Behind The Veil of Depression: Exploring The Roles of Nature and Nurture

Depression can be likened to a psychological veil which shields us off from everyone and everything that matters in the world. The psychic veil of depression can obstruct our breath and vision, leaving us short of energy and unable to experience the world’s beauty around us. Life’s minute tasks become difficult and it’s true challenges, seemingly unbearable. Just how one can unveil and free oneself from this dark and heavy cloak can be difficult to discern, and when you are depressed, you feel isolated; helpless; alone. But you aren’t alone.

Globally, more than 300 million people suffer from some form of depression, including approximately fifteen percent of the adult population in the United States. What’s more, suicide tragically proves to be the second leading cause of death in the world amongst human beings aged 15 to 29 years old, with nearly 800,000 people ending their own lives every year (1). One must wonder—what brings a human being to such a state of psychological pain?

Whoever and wherever you are, I hope you—reader—will think of this post as an attempt to document important and wide-ranging (yet interconnected) portions of the current scientific understanding of depression. I am not a doctor or medical professional, but one of more than 300 million people on this planet who has, at different points in my life, struggled under the psychological veil of depression. The paragraphs below do not consist of medical advice, but of an effort to convey some crucial biological and environmental underpinnings of depression and in the process, shed some light on this dark and all-too-common state of the human mind.

 Photo by: Nolan Septer ( www.septerphoto.com )

Photo by: Nolan Septer (www.septerphoto.com)

Depression has taken on a rather vague definition in recent years, with so much as a spilt cup of coffee being assigned the status of “depressing.” So while the issue seems semantical, I want to take a moment (to attempt) to sort out a workable definition of depression.

The Merriam-Webster Dictionary assigns depression the laughably blunt definition of, “a state of feeling sad.” A secondary definition more reasonably describes depression as, “a mood disorder marked especially by sadness, inactivity, difficulty in thinking and concentration, a significant increase or decrease in appetite and time spent sleeping, feelings of dejection and hopelessness, and sometimes suicidal tendencies.”

According to the criteria established in the Diagnostic and Statistical Manual of Mental Disorders (DSM–5) (2), an individual may be diagnosed as depressed if five or more of the following symptoms persist for a period of two weeks or longer:

  • A sad or depressed mood
  • Loss of interest or pleasure in previously enjoyable activities
  • Change in appetite
  • Excess weight gain or excess weight loss
  • Changes in sleeping patterns—sleeping too much or sleeping too little
  • Increased fatigue
  • Feelings of worthlessness or guiltiness
  • A decline in cognitive ability—difficulty thinking or decision making
  • Thoughts of suicide and/or death

While depression can only reliably be diagnosed by certified medical professionals, human beings certainly experience a wide range of emotions—some of which overlapping with the criteria characterizing depression above—and some of these emotional fluctuations are contextual to the ups and downs of an individual’s life events. Hence, different subtypes of depression may develop under different circumstances—as in the cases of bereavement related depression, postpartum depression, seasonal affective disorder, bipolar disorder, psychotic depression, and persistent depressive disorder.

  • Bereavement-related depression describes the depressive psychological state which often follows the death of a loved one. Depression is not typically diagnosed as being related to bereavement until depressive symptoms have persisted for two or more months following the loss of a loved one (3).
     
  • Postpartum depression is defined as “a mood disorder that can affect women after childbirth.” (4) Mothers experiencing postpartum depression often have extreme feelings of sadness, anxiety, and exhaustion, making daily care activities for both themselves and others potentially problematic.
     
  • Seasonal affective disorder is a form of depression related to a change in the seasons, with depressive symptoms occurring at the same time each year (5). People suffering from seasonal affective disorder often experience more severe depressive symptoms during the winter months and more mild symptoms during the spring and summer months.
     
  • Bipolar disorder—formerly referred to as manic depression—is a subtype of depression in which an individual experiences severe mood swings from the psychologically high states of mania to the low states of depression (6).
     
  • Psychotic depression is a subtype of severe depression in which an individual often experiences some form of psychosis (i.e., hallucinations, delusions, and/or another type of psychological break) and often requires hospitalization (7).
     
  • Persistent depressive disorder describes a subtype of depression which lasts for a period of two years or longer, during which an individual may experience fluctuations in the severity of his or her depressive symptoms (8).

