The human race is now going through the biggest macroeconomic change in history. This change has two faces. First, life expectancies have nearly doubled in the West since the beginning of the 20th century. This change is even more rapid in formerly undeveloped regions as they catch up to Western technologies.

The other aspect is falling birth rates, which seem correlated to longer life spans. Fertility rates (births per woman) have fallen below replacement rates globally for the first time ever. And in many developed countries, fertility rates are alarmingly low.

A fertility rate of at least 2.1 children per woman is needed for native population stability in the West. It can be 2.5 or more where infant mortality is higher.

Japan and Germany are now at about 1.4 children per woman and falling. Singapore, Greece, and Spain are at about 1.3 births per woman. Within decades, whole nations will be at 1 birth per woman.

This means the next generation will be half the size of the last.

Every generation, from now on, will be smaller than the last. For economists and demographers, this problem is represented by the old-age dependency ratio (OADR).
The OADR refers to the number of people in a society who contribute to the economy compared to those who depend on transfer payments of some kind. Most social programs for the aged as well as pension plans were developed when the OADR was much healthier.

As life spans have lengthened, the OADR has deteriorated. There are two reasons for this. Longer lives mean that more people are moving to the dependent column of the balance sheet. At the same time, falling birth rates have reduced the number of workers in the contributor column.

In 1950, there were about 17 workers in America for every retired person. Today, there are less than three contributors to each retired dependent. This ratio continues to worsen simply because people are living longer and birth rates are falling.

In the US today, politicians say that the economy is doing fine. But if that were true, we?d be running budget surpluses. Instead, the US government is borrowing nearly 30 cents of every dollar spent. Transfer payments to the elderly now account for about 30% of federal spending. The roughly $20 trillion dollar national debt continues to grow, and unfunded liabilities are 10 to 20 times that amount (depending on who?s doing the math).

Former head of the Federal Reserve Allen Greenspan has long been known as an optimist. He?s held the view that market forces are robust enough to counter political recklessness. But recently, Greenspan admitted that he has lost his positive outlook. The reason, in his words, is that ?we have a 9% annual rate of increase in entitlements, which is mandated by law. It has got nothing to do with the economy. It has got to do with age and health and the like.?

Our current economic woes aren?t rooted in traditional economic policies. The problem is ?age and health and the like.? In other words, it?s the OADR.

Increasing the number of people on the contributor side of the balance sheet won?t solve the problem. Japan, Germany, Italy, and the Scandanavian countries have spent billions trying to increase birth rates. And they?ve failed. Even if they succeeded, it wouldn?t help in time. It takes decades for newborns to enter the work force.

The best way to prevent the demise of Western economies and the eventual Greek-style collapse of social programs and pension plans is longer life and health spans. If more people can remain healthy and work or invest longer, it would produce the economic growth we need to fund the innovation that will usher in an unparalleled era of prosperity.

Politicians and unions claim that voters won?t accept an increase in retirement ages, but Americans are already working longer than ever before. In fact, the evidence shows that most people would work longer and save more to pay their own way if they could.

According to a study by Zoya Financial, almost two-thirds of Americans have to retire earlier than planned. This is largely due to problems with their health or that of their spouse.

Anti-aging strategies and biotechnologies aren?t just needed from the point of view of the individual. They are, quite literally, the only way to save modern economies from the unintended consequences of increased life spans? the collapsing OADR.

The mainstream scientific community is starting to accept that we must move from a model of disease treatment to anti-aging. Effective anti-aging therapeutics are in labs right now and will greatly increase health spans and working careers, saving Western economies and cultures from ruin in the process.

Bureaucratic and political inertia, though, is slowing the approval and adoption of these life and economy-saving solutions. The establishment will eventually come around, but only kicking and screaming.

Hence the world truly needs more medical professionals, and patients who can spread the word that the old model of treating diseases is obsolete, inhumane, and fiscally suicidal.

