Mark Pine

As women age, their bones often lose calcium and fractures occur more frequently, a condition called osteoporosis. So it seems logical for older women (and men with osteoporosis) to take calcium supplements. Logical … but perhaps not a good idea.

The BMJ (British Medical Journal) published yesterday a meta-analysis (analysis of combined data) of five clinical trials involving 8,000 people who took calcium supplements or placebo pills. The researchers from universities in New Zealand, Scotland and the United States compared the rates of heart attacks among the participants, who were followed for an average of about four years. Those taking the calcium had a 31% higher rate of heart attacks than those taking the placebo.

The researchers also presented a larger analysis involving eleven clinical trials with 12,000 people. Although these trials provided less detailed information about the participants than first five, the results were similar. Those taking calcium had a 27% higher rate of heart attacks. One important caveat: All the trials compared calcium alone to placebo. Calcium is often taken along with vitamin D, and the results may or may not be applicable to the combination.

Cardiologists from two universities in the U.K. reviewed the implications of the meta-analysis in an accompanying editorial. They noted that no increase in mortality rate accompanied the increase in the rate of heart attacks, raising the possibility of a spurious finding, since an increase in heart attacks should result in an increase in mortality. But they also pointed out that although calcium supplements improve bone mineral density, they have not been found to reduce bone fractures. In view of the possibility that they may contribute to heart disease, it would seem wiser not to take them.

The BMJ also published last January a meta-analysis of clinical trials of supplements of vitamin D with or without calcium. Pooling seven clinical trials involving 70,000 participants, Danish medical researchers found that the combination of Vitamin D and calcium reduced the overall rate of bone fractures by 8% and the rate of hip fractures by 16%. Among the patients who took at least 10 mcg of vitamin D with calcium, the rate of hip fracture fell by 26%. Taking vitamin D alone, however, had no effect on fractures.

The reduction in the rate of hip fractures from taking 10 mcg vitamin D plus calcium is substantial, particularly since hip fractures result in considerable disability and increase mortality. Still, the outcome of a benefit-risk analysis that balances the potential benefit of reducing hip fractures against the potential harm of increasing heart attacks is not clear. Although the meta-analysis published by the BMJ yesterday did not investigate heart attacks in people taking calcium along with vitamin D, the possibility that the same increase would also occur with the combination is cause for concern.

The authors of the editorial take the view that calcium supplements “seem to be unnecessary in adults with an adequate diet. Given the uncertain benefits of calcium supplements, any level of risk is unwarranted.” For the time being, the better course would seem to be eating well, including adequate amounts of food containing calcium, but not taking more of the mineral in supplements.

In Mary Shelley’s novel, Dr. Frankenstein is the creator of the monster, not the monster himself. And in the article last week in Scientific American, it is not a single scientist working alone who creates new life (actually that has already been done by Craig Venter), but a consortium of academic institutions launched earlier this year that is working together to assemble standardized parts of living organisms.

The BioFab is a “DNA factory” located within Lawrence Berkeley National Laboratory’s Joint BioEnergy Institute in Emeryville, CA. It is funded by the the laboratory, the National Science Foundation and the BioBricks Foundation. Run by scientists from UC Berkeley and Stanford, it’s website explains that BioFab will “produce broadly useful collections of standard biological parts that can be made freely available to both academic and commercial users.” The name BioFab was inspired by the Fab established by the semiconductor industry to design and manufacture custom chips. According to the BioBricks Foundation,

Using … standard biological parts, a synthetic biologist or biological engineer can already, to some extent, program living organisms in the same way a computer scientist can program a computer.

Gene promoters and ribosome binding sites are two examples of the kind of part that BioFab will design, manufacture, and stock. The former are sequences of nucleotides adjacent to a gene, where RNA polymerase attaches and initiates translation of the DNA into the corresponding messenger RNA. The latter are short sequences of nucleotides of messenger RNA that bind to ribosomes, the catalytic sites where proteins are synthesized by stringing together amino acids, according to the instructions specified in the message.

All proteins have their own sets of genes, promoters, ribosome binding sites, and other similar elements in the DNA and RNA molecules that encode them. BioFab will attempt to catalog and stock as many of these elements as it can.

