Lasers Could Help Identify Malaria and Other Diseases Early.

Combining lasers with a principle discovered by Alexander Graham Bell over 100 years ago, researchers have developed a new way to collect high-resolution information about the shape of red blood cells. Because diseases like malaria can alter the shape of the body’s cells, the device may provide a way to accurately diagnose various blood disorders.

The study relies on a physical principle, known as “the photoacoustic effect,” originally discovered by Bell in 1880. The famed inventor observed that when a material absorbs light from a pulsing light source, it produces sound waves. Since then, scientists have learned that the effect occurs because the object heats up as it absorbs light; the heat causes the object to expand, and this physical change leads to the emission of sound waves.

Today, researchers can induce the photoacoustic effect by using lasers. The most advanced lasers can pulse in the nanosecond range (once every 100 of nanoseconds), generating sound waves from cells and tissues that are at very high frequencies. The higher the frequency, the more information scientists are able to glean about the shape of the object.

Michael Kolios, a photoacoustics scientist at Ryerson University in Toronto, wondered whether he could use the photoacoustic effect to determine the shape of red blood cells. His team developed a laser that pulses every 760 nanoseconds to induce red blood cells to emit sound waves with frequencies of more than 100MHz, one of the highest frequencies ever achieved. Testing the laser on blood samples collected from a group of human volunteers, Kolios and colleagues showed that the high-frequency sound waves emitted by red blood cells in the blood samples revealed the tiniest details about the cells’ shapes. The approach could accurately distinguish samples from a person with malaria, which is characterized by the swelling of red blood cells, from samples from a person with sickle cell anemia, in which the red blood cells distort into a serrated crescent shape, the team reports today in the Biophysical Journal.

The method requires as few as 21 red blood cells. Standard blood tests, in contrast, need more than one drop of blood, and red blood cells need to be analyzed manually by pathologists with a microscope, a task that is slow and prone to human error. The faster diagnosis with Kolios’s technology allows doctors to quickly determine whether the donor’s blood is disease-free immediately prior to blood transfusion. The speed of the approach outperforms standard blood tests by hours, a key advantage for life-saving blood transfusions where every second counts.

Kolios hopes to bring this new device into the clinic. But Nicholas Au, a hematopathologist at the Women’s and Children’s Hospital of British Columbia in Vancouver, says the new technique cannot replace the standard blood test, which reveals more information about the shape of white blood cells and platelets. The shape change in these cells is indicative of diseases like cancer or clotting disorders. Kolios’ team’s method works best with red blood cells because of their biconcave shape, which gives them the unique ability to absorb light better than platelets and white blood cells.

Still, Kolios’ technology holds enormous promise, says Li Hong Wang, a photoacoustics scientist of Washington University in St. Louis. “What’s exciting is the potential application of this method in identifying not only abnormal red blood cells, but also circulating tumor cells,” he says. The latter could be done, he notes, with a pulsing ultraviolet laser, which could accurately measure the amount of a light-absorbing pigment (known as melanin) inside cells using sound waves, allowing scientists to identify circulating tumor cells based on their abnormally high melanin content. While Kolios’s device could be costly, with a price tag of $100,000 for just the laser, Wang is optimistic that the price would go down in light of the growing biomedical demand.



Magnetic fields and the science of biblical creation.

The exponential decay of planetary magnetic fields is one of the strongest scientific arguments that supports the young age of the earth and the solar system. As such it is no surprise that skeptics attack this idea. D.O. from the United States writes concerning some such objections:


Hello Dr. Sarfati:
I have a couple of questions about Humphreys’s rapid decay model of Earth’s magnetic field. I couldn’t find anything on the CMI website that directly addresses these questions, but I apologize if I missed them.

One evolutionist I am debating argued that Lenz’s law implies that nature resists a change in magnetic flux. He used the example of “suddenly turn[ing] on a magnetic field going through a conducting loop, the loop will generate a current to form a magnetic field in the opposite direction to try and keep a magnetic flux of zero.” He says that “changing a magnetic flux generates an electromotive force that tries to oppose the change in flux” and used that to argue that fluctuation is much more likely than exponential decay when it comes to Earth’s magnetic field. Is his argument valid at all?

Also, is it true that if the magnetic field strength of the earth is decaying, its rotation speed must be increasing over time, to conserve angular momentum?

Thanks for your time and help.

Such systems will decay exponentially, as is well known in physics.

CMI’s Dr Jonathan Sarfati responds:

Hi Mr O.

Thank you for asking.

