stopgam's thread
Julia36
22 Jul 2013
Australian Skull May Mean Captain James Cook Wasn't First White

"
A skull unearthed in Australia may belong to the first white man to set foot on the continent -- and it's not who historians might expect.
The skull was found in Taree, a town about 200 miles north of Sydney, in November 2011 by local police, who expected to carry out a murder investigation on the remains. But archaeologists who examined the skull subsequently have said it may be that of a white man born around 1650."


There's enough of a skull there to forensically reconstruct the face and match it with records of sea travellers from Europe.
Edited by Innocent, 22 July 2013 - 06:04 AM.
"
A skull unearthed in Australia may belong to the first white man to set foot on the continent -- and it's not who historians might expect.
The skull was found in Taree, a town about 200 miles north of Sydney, in November 2011 by local police, who expected to carry out a murder investigation on the remains. But archaeologists who examined the skull subsequently have said it may be that of a white man born around 1650."


There's enough of a skull there to forensically reconstruct the face and match it with records of sea travellers from Europe.
Edited by Innocent, 22 July 2013 - 06:04 AM.
Julia36
22 Jul 2013
1hr 38mins Part 1 Australian/German Life of Cook
The aboriginals
2hr 47 mins.
Julia36
22 Jul 2013
Since no-one's died here with Scientific Resurrection coming...history is now in a different light.##
But the world into which men resurrect will be empowered, healthy abundant and accelerating: beyond anything imaginable by people today.
that new world is only 14 years away because machine intelligence is due to advent from 2022, with Intelligence explosion by 2027
But the world into which men resurrect will be empowered, healthy abundant and accelerating: beyond anything imaginable by people today.
that new world is only 14 years away because machine intelligence is due to advent from 2022, with Intelligence explosion by 2027
Julia36
22 Jul 2013
Compensation should be paid to the indigenous peoples who were wiped out and had their lands seized.
SUE THE CELTS who wiped out the ancient Britons
Traces found of the earliest Britons from 900,000 years ago


we're dependent on artefacts to reconstruct the past, but calculation power and growing data bases will enable increasingly realistic simulations.
SUE THE CELTS who wiped out the ancient Britons
Traces found of the earliest Britons from 900,000 years ago


we're dependent on artefacts to reconstruct the past, but calculation power and growing data bases will enable increasingly realistic simulations.
Julia36
23 Jul 2013
Incredible Technology: How Supercomputers Solve Giant Problems
- See more at: http://www.livescien...h.UHEqyqWo.dpuf
You may need to wipe your screen:

Earth & Moon captured from nearly 1 billion miles away
"NASA's Cassini spacecraft captured the color images of Earth and the moon from its perch in the Saturn system nearly 900 million miles (1.5 billion kilometers) away."
Incredible Technology: How Supercomputers Solve Giant Problems

Accurate picture of Venus calculated using data fed into supercomputers. NASA
http://www.technewsd...rcomputers.html
Australia is putting supercomputing into the cloud: you dont need one in your basement - just a terminal anywhere.
"
“The establishment of a cloud alongside the NCI petascale supercomputer and the National High-Performance Data Node of the Research Data Storage Infrastructure (RDSI) initiative will enhance the scale of data-intensive science, leveraging the impact and value of each infrastructure component.
“As the nature of research becomes increasingly collaborative, the cloud will support users with self-service abilities to publish research data, share knowledge and rapidly access software applications."
Metagenomics Used To Recover 'Breakthrough' Genomes
http://www.ibtimes.c...genomes-1355425
"“Most other attempts to recover DNA sequences from historical or ancient samples have suffered from the risk of contamination, because they rely on amplification of DNA in the laboratory, Mark Pallen, a professor of Microbial Genomics at Warwick Medical School in the United Kingdom said in a statement. “The beauty of metagenomics is that it provides a simple but highly informative, assumption-free, one-size-fits-all approach that works in a wide variety of contexts.”
22nd July 2013
More recovery techniques mean more data plotted on the GRID.
More plots mean less calculation needed to complete the grid.
.
Edited by Innocent, 23 July 2013 - 05:44 AM.
Julia36
23 Jul 2013


Science Daily
Geochemical 'Fingerprints' Leave Evidence That Megafloods Eroded Steep Gorge
Ancient Megafloods: Geochemical 'Fingerprints'
July 22, 2013 — The Yarlung-Tsangpo River in southern Asia drops rapidly through the Himalaya Mountains on its way to the Bay of Bengal, losing about 7,000 feet of elevation through the precipitously steep Tsangpo Gorge.
For the first time, scientists have direct geochemical evidence that the 150-mile long gorge, possibly the world's deepest, was the conduit by which megafloods from glacial lakes, perhaps half the volume of Lake Erie, drained suddenly and catastrophically through the Himalayas when their ice dams failed at times during the last 2 million years."
Greening of Earth 4 times older than thought
ibid
Greening of Earth Pushed Way Back in Time
"A new study, led by geologist Gregory J. Retallack of the University of Oregon, now has presented evidence for life on land that is four times as old -- at 2.2 billion years ago and almost half way back to the inception of the planet.
That evidence, which is detailed in the September issue of the journal Precambrian Research
Edited by Innocent, 23 July 2013 - 06:04 AM.
Julia36
23 Jul 2013
Genome editing becomes more accurate

---Understanding begins--->
Lad work is moving into IT and out of test tubes.
This means it will arrive on Moore's Law and accelerate
In 2017 the age of Genomic Medicine will arrive.

"With this technology, scientists can deliver or disrupt multiple genes at once, raising the possibility of treating human disease by targeting malfunctioning genes."
4 years to go!
By the time we can raise the dead (est 2027), the living population will be healthy, non-aging (deployment of discoveries in biotech will roll out as expected, from launch to most people in the world getting them could be down to minutes) and colonising other planets. 2027 science will seem like magic to people of today.


SKYLON
see videos on YouTube or below
https://www.youtube....h?v=0UL4rgq6glE
the British are pushing into space with 2 big projects from Reaction Engines (above)
and Richard Branson
WE are describing the universe in sets of laws and scale and events. When we have enough sufficiently detailed simulations will be built.

Virgin Galactic: Welcome
Booking

Chinese Rocket Engine Test a Big Step for Space Station Project
today
"China has successfully test-fired the rocket engine that will power the next-generation heavy-lift booster, the Long March 5, that will help drive the country's space exploration into the final frontier.
The new rocket engine is closely tied to China's planned space station, and is a big step forward for the country's moon exploration program. The first engine test, carried out on June 29, lasted roughly three minutes from ignition to shutdown, according to the China Manned Space Engineering Office."


Advances in technology demand more physics which will enable the Quantum Archaeology Grid.
Edited by Innocent, 23 July 2013 - 07:08 AM.

---Understanding begins--->
Lad work is moving into IT and out of test tubes.
This means it will arrive on Moore's Law and accelerate
In 2017 the age of Genomic Medicine will arrive.

"With this technology, scientists can deliver or disrupt multiple genes at once, raising the possibility of treating human disease by targeting malfunctioning genes."
4 years to go!
By the time we can raise the dead (est 2027), the living population will be healthy, non-aging (deployment of discoveries in biotech will roll out as expected, from launch to most people in the world getting them could be down to minutes) and colonising other planets. 2027 science will seem like magic to people of today.


SKYLON
see videos on YouTube or below
https://www.youtube....h?v=0UL4rgq6glE
the British are pushing into space with 2 big projects from Reaction Engines (above)
and Richard Branson
WE are describing the universe in sets of laws and scale and events. When we have enough sufficiently detailed simulations will be built.

Virgin Galactic: Welcome
Booking

Chinese Rocket Engine Test a Big Step for Space Station Project
today
"China has successfully test-fired the rocket engine that will power the next-generation heavy-lift booster, the Long March 5, that will help drive the country's space exploration into the final frontier.
The new rocket engine is closely tied to China's planned space station, and is a big step forward for the country's moon exploration program. The first engine test, carried out on June 29, lasted roughly three minutes from ignition to shutdown, according to the China Manned Space Engineering Office."


Advances in technology demand more physics which will enable the Quantum Archaeology Grid.
Edited by Innocent, 23 July 2013 - 07:08 AM.
Julia36
23 Jul 2013


Scientists grow replacement retinas, potentially solving most blindnesses
Your replacement retinas might look like this
today
Edited by Innocent, 23 July 2013 - 06:51 AM.
Julia36
24 Jul 2013

Supercomputer
Prices fall to $99-
Operating system Linix Ubantu: Price : free
This is the shape of things to come. And we're only at the start.
In the 2020's many products will be so cheap they will be NIL and almost NIL cost.






Falling prices are because of falling costs.
Technologies like archaeology move into Information Technology (on computers) and their price then plummets on Moore's Law.
GETTING FROZEN
If you could get frozen for $5 would you?
Sure -Because it's safer.
But it must still be safer at $100,000.
Safety and price are two issues people muddle together, but they aren't related.
Economies of scale haven't kicked in with suspensions because few people are committing to it in death-denial.
Work is associated with cruelling hours of labor, but money rewards unrelated to hours of toil nor effort.
NANO-MAP OF THE WORLD PRODUCEDith 3D Printing
"map of the world at nanoscale resolution, a feat never before achieved with a scanning probe instrument.
Not only that, but closer inspection with a microscope reveals that this image is actually a mosaic of individual chemical formulae made up of nanoscale points." kurzweilai
This will slash existing costs from multi-billions to thousands then hundreds
The world's first full-colour 3D desktop printer
London and New York-based company botObjects recently announced the ProDesk3D, which they claimed to be the first full-colour 3D printer small enough to fit on a desktop
http://futuretimelin...tm#.Ue8ReawW4zV

Scanning instead of freezing:

Brain Presrvation Technology Prize
Acceleration of technologies is counter-intuitive. Your gut feeling or vision of how fast technology is happening is way out.
You can only assess it on paper with the facts.

