One-Minute Workouts

The idea is to interrupt your workday periodically and do a full minute of vigorous exercise. Six times a day would be awesome. I’m working toward once an hour.

Here’s the rationale:

  • Exercise is the single most important thing we can do to improve our quality of life, keep our enthusiasm up, and banish depression.
  • For longevity, exercise is second only in importance to weight control.
  • Many people don’t exercise because they “don’t have time”. Well, these are exercises you can with no investment in time.
  • Exercise triggers avoidance reactions for many people. You know yourself well. For some, it’s easier to commit to a ritual trip to the gym or jog around the neighborhood or yoga before breakfast. For others, the barrier will be lower if you know it’s over in just one minute.I must say that in trying to implement this program myself, I constantly find that it’s difficult to tear myself away from what I’m doing, to interrupt my train of thought. However, I’m almost always glad that I did, because I’m more alert, the thoughts are fresher and more creative after just one vigorous minute.
  • Recent research suggests that, even for people who exercise regularly, hours of sitting poses an independent risk factor.
  • Interval training is a super-efficient way to exercise [Ref 1; Ref 2Ref 3;  Ref 4]. If you’re able to go all-out for periods of a minute or so, working so hard that your heart is pounding and you can’t catch your breath, the CV benefits compare favorably to much longer periods of modest aerobic exercise.

You don’t have to do your one minute as a painful all-out exertion, but if you’re inclined in that direction, the one minute intervals work well.

Here’s a suggestion for how to begin:  Try choosing one of these exercise minutes before every meal.  Vigorous exercise before eating signals the insulin metabolism to burn the energy you are about to consume, rather than store it as fat.

Here are 16 suggested workouts to choose from.  They all require minimal equipment, and can be done in a few square feet in an office or living room.  Mix them up throughout the day.  Some are relatively more accessible than others.  A minute of pull-ups, for example, is a feat of strength that I personally would have to work up to for quite a while.  Maybe in such cases half a minute is enough.

Note: some of these exercises come from the tradition of Kundalini Yoga.  They are accompanied by vigorous breathing.  There are two types of kundalini breathing.  Both involve motion of the stomach only, while the chest and ribcage remain relaxed.  Type 1 (called kapalabhati) is a vigorous exhalation, followed by a passive inhalation as the stomach pops back out of its own accord.  Try coughing with a hand on your belly to get a feel for it.  Type 2 (called bhastrika) is vigorous on both the inhalation and exhalation, pumping the stomach out as well as in, rapidly.

One-minute workouts – a list of exercises

     0.  Stairs are a terrific resource – available almost everywhere people live and work.
Walk or run up, and a minute will feel like a good workout.

  1. Jump rope (you can use an imaginary rope in a pinch)

  2. Sun salutations (from the Hatha yoga tradition)

  3. Kundalini breathing with clasped hands, raised and lowered.
    Extend both arms out in front, both thumbs down, right wrist over left wrist
    Clasp hands, palm to palm
    Inhale and raise straight arms overhead
    Exhale forcibly from the abdomen bringing straight arms down to your lap

  4. Kundalini breathing with knee bends

    Squat with both hands on the ground outside your knees
    Exhale forcibly as you straighten legs, keeping hands on the ground (or close)
    Inhale passively as you return to squatting, catching weight in your hands
    on the way down, (but using legs only on the way up).

  5. Jumping jacks

  6. Pushups  (use handles if you like to avoid wrist strain)

  7. Pullups (chinning bars install in doorways)

  8. Touch opposite toes

Stand with the legs apart, arms extended horizontally
Bend from the waist, knees straight, touching left foot with right hand  (or as far in that direction as flexibility permits)
Lift from the lower back coming up to position one
Repeat alternating left and right

9. Situps or crunches

10. Lie on back, raise legs and arms  to vertical.  Replace legs and stretch arms overhead on the floor.  For extra credit, you can dig heels into the floor and raise tail between leg lifts.

11.  “Marching” from pushup position

alternate sides

12.  Chorus line  

 Step back, right knee to the ground.
Stand and kick right foot to left hand.
Alternate sides.


13.  Pilates ‘swimming’

Lying on stomach, alternately
raise R-hand, L-leg, then
L-hand, R-leg

14. (Kundalini variation)  Body in “planck pose” with straight back, extended legs.
Lift R hand, L leg,  then L hand, R leg   alternating


15.  (The longest minute) Raise both arms overhead and shake hands vigorously from the wrists, while breathing bastrikha style as fast as possible.