This evo really doesn’t know what he’s talking about. Yes, there is such a thing as Lenz’s Law, which states that an induced current is always in such a direction as to oppose the motion or change causing it. But it will not overcompensate the way he is claiming. Rather, the induced current is caused by the field decay, so it will be in the direction of the original field. The decay is a negative of the original, so the induced field will be a positive. But it will never be as great (otherwise a perpetual motion machine would be possible, and this violates the second law of thermodynamics). Thus such systems will decay exponentially, as is well known in physics (as explained in my article The earth’s magnetic field: evidence that the earth is young).

As for the second question, there doesn’t seem to be a connection, because the field has no mass, while angular momentum involves mass.

Hope this helps.

Thank you for your response, it was very helpful. Regarding the second question, I understand what you mean about angular momentum, but the reason I asked it is the evolutionist I was debating said that “a magnetic field is angular momentum density,” and then went on to say that if the magnetic field was decaying, the angular momentum would have to “go somewhere” and would cause an increase in the rotation speed of earth. Is there such a connection between the magnetic field and angular momentum?

Hi again

OK, then ask this critic some questions. We know that the rotational angular momentum of the earth (L0) is given by its angular velocity (ω) times its moment of inertia, which to a good approximation is given by the formula for a solid uniform sphere (I = 2 /5 Mr2 ). See more at Slipshod logic in Creation for Kids? (scroll down a fair way). OK, so what is his formula for the angular momentum of the magnetic field? Let him prove that it would cause a measurable slowdown by working it out quantitatively (if he can even find a formula).

Hope this helps.

Thank you for your insight. I asked the evolutionist what formula he would use for the angular momentum of the earth’s magnetic field, and he said:

“You haven’t had any actual education in electricity and magnetism, have you? A magnetic field is angular momentum density. It’s given by c^-2(r x (E x H) ) r, E, and H being the vectors of the position, electric field, and magnetic field, respectively. Where would the angular momentum go [in Humphreys’s model of magnetic field decay]?” I also found a website that discusses this formula. What am I missing?

The evolutionist also claimed that Lenz’s law would imply that “the nature of magnetism is oscillatory because Nature Abhors A Change In Flux,” and that the correct graph for Humphreys’s model would be a “damped oscillator” rather than an exponential curve. Is this correct?

By the way, I am granting permission to publish any of our email exchange on the CMI website if you wish to, I would just ask that you use my initials and not my full name if you decide to do so.

Hi again

This formula is not relevant to what is being discussed here.

Exponential decay is a very well-known phenomenon, and the way it works here would not be a damped oscillator. Rather, Dr Humphreys himself has written an update in the CRSQ this year, and the main phenomenon is exponential decay (so where would angular momentum go in a typical RI circuit), as per the laws of electromagnetism. There is a small sinusoidal component, which doesn’t affect the long-term energy loss, but nothing like a damped oscillator.


Jonathan Sarfati




Microscopic ‘Tuning Forks’ Could Make the Difference Between Life and Death in the Hospital.

A patient admitted to a hospital with a serious bacterial infection may have only a few hours to live. Figuring out which antibiotic to administer, however, can take days. Doctors must grow the microbes in the presence of the drugs and see whether they reproduce. Rush the process, and they risk prescribing ineffective antibiotics, exposing the patient to unnecessary side effects, and spreading antibiotic resistance. Now, researchers have developed a microscopic “tuning fork” that detects tiny vibrations in bacteria. The device might one day allow physicians to tell the difference between live and dead microbes—and enable them to recognize effective and ineffective antibiotics within minutes.


“It’s a brilliant method,” provided subsequent investigations confirm the researchers’ interpretation of their data, says Martin Hegner, a biophysicist at Trinity College Dublin who was not involved in the work.

The research involves tiny, flexible bars called cantilevers that vibrate up and down like the prongs of a tuning fork when they receive an input of energy. Cantilevers are an important part of atomic force microscopy, which is useful for making atomic scale resolutions of surfaces for use in nanotechnology or atomic physics research. In this technique, a minute needle attached to a cantilever moves across a surface, and the deflection of the cantilever gives information about how atoms are arranged on the surface. It can even be used to shunt atoms around. More recently, however, they have been used without the needle as tiny oscillators, allowing scientists to investigate matter directly attached to the cantilever.