Neuroscientists today can preserve small volumes (<1mm³) of animal brain tissue immediately after death with incredible precision – the features and structure of every synapse within these volumes is well-protected down to the nanometer scale, using an inexpensive, room-temperature process of chemical fixation and plastic embedding, or "plastination." The image to the right is an example of plastination and local circuit tracing, occurring in leading neuroscience labs around the world today. This work immediately raises the question:
* In the types of electron microscopy neuroscientists commonly use (FIBSEM, etc.), preserved neural tissue can be visualized down to about a 6 nanometer resolution. This allows them to directly see each neuron's synapses and dendrites (connections to other neurons). This level of detail also includes the ability to image, directly and indirectly (via molecular probes), many elements of the "synaptome," the number and types of special proteins (vesicles, signaling proteins, cytoskeleton), receptors (Glutamate, etc.), and neurotransmitters (at least six types in human neurons) that are known to be involved in long-term learning and memory at each synapse in the brain, and elements of the "epigenome" (learning-based DNA methylation and histone modifications) in the nucleus of each neuron. It remains an open question in neuroscience exactly which features of the synaptome and epigenome need to be preserved to retain memory and identity in each species. We know simpler connectomes, synaptomes, and epigenomes are used in organisms with simpler memories (C. elegans, Drosophila, Aplysia, etc.), and that the vast majority of neural molecules are not involved in learning and memory, but support other cell functions necessary for life. Chemical fixation and cryonics both preserve the fats, proteins, sugars, and DNA in living neurons, and fix them effectively in place, and relevant membrane receptors stay in their normal distributions as well, as verified by antibody probes. What we don't know yet is if this happens reliably everywhere during whole brain chemical and cryonic preservation. We also don't know the full complement of small molecules and cytoskeletal features in our neurons and glia that are necessary to memory and identity, and which molecular signal states (eg., phosphorylation, methylation) are important. But our knowledge of the molecular basis of learning and memory continues to rapidly grow, aided by exciting new neuroscience techniques (optogenetics, viral tagging, protein microarrays, etc.). Our ability to scan and verify is also rapidly improving. New types of electron microscopy, such as Cryo-TEM, can image at an amazing 3 angstrom resolution, 50 times greater magnification than FIBSEM, a scale where brain proteins and even individual atoms can be directly seen.

Our current Brain Preservation Technology Prize is focused on the connectome, imaged at FIBSEM resolution. As neuroscience advances, we may learn that certain features of the synaptome and epigenome not presently observable by FIBSEM must also be preserved. In that case, the Brain Preservation Foundation will offer additional Technology prizes, and make use of other verification methods and even higher resolution imaging if necessary. Bottom line: As neuroscience continues to advance, BPF will do our best to help science to determine whether reliable and affordable protocols can be found to preserve those brain structures that give rise to our memories and identities, according to our best evidence to date."
http://brainpreservation.org
Not possible in Quantum Archaeology:

Controlling Genes With Light: New Technique
July 23, 2013 — "New technique can rapidly turn genes on and off, helping scientists better understand their function.
Although human cells have an estimated 20,000 genes, only a fraction of those are turned on at any given time, depending on the cell's needs -- which can change by the minute or hour."

Old systems:



the classic primer
Light gene therapy is much cheaper and simpler.
Light is shone directly on the genes and alters them.
It may be possible to do this non-invasively and for the whole body at once evenually.
Julia36
24 Jul 2013
Better pictures from 1 1/2 BILLION kilometres out:

"NASA's Cassini spacecraft has discovered the best evidence yet for a large-scale saltwater reservoir beneath the icy crust of Saturn's moon Enceladus."

Latest Images:
http://www.nasa.gov/cassini

"NASA's Cassini spacecraft has discovered the best evidence yet for a large-scale saltwater reservoir beneath the icy crust of Saturn's moon Enceladus."

Latest Images:
http://www.nasa.gov/cassini
Julia36
24 Jul 2013
World Archaeology Day 2013 invites everyone to dig in
Takes place July 26 2013. Visit dayofarchaeology.com or register to take part.
nearly 7,000 years ago the ancient tombs of
Barnenez


Oldest man-made buildings. Located in northern Finistère and partially restored. According to André Malraux it would have been better named ‘The Prehistoric Parthenon’. The structure are 72 m long, 25 m wide and over 8 m high.[2][3][4] wiki


Artefacts found increase the Archaeological Record and help complete the Quantum Archaeological Grid, from which all dead people will be resurrected as computing accelerates
see
Reference Article on QA
Edited by Innocent, 24 July 2013 - 12:37 AM.
Takes place July 26 2013. Visit dayofarchaeology.com or register to take part.
nearly 7,000 years ago the ancient tombs of
Barnenez
Oldest man-made buildings. Located in northern Finistère and partially restored. According to André Malraux it would have been better named ‘The Prehistoric Parthenon’. The structure are 72 m long, 25 m wide and over 8 m high.[2][3][4] wiki

Artefacts found increase the Archaeological Record and help complete the Quantum Archaeological Grid, from which all dead people will be resurrected as computing accelerates
see
Reference Article on QA
Edited by Innocent, 24 July 2013 - 12:37 AM.
Julia36
24 Jul 2013
Clarke's Three Laws are three "laws" of prediction formulated by the British writer Arthur C. Clarke. They are:
- When a distinguished but elderly scientist states that something is possible, he is almost certainly right. When he states that something is impossible, he is very probably wrong.
- The only way of discovering the limits of the possible is to venture a little way past them into the impossible.
- Any sufficiently advanced technology is indistinguishable from magic.
Julia36
24 Jul 2013


the scale move from nano to quantum may be very fast because machine intelligence will be doing it from 2022
Russia Pioneering Quantum Technologies
MOSCOW -- "This week's International Conference on Quantum Technologies (ICQT) features an all-star cast of quantum researchers, "
Great to see Quantum Communication's listed because signalling should be instant, translational, and free.

from Seth Lloyd, the self-proclaimed quantum mechanic who popularized quantum technology in his book Programming the Universe, to Nicholas Gisim, the founder of first successful quantum computing company, ID Quantique.
"The universe is nothing more than a giant quantum computer," Lloyd, who directs MIT's Center for Extreme Quantum Information Theory, told us. "And once we fully understand the physics necessary to build our own quantum computers, we will be able to create extremely accurate models of anything in the universe."

The Russian Federation's aim is nothing less than to catapult itself to the forefront of quantum technology through its Russian Quantum Center (RQC), a project of the government-sponsored Russian Innovation Hub (Skolkovo Foundation).
July 21st
"Researchers at the University of Calgary recently made a significant step forward in this direction by creating a large system that is in two substantially different states at the same time. Until this point, scientists had only managed to recreate quantum effects on much smaller scales."
""We are still very far from being able to do this with a real cat," he says. "But this result suggests there is ample opportunity for progress in that direction." said researchers
http://www.scienceda...30721161710.htm

Who wins computing wins the galaxy.
Julia36
24 Jul 2013
York launches first hologram city app
"The new technology, called UltraReality, recognises locations to automatically trigger performances of people anchored to the spot. Once the holograms have completed their performance, they can be photographed alongside the app user or their friends, and the shots can be emailed or posted on twitter or facebook."

"
Cleverbot and the Talking Holograms of the Future
In "Nirvana," a short story by Pulitzer winner Adam Johnson appearing in the newest issue of Esquire, a programmer codes an interactive 3D hologram of the president of the United States. Is it possible?
"
Carpenter is the mind behind Cleverbot, an online chat program that might be the closest thing we have today to a hologram that could talk back. Its humanlike dialogue moves beyond nifty into the Turing test gray zone of eerie. (Alan Turing, the father of computer science and AI, said himself that any computer that could successfully converse with a person—without giving away it wasn't human—could be considered 'intelligent.' Cleverbot passed this test in an official 2011 competition.)
Esquire Fact-or-Fiction: Cleverbot and the Talking Holograms of the Future - Popular Mechanics
It only seems fitting that Michael Jackson, the man who brought the world “Thriller,” was resurrected on a Las Vegas stage late Thursday night—in the form of a hologram. (Forbes 4 weeks ago)

The accuracy of data is weak but t wont be in the next 14years - it'll be indistinguishable from the real thing.
You wont be able to tell who is a hologram and who isn't. At that point resurrection is logically accomplished.
Julia36
24 Jul 2013
First look into workings of the Neanderthal brain
"BONES. That is all the passing millennia have left us of the Neanderthals and the more elusive Denisovans. Until recently, the main insights gleaned from these bones have been physical: what our cousins might have looked like, for instance, and how they moved. But cutting-edge genetic science is changing that.
We can now see, for the first time, which genes are switched on in humans but were not in Neanderthals and Denisovans, and vice versa. The findings point to subtle differences between our brain structure and function, and theirs.
The research, presented last week at the Society for Molecular Biology and Evolution meeting in Chicago, reveals that after our ancestors split from Neanderthals and Denisovans, they evolved differences in genes connected with cognitive abilities. Many of those genes are associated with mental disorders in modern humans."
To continue reading this article, subscribe to receive access to all of newscientist.com, including 20 years of archive content.
The study indicates what has been long thought that mental illness and intelligence co-evolved.

Neanderthals Talked -- Like Us
It also is a fair assumption that we wiped them out.
But the genetic discoveries make it possible to reconstruct Neaderthall's mind set.
"BONES. That is all the passing millennia have left us of the Neanderthals and the more elusive Denisovans. Until recently, the main insights gleaned from these bones have been physical: what our cousins might have looked like, for instance, and how they moved. But cutting-edge genetic science is changing that.
We can now see, for the first time, which genes are switched on in humans but were not in Neanderthals and Denisovans, and vice versa. The findings point to subtle differences between our brain structure and function, and theirs.
The research, presented last week at the Society for Molecular Biology and Evolution meeting in Chicago, reveals that after our ancestors split from Neanderthals and Denisovans, they evolved differences in genes connected with cognitive abilities. Many of those genes are associated with mental disorders in modern humans."
To continue reading this article, subscribe to receive access to all of newscientist.com, including 20 years of archive content.
The study indicates what has been long thought that mental illness and intelligence co-evolved.

Neanderthals Talked -- Like Us
It also is a fair assumption that we wiped them out.
But the genetic discoveries make it possible to reconstruct Neaderthall's mind set.
Julia36
24 Jul 2013
Oldest European fort in the inland US discovered in Appalachians
PhysOrg

"On July 22, 2013, archeologists announced evidence of the long-suspected Fort San Juan at Joara, after previous excavations revealed European as well as Mississippian artifacts" wiki
"Fort Tells of Spain’s Early Ambitions"
New York Times, 22 July 2013


Although soldiers of the Caroline fort were massacred by Indians, they are likely to be resurrected with their families in about 2027 with the accelerating pace of technology.


