Healthy Life Extension

Quick Relief from Rheumatoid Arthritis and Irritable Bowel Syndrome?

posted on July 12, 2011

Dear Future Centenarian,

If you suffer from rheumatoid arthritis or IBS, you may be able to get a free sample of a new supplement that can reduce or eliminate the associated inflammation. More in a moment.

Basically, inflammation is a defensive reaction to infections, toxins or injury. The swellings around cuts, sprains or mosquito bites are common examples. It also happens insidiously inside your body.

One of the most prevalent types of damage to your body is caused by a type of molecule referred to as a "free radical" or a "reactive oxygen species" (ROS) that causes oxidative damage, or oxidative stress. These are molecules that are produced on a regular basis in the energy generation part of your cells—the mitochondria. These tiny power plants are the final step in converting the food you eat into a useable form of energy for your cells. During the process, oxygen is used to produce highly reactive molecules that are normally well-contained in your mitochondria, which has multiple antioxidant systems for cleaning them up and making them less reactive.

But as we age, and in times of stress or extreme exertion, these systems cannot always keep up with the amount of ROSs being produced. These molecules, free of the mitochondria, can do tremendous amounts of damage to nearby tissues. This is part of the reason why inflammation can sometimes do more harm than it does good, because it can destroy your own tissue along with the invaders.

Aging people suffer an epidemic of outward inflammatory diseases such as arthritis. But chronic systemic inflammation also damages brain cells, intestines, arterial walls, heart valves, and other structures in the body. Heart attack, stroke, heart valve failure and Alzheimer's senility have been linked to the chronic inflammatory cascade so often seen in aging humans.

Some methods to counteract inflammation are to sleep well. Losing sleep for even part of one night can trigger the key cellular pathway that produces tissue-damaging inflammation.

Also, eat a low-glycemic diet rich in omega-3 and monounsaturated fats, but low in omega-6 and saturated fats (such as salmon, other fatty fish and fish and krill oil; avocados; seeds and nuts; extra virgin olive oil and fresh produce. Since inflammation is caused by free radicals, take supplements that provide omega-3 fatty acids, curcumin, garlic, ginger, glutathione, pomegranate, luteolin, lipoic acid, 5-Loxin, vitamin K, vitamin D and vitamin E. Antioxidants can reduce all types of inflammation, and arthritis in particular.

Avoid eating foods cooked at high temperatures, and minimize foods high in arachidonic acid such as eggs and dairy and the fat in red and white meat. C-reactive protein (CRP) is a sensitive marker of systemic inflammation that has emerged as a powerful predictor of coronary heart disease and other diseases of the cardiovascular system. I suggest you have yours measured the next time you have blood work done.

Inflammation damages your immune system and promotes disease. So, stay away from refined foods. Low-fat varieties are usually high in sugar. Whole grain foods, if you choose to eat them, and fresh fruit have more fiber and are converted to sugars more gradually. Fiber also prevents carcinogens from entering your bloodstream. To control inflammation, lower your blood sugar level, lose weight, exercise more, reduce stress, avoid or cut back on red meat, all grains, coffee and alcohol. Limit egg yolks to ten a week, and take a daily baby or whole aspirin with your biggest meal under a doctor's supervision.

Reducing this body-wide inflammation can slash your chances of heart disease and cancer in half and may be the key to Alzheimer's, arthritis and diabetes. Inflammation lies at the core of most chronic age-related diseases and is the underlying cause of more than 80 diseases. Inflammation ages your entire system. You will live a long, healthy life to the extent you can reduce inflammation.

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If you now suffer from rheumatoid arthritis or any form of IBS, and if you live in the U.S., you can get a free sample of a yet-to-be-released natural supplement that may give you relief within a month. The first twenty people who request a sample with a description of their symptoms can get a sample by sending an email request to Peptidedoc@yahoo.com. Simply put “Free Sample” in the subject line. You will be asked to email your results to the same address within a month after you start using the supplement. The active ingredient is a natural fruit derivative which proved effective in two subjects, but it takes at least twenty to get meaningful results.

Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

AUTOLOGOUS STEM CELLS VERSUS ANGINA Friday, July  8, 2011 http://www.fightaging.org/archives/2011/07/autologous-stem-cells-versus-angina.php
Via EurekAlert!: "injections of adult patients' own CD34+ stem cells reduced reports of angina episodes and improved exercise tolerance time in patients with chronic, severe refractory angina (severe chest discomfort that did not respond to other therapeutic options). The phase II prospective, double-blind, randomized, controlled clinical trial was conducted at 26 centers in the United States. The objective of the trial was to determine whether delivery of autologous (meaning one's own) CD34+ stem cells directly into multiple targeted sites in the heart might reduce the frequency of angina episodes in patients suffering from chronic severe refractory angina, under the hypothesis that CD34+ stem cells may be involved in the creation of new blood vessels and increase tissue perfusion.