Biophysicist Giovanni Longo and colleagues at the Swiss Federal Institute of Technology in Lausanne and the University of Lausanne in Switzerland immersed these cantilevers in a liquid bacterial growth medium and monitored their movement using a laser. They found that the bare cantilever moved very slightly as a result of the thermal movement of the liquid molecules in the medium. They then covered both sides of the cantilever withEscherichia coli bacteria, which can cause food poisoning, and immediately found that the oscillations became much more pronounced. The researchers believe that chemical processes that occur inside the bacteria as they metabolize energy are driving the oscillation. “What we see is that if you have some sort of a moving system on the cantilever, you are going to induce a movement on the cantilever itself,” Longo explains. “Exactly what kind of metabolic movement we see is something that we are still studying.”

To determine if the cantilevers could detect the impact of drugs, the team added ampicillin, an antibiotic that the cultured bacteria were sensitive to. The size of the cantilever’s oscillations decreased almost 20-fold within 5 minutes, the researchers report online today in Nature Nanotechnology. Fifteen minutes later, the scientists flushed the antibiotic out with fresh growth medium, but the movement of the cantilever did not increase again. This, the researchers say, suggests that the antibiotic had killed the bacteria. When they used an ampicillin-resistant strain of E. coli, however, they found that the oscillations initially decreased but returned to normal within about 15 minutes, indicating that the microbes had recovered.

Hegner cautions that the research is still “basic science. … It’s not yet an applied tool which is robust enough to be used in an ER or something.” That, he says, might take another 5 or 10 years.

Before that happens, Hegner says, researchers need to determine what the sensors are picking up and whether that signal can be conclusively linked to the bacteria and their antibiotic resistance. They also need to find out if properties of the medium affect the results, he says. “If you inject a bacterium into a medium with different viscosity and different density, this also might affect the vibration of the sensor.”

The Swiss researchers are continuing to investigate clinical applications of their system. They have recently obtained access to a more secure lab licensed to handle highly pathogenic bacteria and are working on confirming their results in these microbes. They are also thinking beyond the clinic. “Our dream is to send something like this to Mars to see if there is life,” Longo says. “It’s much faster than any other technique one can imagine—you just put some of the martian dirt inside the liquid and whatever attaches to the cantilever, if it moves it’s alive.”


Fat Cells Feel the Cold, Burn Calories for Heat.

Transforming fat cells into calorie-burning machines may sound like the ultimate form of weight control, but the idea is not as far-fetched as it sounds. Unexpectedly, some fat cells directly sense dropping temperatures and release their energy as heat, according to a new study; that ability might be harnessed to treat obesity and diabetes, researchers suggest.


Fat is known to help protect animals from the cold—and not only by acting as insulation. In the early 1990s, scientists studying mice discovered that cold temperatures trigger certain fat cells, called brown adipose tissue, to release stored energy in the form of heat—to burn calories, in other words. Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston. The activation of brown fat seems to start with sensory neurons throughout the body informing the brain of a drop in temperature. In response the brain sends out norepinephrine, the chief chemical messenger of the sympathetic nervous system, which mobilizes the body to cope with many situations. In experimental animals, stimulating norepinephrine receptors triggered brown adipose tissue to release its energy and generate heat, while animals bred to be missing these receptors were unable to mount the same fat cell response.

People also have brown adipose tissue that generates heat when the body is cold. And unlike white fat, which builds up around the abdomen and contributes to many disorders including heart disease and diabetes, this brown fat is found in higher proportions in leaner people and seems to actively protect against diabetes.

In brown fat, the heat-generating process depends on a protein called UCP1; the protein is also thought to be central in brown fat’s ability to prevent diabetes. Researchers are now exploring ways of activating this molecular pathway. But in trying to figure out exactly how fat cells respond to the body being cold, Spiegelman and colleagues discovered that plain old “white” fat cells have a few surprises left. In a study appearing online today in the Proceedings of the National Academy of Sciences, the researchers exposed various kinds of fat cells to cold temperatures directly. “We were a little surprised that no one had tried this before,” Spiegelman says.

The researchers cooled several types of lab-grown human fat cells—brown, white and “beige” (white adipose tissue with some brown cells mixed in)—to temperatures between 27˚ and 39˚C for four hours, eight hours, or up to ten days. White fat cells and beige cells responded to cooling in dramatic fashion. In these cells, levels of the UCP1 were doubled by 8 hours after the treatment. The change in UCP1 also proved to be reversible: Its levels returned to normal once the cells’ temperature was lowered to 37 degrees. But in brown fat cells, no induction of the protein was observed, indicating that cold temperatures don’t mobilize these cells by flipping this particular switch.