In drawing a connection to the Frankenstein novel at the beginning this post, I wanted to point to the issues it raised. Just as Dr. Frankenstein failed to foresee the tragic consequences of his creative work, I find nothing on the BioFab or BioBrick websites that consider the potential negative consequences of making life parts available for order.

I do not disagree that this work should be done. But history shows that the Frankenstein-like “monsters” can and sometimes actually do arise from scientific work. Just as the monster escaped from his creator’s lab and roamed the countryside committing murders, inevitably life actually created in scientific laboratories WILL escape from those facilities and WILL in some instances inflict harm on the planet’s natural life.

If we are to do this work (and I think we should), then our government and others of the world should license and regulate the facilities in which it is done and require effective containment of the new life forms that are created.

New life forms should not be allowed to escape into the environment or to be released intentionally. Once free, life multiplies and mutates. And it is possible that some liberated creations— and their genes—would not die off but persist and spread uncontrollably.

Two potentially significant advancements in drug therapy—both sought for years—were reported this month: an antibiotic and an anti-obesity drug.

A new potential antibiotic was discussed yesterday in an article in ScienceDaily. It kills a broad group of bacteria, including methacillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant bacteria. At the present time, there is no antibiotic available that is completely effective against these microbes.

Bacterial resistance to antibiotics emerged as a significant problem not long after antibiotics were developed. Resistance to penicillin, which first appeared in 1947, was overcome with the introduction of the penicillin-like compounds, methacillin and oxacillin. But then MRSA, a type of Staphylococcus resistant to those drugs, too, appeared in 1961. Until the 1990s, only one drug, vancomycin, could be counted upon to vanquish the resistant bacteria. But eventually vancomycin-resistant bacteria appeared, too. Despite the development of new antibiotics that work against some resistant organisms (e.g., linezolid), there is none available now that works against all of them.

The newly reported antibiotic was derived from the soil bacterium, Microbispora corallina, and is called microbisporicin. It is effective against MRSA, vancomycin-resistant microorganisms, and another difficult-to-treat bacterium that causes severe diarrhea, Clostridium difficile. Microbisporicin is presently undergoing tests in animals. If it passes the tests, it should move into human clinical trials before long.

Another pharmacotherapy advancement, one that involves a potential anti-obesity drug, was reported earlier this month. The new drug is related to rimonabant (Acomplia, Zimulti, et al.), a weight-loss drug that works by blocking cannabinoid receptors. Activity of the endogenous cannabinoid system of neurons is known to induce hyperphagia in animals, an effect which is perhaps related to the notorious “marijuana munchies” observed in humans. Rimonabant counteracts this effect, and human studies have shown that the drug can produce significant weight loss [pdf file] of up to 7 kg in a year, along with improvements in cholesterol and glucose metabolism. But it was also found that rimonabant is associated with a high rate of severe psychiatric adverse effects, including depression and suicidality. Consequently, the drug was not approved in this country.

The new medication is designated TM38837, because it is not yet named. Christian Elling of the Danish drug company, 7TM Pharma, discussed it at the recent International Congress on Obesity in Stockholm. Although it blocks the same cannabinoid receptors as rimonabant, TM38837 does not cross the blood-brain barrier and penetrate into the brain to the same degree. It apparently acts mainly at receptors in the peripheral nervous system. Elling said the compound has produced significant weight loss in studies in mice and rats. It is hoped that the drug will produce weight loss in human studies, too, and because TM38837 does not act in the brain, it will not have the severe psychiatric adverse effects that prevented approval of rimonabant.

The history of weight-loss drugs shows that most medications were beset with significant problems. As one example, dextroamphetamine (Dexedrine), one of the first drugs prescribed for weight loss, caused insomnia, depression and paranoia, and it was addictive. Another example was the drug combination of phentermine and dexfenfluramine, known as Fen-Phen, which was popular for several years in the 1990s. However, dexfenfluramine was withdrawn from the market in 1997 for causing heart valve defects.

At present there are no substantially effective weight loss medications on the market. If TM38837 demonstrates the efficacy and safety that is hoped for, it could indeed become a breakthrough medication.

America and its Afghanistan war allies are trapped in a conflict in which one of those allies is a traitor.

