17 December 2011

Make getting and giving vaccines a holiday tradition



13 November 2011

Eating Pace and Protein to Control Overeating

One matter that most evidence-based nutritionists and dietitians will agree on is that humans have evolved to be experts in the task of seeking out palatable foods, which generally contain a combination of sugar, fat, and salt. These nutrients, usually scarce over the long span of evolutionary time and highly valued, are what helped lead to the development of our senses.

Nowadays, it is still the sight, aroma, and taste of food powered by sugar-fat-salt reward and satisfaction that still guides our eating decisions, except in a modern environment of widely available food and sedentary lifestyles.

The axe that nutritionists have to grind with food manufacturers is the blatant targeting of our senses with   layer upon layer of bold sugar-fat-salt flavors -- think of potato chips dipped in artichoke dip, French fries and ketchup, pizza topped with pepperoni, and so on. According to David Kessler, these foods are so powerfully appealing to our senses that they may even alter our brain chemistry driving our appetites for more.

01 November 2011


Lance Price


09 October 2011

Egg yolks for eye health

Lutein and zeaxanthin are found in egg yolks.


05 October 2011





11 September 2011

Evolution of the "Hero's Journey"



06 September 2011

What chimpanzee predatory behavior can tell us about early human diets




21 August 2011

Living Food Walls for Disadvantaged Youth, Sustainable Communities

The first living wall as it's constructed in South Africa.




12 August 2011

Lindeberg: Focus on Food Choices, Bioactives, not Nutritionism

Dr. Lindeberg weighing a Kitavan man. 



11 August 2011

Intermittent fasting for cardiovascular health



10 July 2011

Phosphorus and food's future

James Elser, Ph.D.
What can we do about phosphorus and food's future?




James Elser, Ph.D., hopes that will change.



25 June 2011

Can we get any smarter? (A conversation with my boy about neuroscience)

A PET image showing energy consumption in the hungry brain. Credit: Wiki
"Can we get any smarter?" That is the question that piqued the interest of a 14-year-old boy yesterday when he saw it on the cover of the July issue of Scientific American. 

What came next was a reading of Douglas Fox's fascinating "The Limits of Intelligence," some heavy thought in a young teenager's head, and a surprised father who rarely has a conversation with his son about neuroscience.

Plus, that same father is rarely met when he comes home from working all day to a welcome like this, "Hi dad. Do you want to go see a cool movie?"

The movie my boy wanted to see (with me!) was Limitless, a science fiction flick he'd seen before about a man who takes a drug that unlocks his ability to use the "other 80 percent of his brain." We went to see it and, as my son pointed out after the movie, all of what was portrayed was just impossible.

How Diet and Lifestyle Influence Telomere Length

Telomere length has a proportional and linear relationship to omega-3 fatty acids.
With all the attention surrounding telomere length as a biomarker of biological aging, it’s worth pointing out that one nutrient may make a lot of difference: fish-derived omega-3 fatty acids.

The higher the blood levels of fish-derived omega-3 acids in patients with coronary heart disease, the longer the telomeres. This was what was found by researchers recently from University of California, San Francisco.


The study (Farzaneh et al. 2010), published in the January issue of JAMA last year, showed that leukocyte telomere length (LTL) was positively associated with higher blood levels of omega-3 fatty acids (see Figure).

“Omega-3 fatty acids may protect against cellular aging in patients with coronary heart disease,” the authors wrote.

This longitudinal study followed 608 patients with stable coronary artery disease for five years. LTL was measured at baseline and again five years later. The baseline levels of omega-3 fatty acids were then used to compare the rates of telomere attrition over the five-year period.

“Association of omega-3 fatty acids with decelerated telomere attrition may lie in the paradigm of oxidative stress, a powerful driver of telomere shortening,” the authors wrote.

Omega-3 fatty acids have been shown to increase levels of catalase and superoxide dismutase (enzymes that serve important antioxidant roles in the body). The researchers hypothesize that omega-3s may even increase the activity of existing telomerase, the enzyme responsible for the addition of base pairs to DNA during replication.

14 June 2011

Updated clinical vitamin D guidelines

Michael Holick, MD, Ph.D., told me in a phone interview nearly a year ago that vitamin D insufficiency and deficiency was "one of the most common medical conditions" and has implications on the health of bones, the heart, the immune system, and likely every cell in the body.