The researchers also found that white fat cells obtained from mice lacking receptors for norepinephrine were still able to respond to cooling by turning on UCP1—showing that the heat-generating pathway is both specific to those fat cells and independent of the sympathetic nervous system .

The finding won’t lead to an antifat pill any time soon, Spiegelman says, but it does give scientists new avenues to explore. “It’s a piece of the basic science, adding to an evolving awareness that fat cells have many lives that we never knew about. Now we know they can sense temperature directly. The next question is, how do they do it, and can that ability be manipulated?”

“The paper is filling in an emerging picture that adipose tissue can be a more flexible, adaptive organ than we once thought,” says Sven Enerbäck, a physician and adipose tissue researcher at the University of Gothenburg in Sweden. “The finding raises the question of whether this new pathway has widespread effects on the animal as a whole.”

Finding that white fat cells directly detect and react to cold is a surprising development, notes cell biologist Peter Tontonoz of the University of California, Los Angeles, because it shows that the sympathetic nervous system isn’t the whole story when it comes to heat generation by adipose tissue. He’s curious whether the heat-generating pathway in white fat is a routine part of everyday temperature regulation. “Even if it isn’t,” he adds, “it could still be targeted by small molecules or other drugs.”




Cholera is Altering the Human Genome.

Cholera kills thousands of people a year, but a new study suggests that the human body is fighting back. Researchers have found evidence that the genomes of people in Bangladesh—where the disease is prevalent—have developed ways to combat the disease, a dramatic case of human evolution happening in modern times.


Cholera has hitchhiked around the globe, even entering Haiti with UN peacekeepers in 2010, but the disease’s heartland is the Ganges River Delta of India and Bangladesh. It has been killing people there for more than a thousand years. By the time they are 15 years old, half of the children in Bangladesh have been infected with the cholera-causing bacterium, which spreads in contaminated water and food. The microbe can cause torrential diarrhea, and, without treatment, “it can kill you in a matter of hours,” says Elinor Karlsson, a computationalgeneticist at Harvard and co-author of the new study.

The fact that cholera has been around so long, and that it kills children—thus altering the gene pool of a population—led the researchers to suspect that it was exerting evolutionary pressure on the people in the region, as malaria has been shown to do in Africa. Another hint that the microbe drives human evolution, notes Regina LaRocque, a study co-author and infectious disease specialist at Massachusetts General Hospital, Boston, is that many people suffer mild symptoms or don’t get sick at all, suggesting that they have adaptations to counter the bacterium.

To tease out the disease’s evolutionary impact, Karlsson, LaRocque, and their colleagues, including scientists from the International Centre for Diarrhoeal Disease Research in Bangladesh, used a new statistical technique that pinpoints sections of the genome that are under the influence of natural selection. The researchers analyzed DNA from 36 Bangladeshi families and compared it to the genomes of people from northwestern Europe, West Africa, and eastern Asia. Natural selection has left its mark on 305 regions in the genome of the subjects from Bangladesh, the team reveals online today in Science Translational Medicine.

The researchers bolstered the case that cholera was the driving force behind the genomic changes by contrasting DNA from Bangladeshi cholera patients with DNA from other residents of the country who remained healthy despite living in the same house as someone who fell ill with the disease. Individuals who were susceptible to cholera typically carried DNA variants that lie within the region that shows the strongest effect from natural selection.

One category of genes that is evolving in response to cholera, the researchers found, encodes potassium channels that release chloride ions into the intestines. Their involvement makes sense because the toxin spilled by the cholera bacterium spurs such channels to discharge large amounts of chloride, leading to the severe diarrhea that’s characteristic of the disease.

A second category of selected genes helps manage the protein NF- kB, the master controller of inflammation, which is one of the body’s responses to the cholera bacterium. A third category involves genes that adjust the activity of the inflammasome, a protein aggregation inside our cells that detects pathogens and fires up inflammation. However, the researchers don’t know what changes natural selection promotes in these genes to strengthen defenses against the cholera bacterium.

Researchers have identified other examples of infectious diseases driving human evolution, such as malaria in Africa favoring the sickle cell allele, a gene variant that provides resistance to the illness. But they are just starting to search the entire genome for signs of disease effects, and this study is the first to use such methods for cholera.

“I think it’s a great example of the impact infectious diseases have had on human evolution,” says infectious disease specialist William Petri of the University of Virginia School of Medicine in Charlottesville, who wasn’t involved with the study. “It’s ambitious, fairly extensive, and very well done,” adds medical microbiologist Jan Holmgren of the University of Gothenburg in Sweden. One strength of the work is that it flags genes, such as those involved with the inflammasome, that researchers have implicated in other intestinal illnesses such as inflammatory bowel disease, says genetic epidemiologist Priya Duggal of the Johns Hopkins Center for Global Health in Baltimore, Maryland. “Overall, they make a very nice case.”

