. My last one was a whopper, and I could have dodged it. That was 4 ½ years ago. Then, last Friday night, I started getting slammed. But by Saturday morning, I was fine.

Aren’t colds supposed to last at least a week or two? Sure, but that was before the “Atom Bomb.”

Let me explain:

Years ago, Bill Faloon, co-founder of Life Extension Foundation, sent me a protocol called the Atom Bomb. It is designed to stop a cold or flu dead in their tracks. The secret is to counter attack at the first sign with a mega dose arsenal of supplements and one OTC drug. If you don’t knock out the cold immediately, stay with this program for a day or two. You have a short window of opportunity, but if you act fast, you can dodge weeks of suffering. I knew this secret 4 ½ years ago… and didn’t use it. I learned a hard lesson and have not been sick with a cold or flu since. When Bill sent me his formula, he had not been sick with either for 13 years!!!

Here is the secret:

Seven Proven Steps to Keep You from Being Struck Down by Colds and Influenza

• Cimetidine (Tagament)—800 to 1,000 mg/day
• Pure Gar brand garlic—9,000 mg once or twice a day
• Kyolic aged garlic extract—3,600 mg/day
• DHEA—200 to 400 mg in the morning
• Lactoferrin—1,200 mg/day
• Zinc—Two 24 mg lozenges every two hours while awake. This is a very high dosage of zinc and may be toxic if taken for long periods. Only take this much zinc for a few days.
• Melatonin—10 to 50 mg at bedtime

 

I suggest you get these supplements from Life Extension. If you’re not already a member, go to www.lef.org/maxlife.

There are many more details. For example, be careful about taking too much zinc as mentioned. I have attached a Word document if you want the full report.

Long Life,
David Kekich
____________________________

LATEST HEADLINES FROM FIGHT AGING!

THE BRAIN PRESERVATION TECHNOLOGY PRIZE Friday, June 17, 2011 http://www.fightaging.org/archives/2011/06/the-brain-preservation-technology-prize.php
From Cryonics Magazine: "As a neuroscientist whose day job is to map neural circuits, I know exactly what type of evidence is needed to convince the scientific community that cryonics preserves the neural circuits encoding our unique memories and personality. What is required is a systematic whole-brain survey with an electron microscope. Recently I, along with my colleagues John Smart and Jacob DiMare, formed the Brain Preservation Foundation (BPF) to promote new scientific research in the field of whole brain preservation for long-term static storage.

The BPF has announced the Brain Preservation Technology Prize (purse currently at $106,000) for the first team to demonstrate that an entire large mammalian brain can be preserved for long-term storage such that the connectivity between neurons remains intact and traceable using today's electron microscopic imaging techniques. A complete set of rules for the prize can be found on our BPF website. This prize is being presented as a challenge to cryonics providers like Alcor and their research partners: 'Demonstrate the quality of your product in a rigorous, independent, and open way to the scientific community and to your customers.' The BPF is hard at work raising funds to promote this prize and to help perform the electron microscopic evaluation required, and we are recruiting a board of scientific advisors and judges that will give the prize credibility."

A CORTICAL NEURAL PROSTHESIS FOR RESTORING AND ENHANCING MEMORY Friday, June 17, 2011 http://www.fightaging.org/archives/2011/06/a-cortical-neural-prosthesis-for-restoring-and-enhancing-memory.php
Researchers are making the first inroads into implanted machinery that can adjust the workings of memory, potentially leading in the years ahead to ways to restore memory function in the old: "Scientists have developed a way to turn memories on and off - literally with the flip of a switch. Using an electronic system that duplicates the neural signals associated with memory, they managed to replicate the brain function in rats associated with long-term learned behavior, even when the rats had been drugged to forget.

Using embedded electrical probes, [scientists] recorded changes in the rat's brain activity between the two major internal divisions of the hippocampus, known as subregions CA3 and CA1. During the learning process, [CA3 and CA1] interact to create long-term memory. Experimenters blocked the normal neural interactions between the two areas using pharmacological agents. The previously trained rats then no longer displayed the long-term learned behavior. The teams then went further and developed an artificial hippocampal system that could duplicate the pattern of interaction between CA3-CA1 interactions. Long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function. In addition, the researchers went on to show that if a prosthetic device and its associated electrodes were implanted in animals with a normal, functioning hippocampus, the device could actually strengthen the memory being generated internally in the brain and enhance the memory capability of normal rats."

WOUND HEALING AS A BIOMARKER OF LONGEVITY Thursday, June 16, 2011 http://www.fightaging.org/archives/2011/06/wound-healing-as-a-biomarker-of-longevity.php
Researchers are very interested in establishing biomarkers of aging and longevity, as at present the only truly reliable way to distinguish between long-lived and not so long-lived individuals is to wait and see what happens - which isn't an efficient way to run studies of potential therapies for aging. Here's an example of one line of investigation: "Wound healing (WH) is a fundamental biological process. Is it associated with a longevity or aging phenotype? In an attempt to answer this question, we compared the established mouse models with genetically modified life span and also an altered rate of WH in the skin.

Our analysis showed that the rate of skin WH in advanced ages (but not in the young animals) may be used as a marker for biological age, i.e., to be indicative of the longevity or aging phenotype. The ability to preserve the rate of skin WH up to an old age appears to be associated with a longevity phenotype, whereas a decline in WH with an aging phenotype. In the young, this relationship is more complex and might even be inversed. While the aging process is likely to cause wounds to heal slowly, an altered WH rate in younger animals could indicate a different cellular proliferation and/or migration capacity, which is likely to affect other major processes such as the onset and progression of cancer. As a point for future studies on WH and longevity, using only young animals might yield confusing or misleading results, and therefore including older animals in the analysis is encouraged."