Dr. Holick added, "If a normal adult isn’t taking at least 1,500 to 2,000 IU from supplement and diet—and you can’t really get it from your diet—then we know you’re vitamin D deficient."


The guidelines follow on the coattails of last November's updated vitamin D recommendations by the Institute of Medicine (IOM), which several experts have condemned as conservative and inadequate. In response, a "Task Force," led by Dr. Holick, reexamined the evidence and compiled new recommendations to provide a more therapeutic emphasis.

The guidelines call for screening populations at risk for vitamin D deficiency and correcting deficiencies with supplementation at levels high enough to maximize effects on calcium, bone and muscle metabolism.

The Task Force recommends maintaining blood concentrations of 25(OH)2D (the active circulating form of vitamin D) consistently above 30 ng/mL. Circulating blood levels below 30 ng/mL are regarded as "insufficient" and below 20 ng/mL as "deficient".

To assist at-risk individuals with meeting blood levels above 30 ng/mL of circulating vitamin D, the Task Force issued new dietary intake recommendations that differ significantly from those given by the IOM:
  • Infants ages 0-1: 400-1,000 IU/day
  • Children ages 1-18: 600-1,000 IU/day
  • Adults ages 18+: 1,500-2,000 IU/day
  • Pregnant or nursing women under 18: 600-1,000 IU/day
  • Pregnant or nursing women 18+: 1,500-2,000 IU/day
  • Obese children and adults: at least 2-3 times the recommendation for their age group
  • Children and adults on anticonvulsants, antifungals and AIDS medications: at least 2-3 times the recommendation for their age group
The Task Force also increased Tolerable Upper Limits for vitamin D to substantially higher levels than what the IOM recommended last fall.

11 June 2011

Depression and telomeres

Reference: Wolkowitz et al. 2011 March.
People who suffer from major depression have a higher risk of age-related illness and earlier mortality (1 &2). Researchers from University of California, San Francisco (UCSF), investigated (1) telomere length in depressed individuals versus matched controls and assessed other biological factors associated with telomere shortening.

Led by Nobel laureate Elizabeth Blackburn, Ph.D., the team of researchers published their findings in the March issue of PLos One. Their hypothesis was that not all depressed subjects would show shortened telomeres equally because of a large variance in depressive episodes over a lifetime. However, they predicted that those who suffered from depression for long durations would have shorter telomeres due to longer exposure to oxidative stress and inflammation induced by psychological stress.

The scientists recruited 18 subjects diagnosed with Major Depressive Disorder (MDD), excluding those with psychosis or bipolar histories, as well as those with Post-Traumatic Stress Disorder to eliminate confounding variables due to interferences with stress hormone regulation. Results from depressed individuals were compared to those of the matched control group.

27 May 2011

Fitness, hunter-gatherer style

Aché man hunting. Credit: Wiki



16 May 2011

How Neandertals Lived, Hunted, and Ate





08 May 2011

Those daily extra cups of joe not linked to hypertension



Diagnosing Darwin's multiple gastrointestinal diseases

Charles Darwin (Credit: Wikimedia)




06 May 2011

Getting off the death chair

My stand-up desk




Safe weight loss for seniors through diet and exercise




03 May 2011

Printing organs for transplants






It's almost sickening.

News that "Nutcracker Man didn't eat nuts" isn't exactly news



See more about Cerling's paper on John Hawks's blog.



02 May 2011

Michael Ruse on "Origins of Human Evolution"

Michael Ruse





Resveratrol Improves Insulin Sensitivity in Humans










29 April 2011

Calcium: U.S. adults still not getting enough




"Adequate lifelong calcium intake is essential to optimizing bone health," remind the study authors, who published their findings in the May 2011 issue of Journal of American Dietetic Association. They also recommend "new approaches to increasing the frequency and level of calcium supplement use to enhance calcium density in diets."





Time and time again, studies have shown that calcium when combined with vitamin D are effective in increasing bone density. However, there's been a lot of back and forth in the calcium world around the topic of supplements, particularly their efficacy and safety. A critical piece lacking in the conversation is of absorption since calcium is one mineral that depends on a few factors -- vitamin D, doses that oversaturate absorption, too much absorbed at once.