While we need to validate these results in phase III studies before definitive conclusions can be drawn, we believe this is an important milestone in considering whether the body's own stem cells may one day be used to treat chronic cardiovascular conditions. At six months after treatment, patients in the low-dose treatment group reported significantly fewer episodes of angina than patients in the control group (6.8 vs. 10.9 episodes per week), and maintained lower episodes at one year after treatment (6.3 vs. 11 episodes per week). Additionally, the low-dose treatment group was able to exercise (on a treadmill) significantly longer at six months after treatment, as compared with those in the control group (139 seconds vs. 69 seconds, on average)." If you want access to this sort of treatment now, and are resident in the US, going abroad as a medical tourist is your only realistic option. Otherwise you may still be waiting five or ten years from now: the FDA moves to approve treatments very slowly, when it moves at all.

CALORIE RESTRICTION SLOWS FERTILITY DECLINE Friday, July  8, 2011 http://www.fightaging.org/archives/2011/07/calorie-restriction-slows-fertility-decline.php
Another example of calorie restriction slowing a specific aspect of the damage of aging: "restricting the caloric intake of adult female mice prevents a spectrum of abnormalities, such as extra or missing copies of chromosomes, which arise more frequently in egg cells of aging female mammals. We found that we could completely prevent, in a mouse model, essentially every aspect of the declining egg quality typical of older females. We also identified a gene that can be manipulated to reproduce the effects of dietary caloric restriction and improve egg quality in aging animals fed a normal diet, which gives us clues that we may be able to alter this highly regulated process with compounds now being developed to mimic the effects of caloric restriction.

The long-term effects of a caloric restriction (CR) diet in humans are being investigated in ongoing studies, but some health improvements, including reductions in cholesterol levels and other cardiovascular risk factors, have already been reported. While the mechanisms by which caloric restriction produces its effects are still being investigated, several of the metabolic pathways involve a regulator of DNA transcription called PGC-1a, which is known to modulate genes involved in controlling mitochondrial number and function. [The researchers] also found that egg cells from female mice lacking a functional PGC-1a gene who were allowed to free feed through adulthood maintained the same egg-cell quality as seen in the CR mice. However, combining CR with PGC-1a inactivation did not increase the effects beyond those achieved separately, which suggests that the two approaches work in a common pathway."

EXPLORING IFG-1 AND LONGEVITY Thursday, July  7, 2011 http://www.fightaging.org/archives/2011/07/exploring-ifg-1-and-longevity.php
Some work here on IFG-1, not to be confused with IGF-1, which is also of interest in longevity: "When researchers at the Buck Institute dialed back activity of a specific mRNA translation factor in adult nematode worms they saw an unexpected genome-wide response that effectively increased activity in specific stress response genes that could help explain why the worms lived 40 percent longer under this condition. Scientists have identified a number of so-called 'longevity' genes active in many species. However, the mechanisms by which those genes impact lifespan remain poorly understood. The majority of research involving those genes has focused on transcription, the first level of cellular activity whereby DNA produces RNA. This research focuses on translation, whereby RNA specifies the production of proteins. [Researchers] inhibited expression of the mRNA translation factor, IFG-1, in adult worms.

IFG-1 is important for growth and development. "Turning down ifg-1 expression flips a switch that turned down growth and reproduction, but increased their healthspan as well as their lifespan. Our primary interest is to understand the biological basis of aging. This will help identify molecular targets that can be used to develop therapeutics that would slow age-related diseases and extend the healthy years of life."

SHORTER TELOMERES, HIGHER CANCER RISK Wednesday, July  6, 2011 http://www.fightaging.org/archives/2011/07/shorter-telomeres-higher-cancer-risk.php
A confirming review of studies: "Telomeres play a key role in the maintenance of chromosome integrity and stability, and telomere shortening is involved in initiation and progression of malignancies. A series of epidemiological studies have examined the association between shortened telomeres and risk of cancers, but the findings remain conflicting. A dataset composed of 11,255 cases and 13,101 controls from 21 publications was included in a meta-analysis to evaluate the association between overall cancer risk or cancer-specific risk and the relative telomere length. The results showed that shorter telomeres were significantly associated with cancer risk compared with longer telomeres.

Studies have showed that telomeres are critical for maintaining genomic integrity and that telomere dysfunction or shortening is an early, common genetic alteration acquired in the multistep process of malignant transformation. In addition, telomere dysfunction has been found to be associated with decreased DNA repair capacity and complex [cellular] abnormalities. Both of animal studies and clinical observations have shown that shorter telomeres were associated with increased risk of cancers, such as epithelial cancers. However, telomere shortening might play conflicting roles in cancer development. For example, the progressive loss of telomeric repeats with each cell division can induce replicative senescence and limit the proliferative potential of a cell, thus functioning as a tumor suppressor. But, once telomeres reach a critical length, it will result in chromosome break, causing genome instability and enhancing potential for malignant transformation."