ARTIFICIAL HEARTS WITHOUT HEARTBEATS Wednesday, June 15, 2011 http://www.fightaging.org/archives/2011/06/artificial-hearts-without-heartbeats.php
The interesting question regarding the removal of the human heartbeat is the impact it will have on other bodily systems. Will it extend life by reducing stress on, for example, vulnerable blood vessels in the brain, or will it shorten life by also eliminating the beneficial response to that stress? Researchers are making progress in artificial hearts, so this question will likely be answered at some point over the next few decades: "The search for the perfect artificial heart seems never-ending. After decades of trial and error, surgeons remain stymied in their quest for a machine that does not wear out, break down or cause clots and infections. But Dr. Billy Cohn and Dr. Bud Frazier at the Texas Heart Institute say they have developed a machine that could avoid all that with simple whirling rotors - which means people may soon get a heart that has no beat.

Inside the institute's animal research laboratory is an 8-month-old calf with a soft brown coat named Abigail. Cohn and Frazier removed Abigail's heart and replaced it with two centrifugal pumps. If you listened to her chest with a stethoscope, you wouldn't hear a heartbeat. If you examined her arteries, there's no pulse. If you hooked her up to an EKG, she'd be flat-lined. .The pumps spin Abigail's blood and move it through her body. The doctors say the continuous-flow pump should last longer than other artificial hearts and cause fewer problems. That's because each side has just one moving part: the constantly whirling rotor. But Cohn says they will still have to convince the world that you don't need a pulse to live. We look at all the animals, insects, fish, reptiles and certainly all mammals, and see a pulsatile circulation. And so all the early research and all the early efforts were directed at making pulsatile pumps. However, the only reason blood must be pumped rhythmically instead of continuously is the heart tissue itself. The pulsatility of the flow is essential for the heart, because it can only get nourishment in between heartbeats. If you remove that from the system, none of the other organs seem to care much."

INVESTIGATING THE GRAYING OF HAIR Wednesday, June 15, 2011 http://www.fightaging.org/archives/2011/06/investigating-the-graying-of-hair.php
If the level of interest the public has in their gray hair could only be transferred to an interest in practical work to repair aging, how much better off we'd be. Here is more research into the biological causes of loss of hair pigmentation with aging: "Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation. We have known for decades that hair follicle stem cells and pigment-producing melanocycte cells collaborate to produce colored hair, but the underlying reasons were unknown.

We discovered Wnt signaling is essential for coordinated actions of these two stem cell lineages and critical for hair pigmentation. The study suggests the manipulation of Wnt signaling may be a novel strategy for targeting pigmentation such as graying hair. The research study also illustrates a model for tissue regeneration. Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color. Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair."

CREATING DOPAMINE NEURONS VIA TRANSDIFFERENTIATION Tuesday, June 14, 2011 http://www.fightaging.org/archives/2011/06/creating-dopamine-neurons-via-transdifferentiation.php
Researchers are making progress in changing cells directly from one type to another: "A research breakthrough has proven that it is possible to reprogram mature cells from human skin directly into brain cells, without passing through the stem cell stage. The unexpectedly simple technique involves activating three genes in the skin cells; genes which are already known to be active in the formation of brain cells at the fetal stage. By reprogramming connective tissue cells, called fibroblasts, directly into nerve cells, a new field has been opened up with the potential to take research on cell transplants to the next level.

We didn't really believe this would work, to begin with it was mostly just an interesting experiment to try. However, we soon saw that the cells were surprisingly receptive to instructions. In experiments where a further two genes were activated, the researchers have been able to produce dopamine brain cells, the type of cell which dies in Parkinson's disease. The research findings are therefore an important step towards the goal of producing nerve cells for transplant which originate from the patients themselves. The cells could also be used as disease models in research on various neurodegenerative diseases. Unlike older reprogramming methods, where skin cells are turned into pluripotent stem cells, known as IPS cells, direct reprogramming means that the skin cells do not pass through the stem cell stage when they are converted into nerve cells. Skipping the stem cell stage probably eliminates the risk of tumors forming when the cells are transplanted. "

LINKING TELOMERES AND PROGERIN Tuesday, June 14, 2011 http://www.fightaging.org/archives/2011/06/linking-telomeres-and-progerin.php
Progerin is the mutant form of lamin-A implicated in the accelerated aging condition progeria. It also shows up in normal aging, to a much lesser degree, and here researchers make progress towards understanding why: "Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin. This study highlights that valuable biological insights are gained by studying rare genetic disorders such as progeria. Our sense from the start was that progeria had a lot to teach us about the normal aging process and clues about more general biochemical and molecular mechanisms.

The mutation that causes progeria strongly activates the splicing of lamin A [or LMNA] to produce the toxic progerin protein, leading to all of the features of premature aging suffered by children with this disease. But modifications in the splicing of LMNA are also at play in the presence of the normal gene. The research suggests that the shortening of telomeres during normal cell division in individuals with normal LMNA genes somehow alters the way a normal cell processes genetic information when turning it into a protein, a process called RNA splicing. To build proteins, RNA is transcribed from genetic instructions embedded in DNA. RNA does not carry all of the linear information embedded in the ribbon of DNA; rather, the cell splices together segments of genetic information called exons that contain the code for building proteins, and removes the intervening letters of unused genetic information called introns. This mechanism appears to be altered by telomere shortening, and affects protein production for multiple proteins that are important for cytoskeleton integrity. Most importantly, this alteration in RNA splicing affects the processing of the LMNA messenger RNA, leading to an accumulation of the toxic progerin protein."

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