27 April 2011

Wake up, Neo-evolution

What would you change about your own naturally evolved, naturally flawed body? Would you choose genetics to avoid diseases like Alzheimer's, diabetes, and cancer? Would you enhance your brain to increase memory and to boost creativity? Would you choose more fast-twitch muscle fibers to run faster or longer? Would you live longer?

These are the questions that Harvey Fineberg, president of the Institute of Medicine, discusses in this new TED talk given in March that was posted only this month. Fineberg says that a new era of neo-evolution -- in which we, as humans, could guide the selection of traits that would define the course of humanity -- is upon us, and he called it "exciting," but "frightening."

I want to answer all of his questions with a "Yes, sign me up!" Who is insane enough to reject a world with an absence of disease, of aging, of dying and death?

Apparently, there are quite a few people. Hava Tirosh-Samuelson, professor of history at Arizona State University, is one of them. Earlier this month, at ASU's Origins Project Science and Culture Festival Tirosh-Samuelson was speaking about a completely different topic when she suddenly surprised us with a few critical words of the "so-called trans-humanist movement."

In a nutshell, her argument is that we still haven't a clue of what humanity is to begin with, so reason suggests against trying to define what it should be in the future. Naturally, after her talk, I decided to ask Tirosh-Samuelson a few questions about her views.

22 April 2011

Health at Telomere's Length












14 April 2011

Stress Awareness Month and the baboon inside you



What African Americans should know about vitamin D and heart health



He said, "I'm in the office all day."

"What do you do at lunchtime?"



OK, he says. "But why outside?"















22 March 2011

Fusing aging theories: Telomere shortening causes mitochondrial dysfunction

New research is adding insight and linking three theories of aging—one that suggests telomere shortening governs lifespan, and two others that suggest dysfunctional mitochondria or oxidative stress leads to aging.

At Harvard-affiliated Dana-Farber Cancer Institute, scientists have gathered data suggesting telomere shortening is the cause of mitochondrial dysfunction and diminished antioxidant defenses. Together, they decrease the body’s energy and diminish organ function, both characteristic of old age.

As telomeres—protective caps at the end of cell chromosomes—shorten with age and begin to fray, cells activate the p53 gene, which signals an “emergency shutdown” chain of events that turns off normal cell growth and division and compromise antioxidant defenses. Going one step further, data from the carefully orchestrated mouse study, published in Nature, show that the p53 gene also represses PGC1-alpha and PGC1-beta. These PCGs are considered the master regulators of metabolism and mitochondrial function.

Repressing PCGs increases the number of dysfunctional mitochondria (with mutated mitochondrial DNA) and leads to a decrease in functional mitochondria distributed throughout in muscles and organs. The dysfunctional mitochondria in aged tissues leak greater amounts of reactive oxygen species and the lack of functional mitochondria hinders normal energy production from cell respiration (the body’s main producer of ATP energy).

“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent from each other,” said Ronald A. DePinho, M.D., a cancer geneticist and senior author of the paper, in a press release.

“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” Dr. DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”

In an article also published in the same issue Nature, Daniel P. Kelly, M.D., scientific director and professor at Burnham Institute for Medical Research-Lake Nona, Orlando, Florida, said that the “intriguing study… unveils a potentially unifying mechanism for cellular ageing.”

Mitigating the Toll of Aging

The new study further supports current thinking that the best defense against aging is to reduce the adverse affects of overproduction of free radicals produced from dysfunctional mitochondria, which cause additional oxidative stress.


Those current targeted therapies include boosting the human body’s antioxidant defenses by eating a healthy diet, reducing calories (by around 25 percent), and supplementing with antioxidant vitamins C and E, as well as with green tea, CoQ10 and resveratrol. These practices not only help to protect against oxidative stress, thereby protecting against telomere shortening, but also help boost generation of new, healthy mitochondria.

When we asked telomere biologist Bill Andrews, Ph.D., to comment on the new study, he answered that it was “tremendous news,” as it supports the need for more research into management of telomeres by activating the genetic expression of the enzyme telomerase, which re-lengthens telomeres.