16.  Sit on the floor with extended legs.

Place hands on the floor behind you, fingers pointed forward.

Lift the tail up off the floor.

Alternately raise the legs and replace them.


Anti-Oxidants can Nullify the Benefits of Exercise

A lot of people still try to understand aging as a kind of accumulated damage, or wear-and-tear.  Theories of oxidative damage are one poular version, and anti-oxidants have been promoted as a remedy for aging by people who should know better.  One trouble with the damage theories is the of things that increase damage, but that lengthen life span.  Exercise is the best example, but there are many others.

For twenty years and more, it has been clear that anti-oxidants don’t lead to longer life.  More recently, there is evidence that anti-oxidants can actually take away the benefits of exercise.  The latest such study was reported just last week.


Writing in her NYTimes column this week, Gretchen Reynolds reported on a Norwegian study* combining vitamin C and E supplements with a vigorous exercise program.  The study recruited people who were already exercising, and intensified their aerobic program for 11 weeks, with both endurance exercise and interval training.  The outcome that they highlighted was in the mitochondrial metabolism.  Mitochondria are tiny “organelles”, hundreds of them in each cell, burning sugar to supply the cell with energy.  One of the things that happens to increase strength and endurance in response to exercise is that the cells grow new mitochondria, and the existing mitochondria become more efficient.  In the Norwegian study, this seemed to be happening on schedule in the test subjects who exercised without vitamin supplements, but not in the group taking vitamins.  Nevertheless, endurance capacity of both groups was imroved by the exercise program.

The first result of this type (that I am aware of) was reported from a German study in 2009 **.  In this study, non-exercisers were given an exercise program for just 4 weeks, and their insulin sensitivity and glutathione both improved; but supplementation with vitamins E and C blocked these benefits.  I think both these are pretty good markers for aging – more basic and more closely-related to aging than mitochondrial markers.  Of course, what we really would like to see would be long-term effects on mortality and longevity.

In between, there have been a number of studies confirming the effect.  Here’s one that found that generation of new mitochondria is blocked by alpha lipoic acid.  Another one related glutathione and mitochondrial markers to vitamin C.  There are studies of old and young people, people who did no exercise prior to the experiment, and people who had exercised regularly, and were challenged with more.  There were also some studies that failed to find an effect [ref for rats; ref for humans]

In one study of mice, very large doses of resveratrol seemed to give the mice great strength and endurance.  However, in a human study last year (from this same Norwegian group), resveratrol diminished the benefits of exercise.

The theory is that temporary elevation of ROS (= free radicals, sources of oxidative damage) is a signal that tells the body to build new muscle, to proliferate mitochondria, and to improve the sensitivity to insulin.  All these changes are plausibly related to better strength and health, and perhaps youthfulness.  The fact that the effects appear when measuring a variety of outcomes from a variety of anti-oxidants (vitamins A, C, E, CoQ10 and resveratrol) lends to the credibility of this idea.  Vitamin C, in particular, is intimately related to the energy metabolism of the mitochondria, lending plausibility to results for vitamin C in particular.


The bottom line, for me, is that results are still quite sketchy, that we don’t know the full story, that some physiological benefits of exercise seem to be blunted for some people, if certain anti-oxiadants are taken in combination with the exercise program.  But the broader context is clear:  Anti-oxidant vitamins have never been shown to increase life span in rodents, or to reduce mortality in humans.  But exercise robustly increases life span in animal studies, and reduces mortality in humans.  For me, the evidence is clear enough to advise against vitamin E and C supplements for people who exercise.  For resveratrol and CoQ10, I remain uncertain.



* I get error messages when I try to pull up the original study in the Journal of Physiology.  If I get a good web reference to the study, I’ll link it above and erase this footnote.

** There are precursors that go back to 1971, when competitive swimmers were given vitamin E, and it was reported to slow them down.  Here’s a 1997 study that reported CoQ10 supplementation dragged down performance improvements from high-intensity sprint training.

A Heavy Hitter Weighs In Against Evolutionary Theory

Demography is the statistical study of population age structures, or the study of aging and fertility through population statistics.  It’s not deep math, but it definitely attracts people who love numbers.  The world’s formost demographer is James Vaupel, an American who has been working at the Max Planck Inst in Germany most of his career.  Annette Baudisch is a brilliantly creative protege of Vaupel, who has come into her own in the last decade*.