We have to recover everyone who's ever lived in history.
Edited by Innocent, 24 July 2013 - 09:08 AM.
PhysOrg
"On July 22, 2013, archeologists announced evidence of the long-suspected Fort San Juan at Joara, after previous excavations revealed European as well as Mississippian artifacts" wiki
"Fort Tells of Spain’s Early Ambitions"
New York Times, 22 July 2013


Although soldiers of the Caroline fort were massacred by Indians, they are likely to be resurrected with their families in about 2027 with the accelerating pace of technology.


We have to recover everyone who's ever lived in history.
Edited by Innocent, 24 July 2013 - 09:08 AM.
Julia36
24 Jul 2013
Spain's Appalachian Outpost - Archaeology Magazine

Julia36
24 Jul 2013
Piles of artifacts are being dug up, mapped analysed and logged.
Thracian Temple Unearthed in Central Bulgaria

"SREDNA GORA, BULGARIA—Archaeologists have discovered a Thracian temple and a sanctuary dedicated to Zeus and Hera in the central region of Bulgaria. The sanctuary of Zeus and Hera dates to the eighth to sixth centuries B.C., and was probably destroyed in the fifth century by Christians who built a church on the site. Pottery fragments and coins have also been recovered."


Zeus
They all join to one another in the
quantum archaeology grid - Google Sites
as enough are found and enough laws of science a complete grid of the past may be possible, deducing things once thought unknowable like human thought.
Archaeological Institute of America
Great resource to see what's going on world wide.
Edited by Innocent, 24 July 2013 - 09:05 AM.
Thracian Temple Unearthed in Central Bulgaria

"SREDNA GORA, BULGARIA—Archaeologists have discovered a Thracian temple and a sanctuary dedicated to Zeus and Hera in the central region of Bulgaria. The sanctuary of Zeus and Hera dates to the eighth to sixth centuries B.C., and was probably destroyed in the fifth century by Christians who built a church on the site. Pottery fragments and coins have also been recovered."

Zeus
They all join to one another in the
quantum archaeology grid - Google Sites
as enough are found and enough laws of science a complete grid of the past may be possible, deducing things once thought unknowable like human thought.
Archaeological Institute of America
Great resource to see what's going on world wide.
Edited by Innocent, 24 July 2013 - 09:05 AM.
Julia36
24 Jul 2013
Gene Therapy Coming of Age?
Scientist-11 Jul 2013
"Using lentiviral vectors to replace mutated genes in blood stem cells, scientists successfully treat two rare diseases apparently without causing harmful side effects.
"Researchers have reported promising results from two gene therapy trials for the treatment of two different rare diseases. The team used lentiviral vectors to swap out faulty genes for working copies in cultures of the patients’ own hematopoietic stem cells (HSCs)—cells that mature into all different types of blood cells—before transfusing the corrected cells back into the patients. In the both trials, 18–32 months after treatment a high precentage of the patients’ blood cells were genetically corrected, and disease progression was arrested."
(-not yet, we're still not expert or comprehensive in identifying errors in genes, relating them to illnesses, and administering gene therapies based on trends and lab work and papers, 2017 will be the age of genetic medicine, where the lame will walk, the blind will see, and some think aging will be halted and reversed. IMO
if that happens there will be explosion in talent as people with experience will be available and knowledge that used to be lost is circulated.
.

By 2027 a land grab for nearest planets which machine intelligence will be able to make habitable may be happening.
Real estate is already being sold on the moon, on Venus and other planets.
Lunar Real Estate For Sale
Entire moons are for sale like phobos:

"Purchasing an entire moon can yield an immediate return on investment."
"Click here to download a .pdf file of NEW pricing for larger properties and planetary moon pricing".
an acre of the moon starts at $2.50 and an entire solar system moon for $25,000.
Ownership security like early settlers is gong to depend on ability to hold it.

Venus

The moon (venus in background)


Saturn

saturn cloud system
As Mars is now known to have has oceans and rivers its climate may be reversible

"Researchers at the California Institute of Technology have analyzed new high-resolution images from the Mars Reconnaissance Orbiter (MRO) and discovered evidence for a delta where a river may once have emptied into an ocean."
Read more: http://www.upi.com/S.../#ixzz2ZxF7BJvC
Edited by Innocent, 24 July 2013 - 09:52 AM.
Lazarus Long
24 Jul 2013
Reading this thread is like reading a graphic novel. Thanks that was fun.
The plot is still developing though.
The plot is still developing though.
Julia36
24 Jul 2013
Cheers. Although I'm playing, I see no scientific reason to think Quantum Archaeology cant be achieved.
Historical information reconstruction past human scales looks certain to be achieved with coming machines.
Better Results than Calorie Restriction Diet
RE: CALORIE RESTRICTION bettered for effectiveness by Intermittent Fasting
ie fasting on one day gorging on the next .
NB this is on rodents, but I bet it;s the same mechanisms in people.
this study was done by US gvmt in 2003:
http://www.ncbi.nlm....cles/PMC156352/
and reported in the BBC docu- film 2013:

Vid:
http://leangainsguid...-1-and-fasting/

Best to read report above, but this is it without graphs
Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake
R. Michael Anson, Zhihong Guo, [...], and Mark P. Mattson
Additional article information
Abstract
Dietary restriction has been shown to have several health benefits including increased insulin sensitivity, stress resistance, reduced morbidity, and increased life span. The mechanism remains unknown, but the need for a long-term reduction in caloric intake to achieve these benefits has been assumed. We report that when C57BL/6 mice are maintained on an intermittent fasting (alternate-day fasting) dietary-restriction regimen their overall food intake is not decreased and their body weight is maintained. Nevertheless, intermittent fasting resulted in beneficial effects that met or exceeded those of caloric restriction including reduced serum glucose and insulin levels and increased resistance of neurons in the brain to excitotoxic stress. Intermittent fasting therefore has beneficial effects on glucose regulation and neuronal resistance to injury in these mice that are independent of caloric intake.
Keywords: caloric restriction‖hippocampus‖insulin‖β-hydroxybutyrate‖ ketosis
Aging refers to the biological changes that occur during a lifetime that result in reduced resistance to stress, increased vulnerability to disease, and an increased probability of death. The rate at which aging occurs is species-specific, suggesting a strong genetic influence. The only environmental variable that has been shown to markedly affect the rate of aging in a wide range of species is caloric intake: Restricting food intake to a level below that which would be consumed voluntarily results in a decrease in the rate of aging and an increase in average and maximum life span (1, 2). Dietary restriction (DR) reduces cancer formation (3, 4) and kidney disease (5) and increases the resistance of neurons to dysfunction and degeneration in experimental models of Alzheimer's and Parkinson's diseases as well as stroke (6–9). Two different DR paradigms have proven effective in increasing life span and disease resistance in rats and mice. In one paradigm animals are provided a daily food allotment that is typically 30–40% less than the ad libitum (AL) consumption of a control population; this limited daily feeding (LDF) paradigm involves a controlled caloric restriction and a corresponding reduction in body weight. In the second paradigm animals are subjected to intermittent (alternate-day) fasting (IF), which in rats results in reduced food intake over time and decreased body weight (10).
Restricting caloric intake causes the restricted population to weigh proportionally less than the AL-fed group. Indeed, weight reduction typically slightly exceeds the degree of food restriction, so that food intake per gram of body weight is reported consistently to be slightly higher in LDF animals than in their AL-fed counterparts (11). Rats and mice usually lose weight when maintained on an IF regimen, although some strains such as C57BL/6 mice may lose little or no weight (12). Both the IF and LDF paradigms are reported to result in dramatic increases in life span in comparison to AL-fed animals (13), but little else is known concerning the similarities and differences in their effects.
It seems reasonable to assume that both LDF and IF paradigms of DR extend life span through a common mechanism. To gain insight into the nature of the underlying mechanism, we compared the effects of LDF and IF diets on several parameters that have been postulated to play a role in the protective effects of DR including body weight, food intake, and fasting levels of serum insulin, glucose, and insulin-like growth factor 1 (IGF-1). In addition, recent studies have shown that rats and mice maintained on an IF regimen exhibit increased resistance of neurons in their brains to insults relevant to the pathogenesis of several different human neurological disorders including epileptic seizures and stroke (6, 8, 14). We therefore performed an experiment to determine whether LDF and IF diets exert similar beneficial effects on neurons in the brain.
Materials and Methods
Animals and Measurements of Body Weight and Food Intake.
Six-week-old C57BL/6 mice were obtained from Charles River Breeding Laboratories, housed in the National Institute on Aging Gerontology Research Center animal colony, and fed a standard NIH-07 diet (Harlan–Teklad, Indianapolis). Food was provided AL until 9 weeks of age. At that time, mice were assigned to one of three groups: AL, fed ad libitum; IF, provided access to food every other day; and LDF, provided with a limited daily food allotment of 60% of that eaten by the AL-fed animals. To control for caloric intake versus periodic food deprivation, a fourth group was added: These pair-fed (PF) mice were provided daily with a food allotment equal to the average daily intake of mice in the IF group. Water was available AL for all groups. The animals were kept in a 12-h light/12-h dark cycle (lights on at 6 a.m. and off at 6 p.m.); food was provided or removed at 10 a.m. Body weight was determined each week on the same day and time. Food intake was measured daily. To keep track of spillage, white bedding was used to allow easy separation of unconsumed food and powder from waste and bedding; spilled food was allowed to dry fully to avoid measurement of wet weight added by urine. Statistical comparisons were made by using ANOVA. All procedures were approved by the National Institute on Aging Gerontology Research Center Animal Care and Use Committee.
Blood Collection and Analyses.
At 29 weeks of age, all mice were fasted for 14 h before blood withdrawal. Blood was removed via intraorbital bleed under isoflurane anesthesia, and serum was isolated. In preliminary studies we found that the glucose concentrations in blood samples from fasted mice collected immediately after the mice succumb to the isoflurane inhalation anesthesia (within 1 min of exposure to the anesthetic) are essentially identical to the glucose concentrations in blood samples from fasted mice killed by decapitation within 10 seconds of removal from their cage. The concentrations of glucose and insulin were determined by using the glucose oxidase method (15) and RIA (16), respectively. IGF-1 concentrations were determined by using an enzyme immunosorbent assay kit (Diagnostic Systems Laboratories, Webster, TX), and β-hydroxybutyrate concentrations were determined by using an assay that measures the oxidation of β-hydroxybutyrate to acetoacetate by using a kit purchased from Sigma. Statistical comparisons were made by using single-factor ANOVA; if significant, pairwise comparisons were made by using a two-tailed t test assuming unequal variance.
Excitotoxin Administration and Quantification of Neuron Damage.
Mice were treated at 30–38 weeks of age. Kainate was injected stereotaxically into the dorsal aspect of the right hippocampus by using the methods described (14). Briefly, mice were anesthetized with Avertin and placed in a stereotaxic head holder, and the skull was exposed along the midline. A convulsant dose of kainate (0.2 μg dissolved in 0.5 μl of PBS, pH 7.2) was injected unilaterally into the dorsal hippocampus (stereotaxic coordinates were 2.0 mm posterior to bregma, 2.4 mm lateral to bregma, and 1.8 mm below the surface of the skull). The contralateral hippocampus of each mouse received an injection of 0.5 μl of PBS. Twenty-four hours after kainate administration, mice were anesthetized with isoflurane and perfused transcardially with saline followed by cold phosphate-buffered 4% paraformaldehyde. Coronal brain sections were cut on a freezing microtome and stained with cresyl violet. Nissl-positive undamaged neurons were counted in three ×40 fields in regions CA3 and CA1. Counts were made in five coronal brain sections per mouse (sections were chosen by unbiased sampling), and the mean number of cells per section was determined such that the value obtained for each animal represents an average total number of neurons counted per section (i.e., sum of six ×40 fields for each hippocampal region). Comparisons of numbers of undamaged neurons in hippocampal regions among treatment groups were made by using ANOVA followed by Scheffé's post hoc and Fisher's tests for pairwise comparisons.
Results and Discussion
By the end of this study, male C57BL/6 mice subjected to IF were consuming essentially the same amount of food in a 48-h period as did those fed AL. On the days they had access to food, the IF mice ate roughly twice as much as did mice fed AL (Fig. (Fig.11a). Mice on the LDF regimen consumed 40% less food as provided: this was reflected in their body weights, which were 49% lower than those of the AL-fed group. In contrast, at the end of the study the body weights of mice maintained on the IF diet or PF on a daily basis were only slightly below those of the AL-fed group (Fig. (Fig.11b). A prominent physiological change that occurs in mammals maintained on reduced-calorie diets is increased insulin sensitivity, which often is reflected in decreased fasting plasma levels of glucose and insulin (17). Fasting serum concentrations of glucose and insulin in mice fed AL in the current study averaged 150 mg/dl and 3,400 pg/ml, respectively (Fig. (Fig.22 a and b). The concentrations of glucose and insulin were decreased significantly, to similar amounts, in mice maintained on either LDF or IF regimens with glucose and insulin concentrations dropping to 100 mg/dl and 700–1,100 pg/ml, respectively (Fig. (Fig.2).2). That similar changes are seen in IF and LDF groups in the current study suggests that despite an overall calorie intake similar to mice fed AL, IF has similar effects on circulating glucose and insulin levels.
Figure 1
Figure 1
Male C57BL/6 mice compensate for periods of fasting by increasing their food intake and gaining weight at rates similar to mice fed AL. Shown are the average daily food intakes (calculated from 14-day intake) (a) and body weights (b) in mice maintained ...
Figure 2
Figure 2
Effects of IF and LDF on serum glucose, insulin, IGF-1, and β-hydroxybutyrate levels. Serum concentrations of glucose (a), insulin (b), IGF-1 ©, and β-hydroxybutyrate (d) were quantified in mice that had been maintained for 20 weeks ...
Levels of circulating IGF-1 were decreased in mice on the LDF diet but increased in mice on the IF diet (Fig. (Fig.22c). These findings are of considerable interest in light of evidence that the insulin signaling pathway is linked to longevity in a variety of species (18), and that IGF-1 levels are reduced in rodents on calorie-restricted diets (19). Because mice on the IF regimen were not calorie-restricted, the difference in IGF-1 levels between the IF and LDF groups suggests a difference in the ways in which IF and caloric restriction influence the growth hormone (GH)–IGF-1 axis and insulin signaling pathways. Because insulin levels were decreased in IF mice to levels even lower than in LDF mice, these two DR regimens reveal a dissociation in the mechanisms regulating IGF-1 and insulin levels. Transgenic rats with reduced levels of GH exhibit a transgene dose-dependent reduction in levels of IGF-1; rats with a moderate reduction in IGF-1 levels live longer, whereas those with a greater decrease in IGF-1 levels have a reduced life span (20). The latter results suggest that there is an optimal level of the GH–IGF-1 axis to maximize survival in mammals. With regard to the neuroprotective effects of IF (see data below and refs. 6–9), studies have reported that IGF-1 signaling is neuroprotective in experimental models of neurodegenerative disorders (21, 22). It will be of considerable interest therefore to determine the mechanisms by which LDF and IF differentially affect IGF-1 levels and insulin signaling and how these changes influence energy metabolism, longevity, and disease resistance.
Fasting is known to result in an increased production of ketone bodies, which can be used as an energy source (23, 24) and are known to provide some protective effects including neuroprotection and resistance to epileptic seizures (25–27). We therefore measured serum levels of β-hydroxybutyrate after an overnight fast in mice that had been maintained on AL, LDF, and IF diets. Mice on the IF diet exhibited a 2-fold increase in the fasting serum concentration of β-hydroxybutyrate compared with mice fed AL (Fig. (Fig.22d). In contrast, the β-hydroxybutyrate concentration of mice on the LDF diet were decreased compared with mice fed AL.
When the excitotoxin kainic acid (KA) is injected into the dorsal hippocampus of mice it induces seizures and damage to pyramidal neurons in regions CA3 and CA1 (14). KA was injected into the dorsal hippocampus of mice that had been maintained for 24 weeks on AL, LDF, and IF diets. All mice exhibited seizures of similar magnitude and duration (data not shown). Mice were killed 24 h after KA administration, tissue sections from their brains were stained with cresyl violet, and the numbers of neurons in regions CA3 and CA1 of each hippocampus were counted. KA caused a marked loss of CA3 and CA1 neurons in mice fed AL. As expected, many neurons in regions CA3 and CA1 of the hippocampus injected with KA degenerated (Fig. (Fig.3).3). There was a significant increase in the survival of CA3 and CA1 neurons in the IF mice compared with mice fed AL (Fig. (Fig.3).3). LDF also protected the CA1 neurons, albeit to a lesser amount than did IF, but did not protect CA3 neurons against KA-induced damage. Interestingly, the mice PF to the IF group also exhibited an increased resistance of CA1 neurons to KA-induced damage relative to either AL-fed or LDF mice. The major difference between the AL-fed and PF groups is that the latter were very slightly restricted early in the study (≈10%). This may imply that there is an optimal level of restriction for neuroprotective effects, a hypothesis that would require further study to verify. The 10% restriction in food intake of mice on the IF regimen may account for the differences between AL-fed and PF mice and also may be a factor in the effects of IF on some physiological parameters in this study.