~ Written by Patrick Cox

Injuries to the spinal cord often cause paralysis and other permanent disabilities because severed nerve fibers do not regrow on their own. During the past few years a number of paralyzed patients have experienced remarkable improvement as a result of Stem Cell Therapy. When their own stem cells or those extracted from cord blood were injected into the spinal column they went straight to the damaged nerves and helped them regenerate. One limitation is that the treatment must be given as soon as possible after the injury. When the same injections were given to patients who had been paralyzed for a year or more they were rarely successful. During the first few months after a spinal injury the nerves lose their ability to regenerate even with the introduction of new stem cells.

Now, scientists of the German Center for Neurodegenerative Diseases (DZNE) have succeeded in releasing a molecular brake that prevents the regeneration of nerve connections. Treatment of mice with Pregabalin, a drug that acts upon the growth inhibiting mechanism, caused damaged nerve connections to regenerate. Researchers led by neurobiologist Frank Bradke report on these findings in the journal Neuron.

Human nerve cells are interconnected in a network that extends to all parts of the body. In this way control signals are transmitted from head to toe, while sensory inputs flow in the opposite direction. For this to happen, impulses are passed from neuron to neuron, not unlike a relay race. Damages to this wiring system can have drastic consequences particularly if they affect the brain or the spinal cord. This is because the cells of the central nervous system are connected by long projections. When severed, these projections, which are called axons, are unable to regrow.

Neural pathways that have been injured can only regenerate if new connections arise between the affected cells. In a sense, the neurons have to stretch out their arms, i.e. the axons have to grow. In fact, this happens in the early stages of embryonic development. However, this ability disappears in the adult. Can it be reactivated? This was the question Professor Bradke and co-workers asked themselves. “We started from the hypothesis that neurons actively down-regulate their growth program once they have reached other cells, so that they don’t overshoot the mark. This means, there should be a braking mechanism that is triggered as soon as a neuron connects to others,” says Dr. Andrea Tedeschi, a member of the Bradke Lab and first author of the current publication.

In mice and cell cultures, the scientists started an extensive search for genes that regulate the growth of neurons. “That was like looking for the proverbial needle in the haystack. There are hundreds of active genes in every nerve cell, depending on its stage of development. To analyze the large data set we heavily relied on bioinformatics. To this end, we cooperated closely with colleagues at the University of Bonn,” says Bradke. “Ultimately, we were able to identify a promising candidate. This gene, known as Cacna2d2, plays an important role in synapse formation and function, in other words in bridging the final gap between nerve cells.” During further experiments, the researchers modified the gene’s activity, e.g. by deactivating it. In this way, they were able to prove that Cacna2d2 does actually influence axonal growth and the regeneration of nerve fibers.

Cacna2d2 encodes the blueprint of a protein that is part of a larger molecular complex. The protein anchors ion channels in the cell membrane that regulate the flow of calcium particles into the cell. Calcium levels affect cellular processes such as the release of neurotransmitters. These ion channels are therefore essential for the communication between neurons.

In further investigations, the researchers used Pregabalin (PGB), a drug that had long been known to bind to the molecular anchors of calcium channels. Over a period of several weeks, they administered PGB to mice with spinal cord injuries. As it turned out, this treatment caused new nerve connections to grow.

“Our study shows that synapse formation acts as a powerful switch that restrains axonal growth. A clinically-relevant drug can manipulate this effect,” says Bradke. In fact, PGB is already being used to treat lesions of the spinal cord, albeit it is applied as a pain killer and relatively late after the injury has occurred. “PGB might have a regenerative effect in patients, if it is given soon enough. In the long term this could lead to a new treatment approach. However, we don’t know yet.”

In previous studies, the DZNE researchers showed that certain cancer drugs can also cause damaged nerve connections to regrow. The main protagonists in this process are the microtubules, long protein complexes that stabilize the cell body. When the microtubules grow, axons do as well. Is there a connection between the different findings? “We don’t know whether these mechanisms are independent or whether they are somehow related,” says Bradke. “This is something we want to examine more closely in the future.”