Major depressive disorder (MMD)—a subtype of depression overlapping significantly with persistent depressive disorder—has been described as a “chronic, remitting syndrome involving widely distributed circuits in the brain,” and is characterized by symptoms such as “depressed mood, anhedonia, disturbed sleep, appetite, and energy, reduced concentration, excessive guilt, and suicidal thoughts.” (9) Major depressive disorder does indeed ‘run in families,’ as the condition displays between 31 and 42 percent heritability (9, 10). However, genetics alone do not account for the complexity of major depressive disorder (or any other subtype of depression for that matter), leaving environmental factors to constitute a significant portion of the biological basis of depression.

 Photo by: Nolan Septer ( www.septerphoto.com )

Photo by: Nolan Septer (www.septerphoto.com)

A number of environmental factors have been linked to the development of depression, including various forms of stressful life events (i.e., early life trauma, sustained stress in childhood, the loss of a loved one, chronic inflammation, medical illness, and so on), and the disparity in environmental conditions underlying the various subtypes of depression highlights a key fact: depression is not a disease of nature or nurture, but a disease of nature and nurture. As biological organisms, we exist in a state of perpetual interplay with our environment, and the input from our environment impacts our physiology in a variety of ways.

As a human being, you have about 20,000 functional genes in your genome and with the exception of mutational events, the order of your genes doesn’t change throughout your lifetime (11). However, the expression of your genes—the manner in which particular genes are “turned on” or “turned off”—is regulated by biological processes referred to in biology speak as “epigenetic modifications.”

The word "epigenetic" is defined as a biological phenomena, "relating to or arising from non genetic influences on gene expression," and when considering the Greek roots of the word, literally means "upon" or "above" genetics (12).

About 100 trillion meters of DNA exists within every adult human being’s body, and each cell within our bodies contains approximately six linear feet of DNA packed into an area of six micrometers (or 0.000236 inches) in diameter—a region known as the nucleus of the cell (13). This seemingly impossible feat occurs as the result of the condensation of our DNA into a structure known as chromatin. Chromatin is then wrapped around proteins called histones and packed even tighter through a process known as methylation, in which methyl groups (-CH<sub>3</sub>; a carbon atom bonded to three hydrogen atoms) are added to specific stretches of DNA, resulting in the inability of these genes to carry out their biological function (a process called down regulation) and this is an example of an epigenetic modification.

Genes are exposed or hidden through the addition or removal of biochemical compounds, allowing for the enhanced or repressed function of specific genes. In this manner, certain genes that should be expressed in skin cells, but not in liver cells, for example, are demethylated in skin cells (allowing for these genes to be expressed) and heavily methylated in liver cells (preventing the expression of these genes in the liver). The same is true of genes which are expressed in our brains, but not in, say, our heart tissue.

So, what does any of this have to do with depression?

The field of epigenetic research has been exploding over the last decade, illuminating epigenetic mechanisms underlying diseases like cancer, heart disease, stroke, dementia, and even depression. The food we eat, the amount and intensity of exercise we get, the number of hours we sleep each night, our stress levels, the variety and quantity of toxins to which we are exposed—nearly everything we experience triggers various epigenetic modifications and some of these effects have been linked to novel theories regarding the causes of depression.

For decades, the explanation of depression went something like this: depressed people have biochemical imbalances of the neurotransmitters norepinephrine, dopamine, and serotonin (popularly referred to as the “happy” chemical) within their brains and low levels of these chemicals are directly responsible for causing the symptoms of depression. In turn, an array of drugs have been developed in order to increase the levels of these neurochemicals (particularly serotonin) in people’s brains with the intention of effectively treating depressive symptoms—and the data shows that these treatment methods actually work pretty well. Millions of people have experienced success in the treatment of their depression with the aid of medications such as selective serotonin re-uptake inhibitors (SSRIs), tricyclic antidepressants, and other medications acting on the serotonin (which is also referred to as 5-hydroxytryptamine), dopamine, or norepinephrine receptors of the brain.

 Photo by: Nolan Septer ( www.septerphoto.com )

Photo by: Nolan Septer (www.septerphoto.com)

However, a significant portion of depressed patients display “treatment resistant depression,” as their symptoms do not improve with the aid of traditional antidepressant medication therapies—and recent research indicates that the neurotransmitters mentioned above constitute only one of the major biological underpinnings of depression.