The point of this is that when such people declare that evolutionary theory doesn’t work, we ought to be listening.  We the evolutionary theorists, we the gerontologists, and we who simply seek a path to a longer, healthier life, and we who have been influenced, perhaps unawarely, by tacit assumptions about evolution.

Essay in Science a year ago, Survey in Nature last month

Last month, these two world-class demographers published a cross-species study correlating fertility with the rate of aging, and they report results that are deeply at odds with the predictions of evolutionary theory.  They are not shy about saying so.

The classic evolutionary theories of aging provide the theoretical framework that has guided aging research for 60 years. Are the theories consistent with recent evidence?

At the heart of the theories lies the observation that the old count less than the young: Unfavorable traits are weeded out by evolution more slowly at higher ages; traits that are beneficial early in life are selected for despite late life costs; and resources are used to enhance reproduction at younger ages instead of maintaining the body at ages that do not matter much for evolution. The decline in the force of selection with age is viewed as the fundamental cause of aging. It is why, starting at reproductive maturity, senescence—increases in susceptibility to death and decreases in fertility—should be inevitable in all multicellular species capable of repeated breeding. Yet, this is not the case. Increasing, constant, and decreasing mortality (and fertility) patterns (see the figure) are three generic variants that compose the rich diversity of life trajectories observed in nature. For vertebrates, reproductive trajectories are commonly hump-shaped, and death rates may start rising much later than reproductive maturity. Thus, a new view on the fundamental causes of aging is needed to explain the clash of theory and data.  [from a 2012 Science essay by the same authors]

This is the kind of condensed academic prose that makes scientific communication so efficient to specialists and so opaque to anyone on the outside trying to figure out what’s going on.  They have captured the core of three evolutionary theories that are currently considered acceptable.  (If you are already familiar with them, you will recognize what they’re talking about; if you would like more detailed accounts of the three theories and their failures, I have written about that here.)  They go on to say that aging in nature has a richness and diversity that these simple theories do not begin to address.  “theories to explain the ultimate evolutionary causes of the varieties of ageing…are in their infancy.”

Baudisch pioneered the study across species of different shapes of life history curves, regardless of the time scale on which they unfold.  In other words, some species have life plans that unfold over days, and others over decades.  Let’s ignore that and stretch out the time axis so that they all fit in the same plot.  Some species (e.g. modern man) have a high rate of survival right up to the end, and then everyone dies in a narrow range of old age; while other species tend to die at a steady rate, unrelated to age, and for some they are actually less likely to die the older they get.  This last case seems strange to us.  Baudisch and Vaupel coined the term “negative senesence”, but it doesn’t have to look like Benjamin Button.  Just think of a pine tree that gets larger and stronger over the decades, and thus more resistant to a drought or a fire or a windstorm, thus less and less likely to die with each passing year.

(You can blow up the figure below to view details.)  The blue line plots fertility over a lifetime:  how many offspring are produced per unit time; the red line plots mortality: what is the probability of an individual dying before the next year or the next day?  These many different plots represent the diversity of different patterns of aging in nature.  The graphs are all stretched out or compressed in time so that each box contains one lifetime, whether that be a day or a decade.

The top row codifies the life plan that is most familiar to us, because it is ours.  Fertility peaks in early life, then declines.  For females, it declines to zero.  Mortality is modest for a long while, then it climbs steeply and everyone dies.  This is the story we take for granted.  It is the form of aging shared by humans, guppies, and certain sea birds.

The next line shows life plans that are similar, but where mortality rises more slowly, so that age of death is spread out over time.  This row contains some familiar mammals like deer, lions, and orcas, but it also contains water fleas and bdelloid rotifers, microscopic creatures famous (at least to biologists) for their chastity.

Further down are stranger and less familiar life plans, including those where fertility rises as mortality falls through most of the life span. According to evolutionary theory, metabolisms aren’t supposed to be able to do this.  The whole reason for aging is (according to theory) the necessity for compromise.  Some organisms can have their cake and eat it.  (Would it be mixing metaphors to call this an evolutionary free lunch?)  When theory accounts for aging in other species as a sacrifice of longevity for fertility, the story rings hollow.  Why are some species but not others compelled to this compromise?