There are now more than 500 stem cell clinics in the United States and the FDA has been holding hearings to decide if they should be closed down or much more strictly regulated. The move comes at an awkward time because research on stem cell treatments is just starting to bear fruit. Tantalizing results from a series of small studies suggest injections with certain types of stem cells may be effective treatments for conditions such as stroke and multiple sclerosis. Also thousands of patients have been able to avoid joint surgery after receiving injections with stem cells and platelet rich plasma. Since Medical Doctors in Stem Cell Clinics generally use cells they?ve isolated from a patient?s own fat, and because those cells are considered only ?minimally manipulated,? the FDA has not regulated the treatments as it would a traditional pharmaceutical.

Patients who want immediate treatment for their conditions and Doctors who perform these treatments say the FDA is being pressured into taking a tough line by academics and pharmaceutical giants who want to control, and profit from, the stem cell industry.

?The problem is, if we do well, it hurts their business plan,? said Dr. Mark Berman, a plastic surgeon in Beverly Hills, California.

Back in 2002, Dr. Berman cofounded a chain of clinics called the Cell Surgical Network. He says he and other physicians in the network have conducted some 5,000 stem cell treatments including on himself and his wife for conditions such as arthritis and hip, back and joint pain. He called the draft regulations arbitrary and hypocritical.

The fight over regulation comes at a time when leading stem cell researchers, after years of disappointing results, are increasingly excited about new studies showing the cells appear to be safe and may be effective in treating a variety of crippling diseases, including macular degeneration and Parkinson?s.

?It?s a very exciting time,? said Sally Temple, a stem cell researcher at the Neural Stem Cell Institute in Rensselaer, N.Y. ?We?re going to see many treatments for diseases that are currently untreatable.?

The results researchers are so excited about are only possible because of decades of tedious work to establish safety protocols, test concepts and learn how to grow, produce, and manipulate stem cells, she said.

?It?s hard to have people understand how long this whole process takes,? said Temple, who also serves as president of the International Society of Stem Cell Research. ?You would not believe what we have to do in my lab to prepare cells properly.?

Stem cells can be extracted from a number of different tissues. They?re highly flexible and can turn into other kinds of cells ? heart cells, say, or retinal cells. That ability lets them act as a kind of internal repair system.

Stem cells extracted from bone marrow have long been used to treat cancer, and blood and immune disorders. Now a variety of types of stem cells are being tested in a slew of other applications.

For example, a team at Stanford and the University of Pittsburgh announced in June in the journal Stroke that they had restored mobility in some stroke patients by injecting a particular kind of modified stem cell directly into their brains. Most stroke patients don?t improve much after six months, but some who received the treatment gained mobility a year or more after their strokes. Some who had been confined to wheelchairs even began to walk.

Dr. Gary Steinberg, a neurosurgeon at Stanford and the study?s lead author, said he thought the cells might be helping by secreting factors that led to the regeneration or reactivation of patient?s cells. ?We didn?t imagine we could restore neurologic function in these chronic stroke patients with severe disability,? said Steinberg.

The study just 18 patients; so Dr. Steinberg is recruiting 156 more for an additional study.

In another promising effort, a team from the University of Southern California announced they had restored some mobility in a 21-year-old man, Kris Boesen, who had become paralyzed from the neck down after a car accident this spring.

The team, led by USC neurosurgeon and bioengineer Dr. Charles Liu, injected 10 million specialized cells created from embryonic stem cells directly into the patient?s spine.

To be sure, it?s unclear whether, or how much, the treatment helped; the patient may also have recovered spontaneously. But whatever the mechanism, the improvement was dramatic: Three months after the treatment, the patient was feeding himself, hugging his family, and using his cell phone.

?The first thing he did when he could use his hands was text his girlfriend,? Liu said.