Numerous theories have been developed in an attempt to understand the mechanisms underlying depression—one of which being the “inflammatory cytokine model of depression,” which posits that chronic inflammation over-activates the hypothalamic pituitary adrenal (HPA) axis (a system of brain structures that triggers the release of stress hormones and stimulates stress responses within our bodies), leading to decreased amounts of neurotransmitters within our brains and the subsequent development of depressive symptoms (14, 15). In response to various forms of stress, chemicals called “pro-inflammatory cytokines”—which function to trigger inflammatory reactions in the body—such as interferon-alpha (INFα), tumor necrosis factor-alpha (TNFα), interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon-gamma (INFγ) are released into the bloodstream and have been linked to the development of a variety of neuropsychiatric symptoms, some of which mirroring the symptoms of depression (14, 16).

A number of links have been established between depression and inflammation. For example, depression frequently presents in patients with inflammatory diseases such as inflammatory bowel disease, rheumatoid arthritis, and psoriasis (17, 18, 19). Additionally, people with increased levels of inflammation have a higher likelihood of developing depression, and the reduction of inflammatory biomarkers in these individuals correlates to the remission of their depressive symptoms (14).

Relating this back to epigenetics: those suffering from depression possess increased levels of pro-inflammatory cytokines in their bloodstreams, and higher levels of these chemicals have been linked to the epigenetic modification of a gene called IL-6 (16). The IL-6 gene codes for the synthesis of the interleukin-6 cytokine and in depressed individuals, this gene is under methylated—resulting in the overexpression of IL-6 and as a result, more of this pro-inflammatory compound in the bloodstreams of depressed people. In addition to IL-6, other pro-inflammatory compounds such as IL-1ra, C-reactive protein (CRP), TNF-α, TNF-β1, and IFN have been epigenetically linked to the development of depressive symptoms (20). In turn, a number of the pro-inflammatory cytokines mentioned above—as well as stress hormones like CRF and glucocorticoids—have been suggested as markers of inflammation which may additionally indicate the presence (or lack thereof) of depressive symptoms (20).

What’s more, antidepressant use has been associated with the increased methylation of the IL-6 gene and treatment with SSRIs have been shown to both reduce circulating levels of pro-inflammatory cytokines (such as IL-1, TNFα, and INFγ) and increase levels of anti-inflammatory cytokines (such as IL-10), further supporting the theory that depression is—at least in part—a symptom of chronic inflammation while potentially uncovering a secondary mechanism of SSRI treatment (14, 20). Although SSRIs have long been known to work on the brain’s serotonin system, the research mentioned above highlights an additional, anti-inflammatory mechanism of action underlying SSRI treatment—a therapeutic effect facilitated by epigenetic modifications.

But the epigenetic roots of depression go even deeper. Autopsies on suicide victims have shown that those who commit suicide often possess increased levels of rRNA (ribosomal RNA) gene methylation within the hippocampus—a region of the brain that regulates emotion, memory, and the activation of the autonomic nervous system—as compared to those who pass away from other causes (21). These rRNA genes are fundamental to learning and memory formation—and the increased methylation of these genes results in fewer proteins being synthesized within the hippocampus, which in turn manifests in the development of depressive symptoms.

Child abuse additionally leaves epigenetic marks on the brain. Similar studies on suicide victims have shown that those who were abused in childhood possess distinct epigenetic markers on the GR gene and these markers have additionally been linked to an increased liklihood of commiting suicide (21). Curiously, similar epigenetic patterns on this gene have been identified in rat pups who were neglected by their mothers (21). 

Patterns of gene methylation aren’t the only epigenetic links to depression, however. In addition to methylation, different forms of epigenetic modifications exist as well, including phosphorylation, ubiquitination, sumoylation, and acetylation. Contrary to methylation, acetylation is an epigenetic modification in which acetyl groups are added to a stretch of DNA and promote the activity of the genes which have been ‘acetylated’. Within the hippocampus, decreased levels of acetylation have been linked to the onset of depressive behavior in response to stress—indicating that acetylation patterns in the hippocampus play important roles in memory formation and behavioral stress response development (22). Acetylation and methylation seem to have important implications in the biology of depression and as a result, growing interests in identifying biomarkers which indicate the epigenetic modification patterns of various brain regions have emerged in the medical field with the intention of developing future diagnostic and treatment methods for depression.

