Are You Spending Money To Die Young?

Healthy Life Extension

Funding Aging Research

Are You Spending Money To Die Young?

posted on August 16, 2011

Dear Future Centenarian,

Healthy food shopping can be inexpensive. Unhealthy food shopping can bankrupt and kill you.

A new study published in the Journal of Health Affairs suggests that increasing the amount of potassium would add $380 per year to the average consumer™s food costs. The Dietary Guidelines for Americans, 2010, outlined the need for Americans to consume more potassium, dietary fiber, vitamin D and calcium, and to eat fewer foods containing saturated fat and added sugar. 

œHard economic times don™t mean you have to eat less healthy foods, says Elizabeth Pivonka, Ph.D., R.D., president and CEO of Produce for Better Health Foundation, the nonprofit entity behind the Fruits & Veggies”More Matters® health initiative. œEating fruits and vegetables is a sound investment in long-term health, and a very inexpensive part of a healthy lifestyle. 

An easy and healthy way to stretch your food budget is to avoid or limit foods that have few vitamins and minerals per calorie, such as chips, cookies and soda, and buy foods that offer higher vitamin, mineral fiber and potassium content per calorie like healthy fruits and vegetables.

A study released earlier this year by the U.S. Department of Agriculture's (USDA) Economic Research Service shows just how affordable fruits and vegetables really are. Getting the recommended amount costs only $2-$2.50 per day. The study used Nielsen Homescan data from 2008 to estimate the average retail price per pound and per cup of 153 commonly consumed fresh and processed fruits and vegetables. They found that average prices ranged from under 20 cents per cup to over $2 per cup depending on the specific fruit or veggie.

Furthermore, according to the U.S. Bureau of Labor Statistics' Consumer Expenditures Survey, the average two person household spends $6,308 on food yearly. Filling half the plate with fruits and vegetables for this two person household would only cost 29 percent of their annual food budget. It costs me a little more, because I buy organic, and I recommend you make this extra investment in your health span.

The types of food Americans choose to eat also directly impacts their lifespan. 

The results of a study issued in July 2011 showed that a diet high in sodium and low in potassium doubles the risk of dying from a heart attack and is associated with a 50% increased risk of death from any cause. The study recorded the diet of 12,000 U.S. adult men and women 20 years and older over a 14-year period. A dietary imbalance of the two minerals posed the greatest risk than simply eating too much salt, because potassium may neutralize the heart-damaging effects of salt.

The results strengthen past studies and research showing a relationship between sodium intake and mortality. The research was conducted by the Centers for Disease Control and Prevention (CDC), Emory University, and Harvard University. 

The researchers noted, œhypertension is the leading global risk factor for death, affecting almost 1 billion people, and commented that œencouraging consumption of unprocessed, potassium-rich fruits and vegetables is the safest and preferred pathway to increasing potassium intake.

Fruits and vegetables are available year-round in fresh, frozen and dried, are affordable, and easy to prepare. 

So flush your poisonous junk food, stock up on what your body thrives on, and¦

¦Long Life,
David Kekich


A novel way to manipulate stem cells: "Though the heart is known to contain some stem cells, they have a very limited ability to repair damage caused by a heart attack [and] researchers have had to look elsewhere. One of the first efforts to use stem cells to reduce heart scarring involved harvesting them from the bone marrow and inserting them back into the heart muscle, close to the heart's blood supply, but this had limited success. Prof. Oron, who has long used low level lasers to stimulate stem cells to encourage cell survival and the formation of blood vessels after a heart attack, was inspired to test how laser treatments could also work to heal the heart.

He and his fellow researchers tried different methods, including treating the heart directly with low level lasers during surgery, and 'shining' harvested stem cells before injecting them back into the body. But he was determined to find a simpler method. After a low-level laser was 'shined' into a person's bone marrow - an area rich in stem cells - the stem cells took to the blood stream, moving through the body and responding to the heart's signals of distress and harm. Once in the heart, the stem cells used their healing qualities to reduce scarring and stimulate the growth of new arteries, leading to a healthier blood flow. To determine the success of this method, Prof. Oron performed the therapy on an animal model. Following the flow of bone marrow stem cells through the use of a fluorescent marker, the researchers saw an increase in stem cell population within the heart, specifically in the injured regions of the heart. The test group that received the shining treatment showed a vastly higher concentration of cells in the injured organ than those who had not been treated with the lasers."

INVESTIGATING THE INDY GENE Thursday, August 11, 2011
The I'm Not Dead Yet (INDY) gene is one of the earlier longevity genes discovered by researchers in course of investigating the effects of calorie restriction. Here is a recent update: "It is known that excess calorie consumption leads to obesity, insulin resistance and increased mortality, whereas calorie restriction reduces accumulation of body fat and improves cellular energy balance and insulin action - reversing obesity and type 2 diabetes, delaying the aging process, and prolonging life in primates and many other species. It has also been shown in the past that reduced expression of the so-called 'INDY' gene in D. Melanogaster flies and C. elegans worms promotes longevity in a manner similar to calorie restriction.

But until now, the cellular mechanism by which this happens was unknown. [Researchers] generated a mouse with the so-called 'INDY' gene deleted. Loss of the gene altered chemical levels in the cellular signaling network in a way that improved mitochondrial action in the liver, metabolism of fatty acids, and cellular energy transport. Overall, these traits protected the mice from diet-related accumulation of body fat and insulin resistance that evolve, as we age, into type 2 diabetes. Discovering how deletion of the INDY gene would impact mitochondrial metabolism in the liver was key, because that is the main organ where the INDY gene does its work."

