Paradigmatic norms and paradigm paralysis

PARADIGMATIC NORMS AND PARADIGM PARALYSIS

“This had made me aware for the first time of the well-disguised myth that they and the academic institutions they represent are bastions of a free exchange of ideas. They are – but only of those ideas that don’t ‘rock the boat’, that refrain from challenging hallowed taboos.”

jack kevorkian

Paradigms have two aspects. The first aspect of a paradigm is that it is a set of shared preconceptions that are assumed to represent objective reality. The second aspect of paradigm refers to a framework for action that encompasses all the values, techniques, and theories shared by the members of a scientific community.

Using Longevity of Surrogate Species as the Predominant Metric

Under the current paradigm, the typical approach to addressing the infirmities of aging is to conduct experiments designed to ascertain how to make lab rats live longer. Two quotes from the blog of the founder of the Longevity Fund,¹ Laura Deming,² illustrate the pervasiveness of this paradigmatic norm.

“So what is the study of aging? I sum it up as the following: trying to figure out what kinds of damage accumulate with age, how to reverse that accumulation and the search for switches that we could flip in human biology…” That quote aligns perfectly with the New Paradigm. How can we correct the environmental conditions that are preventing our maintenance systems from reversing the accumulation of damage that results in FDS? However, her blog is devoted almost entirely to factors that have been shown to extend the lifespan of rats (e.g., “95 things that make mice live longer”).

For someone who is not indoctrinated into the aging paradigm, it seems curious that so much money and energy is being invested in an approach that is wholly reliant upon the assumption that an intervention that would allow mice to live longer would necessarily have a beneficial effect on progressive dysfunctionality/FDS in humans. However, this approach is dictated by the norms of the aging paradigm. The paradigm assumes that the reason that we are afflicted with FDS is that evolution wants us to die someday.³ Thus, under the norms of the aging paradigm, in addressing any issue relating to aging, including FDS, the only relevant metric is longevity. It is very difficult to study human longevity – humans take too long to die. So mice are used as surrogates.

Using simple organisms as surrogates might make sense if there were an aging process that utilized the same mechanisms in all species. But FDS is not caused by any such mechanism. FDS is the result of an environmental agent interfering with the effective functioning of the human maintenance system. The human maintenance system bears as much similarity to the maintenance system of a yeast, fly, worm or lab rat as does the skeletal muscle system or the central nervous system. If the scientific question is, as it must be, what causes FDS in a human, then a great deal of the research using surrogates is off the mark.

For example, caloric restriction has been shown to significantly increase the longevity of lab rats. That makes sense because, by slowing metabolism, caloric restriction will reduce the rate at which intrinsic damage is inflicted. Since the damage side of the equation is more important than the maintenance side in short-lived animals (because they have rudimentary maintenance systems), caloric restriction does extend the life of lab rats. One suspects that lab rats would also do well in a zero gravity environment. However, no study has convincingly demonstrated that caloric restriction extends life in humans, and it is well established that a zero gravity environment has a deleterious effect on humans, akin to greatly accelerated aging. That’s because, in humans, the maintenance side of the equation is the dominant variable. Extreme caloric restriction will not enhance (and may have a negative impact on) the functioning of the human maintenance system. And the absence of gravity, although slowing the rate at which intrinsic damage is inflicted, seriously disrupts one or more of the human maintenance processes.

The Aging Paradigm Rejects Theory

Any given field of physical science typically has two major branches. The theoretical branch attempts to create a conceptual framework that describes and explains objective reality. The experimental branch uses experimental tools to probe individual phenomenon within that framework. The advancement of science generally depends on the interplay between experimental studies and theory.

A fundamental problem with the aging paradigm is that it is not based on theory at all. There is no generally accepted scientific theory that explains why FDS should be part of the human genome. Neither camp in the PA/NPA debate has ever come up with a convincing reason why humans should become progressively less functional with advancing chronological age. They are merely trying (unsuccessfully) to come up with a rationale that would explain how it is even possible that a trait such as FDS, which is so clearly detrimental to survivability and reproductive success, could be genetically inherited.