However, depression is a syndrome of incredible complexity and no single mechanism or biomarker can explain the diverse array of symptoms manifested in those who are depressed. Depressive symptoms—as traditionally established—develop when the concentrations of neurotransmitters such as serotonin and norepinephrine within a person's brain are low. Additionally, increased levels of inflammatory cytokines within an individual’s bloodstream have been shown to over-activate the HPA axis and diminish the amounts of neurotransmitters (such as serotonin and norepinephrine) within the brain—resulting in the onset of depressive symptoms (20). Furthermore, those who experience sustained childhood stress often display higher corticotropin-releasing hormone (CRH) levels within their brains, resulting in an increased stress response in adulthood, as well as diminished neurotransmitter levels within the adult brains of these individuals—which (yet again) triggers the development of depression (20, 23).

In this manner, depression can simultaneously be described as an immune response to chronic inflammation, a neuropsychological response to childhood trauma, and a symptom of biochemical imbalances within a given person's brain.

Herein lies the beauty of epigenetic research—the field allows us to bridge the gaps in our understanding of nature and nurture, illuminating the environmental and biological foundations of diseases like depression, as well as innumerable others. While giving rise to the development of novel, more sophisticated theories regarding the basis of depression, the field of epigenetics has also allowed for the enhancement of more traditional models, as in the case of depression treatment with SSRIs.

And as our understanding of the biological mechanisms underlying depression (or any other disease, for that matter) deepens and complexifies, so too do our definitions of such conditions.

 Photo by: Nolan Septer ( www.septerphoto.com )

Photo by: Nolan Septer (www.septerphoto.com)

Imagine somebody who is visibly depressed. From a base-level, exterior perspective, this person may simply appear to be feeling sad. For decades, those suffering from depression have been told to toughen up, deemed to be lacking in will power. Zoom into the mind of this individual, however, and one realizes that depression is not a choice, but a psychological condition—as mentioned above—characterized predominantly by sadness, inactivity, difficulty thinking, feelings of dejection, hopelessness, and potentially, suicidal thoughts or tendencies. In this manner, depression is indeed a psychological condition (or at least a collection of psychological symptoms).

But keep zooming into the brain of this person. The cortical areas of the brain are responsible for the development of complex cognitive behaviors, personality traits, decision making, and social behavior. The deeper, limbic structures of the brain govern memory formation and our perceptions of emotional sensation. In comparison to a non-depressed person, the cortical regions of the brain—more specifically, the prefrontal cortex—of somebody who is depressed will display a significant decrease in activity, while the limbic structures of his or her brain—such as the amygdala—will be hyperactive (24). Additionally, the volume of an individual's hippocampus has been shown to decrease with both the severity and duration of depressive symptoms (24). In other words, when we are depressed, the regions of our brains which govern and process conscious, rational perceptions are repressed and over-ruled by our more emotional brain areas. Therefore, depression can also be characterized and defined by changes in brain anatomy.

Keep focusing upon a single neuron within this person’s brain. The neurons of this individual's prefrontal cortex transmit fewer neurotransmitters than those of somebody who is not depressed and additionally, the brain cells within this person's prefrontal cortex will have fewer connections to surrounding neurons (24). Furthermore, the neurons of this human being's hippocampus—depending upon the severity of his or her depression—will be atrophied to some degree and some of these neurons will cease to function, effectively resulting in the death of these brain cells (24). Antidepressant medications function to increase the levels of neurotransmitters produced by the neurons within our brains, resulting in a higher efficiency of these neurons, the formation of more connections between brain cells, and the growth of new neurons within the prefrontal cortex and hippocampus—a process known as neurogenesis. When viewed from this perspective, depression can additionally be defined by changes in neurological activity.

Close in on the nucleus of this particular nerve cell and on the DNA inside this nucleus. The methylation patterns on this person’s genes—the epigenetics of this person—differ from those of a non-depressed individual. Genes which activate inflammatory reactions in the body are under-methylated and expressed at higher rates, while those leading to anti-inflammatory reactions are methylated and repressed. Acetylation patterns on genes within the neurons of the hippocampus are reduced and various genes within the brain cells of the prefrontal cortex are heavily methylated (25). Simply put, the gene expression of somebody who is depressed differs from the gene expression of an individual who does not suffer from depression and therefore, depression can be characterized by epigenetic changes, as well.