Of special significance is post-reproductive life span.  Human females go right on living after they have lost their fertility.  This is supposed to be explained by the need to care for her grandchildren.  But in this chart are several other species that also outlive their fertility, including elephants and ground squirrels but also worms and guppies that don’t care for their young at all, let alone their grandchildren.

This poses a big problem for evolutionary theories of aging, because maintaining the body through an extended life span is always presumed to be costly in one way or another – that’s why the body skimps on the job, and the body is permitted to deteriorate with age.  Why, then, would the body take the trouble to preserve itself for a time when it was unable to reproduce, useless to the species and invisible to evolution?  “There should be little or no postreproductive period in the normal life-cycle of any species.”, predicted George Williams in his seminal paper (1957) which has inspired most modern thought on the subject.  (I have written about this topic, suggesting that the post-reproductive segment of the population provides a stabilizing buffer in times of famine, helping to guard against extinction.**)

The bottom line

The bottom line is that nature has been able to do pretty much anything she wants with the metabolism of aging, and the trajectory of mortality that comes from that metabolism.  Most of the evolutionary theory on the subject is based on the idea that natural selection could never affirmatively choose aging if there were a choice.  Aging is bad for the fitness of the organism that suffers aging, and theory says that natural selection should always work against aging.  If most living things suffer decline with age, leading to death, this must have taken place despite natural selection.  There must be some genetic constraints, or physical limitations, or conditions beyond control of the genome.

This survey of Baudisch and Vaupel tells a different story.

For fifteen years now, I’ve been saying that the evolutionary theory of aging doesn’t work, and that it’s high time to stop making excuses for the old theory, to adopt a new theory that fits better with empirical reality.  I have argued from experiments and from field surveys and from general knowledge and from logic, and I have found many people who agree, and maybe a few who have been turned around by my presentation.  But I don’t have the stature that would attract a large readership, or compel anyone to take my word for it.  Maybe they’ll listen to Baudisch and Vaupel.



* I first became aware of Baudisch in 2004.  One of the most common of ancient human follies is to imagine that the way things are is the way things must be.  William D Hamilton – a biologist smart enough to know better – published in 1966 his “proof” from fundamental precepts of evolution that all living things must decline with age.  In a paper provocatively titled, “negative senescence”, Baudisch and Vaupel surveyed a number of animals and plants that don’t decline with age – quite the opposite, they continue to get larger, stronger, and ever more fertile.  “Negative senescence”.  They even included their own “proof” that aging was impossible, and that all living things ought to grow ever stronger and more fertile.
[back to text]

** In this article, I have proposed that population stability is a major part of fitness in nature.  Populations that swing too wildly up and down are in danger of extinction, and it makes sense that such extinctions are a form of Darwinian selection, and they would have left their mark on the genome.  In the case of post-reproductive life span, here’s how it would work:  Sometimes there’s plenty of food, and the population is expanding on a trajectory that’s going to lead to overpopulation and a crash.  Then it’s a good thing to have these older, infertile adults around, because they eat up some of the food, but they don’t contribute to population growth, while the population is growing too fast already.  At other times, food may be scarce and the population is shrinking.  Then the post-reproductive population will be the first to go, because they are old and weak.  They are expendable, from a demographic perspective, because when they disappear there’s no loss to the population’s potential for growth, but there is a benefit when competition for scarce food is reduced.  This is the sense in which a post-reproductive population can provide a buffer, protecting against steep population fluctuations and potential extinction.  [Link to article in Oikos] [back to text]

An easy way to make stem cells, & A new way to eliminate senescent cells

This week, I report on three items from the biomedical literature:

1) Creating pluripotent stem cells may be much easier than we thought.

2) Direct evidence that cancer is not a function of a cell gone rogue, but rather a systemic disease, dependent on cellular environment and chemical context.

3) Nailing the coffin of the theory that aging comes from the accumulation of a lifetime of DNA damage.

In aging science, there are two kinds of “unexpected” results. The first disagrees with theory. These have become commonplace and are no longer really a surprise. Aging “theory” has become so disconnected from experimental results that when contradictions arise, the theorists respond only that “aging is complicated”. But the second is a disagreement with what we thought we knew in the laboratory. These are truly unexpected. In honor of Chinese New Year, I offer this week “Two from Group A and One from Group B”.