The foundational premise of the paradigm – the assumption that FDS is a genetically inherited trait – is based upon a variation on the black-swan fallacy. The black-swan fallacy is an inductive fallacy that states that if something has never been observed, it cannot occur. In other words, just because something has always been observed in a certain way, it is always that way as a matter of universal principle. The example that gave its name to the fallacy is “Every swan that I have ever seen is white; therefore, there can be no black swans.”

Historically, older humans were observed to suffer the progressive dysfunctionality that the Institute labels “FDS.” The black-swan fallacy is the conclusion that since older humans typically suffer from FDS, all older humans must inevitably fall victim to FDS. A series of observations has been turned into a universal principle. That leads to the following logical fallacy, which is at the heart of the aging paradigm – if, as a matter of physical law, all older humans suffer from FDS, then it must be a genetically inherited trait.

There have been a number of advances in scientific knowledge that expose the flaws in that analysis. FDS is not limited to old people. The typical human exhibits diminished functionality early in the third decade of life. So now the onset of FDS is linked to “reproductive maturity.” But lots of humans show no signs of FDS until much later in life. So it’s no longer even a black swan fallacy. Instead, the aging paradigm is based on the dubious conclusion that since most humans start showing signs of FDS soon after reproductive maturity, it is impossible for any human (even those who show no such signs), to have maintenance systems that are effective after the age of 20.

Rather than delve into such issues, normal scientists simply reject the notion that any change to the prevailing paradigm is necessary or even possible. Thus substantially all life scientists are experimenters rather than theoreticians. That’s not to say that researchers do not attempt to explain the results of their experiments. It’s that they reject the possibility that their perception of the big picture could be inaccurate. This attitude is akin to the attitude life scientists had before the acceptance of the Germ Theory, or physicists had before Einstein proposed his theories. Today’s life scientists, like all life scientists throughout history, are comfortable in the knowledge that, at least with respect to the big picture, they already know everything that is knowable. And, based on that knowledge, a number of them have concluded that there will never be a theory of aging.

Reliance on Statistics

Because the aging paradigm precludes the concepts of cause and effect, aging researchers rely almost exclusively on data and statistical probabilities. However, statistical associations are nothing more than statistical associations that can support multiple versions of reality. For example, it is undisputed that the typical human accumulates progressively more intrinsic damage with advancing chronological age. A PA proponent would argue that the progressive accumulation of damage is evidence that supports the notion that there must be a physiological mechanism (i.e., an aging process) that causes that damage. An NPA advocate would argue that the same evidence proves that evolution did not bother to provide humans with a mechanism that would prevent the accumulation of damage after the subject had had an opportunity to reproduce. And the same data is consistent with the Institute’s view that the intrinsic damage is accumulating only because some environmental factor is interfering with the proper functioning of the maintenance system.

A major problem with the aging paradigm is that statistics are used in lieu of theory. For example, a recent statistical survey concluded that the typical human reaches a physiological peak at the age of 27. The survey itself met all of the standards for a peer-reviewed study. Thus, the statement that humans reach a physiological peak during their third decade is reported as an empirical fact. As long as everyone understands that the number is nothing more than a statistical average, no harm is done. The problem is that biology is a natural science. So people assume that there is something more than a statistic behind the statement that it is an empirical fact. Since biology is a “hard science” it’s reasonable to assume that there must be a scientific theory that explains why all humans must start showing signs of aging after that age. But there is no theory and there is no scientific law. There are only statistics and averages.

To illustrate the absurdity of relying solely on statistical associations in lieu of theory, the same study concluded that, on average, a human male’s income reaches a peak at the age of 47 and that the average maximum income is $57,000 per year. The difference between social sciences and natural sciences is that when it comes to the social sciences, everyone understands that statistics are merely statistics. But that statement holds true regardless of what discipline is involved. No one believes that a maximum income of $57,000 per year is a genetically inherited trait. But there is as much scientific support for that proposition as there is for the assumption that the FDS that afflicts a typical 20-year old human is a genetically inherited trait.

Does it make a difference that historically there is a very strong statistical correlation to support the proposition that everyone starts declining by the age of 30? That is still just a statistic, rather than a scientific theory or proof that the decline is hardwired into our DNA.