Depression is simultaneously a molecular, cellular, neurological, psychological, and social condition—and the epigenetic links between depression, inflammation, and chronic stress open up entirely new perspectives with which we can view this tragically common condition of the human psyche. Not only do genetics play an important role in the development of depression, but life factors as wide ranging as the Western diet, gut health, obesity, sleep deprivation, early life trauma, medical illness, and vitamin deficiency have been linked to the development of inflammation within the human body and in turn, the manifestation of depressive symptoms (20). The study of epigenetics is allowing us—for the first time in human history—to connect the dots between our understanding of the biological basis of depression and these widely variable conditions of life.

Additionally—and of equal importance—this new epigenetic perspective with which we can view depression also helps to erase the stigma surrounding this condition. People suffering from the internal struggles of depression can be alleviated from the judgement with which society has—for far too long—viewed those who are depressed. Through understanding the scientific basis of depression (or any other stigmatized psychological condition), we as individuals can better understand and empathize with one another—and we as a society can progress towards the development of quality treatments for this tragically frequent state of the human mind which plagues so many of us.

Depression, as I have attempted to highlight throughout this piece, is a condition of both nature and nurture—of both genetic and environmental origins. An organism cannot exist in a vacuum; we are engaged in an a constant and deeply complex relationship with our environment—whatever those external conditions may be, for better or for worse—and an incredible number of these environmental factors interact with our biology to contribute to the development of depression. Those who are depressed are not physically inferior or psychologically weak, but experiencing a biological response to the conditions of their environment. Remarkably, the epigenetic links between depression, inflammation, and the various conditions of life which contribute to the onset of depressive symptoms are allowing us—as individuals and as a society—to detangle the scientific knots of knowledge which fastens the veil of depression to so many of our minds.

 

References and Recommended Reading:

  1. Depression. (2018, March 22). Retrieved from http://www.who.int/mediacentre/factsheets/fs369/en/
     

  2. What Is Depression? (n.d.). Retrieved from https://www.psychiatry.org/patients-families/depression/what-is-depression
     

  3. Hensley, P. L., & Clayton, P. J. (2008, July 01). Bereavement-Related Depression. Retrieved from http://www.psychiatrictimes.com/bipolar-disorder/bereavement-related-depression
     

  4. Postpartum Depression Facts. (2018). Retrieved from https://www.nimh.nih.gov/health/publications/postpartum-depression-facts/index.shtml
     

  5. M. (2017, October 25). Seasonal affective disorder (SAD). Retrieved from https://www.mayoclinic.org/diseases-conditions/seasonal-affective-disorder/symptoms-causes/syc-20364651
     

  6. Mayo Clinic Staff. (2018, January 31). Bipolar disorder. Retrieved from https://www.mayoclinic.org/diseases-conditions/bipolar-disorder/symptoms-causes/syc-20355955
     

  7. Psychotic Depression. (2018). Retrieved from https://www.webmd.com/depression/guide/psychotic-depression#1
     

  8. Mayo Clinic Staff. (2017, August 08). Persistent depressive disorder (dysthymia). Retrieved from https://www.mayoclinic.org/diseases-conditions/persistent-depressive-disorder/symptoms-causes/syc-20350929
     

  9. Sun, H., Kennedy, P. J., & Nestler, E. J. (2012, June 13). Epigenetics of the Depressed Brain: Role of Histone Acetylation and Methylation. Retrieved from https://www.nature.com/articles/npp201273#abstract
     

  10. Sullivan PF, Neale MC, Kendler KS (2000). Genetic epidemiology of major depression: review and meta-analysis. Am J Psychiatry 157: 1552–1562.
     

  11. Dolgin, E. (2017, November 22). The most popular genes in the human genome. Retrieved from https://www.nature.com/articles/d41586-017-07291-9
     

  12. Epigenetic. (2018). Retrieved from http://www.dictionary.com/browse/epigenetic?s=t
     

  13. Annunziato, A. T. (2008). DNA Packaging: Nucleosomes and Chromatin. Nature Education, 1(1), 26th ser. Retrieved from https://www.nature.com/scitable/nated/article?action=showContentInPopup&contentPK=310.
     