This patient was one of five enrolled in a multicenter clinical trial using cells that support nervous system functioning created from embryonic cells by Asterias Biotherapeutics, which plans to release results from several other patients Wednesday at an International Spinal Cord Society meeting in Vienna.

?If it bears out, it?s going to be huge,? Liu said. ?This was the difference between someone using his hands or not.?

Household dust exposes people to a wide range of toxic chemicals from everyday products, according to a study led by researchers at Milken Institute School of Public Health (Milken Institute SPH) at the George Washington University. The multi-institutional team conducted a first-of-a-kind meta-analysis, compiling data from dust samples collected throughout the United States to identify the top ten toxic chemicals commonly found in dust. They found that DEHP, a chemical belonging to a hazardous class called phthalates, was number one on that list. In addition, the researchers found that phthalates overall were found at the highest levels in dust followed by phenols and flame retardant chemicals.

“Our study is the first comprehensive analysis of consumer product chemicals found in household dust,” says lead author Ami Zota, ScD, MS, assistant professor of environmental and occupational health at Milken Institute SPH. “The findings suggest that people, and especially children, are exposed on a daily basis to multiple chemicals in dust that are linked to serious health problems.” Fortunately there are ways to reduce your exposure.

Chemicals from consumer products are released into the air and get into dust, which can settle on household items or on the floor. People can inhale or ingest small particles of dust or even absorb them through the skin. Infants and young children are particularly at risk for exposure to the chemicals found in dust because they crawl, play on dusty floors, and put their hands in their mouths, the authors say.

Zota and colleagues pooled data from 26 peer-reviewed papers and one unpublished dataset that analyzed dust samples taken from homes in 14 states. They found 45 potentially toxic chemicals that are used in many consumer and household products such as vinyl flooring, personal care and cleaning products, building materials and home furnishings. The meta-analysis combines information from smaller dust studies and thus offers solid conclusions with greater statistical power, the authors say.

The team found that:

? Ten harmful chemicals are found in ninety percent of the dust samples across multiple studies, including a known cancer-causing agent called TDCIPP. This flame retardant is frequently found in furniture, baby products and other household items.

? Indoor dust consistently contains four classes of harmful chemicals in high amounts. Phthalates, substances that are used to make cosmetics, toys, vinyl flooring, and other products, were found in the highest concentration with a mean of 7,682 nanograms per gram of dust-an amount that was several orders of magnitude above the others. Phenols, chemicals used in cleaning products and other household items, were the number two highest chemical class followed by flame retardants and highly fluorinated chemicals used to make non-stick cookware.

? Chemicals from dust are likely to get into young children’s bodies. A flame retardant added to couches, baby products, electronics and other products, TCEP, had the highest estimated intake followed by four phthalates–DEP, DEHP, BBzP and DnBP. The intake numbers in this study probably underestimate the true exposure to such chemicals, which are also found in products on the drug store shelf and even in fast food the authors say.

? Phthalates such as DEP, DEHP, DNBP, and DIBP, are not only found at the highest concentrations in dust but are associated with many serious health hazards. Phthalates are thought to interfere with hormones in the body and are linked to a wide range of health issues including declines in IQ and respiratory problems in children.

? Highly fluorinated chemicals such as PFOA and PFOS are also high on the potential harm scale. These types of chemicals, which are found in cell phones, pizza boxes, and many non-stick, waterproof and stain-resistant products have been linked to numerous health problems of the immune, digestive, developmental and endocrine systems.

? Small amounts can add up. Many of the chemicals in dust are linked to the same health hazards, such as cancer or developmental and reproductive toxicity, and may be acting together. Exposure to even small amounts of chemicals in combination can lead to an amplified health risk, especially for developing infants or young children, the authors say.

“The number and levels of toxic and untested chemicals that are likely in every one of our living rooms was shocking to me,” said co-author Veena Singla, PhD, staff scientist at the Natural Resources Defense Council. “Harmful chemicals used in everyday products and building materials result in widespread contamination of our homes–these dangerous chemicals should be replaced with safer alternatives,” Singla adds.