Especially when an environmental factor could explain the statistical correlation. For example, suppose everyone over the age of 26 suffered from chronic non-acute vitamin C deficiency. In that event, everyone would start showing symptoms of scurvy within a year or two. The result would be a universal physiological peak reached at the age of 27. Moreover, one could conclude from those statistics that scurvy is inevitable, and thus a genetically inherited trait. If the deficiency were never remedied, everyone who did not die prematurely would eventually die from scurvy. Everyone would assume that, like FDS, scurvy was an aging process that was designed to ensure that all humans have a finite lifespan.

Paradigm Paralysis

For well over 160 years, every academician and scientist has known that the core preconception of the aging paradigm – that progressive diminution in functionality is a genetically inherited trait – is diametrically opposed to the principles of natural selection. But they persist in the futile effort to contort the theory to fit the preconception. One might question why, prior to the work of the Institute, no one has publicly questioned the preconception itself. The refusal of the scientific establishment to entertain notions that conflict with the aging paradigm is a classic case of paradigm paralysis.

Per Thomas Kuhn, the preconceptions shared by the practitioners within a paradigm render even the possibility of alternatives counter-intuitive. To a conventional academician or scientist, questioning the paradigm is akin to questioning reality itself. Thus a fundamental characteristic of all paradigms, including the aging paradigm, is that normal scientists cannot and do not question the paradigm.

In the minds of most people, because all humans get old and die, there is an inextricable linkage between the “infirmities of aging” – what the New Paradigm labels “FDS,” and death. Thus our subjective perception is that all complex organisms have a physiological process that is designed to cause death – an “aging process.” This belief is so ingrained that it goes beyond mere subjective perception. There is a metaphysical component. People form religious beliefs to cope with the knowledge that they are going to die. Some higher power wants us to die, and thus FDS must be part of that dying process. To question that preconception, as the Institute does, is blasphemy not only because it is questioning the presumed reality created by a powerful paradigm, but because such questions threaten to trespass beyond science into religion.

Even if a normal scientist were inclined to question the paradigm, he or she would be heavily incentivized not to do so. The reality is that, like everyone else, scientists have to earn a living. That means publishing articles and obtaining research grants for additional studies that generate more published articles. The persons who make decisions regarding granting funds for studies and what articles get published share the preconceptions that render any questioning of the paradigm counter-intuitive. No grant proposal that is inconsistent with the current paradigm would ever be approved for funding. No article questioning the current paradigm would be considered by an academic publication and, if so, it wouldn’t pass peer review.

A related paradigmatic norm is that only a scientist or academician with credentials establishing that such person is, per the Kuhn characterization, a “normal scientist,” and thus thoroughly indoctrinated into the current paradigm, is permitted to express an opinion about the paradigm. If someone who is not a scientist or academician were to discover significant flaws in the paradigm, he or she would have no means of communicating those findings to the world at large. An article written by someone who does not have the proper academic credentials will be rejected by any academic journal or other publication without even having been read. And the only accepted means of communicating any science-related concepts is through the publication of an article in a recognized academic publication.

In other words, no normal scientist or academician would or could publish a paper challenging the current aging paradigm. And no article generated by anyone other than a normal scientist or academician will be considered for publication by any academic journal. These paradigm-protecting norms help explain why such a flawed paradigm has been able to persist for so long.

Why Paradigm Paralysis Is a Problem

The current paradigm provides a comfort zone for scientists. Since “everyone knows” that FDS and the resulting age-associated degenerative diseases are the inevitable consequence of a natural aging process, scientists and the medical establishment feel no pressure to make any progress in the battle against age-associated degenerative diseases. Both sides of the PA/NPA debate accept the misconception that the accumulation of damage that ultimately results in age-associated degenerative diseases is an aspect of a natural, genetically inherited aging process. Thus, assuming that it were possible to declare victory in the PA/NPA debate, the resolution of that sterile debate would have no impact on the real world.