Why are hearts in humans and other higher animals not able to regenerate like salamander hearts? Answering that question would be a step on the road to recreating that ability when needed: "A new study has shed light on why adult human cardiac cells lose their ability to proliferate, perhaps explaining why our heart have little regenerative capacity. The study, done in cell lines and mice, may lead to methods of reprogramming a patient's own cardiac myocytes, or muscle cells, within the heart itself to create new muscle to repair damage.

Recent research suggests that mammals do have the ability to regenerate the heart for a very brief period, about the first week of life. During human development, cardiac myocytes are made by progenitor stem cells and proliferate to form the heart. Once the heart is formed, the myocytes transform from immature cells into mature cells that cannot proliferate. That's not so for newts and salamanders, whose cardiac myocytes can go back and forth between immature, or primitive, states to proliferate and repair damage and then revert back into mature cells once the damage is repaired. [Researchers believe] the reason adult human cardiac myocytes can't do this is quite simple - when the myocytes are in a more primitive state, they are not as good at contracting, which is vital for proper heart function. Because humans are much larger than newts and salamanders, we needed more heart contraction to maintain optimum blood pressure and circulation."

EXERCISE VERSUS MEMORY LOSS Wednesday, August 10, 2011
Another of the many benefits of exercise: a study "shows that a small amount of physical exercise could profoundly protect the elderly from long-term memory loss that can happen suddenly following infection, illnesses or injury in old age. Aging rats that ran just over half a kilometer each week were protected against infection-induced memory loss. Our research shows that a small amount of physical exercise by late middle-aged rats profoundly protects against exaggerated inflammation in the brain and long-lasting memory impairments that follow a serious bacterial infection. Strikingly, this small amount of running was sufficient to confer robust benefits for those that ran over those that did not run. This is an important finding because those of advanced age are more vulnerable to memory impairments following immune challenges such as bacterial infections or surgery.

With baby boomers currently at retirement age, the risk of diminished memory function in this population is of great concern. Thus, effective noninvasive therapies are of substantial clinical value. Past research has shown that exercise in humans protects against declines in cognitive function associated with aging and protects against dementia. Researchers also have shown that dementia is often preceded by bacterial infections, such as pneumonia, or other immune challenges. Previous research has shown that immune cells of the brain, called microglia, become more reactive with age. When the older rats in the study encountered a bacterial infection, these immune cells released inflammatory molecules called cytokines in an exaggerated and prolonged manner. In the current study we found that small amounts of voluntary exercise prevented the priming of microglia, the exaggerated inflammation in the brain, and the decrease of growth factors."

The aging immune system is misconfigured, overpopulated by too many of the wrong sorts of immune cell, while having too few useful cells left to perform the important jobs - such as resisting infections, attacking cancers, and removing senescent cells, for example. One approach to dealing with this problem is to destroy the unwanted cells, and there's evidence for at least some parts of the immune system to show that this is beneficial. Another approach is to use biotechnology to expand the population of useful cells, and this recent release fits into that line of work: "Aging brings about a selective decline in the numbers and function of T cells - a type of white blood cell involved in the immune system's response to infection
and T cells that survive the longest may better protect against infections such as the flu.

The finding may lead to targeting these cells with vaccinations that increase their number and improve protection against disease in older adults. The decline in immune function with age is viewed as the most important contributing factor to older adults' increased susceptibility to infections and decreased responses to vaccinations. We have discovered that aging brings about selective attrition of those T cells that defend us against new infections that we have not encountered before. Not all T cells age the same and the ones that will survive the longest have special features. Finding ways to expand them is our next and final challenge, and our team [should] be able to achieve that in the next few years."

From the SENS Foundation, a look at what might be done to remove damaging cellular aggregates, such as the amyloid beta (Aβ) implicated in Alzheimer's disease (AD), by manipulating the function of lysosomes, the cellular recycling machinery: "Dr. Ben Bahr and his colleagues with the Neurosciences Program and Division of Pharmaceutical Sciences at the University of Connecticut have for some time now been investigating the effects of elevating lysosomal activity using the lysosomal modulator Z-Phe-Ala-diazomethylketone (PADK).  In a new study, Dr. Bahr's group has extended this work into a transgenic mouse model of AD, testing PADK's ability to retard, and to reverse, AD neuropathology and cognitive dysfunction in two models of transgenic AD mice.

Systemic PADK  injection of PADK in both models caused 3- to 8-fold increases in cathepsin B levels and similar elevations in the enzyme's activity in lysosomal cell fractions. Accordingly PADK-induced lysosomal modulations cleared a significant amount of the intra- and extraneuronal burden of Aβ from treated mice, reducing intraneuronal Aβ regions of the hippocampus and piriform cortex by 63 - 73% in younger mice and by ~50% in older ones. As expected, model AD mice also exhibited substantial impairment of performance on cognitive-behavioral tests including the suspended rod, exploratory habituation, and spontaneous alternation behavior in a T-maze tests.

PADK-induced Aβ clearance resulted in the complete restoration of normal function in both young and old animals. As a tribute to the power of the cellular waste-disposal machinery, these results are impressive. Equally, they are not a solution to human brain aging. These animals, like most transgenic models of AD, exhibit no tau pathology nor significant neuronal loss - problems that will also have to be addressed in order to achieve the full prevention of AD and rejuvenation of aging brains."

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