Figure 3
Figure 3
IF is superior to caloric restriction in protecting hippocampal neurons against excitotoxic injury. Mice that had been maintained for 20 weeks on the indicated diets were subjected to an intrahippocampal injection of the excitotoxin KA; PBS was injected ...
A previous study compared the effects of LDF and IF on life span in male C57BL/6 mice, with the two DR regimens resulting in similar life-span extension despite a clear difference in body weight between the two groups (13). However, food intake was not determined, and it was assumed that the difference in body weight was due to some factor other than caloric intake. The present study establishes that it is the ability of this strain of mice to gorge on days when food is provided that allows them to maintain nearly AL body weight when fed every other day, and they thereby avoid a long-term calorie deficit. That IF feeding was more effective than either LDF or PF in protecting neurons from KA-induced damage demonstrates that the IF-feeding schedule itself is neuroprotective independent of overall caloric intake. In a study of F344 rats Masoro et al. (28) found that when calories are explicitly restricted to 60% of the AL intake, altering meal frequency within a 24-h period neither abrogates nor enhances the effect of the net caloric restriction on life span. Although providing evidence that meal frequency does not alter the ability of caloric restriction to extend life span, that study did not allow a conclusion as to whether IF can increase life span independent of overall calorie intake. The present study suggests that in the absence of explicit restriction, fasting may play a role in at least some of the effects of DR.
Because we did not determine life span in this study, we cannot conclude with certainty that the IF regimen used would extend life span. However, a previous study did establish a life-span-extending effect of the identical IF regimen in the identical strain of mice (12). Moreover, a recent study of mice with adipose tissue-selective disruption of the insulin receptor gene showed that the life span of mice can be increased without a reduction in calorie intake (29). Emerging data from this and other laboratories therefore support future studies to determine whether a reduction in caloric intake is the only dietary method to increase longevity or whether IF without caloric restriction might have beneficial effects as well. Thus, although caloric restriction is one important mechanism underlying the effects of different DR regimens on life span and disease susceptibility, at least some beneficial effects of DR regimens may result from a mechanism other than an overall reduction in calorie intake. One such possible mechanism is stimulation of cellular stress-resistance pathways, which are induced strongly by the IF regimen used in this study (7, 8, 14).
A consistent hormonal response to a decrease in food intake in rodents, nonhuman primates, and humans (30, 31) is a reduction in insulin levels and an increase in insulin sensitivity. We found that mice subjected to IF exhibited decreases in serum levels of glucose and insulin to levels at or below those in mice fed daily but with a 40% reduction in caloric intake. The ability of IF to alter fasting levels of insulin and glucose was independent of overall caloric intake. It has been proposed that some beneficial effects of DR result from decreased blood glucose levels (integrated over time) (2). Glucose levels in the blood, integrated over time, have been postulated to lead to high levels of nonenzymatic glycation, a form of protein damage. Higher fuel availability may also lead to an increased frequency of mitochondrial state-four respiration, with consequent increases in reactive oxygen species production from the mitochondrial respiratory chain. DR has been shown to influence oxyradical production and damage (2) and nonenzymatic glycation (32). The present findings are consistent with a role for glucose in the beneficial effects of IF, because the animals spend a large proportion of their life span in a fasted state. However, it might be predicted that on feeding days, when IF mice gorge on food, their levels of oxyradical production and glycation are much higher than in mice on the LDF regimen. Apparently, confining bouts of high caloric intake to a limited time window with long intervening periods of fasting results in adaptive responses that do not occur when meals are more frequent. Previous studies have shown that there are large changes in respiratory quotient as restricted animals move from ingested to stored fuel (33). It may be that alternating periods of anabolism and catabolism play a mechanistic role in triggering increases in cellular stress resistance and the repair of damaged biomolecules or cells. Recent findings suggest that many of the beneficial effects of IF may result from a cellular stress response induced by the fasted state. For example, it was shown that levels of stress protein chaperones (8, 34) and neurotrophic factors (35) are increased in rats and mice maintained on an IF-feeding regimen. The superior neuroprotective efficacy of IF compared with LDF feeding documented in this study is consistent with enhancement of cellular stress resistance that results from the stress associated with fasting rather than an overall reduction in caloric intake.
Interestingly, although IF and LDF DR regimens had similar effects on insulin and glucose levels, they had different effects on serum IGF-1 levels (increased with IF but decreased with LDF) and serum β-hydroxybutyrate levels (increased with IF but decreased with LDF). Decreased IGF-1 levels have been proposed to contribute to the protective effect of DR against carcinogenesis (36). However, IF also protects against tumor growth (37, 38), suggesting that additional mechanisms must be operative in this beneficial effect of IF. Of particular interest with regard to the cytoprotective effect of IF was the large increase in the levels of β-hydroxybutyrate, a fat-derived fuel used when the carbohydrate supply is limiting. It is well known that utilization of these fuels increases in the fasting state in various tissues including the brain (39). Because mice on the IF regimen weigh a great deal more than mice on the LDF regimen they may have larger adipose reserves and a greater ketogenic response than that of LDF mice. This shift to ketogenesis may play a direct role in the cytoprotective effects of IF, because it has been reported that rats fed a ketogenic diet exhibit increased resistance to seizures (25), and that β-hydroxybutyrate protects neurons in rodent models of Alzheimer's and Parkinson's diseases (27). Ketogenic diets are prescribed for some patients with epilepsy (26) and are also implemented in several popular weight-loss programs (40, 41). The findings of this study suggest that IF can enhance health and cellular resistance to disease even if the fasting period is followed by a period of overeating such that overall caloric intake is not decreased.
The ability of both the IF and LDF paradigms to enhance stress resistance and extend life span provides a useful tool for discerning the mechanism by which DR exerts its effect. If a change such as an altered hormone level is proposed to play a fundamental mechanistic role, it should occur in response to both feeding regimes. Comparison of the two paradigms thus provides opportunities for discerning the mechanisms underlying the modulation of aging rate by DR.
Acknowledgments
We thank Dr. Josephine Egan and the Laboratory of Endocrinology at the National Institute on Aging for measurements of serum glucose and insulin and Dr. Julie Mattison for advice and assistance in blood collection.
Abbreviations
DR
dietary restriction
AL
ad libitum
IF
intermittent fasting
LDF
limited daily feeding
IGF-1
insulin-like growth factor 1
PF
pair-fed
KA
kainic acid
Footnotes
This paper was submitted directly (Track II) to the PNAS office.
Article information
Proc Natl Acad Sci U S A. 2003 May 13; 100(10): 6216–6220.
Published online 2003 April 30. doi: 10.1073/pnas.1035720100
PMCID: PMC156352
Neuroscience
R. Michael Anson,*† Zhihong Guo,* Rafael de Cabo, Titilola Iyun, Michelle Rios, Adrienne Hagepanos, Donald K. Ingram, Mark A. Lane,‡ and Mark P. Mattson§
Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224
*R.M.A. and Z.G. contributed equally to this work.
†Present address: Windward Islands Research Institute and St. George's University, University Centre, Grenada, West Indies.
‡Present address: Merck and Company, Inc., Rahway, NJ 07065.
§To whom correspondence should be addressed at: National Institute on Aging, GRC 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224. E-mail: mattsonm/at/grc.nia.nih.gov.
Edited by Anthony Cerami, The Kenneth S. Warren Institute, Kitchawan, NY, and approved March 25, 2003
Received October 18, 2002
Copyright © 2003, The National Academy of Sciences
This article has been cited by other articles in PMC.
Articles from Proceedings of the National Academy of Sciences of the United States of America are provided here courtesy of National Academy of Sciences
References
1. Masoro E J. Exp Gerontol. 2000;35:299–305. [PubMed]
2. Weindruch R, Sohal R S. N Engl J Med. 1997;337:986–994. [PMC free article] [PubMed]
3. Blackwell B N, Bucci T J, Hart R W, Turturro A. Toxicol Pathol. 1995;23:570–582. [PubMed]
4. Mukherjee P, El-Abbadi M M, Kasperzyk J L, Ranes M K, Seyfried T N. Br J Cancer. 2002;86:1615–1621. [PMC free article] [PubMed]
5. Fernandes G, Yunis E J, Miranda M, Smith J, Good R A. Proc Natl Acad Sci USA. 1978;75:2888–2892. [PMC free article] [PubMed]
6. Bruce-Keller A J, Umberger G, McFall R, Mattson M P. Ann Neurol. 1999;45:8–15. [PubMed]
7. Duan W, Mattson M P. J Neurosci Res. 1999;57:195–206. [PubMed]
8. Yu Z F, Mattson M P. J Neurosci Res. 1999;57:830–839. [PubMed]
9. Zhu H, Guo Q, Mattson M P. Brain Res. 1999;842:224–229. [PubMed]
10. Goodrick C L, Ingram D K, Reynolds M A, Freeman J R, Cider N L. Exp Aging Res. 1983;9:203–209. [PubMed]
11. Masoro E J, Yu B P, Bertrand H A. Proc Natl Acad Sci USA. 1982;79:4239–4241. [PMC free article] [PubMed]
12. Goodrick C L, Ingram D K, Reynolds M A, Freeman J R, Cider N. Mech Ageing Dev. 1990;55:69–87. [PubMed]
13. Ingram D K, Reynolds M A. In: Evolution of Longevity in Animals. Woodhead A D, Thompson K H, editors. New York: Plenum; 1987.
14. Duan W, Guo Z, Mattson M P. J Neurochem. 2001;76:619–626. [PubMed]
15. Telfer Brunton W A, Percy-Robb I W. Clin Chim Acta. 1976;69:131–135. [PubMed]
16. Dalpe-Scott M, Heick H M, Begin-Heick N. Can J Biochem. 1982;60:962–966. [PubMed]
17. Kalant N, Stewart J, Kaplan R. Mech Ageing Dev. 1988;46:89–104. [PubMed]
18. Wolkow C A. Trends Neurosci. 2002;25:212–216. [PubMed]
19. Dunn S E, Kari F W, French J, Leininger J R, Travlos G, Wilson R, Barrett J C. Cancer Res. 1997;57:4667–4672. [PubMed]
20. Shimokawa I, Higami Y, Utsuyama M, Tuchiya T, Komatsu T, Chiba T, Yamaza H. Am J Pathol. 2002;160:2259–2265. [PMC free article] [PubMed]
21. Cheng B, Mattson M P. J Neurosci. 1992;12:1558–1566. [PubMed]
22. Hsieh C C, DeFord J H, Flurkey K, Harrison D E, Papaconstantinou J. Mech Ageing Dev. 2002;123:1229–1244. [PubMed]
23. Mitchell G A, Kassovska-Bratinova S, Boukaftane Y, Robert M F, Wang S P, Ashmarina L, Lambert M, Lapierre P, Potier E. Clin Invest Med. 1995;18:193–216. [PubMed]
24. Vazquez J A, Morse E L, Adibi S A. J Clin Invest. 1985;76:737–743. [PMC free article] [PubMed]
25. Bough K J, Valiyil R, Han F T, Eagles D A. Epilepsy Res. 1999;35:21–28. [PubMed]
26. Gilbert D L, Pyzik P L, Freeman J M. J Child Neurol. 2000;15:787–790. [PubMed]
27. Kashiwaya Y, Takeshima T, Mori N, Nakashima K, Clarke K, Veech R L. Proc Natl Acad Sci USA. 2000;97:5440–5444. [PMC free article] [PubMed]
28. Masoro E J, Shimokawa I, Higami Y, McMahan C A, Yu B P. J Gerontol A Biol Sci Med Sci. 1995;50:B48–B53. [PubMed]
29. Bluher M, Kahn B B, Kahn C R. Science. 2003;299:572–574. [PubMed]
30. Grassi G, Seravalle G, Colombo M, Bolla G, Cattaneo B M, Cavagnini F, Mancia G. Circulation. 1998;97:2037–2042. [PubMed]
31. Lane M A, Ball S S, Ingram D K, Cutler R G, Engel J, Read V, Roth G S. Am J Physiol. 1995;268:E941–E948. [PubMed]
32. Cefalu W T, Bell-Farrow A D, Wang Z Q, Sonntag W E, Fu M X, Baynes J W, Thorpe S R. J Gerontol A Biol Sci Med Sci. 1995;50:B337–B341. [PubMed]
33. Duffy P H, Leakey J E A, Pipkin J L, Turturro A, Hart R W. Environ Res. 1997;73:242–248. [PubMed]
34. Guo Z, Ersoz A, Butterfield D A, Mattson M P. J Neurochem. 2000;75:314–320. [PubMed]
35. Lee J, Seroogy K B, Mattson M P. J Neurochem. 2002;80:539–547. [PubMed]
36. Kari F W, Dunn S E, French J E, Barrett J C. J Nutr Health Aging. 1999;3:92–101. [PubMed]
37. Kritchevsky D. Proc Soc Exp Biol Med. 1990;193:35–38. [PubMed]
38. Siegal I, Liu T L, Neopmuceno N, Gleicher N. Cancer Invest. 1988;6:677–680. [PubMed]
39. Pan J W, Rothman T L, Behar K L, Stein D T, Hetherington H P. J Cereb Blood Flow Metab. 2000;20:1502–1507. [PubMed]
40. Anderson J W, Konz E C, Jenkins D J. J Am Coll Nutr. 2000;19:578–590. [PubMed]
41. Willi S M, Oexmann M J, Wright N M, Collop N A, Key L L., Jr Pediatrics. 1998;101:61–67. [PubMed]
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I BELIEVE supplementing nutrients may extend life even further (I've done them for 20 years)
but have only just started alternate day fasts (600 calories one day..anything the next).
As I dont want to get sick as I age: although if QA works dying doesn't bother me:)
i re-stress people shouldn't postpone cryonic suspension preparations IMO
Edited by Innocent, 24 July 2013 - 10:51 PM.
Historical information reconstruction past human scales looks certain to be achieved with coming machines.
Better Results than Calorie Restriction Diet
RE: CALORIE RESTRICTION bettered for effectiveness by Intermittent Fasting
ie fasting on one day gorging on the next .
NB this is on rodents, but I bet it;s the same mechanisms in people.
this study was done by US gvmt in 2003:
http://www.ncbi.nlm....cles/PMC156352/
and reported in the BBC docu- film 2013:

Vid:
http://leangainsguid...-1-and-fasting/

Best to read report above, but this is it without graphs
Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake
R. Michael Anson, Zhihong Guo, [...], and Mark P. Mattson
Additional article information
Abstract
Dietary restriction has been shown to have several health benefits including increased insulin sensitivity, stress resistance, reduced morbidity, and increased life span. The mechanism remains unknown, but the need for a long-term reduction in caloric intake to achieve these benefits has been assumed. We report that when C57BL/6 mice are maintained on an intermittent fasting (alternate-day fasting) dietary-restriction regimen their overall food intake is not decreased and their body weight is maintained. Nevertheless, intermittent fasting resulted in beneficial effects that met or exceeded those of caloric restriction including reduced serum glucose and insulin levels and increased resistance of neurons in the brain to excitotoxic stress. Intermittent fasting therefore has beneficial effects on glucose regulation and neuronal resistance to injury in these mice that are independent of caloric intake.
Keywords: caloric restriction‖hippocampus‖insulin‖β-hydroxybutyrate‖ ketosis
Aging refers to the biological changes that occur during a lifetime that result in reduced resistance to stress, increased vulnerability to disease, and an increased probability of death. The rate at which aging occurs is species-specific, suggesting a strong genetic influence. The only environmental variable that has been shown to markedly affect the rate of aging in a wide range of species is caloric intake: Restricting food intake to a level below that which would be consumed voluntarily results in a decrease in the rate of aging and an increase in average and maximum life span (1, 2). Dietary restriction (DR) reduces cancer formation (3, 4) and kidney disease (5) and increases the resistance of neurons to dysfunction and degeneration in experimental models of Alzheimer's and Parkinson's diseases as well as stroke (6–9). Two different DR paradigms have proven effective in increasing life span and disease resistance in rats and mice. In one paradigm animals are provided a daily food allotment that is typically 30–40% less than the ad libitum (AL) consumption of a control population; this limited daily feeding (LDF) paradigm involves a controlled caloric restriction and a corresponding reduction in body weight. In the second paradigm animals are subjected to intermittent (alternate-day) fasting (IF), which in rats results in reduced food intake over time and decreased body weight (10).
Restricting caloric intake causes the restricted population to weigh proportionally less than the AL-fed group. Indeed, weight reduction typically slightly exceeds the degree of food restriction, so that food intake per gram of body weight is reported consistently to be slightly higher in LDF animals than in their AL-fed counterparts (11). Rats and mice usually lose weight when maintained on an IF regimen, although some strains such as C57BL/6 mice may lose little or no weight (12). Both the IF and LDF paradigms are reported to result in dramatic increases in life span in comparison to AL-fed animals (13), but little else is known concerning the similarities and differences in their effects.
It seems reasonable to assume that both LDF and IF paradigms of DR extend life span through a common mechanism. To gain insight into the nature of the underlying mechanism, we compared the effects of LDF and IF diets on several parameters that have been postulated to play a role in the protective effects of DR including body weight, food intake, and fasting levels of serum insulin, glucose, and insulin-like growth factor 1 (IGF-1). In addition, recent studies have shown that rats and mice maintained on an IF regimen exhibit increased resistance of neurons in their brains to insults relevant to the pathogenesis of several different human neurological disorders including epileptic seizures and stroke (6, 8, 14). We therefore performed an experiment to determine whether LDF and IF diets exert similar beneficial effects on neurons in the brain.
Materials and Methods
Animals and Measurements of Body Weight and Food Intake.
Six-week-old C57BL/6 mice were obtained from Charles River Breeding Laboratories, housed in the National Institute on Aging Gerontology Research Center animal colony, and fed a standard NIH-07 diet (Harlan–Teklad, Indianapolis). Food was provided AL until 9 weeks of age. At that time, mice were assigned to one of three groups: AL, fed ad libitum; IF, provided access to food every other day; and LDF, provided with a limited daily food allotment of 60% of that eaten by the AL-fed animals. To control for caloric intake versus periodic food deprivation, a fourth group was added: These pair-fed (PF) mice were provided daily with a food allotment equal to the average daily intake of mice in the IF group. Water was available AL for all groups. The animals were kept in a 12-h light/12-h dark cycle (lights on at 6 a.m. and off at 6 p.m.); food was provided or removed at 10 a.m. Body weight was determined each week on the same day and time. Food intake was measured daily. To keep track of spillage, white bedding was used to allow easy separation of unconsumed food and powder from waste and bedding; spilled food was allowed to dry fully to avoid measurement of wet weight added by urine. Statistical comparisons were made by using ANOVA. All procedures were approved by the National Institute on Aging Gerontology Research Center Animal Care and Use Committee.
Blood Collection and Analyses.
At 29 weeks of age, all mice were fasted for 14 h before blood withdrawal. Blood was removed via intraorbital bleed under isoflurane anesthesia, and serum was isolated. In preliminary studies we found that the glucose concentrations in blood samples from fasted mice collected immediately after the mice succumb to the isoflurane inhalation anesthesia (within 1 min of exposure to the anesthetic) are essentially identical to the glucose concentrations in blood samples from fasted mice killed by decapitation within 10 seconds of removal from their cage. The concentrations of glucose and insulin were determined by using the glucose oxidase method (15) and RIA (16), respectively. IGF-1 concentrations were determined by using an enzyme immunosorbent assay kit (Diagnostic Systems Laboratories, Webster, TX), and β-hydroxybutyrate concentrations were determined by using an assay that measures the oxidation of β-hydroxybutyrate to acetoacetate by using a kit purchased from Sigma. Statistical comparisons were made by using single-factor ANOVA; if significant, pairwise comparisons were made by using a two-tailed t test assuming unequal variance.
Excitotoxin Administration and Quantification of Neuron Damage.
Mice were treated at 30–38 weeks of age. Kainate was injected stereotaxically into the dorsal aspect of the right hippocampus by using the methods described (14). Briefly, mice were anesthetized with Avertin and placed in a stereotaxic head holder, and the skull was exposed along the midline. A convulsant dose of kainate (0.2 μg dissolved in 0.5 μl of PBS, pH 7.2) was injected unilaterally into the dorsal hippocampus (stereotaxic coordinates were 2.0 mm posterior to bregma, 2.4 mm lateral to bregma, and 1.8 mm below the surface of the skull). The contralateral hippocampus of each mouse received an injection of 0.5 μl of PBS. Twenty-four hours after kainate administration, mice were anesthetized with isoflurane and perfused transcardially with saline followed by cold phosphate-buffered 4% paraformaldehyde. Coronal brain sections were cut on a freezing microtome and stained with cresyl violet. Nissl-positive undamaged neurons were counted in three ×40 fields in regions CA3 and CA1. Counts were made in five coronal brain sections per mouse (sections were chosen by unbiased sampling), and the mean number of cells per section was determined such that the value obtained for each animal represents an average total number of neurons counted per section (i.e., sum of six ×40 fields for each hippocampal region). Comparisons of numbers of undamaged neurons in hippocampal regions among treatment groups were made by using ANOVA followed by Scheffé's post hoc and Fisher's tests for pairwise comparisons.
Results and Discussion
By the end of this study, male C57BL/6 mice subjected to IF were consuming essentially the same amount of food in a 48-h period as did those fed AL. On the days they had access to food, the IF mice ate roughly twice as much as did mice fed AL (Fig. (Fig.11a). Mice on the LDF regimen consumed 40% less food as provided: this was reflected in their body weights, which were 49% lower than those of the AL-fed group. In contrast, at the end of the study the body weights of mice maintained on the IF diet or PF on a daily basis were only slightly below those of the AL-fed group (Fig. (Fig.11b). A prominent physiological change that occurs in mammals maintained on reduced-calorie diets is increased insulin sensitivity, which often is reflected in decreased fasting plasma levels of glucose and insulin (17). Fasting serum concentrations of glucose and insulin in mice fed AL in the current study averaged 150 mg/dl and 3,400 pg/ml, respectively (Fig. (Fig.22 a and b). The concentrations of glucose and insulin were decreased significantly, to similar amounts, in mice maintained on either LDF or IF regimens with glucose and insulin concentrations dropping to 100 mg/dl and 700–1,100 pg/ml, respectively (Fig. (Fig.2).2). That similar changes are seen in IF and LDF groups in the current study suggests that despite an overall calorie intake similar to mice fed AL, IF has similar effects on circulating glucose and insulin levels.
Figure 1
Figure 1
Male C57BL/6 mice compensate for periods of fasting by increasing their food intake and gaining weight at rates similar to mice fed AL. Shown are the average daily food intakes (calculated from 14-day intake) (a) and body weights (b) in mice maintained ...
Figure 2
Figure 2
Effects of IF and LDF on serum glucose, insulin, IGF-1, and β-hydroxybutyrate levels. Serum concentrations of glucose (a), insulin (b), IGF-1 ©, and β-hydroxybutyrate (d) were quantified in mice that had been maintained for 20 weeks ...
Levels of circulating IGF-1 were decreased in mice on the LDF diet but increased in mice on the IF diet (Fig. (Fig.22c). These findings are of considerable interest in light of evidence that the insulin signaling pathway is linked to longevity in a variety of species (18), and that IGF-1 levels are reduced in rodents on calorie-restricted diets (19). Because mice on the IF regimen were not calorie-restricted, the difference in IGF-1 levels between the IF and LDF groups suggests a difference in the ways in which IF and caloric restriction influence the growth hormone (GH)–IGF-1 axis and insulin signaling pathways. Because insulin levels were decreased in IF mice to levels even lower than in LDF mice, these two DR regimens reveal a dissociation in the mechanisms regulating IGF-1 and insulin levels. Transgenic rats with reduced levels of GH exhibit a transgene dose-dependent reduction in levels of IGF-1; rats with a moderate reduction in IGF-1 levels live longer, whereas those with a greater decrease in IGF-1 levels have a reduced life span (20). The latter results suggest that there is an optimal level of the GH–IGF-1 axis to maximize survival in mammals. With regard to the neuroprotective effects of IF (see data below and refs. 6–9), studies have reported that IGF-1 signaling is neuroprotective in experimental models of neurodegenerative disorders (21, 22). It will be of considerable interest therefore to determine the mechanisms by which LDF and IF differentially affect IGF-1 levels and insulin signaling and how these changes influence energy metabolism, longevity, and disease resistance.
Fasting is known to result in an increased production of ketone bodies, which can be used as an energy source (23, 24) and are known to provide some protective effects including neuroprotection and resistance to epileptic seizures (25–27). We therefore measured serum levels of β-hydroxybutyrate after an overnight fast in mice that had been maintained on AL, LDF, and IF diets. Mice on the IF diet exhibited a 2-fold increase in the fasting serum concentration of β-hydroxybutyrate compared with mice fed AL (Fig. (Fig.22d). In contrast, the β-hydroxybutyrate concentration of mice on the LDF diet were decreased compared with mice fed AL.
When the excitotoxin kainic acid (KA) is injected into the dorsal hippocampus of mice it induces seizures and damage to pyramidal neurons in regions CA3 and CA1 (14). KA was injected into the dorsal hippocampus of mice that had been maintained for 24 weeks on AL, LDF, and IF diets. All mice exhibited seizures of similar magnitude and duration (data not shown). Mice were killed 24 h after KA administration, tissue sections from their brains were stained with cresyl violet, and the numbers of neurons in regions CA3 and CA1 of each hippocampus were counted. KA caused a marked loss of CA3 and CA1 neurons in mice fed AL. As expected, many neurons in regions CA3 and CA1 of the hippocampus injected with KA degenerated (Fig. (Fig.3).3). There was a significant increase in the survival of CA3 and CA1 neurons in the IF mice compared with mice fed AL (Fig. (Fig.3).3). LDF also protected the CA1 neurons, albeit to a lesser amount than did IF, but did not protect CA3 neurons against KA-induced damage. Interestingly, the mice PF to the IF group also exhibited an increased resistance of CA1 neurons to KA-induced damage relative to either AL-fed or LDF mice. The major difference between the AL-fed and PF groups is that the latter were very slightly restricted early in the study (≈10%). This may imply that there is an optimal level of restriction for neuroprotective effects, a hypothesis that would require further study to verify. The 10% restriction in food intake of mice on the IF regimen may account for the differences between AL-fed and PF mice and also may be a factor in the effects of IF on some physiological parameters in this study.