As discussed in the essay entitled “Pharmaceutical Interventions for Age-Associated Disorders,” the pharmaceutical industry generates enormous profits marketing drugs that purportedly treat symptoms , but have no direct effect on the root causes, of age-associated degenerative diseases. But everyone is comfortable with that because the root cause is assumed to be aging and aging remains a complete mystery. The concepts set forth in the New Paradigm are a direct challenge to that comfort zone. If a sizeable portion of the public came to understand that FDS is in fact a preventable and curable degenerative disorder, they would demand solutions.

Confirmation Bias

Kuhn identified confirmation bias as another mechanism that (intentionally or unintentionally) results in the perpetuation of an existing paradigm. Confirmation bias is the tendency to search for, interpret, favor, and recall information in a way that confirms one’s preexisting beliefs. The effect is especially strong for emotionally charged issues and deeply entrenched beliefs, such as the aging paradigm.

For example, the reason “everyone knows” that FDS is a genetically inherited trait is that “all” older humans exhibit symptoms of FDS. Assuming the factual premise were accurate, the conclusion would be a classic example of the black swan fallacy – the false conclusion that if a phenomenon has not been observed then it must be impossible.

Aside from the logical fallacy, there is a significant element of confirmation bias in the premise itself. There are in fact older humans who do not have any symptoms of FDS. But any evidence of the existence of such persons is ignored because our preconceptions tell us that their existence is impossible. When actually confronted by such a person, the person is dismissed as an anomaly, or the reaction is limited to the observation that the person is fortunate that he or she doesn’t age as fast as others. But in order for a 60-year old person to have no symptoms of FDS, that person would have to be endowed with a maintenance system that was fully effective. Evolutionary principles dictate that if even one such person exists, then all humans have the same genetic capability, and thus FDS is not a genetically inherited trait. But conventional scientists choose to ignore or discount the evidence.

Another critical example of conventional scientists’ confirmation bias relates to the potential effectiveness of maintenance systems. NPA proponents generally concur that biological aging is the result of maintenance processes failing to do a sufficiently good job of preventing and/or correcting intrinsic damage, thus allowing the damage to accumulate. But rather than examining the enormous amount of readily available information regarding human maintenance processes, they ignore it. Instead, they simply assume that that since most species appear to lose functionality with advancing chronological age, maintenance systems are inherently ineffective.

But NPA proponents have for decades indirectly cited the effectiveness of maintenance systems in their debate against PA proponents. Since the 1950s, a core NPA argument is based on the fact that, in the natural world, all organisms die of non-aging related causes (predators, starvation, etc.) before exhibiting any symptoms of FDS. Thus, they argue, even if a finite lifespan would benefit a species, there is no need for an aging mechanism, because nature has already ensured that all individuals comprising any particular species have a finite lifespan. That argument is an effective counter to the PA argument. However, using the applicable data for that purpose and ignoring its broader implications is a classic example of confirmation bias. Intrinsic damage is inexorable. Thus, if no species shows any signs of FDS in the evolutionary environment, then one must conclude that all species are endowed with effective maintenance systems.

Only when an animal becomes domesticated and outlives its natural lifespan (the natural lifespan of a species is the time period before substantially all members of the species would die from non-aging related causes in the evolutionary environment) does it begin to show any age-related diminution in functionality. Principles of natural selection mandate that each species is endowed with a maintenance system that has a chronological limitation, with that limitation being a function of the natural lifespan of that species. The inescapable conclusion implied by the fact cited by the NPA proponents to refute the PA argument – that all species are endowed with maintenance systems that are effective throughout the natural lifespan of that species – completely undercuts their foundational assumption that all maintenance systems are inherently ineffective.

The Longevity Fund is a venture capital firm that invests in start-up companies that aim to prevent or cure age-associated diseases.
Ms. Deming’s blog can be accessed at ldeming.com/longevityfaq.
As noted elsewhere on this website, no mammal ever exhibits any symptoms of FDS during its natural lifespan. See the essay entitled “Aging in Other Species.” If the goal is to learn why relatively young humans suffer from FDS, it is nonsensical to use organisms that never suffer from FDS (at least in their evolutionary environment) as surrogates.

This is the final essay in this Section. The next Section is “The Case for Paradigm Shift.”