In the meantime, consumers who want to reduce their exposure to chemicals in household dust and the environment around them can take a few simple steps:

1. Keep dust levels low by using a strong vacuum with a HEPA filter and vacuum frequently. The HEPA filter is important because with ordinary vacuums many of the chemicals will go right back into the air you breathe instead of staying in the bag or filter.

2. Wash hands frequently

3. Avoid personal care and household products that contain potentially dangerous chemicals. Examples include cleaning solvents, pesticides, chlorine bleach (use hydrogen peroxide bleach), toxic drain cleaners (use the enzyme based kind from the health food store), many cleaning products (buy those based on non-toxic ingredients), and many cosmetics.

4. Change the furnace filter regularly

5. Install a HEPA air purifier in any room you spend a lot of time in or better yet put a whole house unit on the furnace.

6. Open windows a few inches when weather permits to bring in fresh air. Most homes are more polluted than outdoors.

7. Have your carpets cleaned once a year by an environmentally friendly company like Chem-Dry that uses safe natural cleaning solutions.

“Consumers have the power to make healthier choices and protect themselves from harmful chemicals in everyday products,” says Robin Dodson, an environmental exposure scientist at Silent Spring Institute. “These things can make a real difference not only in their health but also in shifting the market toward safer products.”

Researchers from Rome’s Sapienza University and the San Diego School of Medicine spent six months studying the residents of Acciaroli in order to determine why over 10% of the population is more than 100 years old. This small village in Italy is best known for its natural beauty and healthy fruits and vegetables.

With a population of 700 people Acciaroli is part of an area that thrives on a diet of Mediterranean foods, such as fresh fruits and vegetables, fish, and olive oil. This is where Ancel Keys, a nutritionist from the United States, found convincing proof that the Mediterranean diet provides excellent health benefits. Researchers also found that the people living in these small communities, and in nearby villages appear to be almost immune to chronic illnesses, such as heart disease and dementia. These illnesses are common among aging citizens living in the Western World.

The Researchers discovered that Adrenomedullin, a hormone that widens blood vessels, was found to be present in small quantities in the test subjects. Adrenomedullin is present “in a much reduced quantity in the subjects studied and seems to act as a powerful protecting factor, helping the optimal development of microcirculation”, or capillary circulation, they said in a statement. In older people, capillary blood vessels usually degenerate, but the seniors in Cilento had capillaries of the sort found in much younger people, even those in their 20s.

The study also describes “metabolites present (in the bodies of those studied) which may have a positive influence on longevity and the well-being of Cliento’s centenarians”, without giving further details. The research has been expanded to include more data from blood tests, neurological reading and cardiac exams.

The scientists are looking into whether genetics could combine with lifestyle factors including diet and physical activity to extend the villager’s longevity.
The residents eat rosemary almost every day, which is known to improve brain activity. Walking, gardening, fishing and other physical activities are other important ingredients for a long, healthy, prosperous life that are practiced regularly by the residents.

Quality of life and longevity tend to improve the more people eat unprocessed natural foods with lots of vegetables, fruits, beans, whole grains, nuts, and seeds. Most centenarians are not vegetarians, but generally eat a relatively small amount of meat.

The researchers have decided to extend the study and expand their research, including by launching a fundraising campaign. Aside from blood tests, the researchers also carried out cardiac and neurological tests, Alan S. Maisel, the San Diego cardiologist heading up the project.

Researchers have used CRISPR a revolutionary new genetic engineering technique to convert cells isolated from mouse connective tissue directly into neuronal cells.

In 2006, Shinya Yamanaka, a professor at the Institute for Frontier Medical Sciences at Kyoto University at the time, discovered how to revert adult connective tissue cells, called fibroblasts, back into immature stem cells that could differentiate into any cell type. These so-called induced pluripotent stem cells won Yamanaka the Nobel Prize in medicine just six years later for their promise in research and medicine.

