Anomalies

This website uses the term “anomaly” a lot.  An anomaly, loosely defined, is any phenomenon that deviates from a common form or that displays inconsistency with what is expected.  When discussing scientific theories, an anomaly is an observation that is inconsistent with what the theory predicts.  Why are anomalies so important?

In the natural sciences, anomalies are what cause scientists to revise and update theories and paradigms.  The life sciences work a little differently.  The life sciences generally ascribe to a paradigm that relies upon statistical associations.  No drug works perfectly, so unexpected results are easily dismissed. Everything is driven by big data.  Big data buries anomalies.  In physics, a significant anomaly leads to a re-examination of the underlying scientific theory.  In the life sciences, anomalies are typically ignored.  “Humans are complicated.”

The conventional approach is to equate genotype with statistical averages of phenotype, as shown by big data.  The Hypothesis uses the term genetic potential, rather than genotype, and makes a big distinction between genetic potential and phenotype.  To illustrate the distinction, take a nonhuman example.  Chickens have the genetic potential to fly.  That genetic potential does not change throughout a chicken's lifespan.  But, as a general rule, chickens don't fly.  They don't fly because of environmental reasons.  Big data will cancel out the anomalous result of the chicken that does fly on occasion.  The approach of the Hypothesis is to study the anomaly.  The chicken that does fly will tell us more about whether chickens have the genetic potential to fly than years of research into roundworms and fruit flies.  

The Institute was created to examine a specific anomaly.  The current paradigm is based on the presumption that progressive loss of function is the inevitable result of the passage of time.  The experience of the founder, and thousands of others like him, is inconsistent with that paradigm.  The result is so inconsistent – such a significant anomaly - that the founder determined that it could not be ignored.

There is no generally accepted scientific theory that explains why we lose function as we age.  There are numerous hypotheses, but no single hypothesis has become generally accepted as providing a comprehensive explanation.  A primary reason is that all of the hypotheses that have been advanced to date have anomalies that are too significant to ignore. 

 

Exercise is the universal anomaly when it comes to hypotheses relating to the aging process.  A ubiquitous statement is that humans lose x% of their muscle mass every decade after the age of 30.  The more complete statement is of course to qualify the general statement by adding the words “unless they exercise.” 

The same caveat is necessary with respect to every hypothesis or general statement related to the aging process.  One hypothesis of aging is that we are fated to die because our telomeres (protective caps on the ends of chromosomes) get shorter each time our cells divide.  That creates a finite number of times that cells can divide, and thus an outside limit on aging commonly known as the "Hayflick limit".  However, moderate, steady state exercise has been shown to slow the shortening of telomeres.  Intense exercise lengthens telomeres.  So the correct statement is not that telomeres get shorter with age, it is that telomeres get shorter with age, unless we exercise.

For years, the predominant theory of aging was the mitochondrial free radical theory of aging (MFRTA).  Mitochondria are the organelles within cells that generate energy through aerobic metabolism.  Mitochondrial dysfunction has been conclusively linked to the aging process.  MFRTA posits that mitochondria malfunction because of something called free radicals (that’s why antioxidants are supposed to be good for you).  Intense exercise results in cascades of free radicals, which would be expected to aggravate mitochondrial dysfunction.  But study after study has conclusively demonstrated that nothing promotes mitochondrial health as much as exercise. 

 

Another general statement relating to aging is that older people progressively lose homeostatic capability, as measured by heart rate variability.  People who exercise with intensity increase heart rate variability.     

Until recently, it was almost universally accepted by biogerontologists that most of the effects of aging could be ascribed to wear and tear.  Physical activity, and more specifically the burning of calories through exercise, accelerates the rate at which cells die.  With that breakdown should come an acceleration in the onset of aging-associated diseases and ultimately death.  A comprehensive study on the presumed effects of exercise on cellular atrophy provides confirmation.  That study concludes that the lifespan to limit entropy (death as a result of the aging process) for a sedentary male would be 85.05 years, while the lifespan to limit entropy for a very active male would be 53.20 years.  The numbers for women were 95.75 years and 57.68 years respectively.  The authors of the study acknowledged that there appeared to be some inconsistency between their results and the fact that physical activity is universally acknowledged to lower the risk of all aging-associated diseases. 

The same study predicted changes to the expected lifespan of an astronaut based on the time the astronaut is exposed to the weightless condition.  Gravity plays a significant role in entropy, so it was assumed that the absence of gravity would play the same life-extending role as does the absence of physical activity.  The study predicted that a male astronaut would extend his life span one year for every 9.5 years he spent in space.  For a female astronaut, this time was estimated as 7.5 years.  These predictions are also wildly inconsistent with reality.  The initial astronauts who were housed aboard space stations suffered greatly accelerated FDS, characterized by significant bone loss, loss of muscle mass, etc.  The symptoms were described as an acceleration of aging.  NASA immediately recognized the problem as a lack of exercise.   Simply fighting the effects of gravity is a significant form of exercise.  Now all occupants of the space station are required to exercise periodically.

The Hypothesis has a simple means of reconciling all of these apparent anomalies.  These other hypotheses do not tell us anything about why the aging process occurs.  They are all merely descriptions of symptoms of FDS.  If one fails to periodically activate the Growth Process through intense exercise, one will suffer from FDS.  Among the symptoms of FDS are that one will lose muscle mass, one’s telomeres will get shorter, one’s mitochondria will become damaged and dysfunctional and the forces of entropy will prevail.  But if one does periodically activate the Growth Process, the aging process will not occur and none of these symptoms will appear.