The findings probably won’t lead to new cholera treatments, says LaRocque, because current measures—which rapidly replace the water and electrolytes patients lose—work very well. “The real issue with cholera,” she says, “is how do we prevent it,” a difficult problem in areas without clean water supplies. But understanding how humans have evolved in response to cholera might help researchers devise more potent vaccines that would provide better protection against this killer, she says.



Hypersensitive Wires Feel the (Electromagnetic) Force.

The ability to pack bits of data on computer hard drives has skyrocketed more than 10,000-fold over the past 3 decades. You can now fit more than 100 Hollywood movies on the average machine. One reason has been the steady improvement in sensors used to read and write bits of data in the magnetic materials used to make the disks. Now researchers describe the most powerful such sensing material yet to work at room temperature. The discovery may open the door not just to reading out smaller data bits, but also to a wide range of improved magnetic technologies such as making cheaper touch screen displays.

At the heart of data reading and recording devices is a property called magnetoresistance (MR), in which the electrical resistance of a material changes in response to the presence of an external magnetic field. Turn on a magnetic field, and the material’s ability to carry an electric current skyrockets or plummets in response. Early MR materials changed their resistance only by a few percent at room temperature. Giant magnetoresistive materials discovered in the late 1980s pushed the number up to 110%. And researchers in Japan raised it to 600% in 2002 with the discovery of materials that carry out something called tunnel magnetoresistance. But now all those numbers pale in comparison, as a paper published online today inScience reports that molecular wires are capable of a 2000% magnetoresistance change at room temperature .

Ironically, the new molecular wires aren’t made with magnetic materials at all. Rather, their MR effect relies on the conductivity of nonmagnetic organic dye molecules called DXP, which the Italian automaker Ferrari once used to give their roadsters their trademark red color. Unlike conventional inorganic metals in which electrons zip through a crystalline lattice, in organics electrons must hop from one molecule to another, like pails of water being passed by a bucket brigade. To create a MR, material researchers need to switch off that bucket brigade in the presence of a magnetic field.

In organic materials researchers do this with a little help from quantum mechanics. A tenet of quantum mechanics called the Pauli Exclusion Principle states that no two fermions (particles in a family that includes electrons) can occupy the same quantum state. If two electrons with the same quantum state try to hop onto the same DXP, they can’t. The bucket brigade turns off and resistance skyrockets.

But over the past several years, researchers have found that thin films of DXPs or other organic conductors have an MR well below the competition. The reason for this turned out to be another quantum mechanical property. In addition to carrying a negative electric charge, electrons also carry spin, which can point up or down like a tiny bar magnet. If two electrons have the same spin, they can’t hop on the same DXP together. But if one electron’s spin flips to the opposite direction, then it’s no problem. The two can hop on one DXP together, and the bucket brigade continues.

In their work with films of DXPs and other organics, researchers found that two problems prevented the films from acting like good MR materials. First, thermal fluctuations at room temperature flipped electron spins. And second, even if electrons did share the same spin direction—and were thus blocked from hopping onto the same DXP—they just jumped to a neighbor that wasn’t blocked. “If it’s a 3D film, you can always go around the blockade,” says Markus Wohlgenannt, a physicist at the University of Iowa in Iowa City, whose team was one of the first to discover organic MR materials.

To prevent this runaround, researchers led by Wilfred van der Wiel, a physicist at the University of Twente in the Netherlands sought to arrange the DXPs in straight lines. To do so, they essentially shoved them inside the narrow pores of a zeolite, a lattice-like mineral, in which the confines were so tight the organics had no choice but to line up. They then placed their zeolite atop a conductive surface with the pores facing up and used the tip of an atomic force microscope to make contact with individual DXPs at the top end of single pores. The lineup of DXPs obviously meant that electrons could no longer hop around a blockade. But they also found that even very small magnetic fields were enough to prevent thermal fluctuations from flipping electron spins. And the result was that when electrons encountered blockages, they were unable to work around them, and the resistance of the material shot upwards.