  14. Kresser, C. (2017, January 10). Is Depression a Disease-or a Symptom of Inflammation? Retrieved from https://chriskresser.com/is-depression-a-disease-or-a-symptom-of-inflammation/
     

  15. Smith, R. S. (1997). Cytokines and Depression. Retrieved from http://www.cytokines-and-depression.com/chapter7.html
     

  16. Ryan, J., Pilkington, L., Neuhaus, K., Ritchie, K., Ancelin, M., & Saffery, R. (2017). Investigating the epigenetic profile of the inflammatory gene IL-6 in late-life depression. BMC Psychiatry, 17(1). doi:10.1186/s12888-017-1515-8
     

  17. Lichtenstein, G. R. (2017). Depression and Inflammatory Bowel Disease. Gastroenterology & Hepatology, 13(3), 143.
     

  18. Margaretten, M., Julian, L., Katz, P., & Yelin, E. (2011). Depression in patients with rheumatoid arthritis: description, causes and mechanisms. International Journal of Clinical Rheumatology, 6(6), 617–623. http://doi.org/10.2217/IJR.11.6
     

  19. Golpour, M., Hosseini, S. H., Khademloo, M., Ghasemi, M., Ebadi, A., Koohkan, F., & Shahmohammadi, S. (2012). Depression and Anxiety Disorders among Patients with Psoriasis: A Hospital-Based Case-Control Study. Dermatology Research and Practice, 2012, 381905. http://doi.org/10.1155/2012/381905
     

  20. Jeon, S. W., & Kim, Y. K. (2016). Neuroinflammation and cytokine abnormality in major depression: Cause or consequence in that illness? World Journal of Psychiatry, 6(3), 283–293. http://doi.org/10.5498/wjp.v6.i3.283
     

  21. Epigenetics & the Human Brain. (2018). Retrieved from http://learn.genetics.utah.edu/content/epigenetics/brain/
     

  22. Sun, H., Kennedy, P. J., & Nestler, E. J. (2012). Epigenetics of the Depressed Brain: Role of Histone Acetylation and Methylation. Neuropsychopharmacology, 38(1), 124-137. doi:10.1038/npp.2012.73
     

  23. Carpenter LL, Tyrka AR, McDougle CJ, Malison RT, Owens MJ, Nemeroff CB, Price LH. Cerebrospinal fluid corticotropin-releasing factor and perceived early-life stress in depressed patients and healthy control subjects. Neuropsychopharmacology. 2004;29:777–784.
     

  24. (2018). Retrieved from http://thebrain.mcgill.ca/flash/d/d_08/d_08_cr/d_08_cr_dep/d_08_cr_dep.html
     

  25. Castren, E., Voikar, V., & Rantamaki, T. (2007). Role of neurotrophic factors in depression. Current Opinion in Pharmacology, 7(1), 18-21. doi:10.1016/j.coph.2006.08.009

Directed Panspermia: A Long Strange Trip

Since humans have been human, the beauty of the cosmos has overwhelmed us with wonder. The awe-inspiring expanse of space and time in which we are embedded, from which we arose, dissolves the human ego with reliability; as it should when gazing into the cosmic soup that birthed all of life on this planet—all of life in the known universe. Carl Sagan famously stated that the "origin and evolution of life are connected in the most intimate way with the origin and evolution of the stars."1 We are one of many manifestations of universal expansion, reflecting back upon our cosmic path to existence.

But what if life on this planet arose by a more intimate and expedited means? The theory of Directed Panspermia—the notion that life on earth was intentionally inoculated with microorganisms by an intelligent, extraterrestrial civilization (despite proving the stuff of fascinating science fiction)—was first popularized as a legitimate scientific inquiry by the Nobel laureate and co-discoverer of the double helical structure of DNA, Francis Crick. In 1972, Along with British chemist, Leslie Orgel, Crick published a paper entitled, Directed Panspermia, in which the two scientists considered the evidence regarding, "the theory that organisms were deliberately transmitted to the earth by intelligent beings on another planet."2

Double Helix.jpg

Crick and Orgel argue that a spaceship containing large samples of microorganisms may have been sent throughout space with the intention of seeding life on habitable planets, one of which being our home, Earth.

"The radius of our galaxy is about 105 light years, so we could infect most planets in the galaxy within 108 yr by means of a spaceship traveling only one-thousandth of the velocity of light," Crick and Orgel wrote, going on to posit that, “several thousand stars are within a hundred light years of the Earth and could be reached within as little as a million years by a spaceship travelling at only 60,000mph, or within 10,000yr if a speed of one-hundredth of that of light were possible.”

Aside from the theoretical technology required to transport microorganisms throughout space, an additional question arises; can microorganisms, particularly bacterial and fungal spores, survive in the vacuous, irradiated landscape of the cosmos?