Dr. Andrews wrote, “It’s the best support ever for the fact that telomere elongation’s role in aging far exceeds the roles played by mitochondria and oxidative stress.” In effect, telomere shortening is the root cause of the others.

Mitochondria become dysfunctional when telomeres shorten and fray, a new study suggests. In an article to be published in a forthcoming issue of IsaNews magazine, Dr. Andrews writes, “Mitochondrial dysfunction causes aging—but telomere shortening has turned out to be the primary cause of mitochondrial dysfunction. And humans’ natural defenses against oxidative stress are really quite exceptional (for example, our cells produce ten times more superoxide dismutase, a potent natural antioxidant, than mice)—until telomere shortening begins to degrade those defenses inside our bodies.”

He added that while “anti-aging therapies of years past merely treated the symptoms of aging. New research is devoted to identifying a new class of therapies that treat aging at its root cause, and hold great promise of one day allowing us to feel young and healthy at 120 years of age and beyond.”

An earlier study, of which Dr. DePinho was also the senior author, gives testimony to the benefits of telomerase, as found in mice that were genetically engineered to produce the enzyme. The study found that when the telomerase was restored in the mice, their age-related symptoms disappeared and several organs including the brain were rejuvenated.


Kelly DP. Cell biology: Ageing theories unified. Nature 2011;470:342-3.

Sahin E, Colla S, Liesa M et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470:359-65.

Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature 2010;464:520-8.

Jaskelioff M, Muller FL, Paik JH et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011;469:102-6.

16 March 2011

Potassium iodide: Why you should avoid it

Ever since the news of Japan's nuclear crisis, there have been several claims made over the Internet that have panicked people in the U.S. about potential exposure to radiation (one culprit is this viral e-mail), which has led to me being the recipient of questions about whether or not people should be taking potassium iodide supplements to avoid absorption to radioactive iodine.

Should you take potassium iodide pills? My answer has been an unequivocal, "No, it's not necessary. There is little risk of any level of radiation exposure to worry about anywhere else other than in Japan near the reactors. If you're worried about getting cancer, try thinking more about losing weight, eating more dietary fiber, and eating more fruits and vegetables."

In the process of answering questions, I did find myself interested in learning more about radiation and health. By far the best, most in-depth article I've read on "How Radiation Threatens Health" is this one written by Nina Bai and published by Scientific American. Bai's article gives readers an excellent understanding on the typical radiation levels that people are currently exposed to (0.2 to 0.3 milliSieverts), how much they are exposed to by a typical CT scan (1 milliSievert) and what kinds of levels people should really be worried about—the kind of levels that lead to symptoms of radiation sickness ("a whole body dose of 3 sieverts, that is, 3,000 times the recommended public dose limit per year") and the kind that kills people within weeks (5 to 10 sieverts).

Yes, there are concerns over low-dose radiation over time, but as Bai's article points out, the increase of cancer risk is small and basically comes out to about an increase of eight potential cancer cases per 10,000 people. And, the point is that even if any radiation made it over the ocean and to the U.S. (which is unlikely) it would be at levels too low to cause concern.

As for potassium iodide (KI) supplements (not addressed in Bai's article), there is cause for concern because I keep reading that these are "flying off the shelves" in various articles.

The way KI works is by flooding iodine into the thyroid gland to become trapped by the thyroid's receptors, which blocks the uptake and accumulation of radioiodine that could lead to possible thyroid diseases or cancer. This is particularly important in children who are more at risk for radioiodine-induced cancer (as is what happened with the Chernobyl incident because of radioiodine0contaminated milk). The doses for preventing radioidine uptake are high: 50 to 100 milligrams for adults. If exposure is pretty certain, then supplementation with these pills make sense.

But consider that the Upper Limit for adults is 1.1 milligram per day. These pharmacologic doses could be potentially detrimental since excessive iodine can actually lead to hyper- or hypothyroidism and have been known to increase risk of thyroid cancers. Taking these doses should not be considered a safe precautionary measure, as marketed. There is a risk!

My concern is this: that the irresponsible Internet claims are leading people to actually take the high doses of the KI and that retail outlets selling them (like this one with 130 milligram per tablet!) are doing so without giving people any sense of what the risks are when taking high amounts.