 Aging is not caused by mutations in the cellular DNA accumulating over a lifetime*

An old theory of aging says that there is a chance of DNA mutation with every cell replication. The “germ line” consists of egg and sperm cells that will be passed to the next generation and on and on, so natural selection has been strong to assure replication is super-accurate. But within a single lifetime there are cells that are used to build the body. Skin and muscle and blood cells will all die with the body, so there is less evolutionary pressure to keep their DNA pristine. It’s more important to the individual’s success that the replication take place fast and efficiently, even at the expense of accuracy (so the theory goes). So we might expect that little inaccuracies might accumulate over a lifetime, leading to dysfunction.

This theory dates all the way back to 1959, proposed by a nuclear physicist named Leó Szilárd**.  Szilárd assumed that all cells in the body make copies of themselves – skin cells make more skin cells and liver cells make more liver cells. Stem cells had not yet been discovered. Like a good physicist, he worked out the mathematical consequences of the theory in the abstract. Almost nothing was known about mutation rates at the time, so he could fill in parameters that made the theory work.

So why does aging proceed only gradually for most of a lifetime, and then just at the time when an old individual is slowed down, both in activity and in cell replication, aging begins to proceed at an accelerating pace, becoming catastrophic in the late stages? A few years after Szilárd, Leslie Orgel answered this question and the theory of somatic mutations became known thereafter as Orgel’s Hypothesis. What Orgel added to the Szilárd theory was that some mutations are more important than others. Indeed, some mutations affect replication itself, and they cause more inaccuracy. Thus inaccuracy in the particular genes that affect DNA replication cause ever more mutations, and more inaccuracies in a vicious cycle. This was Orgel’s explanation for the fact that aging does not proceed steadily over a lifetime, but starts slow and then accelerates, plunging toward death.

Of course, once stem cells were discovered (just a few years after Orgel’s paper), there was no longer any reason for copying errors to beget copying errors, and no basis for the accelerating schedule that characterizes aging. (Indeed, this is thought to be the reason that the body uses specialized stem cells.) This should have been a mortal blow to the theory. And further, the theory also conflicted directly with experiment. Cells from old mice and young were infected with a virus. The virus commandeers the host cell’s machinery to copy and transcribe its own DNA; so it was thought that if this machinery becomes less efficient with age, then the virus would spread more slowly through the old cells than the young. No such effect was found. [Rabinovitch & Martin, 1982] Another lab set out very deliberately to test the Orgel hypothesis by culturing cells over a long period, then counting the transcription errors in younger and older cell lines. They found no difference. [Harley et al, 1980]

So how surprised can we be with this week’s results?  Genomes were compared for pairs of identical twins 40 years old and 100 years old. The assumption is that, at birth, the genomes of each pair were identical, but that a lifetime of random mutations could cause the twins’ genomes to diverge. The result was no detectable mutations in the 40-year-old pair, and only 8 mutations out of 3 billion base pairs in the centenarians. 5 of the 8 were in non-coding regions of DNA.  Mutations at this level are likely to be utterly insignificant.

For me, the interesting question is why theories like this are still considered viable, though they have been falsified on multiple occasions.


Cancer begins not with a single rogue cell, but with a weak or toxic metabolic environment.

Just a few years ago, the mainstream view of cancer was that it was the result of a rare accident, a cell that just happened to mutate in such a way as to make it reproduce out of control. Once the mutation took place (so the theory went), any single cell would become an unstoppable parasite, spreading through the body and halting only with the patient’s death.

It has come to light more recently that the body has many defenses against cancer cells, even after they have become malignant. Hence, cancer should be regarded as a systemic disease, not a cellular anomaly.  Now, many cancer biologists believe that these mutations to a cancerous state are common occurrences, but that most cells are smart enough to detect their own diseased state, and this triggers apoptosis=programmed cell death. For those few that escape apoptosis, a healthy immune system is able to detect them and attack them in the same way foreign microbes are targeted and killed [ref].  Hence immune therapies for cancer have become the most promising line of research in oncology today. (It was Science Magazine’s “breakthrough of the year” a few weeks ago.)

In an Italian study published last week, rats were treated with a chemical that reliably causes liver cancer. Half of them developed the disease. Another group of rats was treated with the same chemical, but they were also injected with 8 million normal liver cells (= a fraction of a ml — a lot for a rat). These were not stem cells, just end-differentiated liver cells. (It is known that such cells find their way to the liver – we don’t know how.) But none of the treated rats developed cancer, compared to half the untreated animals.