Pakistan, an essential partner in the war effort, is internally split in two. One of those two parts appears to be actively working to aid the enemy, the Afghan Taliban. That is a main conclusion to be inferred from the Afghan War Diary, 2004-2008, a trove of documents written by American soldiers and intelligence officers fighting in the Afghanistan conflict. The documents were recently leaked from American military files to the Guardian, the NY Times, and Der Spiegel, leading news organizations in nations involved in the war effort.

A report on the documents in the Times on Sunday recounted several of them describing a component Pakistan’s intelligence service (ISI), the “S Wing,” planning and carrying out attacks on American forces.

One of the documents told how a former director of the ISI, Hamid Gul, met with militants in a city near the Afghanistan border, Wana in South Waziristan in January 2009. There they planned an attack to retaliate against a CIA drone attack on militants a few weeks earlier.

The Times article also said that Gul offered to allow the Taliban to use the Pakistan border region as a base if they concentrated their attacks inside Afghanistan. And it said that the ISI established networks of suicide bombers for attacking in Afghanistan.

On Sunday, the British news organization, the Guardian, also published an article on the documents. Some of them disclosed embarrassing details of the American effort in Afghanistan, including drone attacks and special forces missions to assassinate Taliban leaders.

Should America withdraw from Afghanistan? If Pakistan—or at least one part of that nation’s fragmented, schizophrenic government—continues to allow Taliban militants to use its territory as a base of operations from which to attack American and coalition forces in Afghanistan, then our military efforts there may be futile. Moreover, if America continues to commit questionable actions that some might consider war crimes, then in losing the war, our nation will also lose international influence and moral standing.

Most Americans want the U.S. to set a timetable for withdrawal of our forces, according to a CBSNews poll earlier this month. Unfortunately, it’s not as simple as pulling our troops out.

Pakistan is playing a double game. The nation is ostensibly our ally in the war against the terrorists. But, as the Times explained in an editorial yesterday, the ISI is maintaining its influence in Afghanistan in the expectation of an American withdrawal. But the means by which the ISI tries to hold onto power in Afghanistan works to undermine America’s position there.

The problem this presents to our nation, however, is as much a problem in Pakistan as Afghanistan. Pakistan has nuclear weapons, and the greatest danger for America and many other nations is the possibility that Pakistan’s nuclear force would come under the control of Islamic militants in that nation. To my mind, such a danger constitutes a far greater threat to us than our losing the Afghan conflict.

Our effort in Afghanistan is most importantly one theater of conflict in a fight going on in Pakistan, as well. We are waging a shooting war against the Afghanistan Taliban, but we are also waging a war of influence in the conflict between pro-West, pro-democracy groups and anti-Western Islamic factions in Pakistan.

Right now, the Times says, the Obama administration is working to strengthen our good relations with Pakistan through economic aid and a fragile military alliance. At the same time, we trying to destroy the Afghan assets of the anti-Western factions of the Pakistani government and thus working to neutralize them. This may be the most far-reaching aspect of our efforts in that region. Because of the potential consequences—the possibility that the terrorists might gain control of a nuclear armamentarium—they are not efforts we can withdraw from.

Galen Strawson, a philosophy professor at Reading University, penned an opinion column in the NY Times last week making an argument that we are not morally responsible for our actions, because we are not truly free to choose.

The argument asserts that all our decisions are grounded in our nature, and our nature is determined, ultimately, by factors over which we have no control. His view seems to be a kind of fuzzy determinism, although he never says whether he accepts full-fledged determinism, which he defines as “the theory that absolutely everything that happens is causally determined to happen exactly as it does by what has already gone before.” Whatever he believes, he presents an argument which rules out free will and abrogates moral responsibility.

Galen seems to believe that determinism is either true or false. He writes, “Current science gives us no more reason to think that determinism is false than that determinism is true.”

In fact quantum mechanics – the fundamental, well-verified theory of the nature of reality – indicates that determinism is true to some extent AND the opposite, freedom or free will, is also true to some extent. The bottom line: There is ENOUGH freedom in the universe for us to be responsible for what we do.