02 March 2011

Vitamin K2: Building bones while beating back arterial calcification

Vitamin K2's time to shine has come—move over vitamin D! Once only known for its role as a "koagulation" factor in blood clotting, vitamin K2 is emerging as another fundamental anti-aging nutrient. While vitamins D and E have garnered the majority of interest in the last decade, the impact of vitamin K2 on aging bones and hearts demands that we give it equal attention.

Whereas most vitamin and mineral supplements use vitamin K in its form of K1 (phylloquinone sourced from plants) because it is easily available and cheap, it is the natural form of K2 (menaquinone sourced from friendly bacteria) that is the most biologically active and shown to enhance both bone formation and vascular health.

The full compilation of recent research underscores the idea that K1 and K2 should be appreciated as separate nutrients with distinct physiological actions and benefits. K1 is the more familiar vitamin known for its key role in directing blood-clotting in the body and the one given as a shot at birth (a common practice in many countries to curtail hemorrhage incidents in newborns.) The picture for K2 seems to be a bit more varied and is key in regulating calcium balance.

Vitamin K2 acts by activating the bone-building hormone (carboxylating osteocalcin) to clear calcium from the arteries and use it in bone mineralization. It effectively removes calcium that would otherwise end up deposited in arterial plaques. Since protecting arteries and soft tissues from calcification is one of the most important ways to stave off the ravages of aging on the body, consuming enough vitamin K2 daily is key for a long, healthy life.

Getting Enough K2

Because vitamin K2 is synthesized by friendly bacteria in the intestine, nutrition scientists have long assumed that that deficiencies were rare. However, new data are showing that intestinally synthesized vitamin K is not absorbed as easily as previously thought. Vitamin K also preferentially accumulates in the liver where it does have a clotting factor role.

In fact, once overlooked because "time to clot" was the test for vitamin K status, it is here where we are now seeing new signs of vitamin K deficiency previously only seen with vitamin D deficiency—fragile, brittle bones and increased fractures—even with adequate calcium and vitamin D.

Most people in North America should increase amounts consumed daily. The evidence finds that only with much higher intake do bone cells get their share and the same holds true for removal of calcium in arteries.

People can obtain enough vitamin K2 by eating plenty of fermented foods such as cheese, sauerkraut, and natto (a traditional Japanese soy-based food). Supplementation is another viable option as achieved with a quality multivitamin.

Regardless of how one gets it, it’s important not to underestimate value of this underdiscussed nutrient and to understand that most people are not getting enough. Consuming sufficient amounts of K2 along with a healthy diet will increase odds of a healthier life with clear arteries and stronger bones.


McCann and Ames. Vitamin K, an example of triage theory: is micronutrients inadequacy linked to diseases of aging?. Am J Clin Nutr 90:889-907, 2009.
Vitamin K2. Monograph. Alternative Medicine Review 14(3):284-293, 2009.
Koitaya. Et al. Effect of low dose vitamin K2 (MK-4) supplementation on bioindices in postmenopausal Japanese women. J Nutr Sci Vitaminol. 55:15-21, 2009.
Gast, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovas Dis 19:504-510, 2009.
Shea, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 89: 1799-1807, 2009.
Shea MK, Booth SL Update on the role of vitamin K in skeletal health. Nutr Rev 66(10):549-57, 2008.

25 February 2011

Is there a link between telomeres and dietary fiber?

New evidence published in Archives of Internal Medicine has it that eating more dietary fiber, particularly from whole grains, could lead to a longer life. The large study found a high-fiber diet reduced risk of heart disease and cancer, as well as infectious and respiratory illnesses.

This is great news for those eating diets high in fiber. What’s also interesting is that another reason why dietary fiber is protective to health is because of its influence on telomeres. Telomeres are the protective caps at the end of chromosomes, and their length is considered the closest way to measure lifespan in humans.

As reported in a prospective cohort study published in the March 2010 issue of American Journal of Clinical Nutrition (AJCN), telomere length is positively associated with higher fiber intake in women. Dietary fiber from whole grains appears to provide the strongest benefit.

In addition, in the AJCN study, the researchers found telomere length was negatively associated with increased waist circumference and higher intake of omega-6 fatty acids in the diet.