Increasing evidence indicates that carcinogenesis is dependent on the tissue context in which it occurs, implying that the latter can be a target for preventive or therapeutic strategies. We tested the possibility that re-normalizing a senescent, neoplastic-prone tissue microenvironment would exert a modulatory effect on the emergence of neoplastic disease.


Rats were exposed to a protocol for the induction of hepatocellular carcinoma (HCC). [One] group of animal was then delivered 8 million normal hepatocytes, via the portal circulation. Hepatocytes transplantation resulted in a prominent decrease in the incidence of both pre-neoplastic and neoplastic lesions. At the end of 1 year 50% of control animals presented with HCC, while no HCC were observed in the transplanted group.

Extensive hepatocyte senescence was induced by the carcinogenic protocol in the host liver; however, senescent cells were largely cleared following infusion of normal hepatocytes.


Note the last sentence. Senescent cells are cells with short telomeres, and they are known to be a risk factor for all diseases of aging. In a 2011 experiment from Mayo Clinic, a genetically-engineered trigger was introduced to allow the experimenters to eliminate senescent cells at will; the result was that disease was avoided and life span extended. This week’s experiment raises the possibility that simply introducing healthy, young cells can signal the body to eliminate the bad actors. How does this work? Is it through chemical signaling that can be induced without the cells? This is a promising avenue for research.

Group B

An easy path to stem cells?

Background: The cells in our bodies are mostly specialized to perform a task. Nerve cells or muscle cells or skin cells or blood cells do their particular jobs. There are also stem cells, whose job is to grow more of every other kind of cell. Stem cells are important for renewing body tissues and for healing. Specialized stem cells can grow into several kinds of tissue, for example white or red blood cells. The most powerful stem cells are completely undifferentiated, and they have the potential to grow into any other kind of cell the body might happen to need. They are called pluripotent stem cells.

Before the Republicans, with their superior ethics, took over the rules of research at NSF, there was an abundant supply of stem cells for research, gleaned from aborted and stillborn fetal tissue. At the beginning of the GWBush Administration, that source was cut off (for reasons that seemed more political than moral). But then the Law of Unintended Consequences kicked in. There was a surge of interest in the basic science of stem cells, with a practical focus on the question: Is it possible to turn an ordinary differentiated cell back into the stem cell from which it was derived? There ensued a race to create IPS cells in the lab. (IPS stands for “INDUCED pluripotent stem cells”.)

The race was won by a Korean lab, which first created IPS cells by careful doctoring of ordinary skin cells. The next breakthrough came from a Japanese lab. Their technique was refined and streamlined until, a few years ago, it was common to say that just 4 chemicals are needed to turn a skin cell back into a stem cell.

In Nature this week is an article about another Japanese group that claims an even easier path to create stem cells, just by starting with ordinary skin cells and reading them the Riot Act. No specific chemical treatment was used, but the cell did the job itself in response to stress. They report that the specific stress that seems to work best is an acid bath.

IPS cells created in this way were introduced into an embryo, in order to demonstrate that they have the ability to grow into any of the body’s tissues. They were able to produce a chimeric mouse, meaning that different cells in the mouse’s body were derived from different parents.

This result was truly unexpected. Many labs have worked for years to come up with a reliable technique for creating stem cells. None of them has reported that it was easy. Why this should work is yet a deeper mystery. It is reminiscent of certain species of jellyfish and beetles that revert to their larval state when stressed, and, when conditions improve, can begin life anew with a full life span ahead of them.


* Confusingly, this hypothesis has nothing to do with the “Mutation Accumulation Theory of Aging”. The latter concerns random, detrimental mutations that (hypothetically) only affect the organism late in life, after most have died of other causes. Therefore these become invisible to natural selection, and they accumulate as part of what is called “genetic load”. The present article is about a metabolic theory, not a genetic theory. It is the hypothesis about mutations that accumulate over a single lifetime, not in the genetic material but in the stem cells that renew the body’s tissues.

**Szilárd was a Hungarian-American who first suggested the possibility that nuclear fission could be realized as a self-sustaining chain reaction, which is the basis for both nuclear bombs and nuclear power. As a Jewish refugee, a brilliant physicist, and a grateful American, Szilárd worked on the Manhattan Project during World War II; but he personally urged President Truman not to use the superweapon he had helped create against the Japanese people, but to demonstrate it instead in Tokyo Harbor. After the war, he helped found the Council for a Livable World—an early, high-profile disarmament advocacy group—as he spent the last years of his life studying not physics but biochemistry.