At the heart of the argument Galen presents against free will and moral responsibility and in favor of determinism of some kind is this proposition:

“(ii) When one acts for a reason, what one does is a function of how one is, mentally speaking. (It’s also a function of one’s height, one’s strength, one’s place and time, and so on….”

So consider this simple example: I am free to choose to jump up or not. I can jump up 2 inches or 2 feet. But I cannot jump up 10 feet high or minus 10 feet below the floor. I am free to choose to jump within a range of freedom. The range is limited, as Galen points out, by my physical body, my mental state, my time and place. But within that range, I AM free, and nothing in my past determines beforehand my actual choice, which I make spontaneously in the instant that I choose.

Quantum mechanics indicates that this is true. Freedom exists within a range and determinism exists by placing limits on the range of freedom. Events in the universe occur as the outcome of the evolution of a wave function (state vector). The evolution of the wave function of an event and the range it specifies for the outcome of the event are completely deterministic. But the actual occurrence of the event at some point within the range is probabilistic and free.

The wave function assigns probabilities to the points at which the event can take place. But there is nothing that determines in advance at which point exactly the event will happen.

Since we humans exist in the universe and our decisions are made within it, the same circumstances apply to us. We are constrained by determinism to choose within ranges of outcomes that are not so improbable that that they are impossible. But within those limits, nothing determines in advance what we choose.

Galen’s argument fails in assuming the truth of this phrase:

“…what one does is a function of how one is…”

Although this assertion seems self-evident, it is false. And QM says it cannot be true. Nothing determines in advance the actual, particular outcome in reality of the evolution of the wave function of an event like a decision.

How we are places limits on what we choose, constraining our choices to a particular set of possibilites. But nothing determines in advance our actual decisions. They are made completely spontaneously in the instant they are made.

Two research studies on rodents appearing this month show that small RNA molecules found in most cells—known as microRNAs—can stimulate or reduce craving for cocaine and cocaine-seeking behavior.

In one of the studies, conducted by scientists at Rockefeller University and published online Monday in the Journal of Experimental Medicine, the researchers made cocaine available to mice, a species known self-administer the drug. But when they used mice, the neurons of which had been modified to lack a protein necessary for making microRNAs, the animals consumed less of the drug. The scientist then identified a particular group of microRNAs likely to be involved in mediating the animals’ craving for cocaine.

Earlier this month, Scripps Research Institute scientists reported a study of rats in the journal Nature, in which they discovered a particular microRNA with the opposite effect. They found that rats given access to cocaine for extended periods produced increasing levels of a microRNA, designated microRNA-212, in the neurons of the dorsal striatum, a brain region involved in reward-seeking behavior and cocaine addiction. But as the levels of microRNA-212 rose, the rats showed an increasing dislike for the drug, which limited its consumption. In contrast, when the levels of this microRNA decreased, the rats consumed more drug and showed compulsive cocaine-seeking behavior.

MicroRNAs are short RNA molecules averaging around 20 nucleotides in length. They are found in every cell and like proteins are produced by translation of the genetic code. They regulate gene expression by interfering with and turning off the translation of a gene’s DNA code by binding to complementary sequences of the corresponding messenger RNA.

The discovery that microRNAs are involved in rodents’ cocaine-seeking behavior points to the possibility of developing treatments for human cocaine addiction. MicroRNA-212 has been found in the dorsal striatum of humans as well as rats. Thus, one possibility would be developing a drug that stimulates production of that molecule. Or drugs might be found that would inhibit production of microRNAs that stimulate drug-seeking behavior, such as those identified in the mouse study.

And since microRNAs are synthesized within cells by translation of DNA, there is also the possibility of developing a gene therapy for cocaine addiction, in which the DNA template for a desired microRNA would be inserted into a person’s cells.

Our hi-tech civilization makes use of tens of thousands of chemicals, most of which haven’t been tested for noxious effects. Inhaled, ingested, or in contact with skin, the substances sometimes cause respiratory disease, damage the nervous system, interfere with hormones, or trigger cancer. In a Scientific American article Tuesday, Paul Blanc, a professor of occupational and environmental medicine at U.C. Berkeley, answered questions about toxic chemicals.

People may get exposed to harmful chemicals in common consumer products, Blanc said. He mentioned waterproofing sprays used on shoes and leather, as one good example. The aerosols contain fluoropolymers that can cause severe lung damage.