Figure 3
Figure 3
IF is superior to caloric restriction in protecting hippocampal neurons against excitotoxic injury. Mice that had been maintained for 20 weeks on the indicated diets were subjected to an intrahippocampal injection of the excitotoxin KA; PBS was injected ...
A previous study compared the effects of LDF and IF on life span in male C57BL/6 mice, with the two DR regimens resulting in similar life-span extension despite a clear difference in body weight between the two groups (13). However, food intake was not determined, and it was assumed that the difference in body weight was due to some factor other than caloric intake. The present study establishes that it is the ability of this strain of mice to gorge on days when food is provided that allows them to maintain nearly AL body weight when fed every other day, and they thereby avoid a long-term calorie deficit. That IF feeding was more effective than either LDF or PF in protecting neurons from KA-induced damage demonstrates that the IF-feeding schedule itself is neuroprotective independent of overall caloric intake. In a study of F344 rats Masoro et al. (28) found that when calories are explicitly restricted to 60% of the AL intake, altering meal frequency within a 24-h period neither abrogates nor enhances the effect of the net caloric restriction on life span. Although providing evidence that meal frequency does not alter the ability of caloric restriction to extend life span, that study did not allow a conclusion as to whether IF can increase life span independent of overall calorie intake. The present study suggests that in the absence of explicit restriction, fasting may play a role in at least some of the effects of DR.
Because we did not determine life span in this study, we cannot conclude with certainty that the IF regimen used would extend life span. However, a previous study did establish a life-span-extending effect of the identical IF regimen in the identical strain of mice (12). Moreover, a recent study of mice with adipose tissue-selective disruption of the insulin receptor gene showed that the life span of mice can be increased without a reduction in calorie intake (29). Emerging data from this and other laboratories therefore support future studies to determine whether a reduction in caloric intake is the only dietary method to increase longevity or whether IF without caloric restriction might have beneficial effects as well. Thus, although caloric restriction is one important mechanism underlying the effects of different DR regimens on life span and disease susceptibility, at least some beneficial effects of DR regimens may result from a mechanism other than an overall reduction in calorie intake. One such possible mechanism is stimulation of cellular stress-resistance pathways, which are induced strongly by the IF regimen used in this study (7, 8, 14).
A consistent hormonal response to a decrease in food intake in rodents, nonhuman primates, and humans (30, 31) is a reduction in insulin levels and an increase in insulin sensitivity. We found that mice subjected to IF exhibited decreases in serum levels of glucose and insulin to levels at or below those in mice fed daily but with a 40% reduction in caloric intake. The ability of IF to alter fasting levels of insulin and glucose was independent of overall caloric intake. It has been proposed that some beneficial effects of DR result from decreased blood glucose levels (integrated over time) (2). Glucose levels in the blood, integrated over time, have been postulated to lead to high levels of nonenzymatic glycation, a form of protein damage. Higher fuel availability may also lead to an increased frequency of mitochondrial state-four respiration, with consequent increases in reactive oxygen species production from the mitochondrial respiratory chain. DR has been shown to influence oxyradical production and damage (2) and nonenzymatic glycation (32). The present findings are consistent with a role for glucose in the beneficial effects of IF, because the animals spend a large proportion of their life span in a fasted state. However, it might be predicted that on feeding days, when IF mice gorge on food, their levels of oxyradical production and glycation are much higher than in mice on the LDF regimen. Apparently, confining bouts of high caloric intake to a limited time window with long intervening periods of fasting results in adaptive responses that do not occur when meals are more frequent. Previous studies have shown that there are large changes in respiratory quotient as restricted animals move from ingested to stored fuel (33). It may be that alternating periods of anabolism and catabolism play a mechanistic role in triggering increases in cellular stress resistance and the repair of damaged biomolecules or cells. Recent findings suggest that many of the beneficial effects of IF may result from a cellular stress response induced by the fasted state. For example, it was shown that levels of stress protein chaperones (8, 34) and neurotrophic factors (35) are increased in rats and mice maintained on an IF-feeding regimen. The superior neuroprotective efficacy of IF compared with LDF feeding documented in this study is consistent with enhancement of cellular stress resistance that results from the stress associated with fasting rather than an overall reduction in caloric intake.
Interestingly, although IF and LDF DR regimens had similar effects on insulin and glucose levels, they had different effects on serum IGF-1 levels (increased with IF but decreased with LDF) and serum β-hydroxybutyrate levels (increased with IF but decreased with LDF). Decreased IGF-1 levels have been proposed to contribute to the protective effect of DR against carcinogenesis (36). However, IF also protects against tumor growth (37, 38), suggesting that additional mechanisms must be operative in this beneficial effect of IF. Of particular interest with regard to the cytoprotective effect of IF was the large increase in the levels of β-hydroxybutyrate, a fat-derived fuel used when the carbohydrate supply is limiting. It is well known that utilization of these fuels increases in the fasting state in various tissues including the brain (39). Because mice on the IF regimen weigh a great deal more than mice on the LDF regimen they may have larger adipose reserves and a greater ketogenic response than that of LDF mice. This shift to ketogenesis may play a direct role in the cytoprotective effects of IF, because it has been reported that rats fed a ketogenic diet exhibit increased resistance to seizures (25), and that β-hydroxybutyrate protects neurons in rodent models of Alzheimer's and Parkinson's diseases (27). Ketogenic diets are prescribed for some patients with epilepsy (26) and are also implemented in several popular weight-loss programs (40, 41). The findings of this study suggest that IF can enhance health and cellular resistance to disease even if the fasting period is followed by a period of overeating such that overall caloric intake is not decreased.
The ability of both the IF and LDF paradigms to enhance stress resistance and extend life span provides a useful tool for discerning the mechanism by which DR exerts its effect. If a change such as an altered hormone level is proposed to play a fundamental mechanistic role, it should occur in response to both feeding regimes. Comparison of the two paradigms thus provides opportunities for discerning the mechanisms underlying the modulation of aging rate by DR.
Acknowledgments
We thank Dr. Josephine Egan and the Laboratory of Endocrinology at the National Institute on Aging for measurements of serum glucose and insulin and Dr. Julie Mattison for advice and assistance in blood collection.
Abbreviations
DR
dietary restriction
AL
ad libitum
IF
intermittent fasting
LDF
limited daily feeding
IGF-1
insulin-like growth factor 1
PF
pair-fed
KA
kainic acid
Footnotes
This paper was submitted directly (Track II) to the PNAS office.
Article information
Proc Natl Acad Sci U S A. 2003 May 13; 100(10): 6216–6220.
Published online 2003 April 30. doi: 10.1073/pnas.1035720100
PMCID: PMC156352
Neuroscience
R. Michael Anson,*† Zhihong Guo,* Rafael de Cabo, Titilola Iyun, Michelle Rios, Adrienne Hagepanos, Donald K. Ingram, Mark A. Lane,‡ and Mark P. Mattson§
Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224
*R.M.A. and Z.G. contributed equally to this work.
†Present address: Windward Islands Research Institute and St. George's University, University Centre, Grenada, West Indies.
‡Present address: Merck and Company, Inc., Rahway, NJ 07065.
§To whom correspondence should be addressed at: National Institute on Aging, GRC 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224. E-mail: mattsonm/at/grc.nia.nih.gov.
Edited by Anthony Cerami, The Kenneth S. Warren Institute, Kitchawan, NY, and approved March 25, 2003
Received October 18, 2002
Copyright © 2003, The National Academy of Sciences
This article has been cited by other articles in PMC.
Articles from Proceedings of the National Academy of Sciences of the United States of America are provided here courtesy of National Academy of Sciences
References
1. Masoro E J. Exp Gerontol. 2000;35:299–305. [PubMed]
2. Weindruch R, Sohal R S. N Engl J Med. 1997;337:986–994. [PMC free article] [PubMed]
3. Blackwell B N, Bucci T J, Hart R W, Turturro A. Toxicol Pathol. 1995;23:570–582. [PubMed]
4. Mukherjee P, El-Abbadi M M, Kasperzyk J L, Ranes M K, Seyfried T N. Br J Cancer. 2002;86:1615–1621. [PMC free article] [PubMed]
5. Fernandes G, Yunis E J, Miranda M, Smith J, Good R A. Proc Natl Acad Sci USA. 1978;75:2888–2892. [PMC free article] [PubMed]
6. Bruce-Keller A J, Umberger G, McFall R, Mattson M P. Ann Neurol. 1999;45:8–15. [PubMed]
7. Duan W, Mattson M P. J Neurosci Res. 1999;57:195–206. [PubMed]
8. Yu Z F, Mattson M P. J Neurosci Res. 1999;57:830–839. [PubMed]
9. Zhu H, Guo Q, Mattson M P. Brain Res. 1999;842:224–229. [PubMed]
10. Goodrick C L, Ingram D K, Reynolds M A, Freeman J R, Cider N L. Exp Aging Res. 1983;9:203–209. [PubMed]
11. Masoro E J, Yu B P, Bertrand H A. Proc Natl Acad Sci USA. 1982;79:4239–4241. [PMC free article] [PubMed]
12. Goodrick C L, Ingram D K, Reynolds M A, Freeman J R, Cider N. Mech Ageing Dev. 1990;55:69–87. [PubMed]
13. Ingram D K, Reynolds M A. In: Evolution of Longevity in Animals. Woodhead A D, Thompson K H, editors. New York: Plenum; 1987.
14. Duan W, Guo Z, Mattson M P. J Neurochem. 2001;76:619–626. [PubMed]
15. Telfer Brunton W A, Percy-Robb I W. Clin Chim Acta. 1976;69:131–135. [PubMed]
16. Dalpe-Scott M, Heick H M, Begin-Heick N. Can J Biochem. 1982;60:962–966. [PubMed]
17. Kalant N, Stewart J, Kaplan R. Mech Ageing Dev. 1988;46:89–104. [PubMed]
18. Wolkow C A. Trends Neurosci. 2002;25:212–216. [PubMed]
19. Dunn S E, Kari F W, French J, Leininger J R, Travlos G, Wilson R, Barrett J C. Cancer Res. 1997;57:4667–4672. [PubMed]
20. Shimokawa I, Higami Y, Utsuyama M, Tuchiya T, Komatsu T, Chiba T, Yamaza H. Am J Pathol. 2002;160:2259–2265. [PMC free article] [PubMed]
21. Cheng B, Mattson M P. J Neurosci. 1992;12:1558–1566. [PubMed]
22. Hsieh C C, DeFord J H, Flurkey K, Harrison D E, Papaconstantinou J. Mech Ageing Dev. 2002;123:1229–1244. [PubMed]
23. Mitchell G A, Kassovska-Bratinova S, Boukaftane Y, Robert M F, Wang S P, Ashmarina L, Lambert M, Lapierre P, Potier E. Clin Invest Med. 1995;18:193–216. [PubMed]
24. Vazquez J A, Morse E L, Adibi S A. J Clin Invest. 1985;76:737–743. [PMC free article] [PubMed]
25. Bough K J, Valiyil R, Han F T, Eagles D A. Epilepsy Res. 1999;35:21–28. [PubMed]
26. Gilbert D L, Pyzik P L, Freeman J M. J Child Neurol. 2000;15:787–790. [PubMed]
27. Kashiwaya Y, Takeshima T, Mori N, Nakashima K, Clarke K, Veech R L. Proc Natl Acad Sci USA. 2000;97:5440–5444. [PMC free article] [PubMed]
28. Masoro E J, Shimokawa I, Higami Y, McMahan C A, Yu B P. J Gerontol A Biol Sci Med Sci. 1995;50:B48–B53. [PubMed]
29. Bluher M, Kahn B B, Kahn C R. Science. 2003;299:572–574. [PubMed]
30. Grassi G, Seravalle G, Colombo M, Bolla G, Cattaneo B M, Cavagnini F, Mancia G. Circulation. 1998;97:2037–2042. [PubMed]
31. Lane M A, Ball S S, Ingram D K, Cutler R G, Engel J, Read V, Roth G S. Am J Physiol. 1995;268:E941–E948. [PubMed]
32. Cefalu W T, Bell-Farrow A D, Wang Z Q, Sonntag W E, Fu M X, Baynes J W, Thorpe S R. J Gerontol A Biol Sci Med Sci. 1995;50:B337–B341. [PubMed]
33. Duffy P H, Leakey J E A, Pipkin J L, Turturro A, Hart R W. Environ Res. 1997;73:242–248. [PubMed]
34. Guo Z, Ersoz A, Butterfield D A, Mattson M P. J Neurochem. 2000;75:314–320. [PubMed]
35. Lee J, Seroogy K B, Mattson M P. J Neurochem. 2002;80:539–547. [PubMed]
36. Kari F W, Dunn S E, French J E, Barrett J C. J Nutr Health Aging. 1999;3:92–101. [PubMed]
37. Kritchevsky D. Proc Soc Exp Biol Med. 1990;193:35–38. [PubMed]
38. Siegal I, Liu T L, Neopmuceno N, Gleicher N. Cancer Invest. 1988;6:677–680. [PubMed]
39. Pan J W, Rothman T L, Behar K L, Stein D T, Hetherington H P. J Cereb Blood Flow Metab. 2000;20:1502–1507. [PubMed]
40. Anderson J W, Konz E C, Jenkins D J. J Am Coll Nutr. 2000;19:578–590. [PubMed]
41. Willi S M, Oexmann M J, Wright N M, Collop N A, Key L L., Jr Pediatrics. 1998;101:61–67. [PubMed]
++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
I BELIEVE supplementing nutrients may extend life even further (I've done them for 20 years)
but have only just started alternate day fasts (600 calories one day..anything the next).
As I dont want to get sick as I age: although if QA works dying doesn't bother me:)
i re-stress people shouldn't postpone cryonic suspension preparations IMO
Edited by Innocent, 24 July 2013 - 10:51 PM.
Julia36
24 Jul 2013
THEY'VE DONE IT!
Quantum Entanglement Made Visible
MOSCOW -- The co-founder of the first successful quantum technology company claimed this week to have demonstrated macroscopic quantum entanglement,"
NB this is MACRO (BIG) entanglements