MAKING BETTER CELLS FOR TISSUE ENGINEERING Wednesday, July  6, 2011 http://www.fightaging.org/archives/2011/07/making-better-cells-for-tissue-engineering.php
Altering cells used in tissue engineering so as to obtain a better result is a very viable prospect, as demonstrated in a recent investigation of tendon regeneration: "The basic function of tendon is to transmit force from muscle to bone, which makes limb and joint movement possible. Therefore tendons must be capable of resisting high tensile forces with limited elongation. The mechanical properties of tendons are related to the fibril diameter distribution, large fibrils could withstand higher tensile forces. In the healing tendon, a uniform distribution of small diameter collagen fibrils has been found with poorer mechanical properties than native tissue and shows no improvement of mechanical properties with time.

The present study for the first time demonstrated the use of a scaffold-free tissue engineered tendon model for investigating the biological function of collagen V in tendon fibrillogenesis. Conclusively, it was demonstrated that Col V siRNA engineered tenocytes improved tendon tissue regeneration. These findings present a good example of in vitro tissue engineering model for tendon biology investigation and may provide basis for future development of cell or gene therapy for tendon repair."

MORE ON STEM CELL AGING AND ENVIRONMENTAL CUES Tuesday, July  5, 2011 http://www.fightaging.org/archives/2011/07/more-on-stem-cell-aging-and-environmental-cues.php
Researchers are making inroads into showing that stem cell decline with aging is a function of the surrounding environment - you might recall the experiments in which old mice were given young blood, for example. Here is another research report: "Increasing studies have demonstrated the importance of extrinsic cellular factors on the aging of adult stem cells. Aged mouse spermatogonial stem cells have been transplanted into young recipient hosts for over three years without any decline in function.

Serum from old mice markedly induces embryonic stem cell dysfunction. However, the effects of the aged environment on [mesenchymal stem cell (MSC)] senescence and function have not yet been reported. In the present study, the young and the old systemic milieu were mimicked by adding 20% [young rat serum (YRS) and old rat serum (ORS)] into the culture medium respectively. The results show that the ORS culture clearly promoted senescence and [reactive oxygen species] production in the MSCs compared with those cultured with YRS. The proliferation and survival ability of the MSCs were also significantly inhibited in the ORS group compared with that in the YS group. Therefore, ORS induces MSC senescence, as well as inhibit their proliferation and survival ability."

THE SEARCH FOR WAYS TO SPUR STEM CELLS INTO ACTION Monday, July  4, 2011 http://www.fightaging.org/archives/2011/07/the-search-for-ways-to-spur-stem-cells-into-action.php
Based on work to date, it should be expected that there are effective ways to provoke existing stem cell populations in the body into greater feats of healing than normally take place. This research is an example of the type: "Injecting proteins similar to insulin directly into the heart can cause damaged cells to repair themselves and begin regenerating again, researchers said. Tests on pigs showed that the dormant cells could begin regrowth following a 'regenerative medicine' treatment using certain growth factors - naturally occurring proteins which cells use to communicate with their environment. Experts from Liverpool John Moores University (LJMU) said the four-year study presented a 'significantly different' therapy to those currently being developed by scientists.

The findings, produced with teams from Italy and Spain, could lead to simple and affordable treatments for heart attacks. This new approach by LJMU could ultimately lead to a clinical myocardial regenerative therapy which is effective, simple, affordable, readily and widely available and easy to apply and compatible with the current clinical standard of cardiac care. The research shows that injecting growth factors IGF-1 and HGF caused significant 'anatomical, histological and physiological' regeneration of damaged hearts and 'sets the path' for testing clinical trials. Another member of the LJMU BioStem research team, Dr Georgina May Ellison, said funding had been secured for clinical tests of the new method to begin at the Vall d'Hebron University Hospital in Barcelona."

THE GOAL: BRING AGING UNDER MEDICAL CONTROL Monday, July  4, 2011 http://www.fightaging.org/archives/2011/07/the-goal-bring-aging-under-medical-control.php
Reuters reports on a recent presentation by Aubrey de Grey of the SENS Foundation: "'I'd say we have a 50/50 chance of bringing aging under what I'd call a decisive level of medical control within the next 25 years or so,' de Grey said in an interview before delivering a lecture at Britain's Royal Institution academy of science. And what I mean by decisive is the same sort of medical control that we have over most infectious diseases today.

De Grey sees a time when people will go to their doctors for regular 'maintenance,' which by then will include gene therapies, stem cell therapies, immune stimulation and a range of other advanced medical techniques to keep them in good shape.

The idea is to engage in what you might call preventative geriatrics, where you go in to periodically repair that molecular and cellular damage before it gets to the level of abundance that is pathogenic. For some, the prospect of living for hundreds of years is not particularly attractive, either, as it conjures up an image of generations of sick, weak old people and societies increasingly less able to cope. But de Grey says that's not what he's working for. Keeping the killer diseases of old age at bay is the primary focus.  This is absolutely not a matter of keeping people alive in a bad state of health. This is about preventing people from getting sick as a result of old age. The particular therapies that we are working on will only deliver long life as a side effect of delivering better health."

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