Wohlgenannt calls the new work “a groundbreaking paper.” That said, he adds that it’s not clear if this will lead to higher capacity disc drives. For starters, researchers must first pull off the effect without the use of atomic force microscopes, which aren’t a practical addition to disk drive technology. Researchers will probably also need to figure out ways to push higher electrical currents through the molecular wires to make magnetic sensors that can compete with current technology. But even if the new materials aren’t ideal for making better disk drives, Wohngenannt and van der Wiel say the powerful MR effect might still make them useful for other electronics applications such as pen-based touch screens that are responsive to a magnetic stylus or perhaps even improved magnetic sensors in smart phones that are able to pick up the Earth’s magnetic field and use that for improved navigation.



Where Corn Is King, a New Regard for Grass-Fed Beef.

Story at-a-glance

  • Grass-fed beef represents a sought-after solution to unsustainable agricultural practices – one that could not only drastically reduce pollution but also produce a nutritionally superior meat
  • While far from the norm at this point, a new appreciation for grass-fed meat, and all that it stands for, is steadily growing and these so-called ‘unconventional’ ranchers are now becoming mainstays in the industry
  • Grass-fed beef is higher in certain vitamins and minerals, lower in total fat, and has a more balanced omega-3 to omega-6 ratio than grain-fed beef
  • Grass-fed beef is now widely available via farmer’s markets, food coops, direct farm-to-consumer sales, and even online.
  • grass-fed-cows

In the grand scheme of all that is wrong with modern agriculture, the unnatural transition that turned cattle (which naturally eat grass) into grain-eating ruminants is at the top of the list.

When a cow is left to eat on its own, it doesn’t choose corn or soy to munch on… it selects grass, but in the twisted realm of agribusiness, raising grass-fed cows, especially in the heart of ‘corn country’ (the Midwest) is now regarded as a specialty industry “for the crazies,” as the New York Times recently reported.1

“Where the great cattle herds once roamed, grass finishing — an intricate and lengthy ballet involving the balance of protein and energy derived from the stalk, with the flavor rendered by earth, plants and even stress — is a nearly lost art.

…said Fred Kirschenmann, a distinguished fellow at the Leopold Center for Sustainable Agriculture at Iowa State University… ‘The attitude out there is that grass-fed is for the crazies.’”

Yet, far from being ‘crazy,’ grass-fed beef represents a sought-after solution to unsustainable agricultural practices – one that could not only drastically reduce pollution but also produce a nutritionally superior meat.

While far from the norm at this point, a new appreciation for grass-fed meat, and all that it stands for, is steadily growing and these so-called ‘unconventional’ ranchers are now becoming mainstays in the industry.

Change to the Cattle Industry Must Come ‘From Educated People From the Outside’

Concentrated Animal Feeding Operations (CAFOs), in which the majority of US beef (and pork, chicken and eggs) is raised, contribute directly to global warming by releasing vast amounts of greenhouse gases into the atmosphere – in fact, more than the entire global transportation industry.

They also contribute to climate disruption by their impact on deforestation and draining of wetlands, and because of the nitrous oxide emissions from huge amounts of pesticides used to grow the genetically engineered corn and soy fed to animals raised in CAFOs.

The cows are fattened for slaughter on giant feed lots as quickly as possible (on average between 14 and 18 months) with the help of grains, as CAFOs represent a corporate-controlled system characterized by large-scale, centralized, low profit-margin production, processing and distribution systems.

Contrary to popular arguments, factory farming is not a cheap, efficient solution to world hunger. Feeding huge numbers of confined animals actually uses more food, in the form of grains that could feed humans, than it produces. For every 100 food calories of edible crops fed to livestock, we get back just 30 calories in the form of meat and dairy. That’s a 70 percent loss.

With the Earth’s population predicted to reach 9 billion by mid-century, the planet can no longer afford this reckless, unhealthy and environmentally disastrous farming system. And as Prescott Frost, great-grandson of poet Robert Frost who has entered the grass-fed meat business, told the New York Times:2

“If change is going to come to the cattle industry, it’s got to come from educated people from the outside,” Mr. Frost said, quoting from Allan Nation, the publisher of The Stockman Grass Farmer, considered the grazier’s bible.”