"
Schrödinger's 'kittens' made in the lab from photons
"
The rules of quantum mechanics may extend to much larger objects than we thought – and this may have practical uses"
This is a MASSIVE breakthrough

Adult version of this thread:
Reference Article on QA
Quantum Entanglement Made Visible
MOSCOW -- The co-founder of the first successful quantum technology company claimed this week to have demonstrated macroscopic quantum entanglement,"
NB this is MACRO (BIG) entanglements

"
Schrödinger's 'kittens' made in the lab from photons
"
The rules of quantum mechanics may extend to much larger objects than we thought – and this may have practical uses"
This is a MASSIVE breakthrough

Adult version of this thread:
Reference Article on QA
Julia36
25 Jul 2013
Super-organs: building body parts better than nature
"
FANCY a liver that works a little harder? Synthetic DNA circuits inserted into human stem cells could soon allow us to build new organs with unprecedented precision and speed. The circuits can be designed on a computer and assembled from ready-made parts ordered online. The technique could prove an efficient way of making organs for transplant without the worry of rejection, and raises the tantalising possibility that it might one day be possible to upgrade the organs we were born with. Human cells have already been used to create a tiny liver and a set of neurons.
"At the moment, the aim is to normalise cells, but in future, enhancement has to be on the menu," says Chris Mason, a professor of regenerative medicine at University College London, who wasn't involved in the work.
"Everything we have in our bodies is hardwired," says synthetic biologist Patrick Guye at ...
To continue reading this article, subscribe to receive access to all of newscientist.com, including 20 years of archive content."

"
FANCY a liver that works a little harder? Synthetic DNA circuits inserted into human stem cells could soon allow us to build new organs with unprecedented precision and speed. The circuits can be designed on a computer and assembled from ready-made parts ordered online. The technique could prove an efficient way of making organs for transplant without the worry of rejection, and raises the tantalising possibility that it might one day be possible to upgrade the organs we were born with. Human cells have already been used to create a tiny liver and a set of neurons.
"At the moment, the aim is to normalise cells, but in future, enhancement has to be on the menu," says Chris Mason, a professor of regenerative medicine at University College London, who wasn't involved in the work.
"Everything we have in our bodies is hardwired," says synthetic biologist Patrick Guye at ...
To continue reading this article, subscribe to receive access to all of newscientist.com, including 20 years of archive content."

Julia36
25 Jul 2013
Scientists Generate Database to Reconstruct Fingers from Drawings
- If we cant bring Da Vinci back for 14 years..at least we can resurrect his finger.
"The fingers of thousands of people who created sketches of Brad Pitt and Angelina Jolie on their iPhones can collectively guide and correct the drawing strokes of subsequent touchscreen users in a new application created by researchers."


Knowing Da Vinci he probably used his toes
Edited by Innocent, 25 July 2013 - 12:15 AM.
- If we cant bring Da Vinci back for 14 years..at least we can resurrect his finger.
"The fingers of thousands of people who created sketches of Brad Pitt and Angelina Jolie on their iPhones can collectively guide and correct the drawing strokes of subsequent touchscreen users in a new application created by researchers."


Knowing Da Vinci he probably used his toes
Edited by Innocent, 25 July 2013 - 12:15 AM.
Julia36
25 Jul 2013
'Dead' Gene Comes to Life
"July 23, 2013 — A gene long presumed dead comes to life under the full moon of inflammation, Stanford University School of Medicine scientists have found."

"July 23, 2013 — A gene long presumed dead comes to life under the full moon of inflammation, Stanford University School of Medicine scientists have found."

Julia36
25 Jul 2013
Scientists reach holy grail in label-free cancer marker detection: Single molecules
These accelerating breakthroughs are not going to stop. They aren't going to slow down. They aren't going to stay the same:
"months after setting a record for detecting the smallest single virus in solution, researchers at the Polytechnic Institute of New York University (NYU-Poly) have announced a new breakthrough: They used a nano-enhanced version of their patented microcavity biosensor to detect a single cancer marker protein, which is one-sixth the size of the smallest virus, and even smaller molecules below the mass of all known markers. This achievement shatters the previous record, setting a new benchmark for the most sensitive limit of detection"

Edited by Innocent, 25 July 2013 - 12:37 AM.
These accelerating breakthroughs are not going to stop. They aren't going to slow down. They aren't going to stay the same:
"months after setting a record for detecting the smallest single virus in solution, researchers at the Polytechnic Institute of New York University (NYU-Poly) have announced a new breakthrough: They used a nano-enhanced version of their patented microcavity biosensor to detect a single cancer marker protein, which is one-sixth the size of the smallest virus, and even smaller molecules below the mass of all known markers. This achievement shatters the previous record, setting a new benchmark for the most sensitive limit of detection"

Edited by Innocent, 25 July 2013 - 12:37 AM.