Since then, researchers have discovered other ways to convert cells between different types. This is mostly done by introducing many extra copies of “master switch” genes that produce proteins that turn on entire genetic networks responsible for producing a particular cell type.

Now, researchers at Duke University have developed a strategy that avoids the need for the extra gene copies. Instead, a modification of the CRISPR genetic engineering technique is used to directly turn on the natural copies already present in the genome. This is important because one of the risks of using current IPS cells for stem cell therapy is introducing genetically altered DNA into a person’s body. This method does not require adding any new genes to the cells.

These early results indicate that the newly converted neuronal cells show a more complete and persistent conversion than the method where new genes are permanently added to the genome. These cells could be used for modeling neurological disorders, discovering new therapeutics, developing personalized medicines and, perhaps in the future, implementing cell therapy.

The study was published on August 11, 2016, in the journal Cell Stem Cell.

“This technique has many applications for science and medicine. For example, we might have a general idea of how most people’s neurons will respond to a drug, but we don’t know how your particular neurons with your particular genetics will respond,” said Charles Gersbach, the Rooney Family Associate Professor of Biomedical Engineering and director for the Center of Biomolecular and Tissue Engineering at Duke. “Taking biopsies of your brain to test your neurons is not an option. But if we could take a skin cell from your arm, turn it into a neuron, and then treat it with various drug combinations, we could determine an optimal personalized therapy.”

“The challenge is efficiently generating neurons that are stable and have a genetic programming that looks like your real neurons,” says Joshua Black, the graduate student in Gersbach’s lab who led the work. “That has been a major obstacle in this area.”

In the 1950s, Professor Conrad Waddington, a British developmental biologist who laid the foundations for developmental biology, suggested that immature stem cells differentiating into specific types of adult cells can be thought of as rolling down the side of a ridged mountain into one of many valleys. With each path a cell takes down a particular slope, its options for its final destination become more limited.

If you want to change that destination, one option is to push the cell vertically back up the mountain — that’s the idea behind reprogramming cells to be induced pluripotent stem cells. Another option is to push it horizontally up and over a hill and directly into another valley.

“If you have the ability to specifically turn on all the neuron genes, maybe you don’t have to go back up the hill,” said Gersbach.

Previous methods have accomplished this by introducing viruses that inject extra copies of genes to produce a large number of proteins called master transcription factors. Unique to each cell type, these proteins bind to thousands of places in the genome, turning on that cell type’s particular gene network. This method, however, has some drawbacks.

“Rather than using a virus to permanently introduce new copies of existing genes, it would be desirable to provide a temporary signal that changes the cell type in a stable way,” said Black. “However, doing so in an efficient manner might require making very specific changes to the genetic program of the cell.”

In the new study, Black, Gersbach, and colleagues used CRISPR to precisely activate the three genes that naturally produce the master transcription factors that control the neuronal gene network, rather than having a virus introduce extra copies of those genes.

CRISPR is a modified version of a bacterial defense system that targets and slices apart the DNA of familiar invading viruses. In this case, however, the system has been tweaked so that no slicing is involved. Instead, the machinery that identifies specific stretches of DNA has been left intact, and it has been hitched to a gene activator.

The CRISPR system was administered to mouse fibroblasts in the laboratory. The tests showed that, once activated by CRISPR, the three neuronal master transcription factor genes robustly activated neuronal genes. This caused the fibroblasts to conduct electrical signals — a hallmark of neuronal cells. And even after the CRISPR activators went away, the cells retained their neuronal properties.

“When blasting cells with master transcription factors made by viruses, it’s possible to make cells that behave like neurons,” said Gersbach. “But if they truly have become autonomously functioning neurons, then they shouldn’t require the continuous presence of that external stimulus.”

The experiments showed that the new CRISPR technique produced neuronal cells with an epigenetic program at the target genes matching the neuronal markings naturally found in mouse brain tissue.