Because the study was only observational, the authors reported that further investigation is necessary to further illuminate the link between dietary fiber and telomere length.

Whole grains examples are rolled oats, buckwheat, whole wheat, and wild rice. The grains contain the entire grain kernel, which include the bran, germ and endosperm. Less than 5 percent of Americans consume the minimum recommended amount of whole grains, which is about 3 ounce-equivalents per day, according to U.S. Department of Agriculture.

Americans barely receive half the amounts of dietary fiber recommended daily. How much dietary fiber is enough? The recommended amounts are 25 grams of fiber for women and 38 grams of fiber for men.
The AJCN study was among the first to document the relationship between diet and telomere length. The authors of the study concluded that the results provided more support that an improved diet and lifestyle would indeed help to slow the aging process.

"Telomere shortening is accelerated by oxidative stress and inflammation, and diet affects both of these processes," the authors report.

Studies have also found that the following changes in diet and lifestyle are all positively associated with telomere length:
  •  not smoking
  • exercising regularly
  • maintaining a normal body weight
  • healthy management of stress
  • consuming sufficient long-chain omega-3 fatty acids from fish weekly
  • maintaining a healthy vitamin D status
  • consuming a quality multivitamin daily
  • consuming antioxidants such as CoQ10 and green tea

Cassidy A, De V, I, Liu Y et al. Associations between diet, lifestyle factors, and telomere length in women. Am J Clin Nutr 2010;91:1273-80.

Post originally written to be posted here.

22 February 2011

Pornography in the Primordial Soup

Panel of scientists debate on "What is Life?"

Sometime between 4 and 3.5 billion years ago, the emergence of life had intense beginnings on a young planet in the midst of a so-called primordial soup—consisting of water vapor, carbon monoxide, carbon dioxide, nitrogen, and ammonia and shaped by strong winds, electrical storms, volcanic eruptions, and ultraviolet radiation.

In 1953, Stanley Miller and Harold Urey put Earth's primitive conditions to test for the first time in a famous laboratory experiment. It yielded variety of amino acids and organic compounds. The researchers realized something more: that no early form of life could have ever survived the world of today, because of the presence of oxygen that directly attacks at the bonds that holds together complex molecules.

Scientists also now know that the original blueprint of life was not DNA, but short RNA strands that may have also served as their own biological catalysts, before enzymes ever evolved, providing for self-replication. This early RNA world would eventually give rise to DNA, which used RNA as its template for encoding the genetic information to build proteins.

Still, there are several other questions that remain surrounding life's origins such as How can life be defined? Where did it happen? What came first: replication or metabolism? Could life have happened elsewhere in the universe? What would an alternative form of life and biochemistry look like?

Last weekend, to discuss the questions, a small panel of six scientists gathered at workshop at Arizona State University with a major goal of charting out the steps between the RNA world and greater complexity. Some would say theirs was a hopeless cause and a waste of time.

Then, on Saturday, February 12, a public debate  took place between them with an overarching theme entitled, "What is Life?" Theoretical physicist and cosmologist Lawrence Krauss, ASU professor and director of ASU's Origins Project defended the exercise as uniquely human.

"It's a profound and deep question that hits at everything we think about," Krauss said, noting how the question has a powerful draw. "It sounds like a simple question, the answer isn't so simple. In fact, every time I think about that question, I think about pornography."

He referred to a 1964 Supreme Court case where Justice Potter Stewart once was asked to explain the definition obscene pornography. "I know it when I see it," the judge responded. Krauss said, "In some sense, life is like that."  

Life: Complexity with a Specified Direction

Evolutionary biologist Richard Dawkins further  elucidated the significance of the question in characteristic eloquence, "This may be the only planet in the universe that contains eyes to see it, brains to think about it, and wonder about it. I don't believe that. I suspect there is plenty of life in the universe, but this is the only kind of life we know about."

According to Dawkins, because the laws of physics apply all over the universe, it is likely that life could have materialized many times by the process of evolution by natural selection. Life, then, would have to be defined as anything that is highly statistically improbable, but that appears to have a specified direction.