Grass-Fed Beef Is Better for You, Better for the Planet and Better for the Cows

A joint effort between the US Department of Agriculture (USDA) and Clemson University researchers determined a total of 10 key areas where grass-fed is better than grain-fed beef for human health.3 In a side-by-side comparison, they determined that grass-fed beef was:

Lower in total fat Higher in beta-carotene Higher in vitamin E (alpha-tocopherol)
Higher in the B-vitamins thiamin and riboflavin Higher in the minerals calcium, magnesium and potassium Higher in total omega-3s
A healthier ratio of omega-6 to omega-3 fatty acids (1.65 vs 4.84) Higher in CLA (cis-9 trans-11), a potential cancer fighter Higher in vaccenic acid (which can be transformed into CLA)


Another troubling aspect of grain-fed cattle involves the well-being of the animal and, consequently, the health effect this has on you. Common consequences among grain-fed cattle include:4

  1. Acidosis. During the normal digestive process, bacteria in the rumen of cattle produce a variety of acids. Saliva neutralizes the acidity from grass-based diets, but grain-based eating in feedlots prohibits saliva production. The net result is “acid indigestion.”

Animals with this condition are plagued with diarrhea, go off their feed, pant, salivate excessively, kick at their bellies, and eat dirt. Over time, acidosis can lead to a condition called “rumenitis,” an inflammatory response to too much acid and too little roughage and results in inefficient nutrient absorption.

  1. Liver abscesses. From 15 to 30 percent of feedlot cattle have liver abscesses, which result when bacteria may leak out through ulcerated rumen in cattle and are ultimately transported to the liver.
  2. Bloat. During digestion, cows produce gas and when they are on pasture, they belch up the gas without any difficulty. Grain-based feeding causes these gasses to become trapped, and results in bloat. In more serious cases of bloat, the rumen becomes so distended with gas that the animal is unable to breathe and dies from asphyxiation.
  3. Feedlot polio. A highly acidic digestive environment may result in the production of an enzyme called “thiaminase,” which destroys vitamin B1, starving the brain of energy and creating paralysis.
  4. Dust pneumonia. In dry weather, the feedlot can become a dust bowl, which springs the cattle’s immune system into action and keeps it running on a constant basis, ultimately resulting in respiratory ailments and even death.
  1. Virginia farmer Joel Salatin is a living example of how incredibly successful and sustainable natural farming can be. He produces beef, chicken, eggs, turkey, rabbits and vegetables. Yet, Joel calls himself a grass farmer, for it is the grass that transforms the sun into energy that his animals then feed on. By closely observing nature, Joel created a rotational grazing system that not only allows the land to heal but also allows the animals to behave the way the were meant to — expressing their “chicken-ness” or “pig-ness,” as Joel would say.
  2. Cows are moved every day, which mimics their natural patterns and promotes revegetation. Sanitation is accomplished by birds. The birds (chickens and turkeys) arrive three days after the cows leave — via the Eggmobile — and scratch around in the pasture, doing what chickens do best.
  3. No pesticides. No herbicides. No antibiotics. No seed spreading. Salatin hasn’t planted a seed or purchased a chemical fertilizer in 50 years. He just lets herbivores be herbivores and cooperates with nature, instead of fighting it. It’s a different and refreshing philosophy. When cows are raised on a ‘salad bar’ of natural grasses, the meat takes on different flavors that cannot be achieved with grain. Frost told the New York Times:5
  4. “’When the wine industry started out in California, nobody had a language for what a bouquet was,’ Mr. Frost, 55, said. ‘Vintners had to come up with a way an audience could have a conversation about hints of raspberries, of chamomile. And that’s what we have to do with beef.’”
  5. Farming done in this type of sustainable manner can be incredibly profitable, too. Instead of making $150 per acre per year from a crop that produces food for three months, but lays fallow for the rest of the year, Salatin’s making $3,000 per acre by rotating crops throughout the year, thereby making use of his land all 12 months — and maintaining its ecological balance at the same time. This generates complementary income streams for the small farmer and allows them to compete with CAFO operations, while protecting the land from ecological disasters.
  6. Where Can You Find Grass-Fed Beef?
  7. Currently, meat in supermarkets will be labeled 100% grass-fed if it came from pasture, but if it contains no label it’s probably CAFO-raised. In 2013, a new alliance of organic and natural health consumers, animal welfare advocates, anti-GMO and climate-change activists will tackle the next big food labeling battle: meat, eggs and dairy products from animals raised on factory farms, or CAFOs.
  8. This campaign, which aims to have CAFO foods labeled, will start with a massive program to educate consumers about the negative impacts of factory farming on the environment, on human health and on animal welfare, and then move forward to organize and mobilize millions of consumers to demand labels on beef, pork, poultry and dairy products derived from these unhealthy and unsustainable so-called “farming” practices.
  9. In the meantime, you can boycott food products from CAFOs and choose to support farmers who produce healthful grass-fed meat, eggs and dairy products using humane, environmentally friendly methods. You can do this not only by visiting the farm directly, if you have one nearby, but also by taking part in farmer’s markets and community-supported agriculture programs, many of which offer grass-fed beef. The following organizations can also help you locate grass-fed beef and other farm-fresh foods in your local area, raised in a humane, sustainable manner.