Interestingly, spores of both the Bacillus pumilus SAFR-032 and Bacillus subtillis 168 bacterial species have been shown to survive in space for eighteen months,3 and spores of the Bacillus subtillis species can survive for up to six years in the interstellar conditions of the cosmos.4

Fungal spores display an even more notable resilience in space, as cells of the Cryptococcus neoformans species have been shown to grow more quickly than normal when exposed to radiation 500 times the background rate of interstellar space.5,6 While modern science is currently unable to conduct studies on the scale needed for panspermia to occur—durations of thousands to millions of years—these preliminary studies support the physical viability of lithopanspermia (the interplanetary transfer of microorganisms within meteorites)7 and in turn, the theory of Directed Panspermia, as well.

Mars.jpg

And bear in mind, this is not my theory, or the theory of another similarly unqualified individual, but a theory developed and considered with serious scientific scrutiny by a man partially responsible for one of the most significant scientific discoveries in human history. Scientific breakthroughs, if truly breakthroughs, must question and counter the accepted nature of reality to a degree bordering upon absurdity when viewed through the lens of the cultural perspective of the time.

Crick and Orgel additionally call upon chemical and biological evidence to support their theory of Directed Panspermia.

"The universality of the genetic code," Crick and Orgel argued, "follows naturally from an 'infective' theory of the origins of life." If the earth was indeed inoculated directly with extraterrestrial microorganisms, subsequent life forms must have then arose from the same genetic pool, eventually evolving into the variety of single-celled and subsequently, multicellular organisms found throughout the various ecosystems of modern-day Earth. In the words of Crick and Orgel, "Life on Earth would represent a clone derived from a single extraterrestrial organism."

Just 200-400 million years after the formation of the Earth’s crust, life had already begun taking a foothold in the available niches of this young planet—an incredibly rapid rate for the novel arisal of life in the universe. While Bacillus subtillus spores have been indicated to possess the potential to survive for several hundred years under the temperature and ultraviolet radiation conditions of interstellar space, these same spores could potentially survive in dark, molecular clouds—protected from the bombardment of cosmic radiation—for periods of hundreds of millions of years, rendering interstellar microbial transportation and in turn, directed panspermia a biological possibility.8,9

An additional clue indicating the potential extraterrestrial origins of life on Earth includes molybdenum; an essential trace element that facilitates a variety of enzymatic functions in nearly all known life forms. The biochemistry of an organism must to some degree reflect the environment in which that organism evolved and particularly, rare chemical elements which display a crucial biological function may indicate evolutionary clues regarding the nature of that early evolutionary environment. Earth displays a 0.02% abundance of molybdenum and therefore, as Crick and Orgel argued, "if it could be shown that the elements represented in terrestrial living organisms correlate closely with those that are abundant in some class of star—molybdenum stars, for example—we might look more sympathetically at 'infective' theories."

In other words, the ubiquity of molybdenum amongst life on Earth may indicate that our earliest prokaryotic ancestors evolved in an environment rich in this element; an environment with a significantly higher abundance of the stuff than Earth.

Despite its being a theory regarding the evolutionary origins of life, the theory of Directed Panspermia signifies a deeply ingrained aspect of human psychology; the need to persist. As human beings, we reproduce, have children, build families, write books, erect monuments, invent, create—all as a means of guaranteeing the existence of an aspect of ourselves beyond that of our physical being. The future possibility of colonizing Mars has provoked notable excitement in recent decades, but beyond the colonization of another planet by our own species, we possess the potential capability to spread life throughout the reaches of the universe, ensuring the sustenance of this most beautiful of universal phenomena.

Consider this: a meteorite is identified to be on a collision course with Earth. Without a means of deflecting this incoming projectile and risking the annihilation of our species, along with potentially all of life on Earth, might we attempt to send microorganisms throughout the universe with some hope, however minute, of successfully sustaining the beauty of life in the universe?

Christian Orlic, a zoologist studying experimental evolution and currently developing an extended history of Crick and Orgel’s theory of Directed Panspermia, summarized the motives of such actions eloquently:

“The demise of our kind is hard enough to accept but the prospect of a lifeless universe, a universe that could never come to know itself, a universe so grand and yet with no one to admire it or even dwell in it could be too much to bear.”1

Perhaps intelligent life elsewhere in the universe would relate to this sentiment. In the words of Crick and Orgel, the motivation for an intelligent, extraterrestrial civilization to populate the galaxy, “would be strong, if they believed that all or even the great majority of inhabitable planets could be given life by Directed Panspermia.”