"You have to add that 'specified direction' because with hindsight you could say any old heap of rubbish is statistically improbable in that there has never been a heap of rubbish exactly the same," Dawkins said. "What's special about life is that living things are statistically improbable in a direction, which you could have specified in advance. It's not always exactly the same, but birds are good at flying, fish are good at swimming, moles are good at digging. All living thins are good at something, whereas lumps of rock aren't.    

Whatever life is, it is characterized by its complex molecules that must somehow create the energy to convert raw material into a structure, all while excluding anything that may be toxic to those reactions of metabolism and reproduction. This is why geneticist and Nobel Laureate Lee Hartwell argued, "Inevitably, life will be cellular. Cells will have been selected to have an optimum size and optimum structure for whatever lifestyle they happen to have."

Searching for a Second Genesis

A sort of definition of what to look for was heartening for NASA planetary scientist Chris McKay, "What Lee said was a beautiful synthesis of how we can search for life, and I want to take that to the specifics of how do we do it in near tem missions in our solar system."

There is an advantage to finding other forms of life in our own solar system, argued McKay, because "then we'd know that life is common in the universe." The task of finding other forms of life in the solar system, even on our own planet, is one promoted by cosmologist and astrobiologist Paul Davies.

Davies doesn't see things quite the same way as McKay. "How can we find this second sample of life? Chris has said one way you can do that is you can go somewhere else in the solar system and find it there. That's great. But it's also very expensive. Is there another way? Well, no planet is more Earth-like than Earth itself. Shouldn't it have occurred many times right here on our home planet? How do we know it didn't?"

While Davies looks for alternative life on Earth—a process that he boldly claims can be completed in less than a decade—biologist and entrepreneur Craig Venter is more interested in creating synthetic life.

Venter explained how he and his colleagues synthesized DNA and chromosomes and inject it into E. coli, which he likened to creating a computer program that builds its own computer, or as he puts it, "A situation where the software actually leads to building its own hardware, but we're trying to go much further. We had to learn how to boot up this bacterial genome."

Change the DNA, change the software, and you change the species, Venter explained, and as others have pointed out, his team did use a living cell, but the cell was the first one to ever have synthetic DNA.

Living Artificial Intelligence

Among these scientists, one thing was certain: the definition of life could not be agreed upon in the face of alternative forms of life in the universe, in our own solar system, on the Earth, or from creating life from scratch. But, perhaps, a definition of life isn't needed after all because, as Krauss put it, anyway, it could change.

"Let me throw it in a completely different direction," Krauss offered in the debate."When computers become conscious, which they will—my Mac is far closer than the PC—will we call them life? And they'll object if we don't, I suspect. I think the definition is a moving target."

After all, the difference from what Venter is accomplishing—with software that makes its own hardware—and computers is that computers simply haven't done that yet (made their own hardware), but when they do, which will happen in at least one or two decades, Krauss said, "they will become the dominant forms of intelligent life on the planet and biology will have to incorporate that in order to keep up."

At the end of the debate, the inevitability of life in the universe was the lesson really learned, given that there could be life lurking almost anywhere.

Be it in a biological world, a  synthetic world, or another kind, life can defined as simply… we'll just know it when we see it.

To read more about the entire weekend conference on origins of life, see Dennis Overbye's article in the New York Times.

UPDATE: the science network has now published the video of this debate. Click on the video to watch below.

20 February 2011

Evolution of Lactose Tolerance in Africa

Sarah Tishkoff



But shortly after weaning, the expression of lactase decreases sharply -- that is, except in populations that are lactase persistent. In 2002, an elegant genetic study found the gene for lactase in European populations.

Tishkoff showed us in charts and on a map how she performed genetic studies on the African pastoralist populations with lactase tolerance. Based on the findings, she found a perfect example of convergent evolution -- that several of the populations had developed lactose tolerance in different ways genetically -- because of strong selective pressures to drink milk.

With her latest study and archeological data, she is now tracking the origins of pastoralism. She showed us a map (Smith 1992) where it's clear that most lactose tolerance emerged only in the last few thousand years, but at different times. Her research confirms that pastoralism was brought into southern Africa only recently, most likely from the Great Lakes region.

"So, are humans still evolving? Yes," Tishkoff said.