Paralyzing Comatose Cardiac Arrest Survivors Improves Outcomes.

Neuromuscular blockade for at least 24 hours improved in-hospital survival rate.
The 2010 American Heart Association guidelines recommend limiting neuromuscular blockade (NMB) in patients with return of spontaneous circulation (ROSC) because it could be harmful. However, NMB is often used to prevent shivering in post–cardiac arrest patients receiving therapeutic hypothermia. Researchers performed a post-hoc analysis of a prospective, observational study of comatose adults with nontraumatic out-of-hospital cardiac arrest who had sustained ROSC (palpable pulses for ≥20 minutes) and were transported to four centers over a 9-month period.

Of 111 patients, 18 received NMB for at least 24 hours after ROSC (sustained NMB), 59 received NMB for less than 24 hours, and 34 received no NMB. In-hospital survival was higher in patients who received NMB at any point than in those who received no NMB (52% vs. 35%). Patients who received sustained NMB were more likely to survive than the other two groups combined (78% vs. 41%). Fifty percent of those who received sustained NMB and 28% of the other two groups had favorable neurologic outcomes (not a significant difference). The sustained-NMB group had similar prognostic scores but shorter time from collapse to ROSC, higher baseline blood pH, and lower incidence of chronic obstructive pulmonary disease than the other two groups combined. Multivariable analysis showed that sustained NMB was independently associated with survival (adjusted odds ratio, 7.23) and improvement in lactic acidosis.

The authors postulate that NMB reduces metabolic demand and global oxygen consumption, improves pulmonary gas exchange, and prevents ventilator dyssynchrony, thereby protecting against episodic rises in intracranial pressure.


Although some studies have suggested that long-term neuromuscular blockade may lead to critical illness, polyneuropathy, or generalized muscle weakness, this study suggests it may have benefit in post–cardiac arrest patients. A note of caution, however: Be sure that any patient with a chance of awareness is adequately sedated before paralysis!




More Information on Thrombolysis Benefits for Ischemic Stroke.

Two studies using large databases provide details on timing and outcomes.

Clinical trials of thrombolysis for acute ischemic stroke typically have included fewer than 1000 patients. Two new studies involved larger datasets, allowing investigators to analyze important clinical issues in greater detail.

Saver and colleagues analyzed data from the national Get With The Guidelines–Stroke (GWTG-Stroke) database on 58,353 patients (median age, 72; 50.3% women) treated with tissue plasminogen activator (TPA) within 4.5 hours of symptom onset over a 9-year period. The median time from symptom onset to TPA administration was 144 minutes. Factors associated with earlier treatment included greater stroke severity, arrival by ambulance, and arrival during regular hours. Intracranial hemorrhage occurred in 4.9% of patients; 38.6% were discharged home. Earlier treatment, measured in 15-minute increments, was associated significantly with reduced mortality (odds ratio, 0.96), reduced intracranial hemorrhage (OR, 0.96), increased chance of independent ambulation at discharge (OR, 1.04), and increased rate of discharge to home (OR, 1.03).

The IST-3 collaborative group examined the effects of thrombolysis on 18-month quality-of-life and functional outcomes. Among more than 2300 patients from 10 countries who were randomized to usual care or thrombolysis within 6 hours of stroke, the adjusted odds of being alive and independent at 18 months were 28% greater with thrombolysis. Survival at 18 months did not differ. On a scale measuring mobility, self care, activity, pain, and anxiety, patient or caregiver reports of wellbeing improved significantly more between 6 and 18 months after stroke, and were better at 18 months, in the thrombolysis group, although anxiety was not lower.


The data from the large GWTG-Stroke database emphasize the importance of timely intervention for acute ischemic stroke. Currently, fewer than one third of patients are treated with thrombolysis with a door-to-needle time of <60 minutes (Stroke 2011; 42:2983). The Target: Stroke initiative of the American Heart Association/American Stroke Association aims to improve this rate to 50% in the next few years. Accelerating the pace of treatment will have multiple important benefits, including lower mortality and improved functional outcomes.

The study from the IST-3 investigators shows long-term benefits for functional status with prior thrombolytic therapy. Although multiple factors can affect health status 18 months after stroke (such as cardiac issues and infectious complications), the persisting improvements in functional status with prior thrombolytic therapy are reassuring.