“The method that introduces extra genetic copies with the virus produces a lot of the transcription factors, but very little is being made from the native copies of these genes,” explained Black. “In contrast, the CRISPR approach isn’t making as many transcription factors overall, but they’re all being produced from the normal chromosomal position, which is a powerful difference since they are stably activated. We’re flipping the epigenetic switch to convert cell types rather than driving them to do so synthetically.”

The next steps, according to Black, are to extend the method to human cells, raise the efficiency of the technique and try to clear other epigenetic hurdles so that it could be applied to model particular diseases.

“In the future, you can imagine making neurons and implanting them in the brain to treat Parkinson’s disease or other neurodegenerative conditions,” said Gersbach. “But even if we don’t get that far, you can do a lot with these in the lab to help develop better therapies.”

Reference: Joshua B. Black, Andrew F. Adler, Hong-Gang Wang, Anthony M. D?Ippolito, Hunter A. Hutchinson, Timothy E. Reddy, Geoffrey S. Pitt, Kam W. Leong, Charles A. Gersbach. Targeted Epigenetic Remodeling of Endogenous Loci by CRISPR/Cas9-Based Transcriptional Activators Directly Converts Fibroblasts to Neuronal Cells. Cell Stem Cell, 2016; DOI: 10.1016/j.stem.2016.07.001

Fasting as little as eight days a year could help bodies become healthier, according to new research from the University of Southern California.

Fasting two to four days at a time every six months causes stem cells to awake from their normal dormant state, and start regenerating. Researchers discovered this practice eliminated damaged and older cells, and caused new cells to be born, effectively renewing the immune system. This is the first time any natural intervention has ever been shown to trigger this self-renewal.

In mice and humans, white blood cell counts were significantly lowered after long periods without food. These bodies are vital to the human immune system. But, when their numbers decline to a critical point, pathways for hematopoietic stem cells were switched on. These cells manage the immune system and generate new blood.

“When you starve, the system tries to save energy, and one of the things it can do to save energy is to recycle a lot of the immune cells that are not needed, especially those that may be damaged,” Valter Longo of the USC Davis School of Gerontology, said.

Going without food for 48 to 96 hours shifts human bodies to consume stores of fat, glucose (sugar), and ketones (created when fats are broken down for energy). Unhealthy white blood cells are also broken down, so that their components can be reused for the next generation of cells. This process is akin to recycling for the immune system.

After a period of fasting, human immune systems generate new blood cells when nutrients start flowing back into the body. Researchers at USC wanted to know what drives body systems to rebuild the cells.

Protein kinase A, an enzyme known to inhibit cell regeneration, was reduced in the systems of people who are fasting, the study found. Concentrations of a growth-factor hormone called IGF-1 were also lowered in those who have not eaten in days.

Of course most people would not want to fast on only water for two to four days at a time and it is probably not safe except under medical supervision. There are several alternatives that produce some of the same benefits including juice fasting and time restricted eating for people that are healthy enough to do a less extreme form of fasting.

Juice fasting involves drinking raw fruit and vegetable juices usually for one day at a time. Some people juice fast once a week and others once a month. It is important to use at least 50% vegetables to make juice and not overdue the fructose sugars that are concentrated in fruit juice. Typically between 2 and 3 quarts of juice are consumed per day. There are now many brands of pressure pasteurized juices available in health food stores that are raw. High pressure is used to destroy the bacteria instead of heat. Water is not restricted on a juice fast.

Another approach to fasting which has produced beneficial results is time restricted eating. It involves eating with no limit on quantity during an 8 hour consecutive period and then going without food until the next day. Water is available to drink 24 hours each day and not restricted. Some people eat this way every day. A scientific study of time restricted eating which showed impressive results was published in Cell Metablolism.

Reference: Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression. Cell Stem Cell, Volume 14, Issue 6, p810?823, 5 June 2014