Why was milk selective pressure so strong? There has been a lot of debate, Tishkoff said, such as whether it is the source of water, protein, or calcium. But it's not everywhere, so there has to have been a cultural transformation in each region.

"There's only some environments that can handle that cultural development," Tishkoff said, but in each case, there has to be an underlying genetic variation and the different variants suggest that perhaps for some populations had a more difficult time with the change or took longer to adapt to it than others.

The Nature of Human Skin Pigmentation

Nina Jablonsky
On Sunday morning at #AAASmtg in Washington DC, Nina Jablonski talked to use about human skin pigmentation as an example of natural selection.

"Human skin is colorful, it's mostly naked, it's sweaty, and it's tough yet sensitive," Jablonski said. The gradient of human skin pigmentation is very clear in the old world, as it's lighter in the northern countries and darker in Africa.



When Homo ergaster 1.6 mya was foraging in the savannah, the species would have needed more naked and sweaty skin for keeping cool. In addition, Jablonski's research has found that permanent dark pigmentation evolved 1.2 mya, at the same time as these other developments -- an interesting development!.


Ultraviolet radiation (UVR) had a lot to do with the advent of darker skin pigmentation. On a map (by George Chaplin based on NASA TOMS7 satellite data) of annual average UVR, Jablonski was able to clearly show the strength of UVR.

"We evolved initially in equatorial Africa and then we had two waves of dispersal from Africa," Jablonski said. "This really changed the selective genes for human skin fundamentally."






Indeed, we have an independent evolution of depigmentation of humans in Asia and in Europe. And we also know that the Neandertals experienced the same selection of depigmentation. There are many genes involved in pigmentation and Jablonski said she has even found in some populations, where the amount of UVR changes by season, that people have adapted to change the amount of melanin in their skin throughout the season

Nowadays, accelerated rates of movement around the world, has put humans in environments that are poorly matched, Jablonski said, which has created serious health problems such as with rickets in children, birth defects, and even metabolic syndrome.



19 February 2011

Designing biology

Photo credit: Sara Fulcher on Flickr
Where can we find a cure for cancer, new semiconductor technology, or the solution for turning waste plant materials into biofuels? The answer is enzymes that are produced through "directed evolution," according to Frances H. Arnold, professor of chemical engineering and biochemistry at the California Institute of Technology.

Arnold's lab doesn't synthesize enzymes as other labs do. She and her team "evolve them" toward a certain desired goal in the same way that nature has done it for 3.5 billion years.

Aronold presented an overview of her budding field of work to an audience at American Association for the Advancement of Science annual meeting (#AAASmtg) in Washington DC. The field of directed evolution is relatively new and includes few people at the present time, but Arnold sees high hopes for the future.

"When I started engineering proteins a long time ago, there appeared to me an algorithm that dos a really good job and that's evolution," she said. "Evolution works because the regions that life has discovered and explored are rich in function. Directed evolution exploits smooth paths in the fitness landscape."

The fact is, DNA is cheap and easy. Designing it isn't.

"We're getting really good at making DNA. The price is dropping every day," Arnold said. "But we don't know what to write. We can synthesize any sequence. We can insert new code (referring to Craig Venter's recent success), but we don't know how to write it. We don't even know how to write a single protein."

And, when it comes to enzymes for use inside a complex biological system, she says,"Details matter. We don't understand the details."

Freed from constraints of worrying about biological function, directed enzyme evolution allows Arnold's team to explore new pathways and possibilities.

Arnold presented a few of her enzymes that have been created through directed evolution. Her source materials are from every possible place -- the "heel of your shoe," for example -- and she doesn't limit herself to what's available.

Frances Arnold
By combining several different enzymes and selecting for specific active sites, she can produce more stable proteins that perform practical work.

Where is directed enzyme evolution going in the future? Arnold says that functional protein can be used in several ways. One example Arnold gives is in materials chemistry, such as the work of Angela Belcher of MIT, who uses virus proteins to enrobe minerals onto protein coats.

"You can make a virus that really loves to bind to a single-walled carbon nanogen," Arnold said, which would be a boon for semiconductor technology.

There is really no end to the influence that directed enzyme evolution could have on the world, from highly specific targeting in biological systems to technology.

In short, there's no doubt of an exciting future in intelligently designing new biology.