I used one such product two days ago, Kiwi Protect-all from Sara Lee Household and Body Care. At that time, I had no idea that severe lung damage could result from ingredients in the can. This morning, I checked the label, which says only that it contains “petroleum distillates,” hardly informative. I also went to the the Kiwi website, but that divulges even less info. However, my call to a telephone number on the can to contact for “questions” confirmed that Protect-all does contain fluoropolymers.

When I applied the spray to new running shoes, I did take the precaution of using it in a screened porch with lots of airflow. Still, if I had known, I would have taken more care, like holding my breath while spraying and leaving the porch before taking a breath.

What can be done to control the use of toxic substances and increase the information available to consumers?

The Congress is now considering new legislation to overhaul the decades old Toxic Substances Control Act. It is “an antiquated law that in its current state, leaves Americans at risk of exposure to toxic chemicals,” according to Sen. Frank Lautenberg (D-NJ), who introduced the new bill, the Safe Chemicals Act of 2010. He explains on his website that the Environmental Protection Agency “does not have the tools to act on dangerous chemicals and the chemical industry has asked for stronger laws so that their customers are assured their products are safe.” The description of the bill says:

The “Safe Chemicals Act of 2010” requires safety testing of all industrial chemicals, and puts the burden on industry to prove that chemicals are safe in order stay on the market. Under current policy, the EPA can only call for safety testing after evidence surfaces demonstrating a chemical is dangerous. As a result, EPA has been able to require testing for just 200 of the more than 80,000 chemicals currently registered in the United States and has been able to ban only five dangerous substances. The new legislation will give EPA more power to regulate the use of dangerous chemicals and require manufacturers to submit information proving the safety of every chemical in production and any new chemical seeking to enter the market.

Even if the bill were to become law soon (probably unlikely in this election year), the U.S. would be catching up to Europe. In 2007, the EU’s European Chemical Agency (ECHA) inaugurated REACH, a program for “Registration, Evaluation, Authorisation and Restriction of Chemicals.”

According to the ECHA website, REACH

applies to all chemicals: not only chemicals used in industrial processes but also in our day-to-day life, for example in cleaning products, paints as well as in articles such as clothes, furniture and electrical appliances. … All manufacturers and importers of chemicals must identify and manage risks linked to the substances they manufacture and market.

Concern about thousands of potentially harmful chemicals in consumer products growing in this country, too. In May, Nicholas Kristof, the NY Times columnist wrote about a new report from the President’s Cancer Panel, which warns that “our lackadaisical approach to regulation may have far-reaching consequences for our health.”

Perhaps something will get done, and before long, I won’t be surprised by a news article informing me that a consumer product I used just a couple days previously might possibly cause me to suffer from a severe disease.

This year Washington, DC, experienced the hottest June on record, and the records go back to 1872. Yet, when it comes to taking action to reduce the CO₂ emissions that are contributing to global warming, the senators in the city are frozen in inaction. That’s the pessimistic opinion today of David Leonhardt, a business columnist of the NY Times. He writes that the 60 votes needed to pass climate legislation are not to be had at the present time. Leonhardt discusses the futility of trying to pass a bill to put a price on carbon, like cap-and-trade legislation, and he asks whether it makes sense for now just to try to legislate some rules, similar to vehicle mileage standards, that would to curb fossil fuel consumption.

What can be done and how it might be accomplished was also the subject of a Scientific American article last week. It depends, the piece suggested, on how much global warming we Americans are willing to accept. The article reviewed a new report of the National Research Council on the impacts of every degree Celsius of global temperature increase. These are a few of them:

• A 5 to 15 percent lower yield for some crops, including corn in Africa and the U.S., and wheat in India
• A 3 to 10 percent increase in heavy rainfall globally
• A 5 to 10 percent drop in rainfall in southwestern North America, southern Africa and the Mediterranean
• A 5 to 10 percent change (increases in some regions, decreases in others) in stream flow in many river basins globally
• A 15 to 25 percent decrease in the extent of Arctic Ocean sea ice

The report presents the hazards in terms of temperature changes rather than atmospheric CO₂ levels. Perhaps doing that might make the consequences easier for the public and the senators to grasp and evaluate. The report’s authors believe that doing so removes some of the uncertainty clouding the debate. Whatever the cause of the warming, the report indicates, a 3-degree increase in global average temperature means arctic ice is gone.