Life on Earth.jpg

The generally accepted age of the universe as indicated by modern physics is approximately 13.8 billion years,11 ample time for life to arise, evolve, and decimate on numerous planets throughout the cosmos. Nobel Prize winning physicist Enrico Fermi, in addition to a wealth of contribution made to twentieth-century science, popularized a theory known as Fermi’s Paradox—an observation of conflict between the notably high probability of the existence of intelligent extraterrestrial life and the utter lack of accepted scientific evidence on the matter. “Where is everybody?” Fermi famously questioned.12

What if, however, as is indicated by Crick and Orgel’s theory of Directed Panspermia, life itself signifies the existence of such intelligent extraterrestrial life? I know, all of this seems completely crazy and if you are skeptical of the evidence supporting the theory of Directed Panspermia, you are certainly not alone. Crick and Orgel themselves describe their own arguments as being, “of necessity, somewhat sketchy.”

That being said, Crick, a man well acquainted with the frontiers of scientific advancement, might have responded to such scrutiny by retorting that his, “message to experimentalists is: Be sensible but don’t be impressed too much by negative arguments. If at all possible, try it and see what turns up.”13 The fortune of scientific advancement befalls those bold enough to question the paradigms of the time, and proceed to act accordingly.

And as science advances—as we enhance our understanding of the world around us—the complexity of our existence and interreliance on innumerable exterior factors for our survival begins to emerge with clarity. While human beings seldom resist assuming an identity of cosmic significance, perhaps it is not humanity which symbolizes the pinnacle of universal existence, but rather it is simply the existence of life itself—in all of its forms—which proves most miraculous. An intelligent civilization, if faced with an existential threat to its home planet, would not only act in order to sustain the survival of its own species, but of life itself.

References:

  1. Orwig, J. (n.d.). These Quotes From Carl Sagan Will Make You Feel at One With The Cosmos. Retrieved March 21, 2018, from
     
  2. Crick, F., & Orgel, L. (1973). Directed panspermia. Icarus, 19(3), 341-346. doi:10.1016/0019-1035(73)90110-3
     
  3. Rainey, K. (2014, April 30). Space Station Research Shows That Hardy Little Space Travelers Could Colonize Mars. Retrieved March 21, 2018, from https://www.nasa.gov/mission_pages/station/research/news/eu_tef/
     
  4. Horneck, G., Bücker, H., & Reitz, G. (1994). Long-term survival of bacterial spores in space. Advances in Space Research, 14(10), 41-45. doi:10.1016/0273-1177(94)90448-0
     
  5. Wang, T. (2015, June 02). Astromycology: The "Fungal" Frontier. Retrieved March 21, 2018, from https://harvardsciencereview.com/2015/06/02/astromycology-the-fungal-frontier/
     
  6. Dadachova, Ekaterina, and Arturo Casadevall. “Ionizing Radiation: How Fungi Cope, Adapt, and Exploit with the Help of Melanin.” Current Opinion in Microbiology11.6 (2008): 525-31.
     
  7. Horneck, G., Klaus, D. M., & Mancinelli, R. L. (2010). Space Microbiology. Microbiology and Molecular Biology Reviews, 74(1), 121-156. doi:10.1128/mmbr.00016-09
     
  8. Corliss, W. R. (n.d.). Can spores survive in interstellar space? Retrieved March 21, 2018, from http://science-frontiers.com/sf042/sf042p11.htm
     
  9. Weber, Peter, and Greenberg, J. Mayo; "Can Spores Survive in Interstellar Space?" Nature, 316:403, 1985.
     
  10. Orlic, C. (2013, January 09). The Origins of Directed Panspermia. Retrieved March 21, 2018, from https://blogs.scientificamerican.com/guest-blog/the-origins-of-directed-panspermia/
     
  11. Redd, N. T. (2017, June 07). How Old is the Universe? Retrieved March 21, 2018, from https://www.space.com/24054-how-old-is-the-universe.html
     
  12. Fermi Paradox. (n.d.). Retrieved March 21, 2018, from https://www.seti.org/seti-institute/project/details/fermi-paradox
     
  13. Crick, F. (1988). What mad pursuit: A personal view of scientific discovery. Basic.