The SciAm article also makes the essential point that action on climate in the Congress and the country as a whole depends on the attitude of the public toward the issue.

In that connection, researchers at the Center for Climate Change Communication at George Mason University in Fairfax, VA, may have discovered a way to boost support for taking action. The scientists interviewed 70 volunteers, who each read an essay on climate change as a health issue.

The study included approximately equal numbers of people who fell into each of six attitude groups in regard to the global warming debate. Three groups accepted that it is occurring—those who felt “alarmed,” “concerned,” or “cautious” about the consequences, and three other groups had doubts—those who felt “disengaged,” “doubtful,” or “dismissive” toward the issue. The scientists interviewed each person after the reading and assessed their opinions, positive or negative, toward the essay as a whole and each of 18 sentences.

Remarkably many of the volunteers in every group “reacted positively to the information.” For example, 44% of the disengaged subjects “indicated that the essay reflected their personal point of view, was informative or thought-provoking, or offered valuable prescriptive information on how to take action relative to the climate problem.” But even more surprising was the response to the four sentences in the essay that focused on the benefits to health of curbing climate change. Most of the volunteers—both the acceptors and the doubters—reacted positively to this information. In contrast, the doubters reacted negatively to 14 other sentences in the essay, including seven that described threats to health of continuing climate change (as opposed to the benefits of stopping it), five introductory sentences and two concluding ones.

The research points to an impediment that may be interfering with building support for action on climate change. The debate so far has mostly been presented in rather abstract terms, like emissions and concentrations of CO₂ or conditions distant in place and time, like the melting of arctic ice or the expansion of deserts. Discussing the issue that way makes the consequences seem far removed. It would be better, perhaps, to talk in personal terms, like the potential benefits to people’s health. That might help to bring the issue home.

This month I officially became a senior citizen and enrolled in Medicare. So I am interested to discover that the federal government has just released a comprehensive statistical report on the age group of which I am now a member. Who are we and how do we fare? While there are few surprises in the new report, I think the data are worth checking.

In 2008, 39 million people in the U.S. were age 65 and over, 13% of the population.

We seniors live in all cities, states and regions, but the highest concentrations of us, up to 1/3 of the local populations, reside in the sun states (Florida, Arizona, New Mexico, Texas), the Great Plains from far north to the deep south, and along the East and Northwest coasts.

Eighty percent of us are non-Hispanic whites, 9% are black and 7% Hispanic. More than half of us are married, but more men are married than women, who more often have lost spouses to death. About 40% of the women live alone, compared to 20% of the men.

Three-quarters of us have at least a high school education, and one-fifth have a bachelor’s degree. These educational rates have tripled and quadrupled since 1965.

Older Americans’ income has been increasing. During the last four decades, the proportion of us living in poverty has gone down from 15% to 10%. The poverty rate of seniors is now about the same as that of all Americans. The proportion of seniors in the low-income category has declined from one-third to one-quarter. In contrast, high-income seniors have increased from less than one-fifth of us to more than one-third.

Among white Americans, median household income for older Americans is $29,000. In 2007, the median household net worth was $280,000, which was six times that of older black households, $46,000.

The proportion of men still working has been trending upward and is now near 40% among 65-69 year-olds and more than 10% for those over 70. The proportion of the women still working is growing also and is now near 25% of 65-69 year-olds, but it is less than 10% of those over 70. Forty percent of seniors’ income is derived from Social Security, 1/3 from earnings and 1/5 from pensions. Social Security provides more than half the income of 60% of seniors.

The current life expectancy at age 65 in the U.S. is 18.5 years, which is less than many other industrialized nations by a year or two. It is longer for women than men by around 5 years. Life expectancy at age 85 is about 6-7 years.

Death comes most frequently due to heart disease, cancer, stroke, respiratory illness, Alzheimer’s disease, and diabetes. Hypertension, arthritis, heart disease, cancer, diabetes, and respiratory diseases are the most common chronic diseases. But more than half of seniors of all ages rate their own health as good to excellent.

Most seniors in America have adequate diets. But few get regular physical exercise—only about 1/5 do, compared to 1/3 of younger adults. And obesity is increasing. It currently affects 32% of us, compared with 22% in 1988–1994.

Health care costs are rising fast for older Americans, going from $9,224 in 1992 to $15,081 in 2006. The fraction of older Americans’ income going to health care has also increased for those in or near poverty, growing from 12% to 28% during the last three decades.

Cyclists also grow old (a side note, but one that is marginally related to the content of this post):

I’ve been following the Tour de France all month. The race for the yellow jersey has been a struggle between two young powerful riders, Alberto Contador (Spain) and Andy Schleck (Luxembourg), who are now less than 8 seconds apart in cumulative time. Lance Armstrong, at age 38, has not played a prominent role. He suffered through two crashes during one stage more than a week ago, and as a result, he lost much time. He is now out of the running for the podium.

But today, during a mountain stage in the Pyrenees, Lance broke away from the pack and attempted show his stuff is still strong and win the stage. Several other riders joined him in the breakaway, and the group moved 8-10 minutes ahead of the peloton. In the last few kilometers, the riders in the group sprinted for the finish line, each trying to win. Lance tried his best but came in sixth.

Interviewed after the race, the great cyclist was clearly feeling his age. “I wasn’t the oldest rider in the group,” he said, referring to another cyclist, 39, who also joined the breakaway. Those were his last words to the camera today.

A typical vaccine against a viral illnesses, like those against measles or polio, stimulate the immune system to respond to respond to viral antigens—usually proteins making up the outer envelope or coat of the virus—which are shared by all virus particles of that type. For that reason, being vaccinated against either of those illnesses can protect someone against all measles or polio viruses that a person might encounter.

But that kind of protection doesn’t develop with vaccines against HIV, the AIDS virus, or against influenza A virus. HIV is extremely variable, and the virus can rapidly evolve and change the composition and structure of its envelope proteins, even as it reproduces itself inside an infected person. This ability of HIV is a major reason why efforts to develop a vaccine for AIDS have so far failed.

Influenza A virus is also a highly variable but for a different reason. Two proteins that make up its viral envelope, the hemagglutinin (HA) and the neuraminidase (NA), exist in multiple forms. There are 16 HAs and 9 NAs. From year to year, the particular combination of HA and NA that make up an influenza virus in circulation may change. For that reason, at the beginning a flu season, we need to get re-vaccinated in order to have immunity against that year’s type of flu virus.

But two research reports this from the National Institute of Allergy and Infectious Diseases (NIAID, one of the National Institutes of Health) indicate that scientists are trying to find ways to get around the variability of HIV and influenza A by developing vaccines that stimulate immunity against parts of the viral envelopes that do not change.

As reported in ScienceDaily, NIAID researchers isolated antibodies from the blood of persons infected with HIV that proved to be effective at counteracting the infectivity of 90% of all strains of the virus circulating worldwide. Then they determined the chemical structure of those antibodies when they were attached to the virus. They discovered that “the antibodies attach to a virtually unchanging part of the virus, and this explains why they can neutralize such an extraordinary range of HIV strains,” according to John R. Mascola, one of the scientists.

In the case of the influenza A vaccine, other NIAID researchers isolated antibodies effective at counteracting the infectivity of potentially all strains of the viruses from animals—mice, ferrets, and monkeys—by stimulating them to produce the antibodies with a two-step vaccination technique. First they “primed” the animals’ immune systems by injecting viral DNA encoding the influenza HA protein. Then they boosted the animals’ immune response to the DNA primer by injecting seasonal influenza vaccine or a weakened cold virus containing the HA protein.

After obtaining the antibodies from the animals, the scientists determined that these broadly effective antibodies target a portion of the HA protein that varies very little among strains of the virus.

The HIV researchers hope to utilize their knowledge of the structure of the broadly effective anti-HIV antibodies to design vaccines that are effective and work against many strains of HIV. And the influenza researchers are now testing their prime-boost immunization technique in humans to learn whether the process will work in humans also to stimulate the production of antibodies effective against many strains of influenza A virus. If they are successful, yearly flu vaccination may no longer be necessary.