Commusings: Why Do Giraffes Have Long Necks? by Jeff Krasno

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Dear Commune Community,

Epi means above. Genetics refer to my coding – or genome. Epigenetics, then, is what exists “above my genes” – which is why sometimes I call my pinchable muffin tops my “epigenome,” as this (now greatly diminished) fat innertube exists “above my jeans.”

[CODE RED DAD JOKE]

Last Sunday, I published the first installment of my excavation into epigenetics. Specifically, I explored how genes express themselves differently in relation to behavior and the environment. The term epigenetics is also used to refer to the transgenerational inheritance of acquired traits. This is the focus of today’s musing.

In both contexts, epigenetics casts a shadow on our conventional understanding of genetic determinism and evolution. The phenomenon points to a new understanding of the human organism not as a fixed entity with a sealed fate but as a fluctuating process changing in relation to its exposome – the foods we eat, stress, our relationships, environmental toxins, our feeling and thoughts.

This is both empowering and scary for the same reason. We have more agency over our health – for better and worse – than we ever thought. This agency applies not only to our own health but potentially to the health of our children.

Here at [email protected] and evolving on IG @jeffkrasno.

In love, include me,
Jeff

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Why Do Giraffes Have Long Necks?

 

While the term epigenetics often refers to how genes change in relationship to environmental conditions and inputs, it also bears another meaning. The auxiliary definition of epigenetics refers to the transgenerational inheritance of acquired traits. In this sense, proponents of epigenetics theorize that certain characteristics that are acquired in response to experiences and environmental circumstances can be passed down to the next generation. 

This concept is at odds with strict Neo-Darwinism. 

Classical Darwinism describes a philosophy in which organisms evolve through the natural selection of small, hereditary variations. Those genetic mutations that help an individual survive and reproduce are passed on through reproduction. This process of natural selection slogs on from generation to generation.

Darwinism is classically pitted against the theories of the early 19-century French biologist Jean Baptiste Lamarck. Lamarckism posits that certain environmental circumstances create needs to which organisms respond and then those acquired traits are passed on to its offspring. This concept is commonly illustrated by way of giraffes. This theory posits that the giraffe originally looked like a horse with a small neck and forelimbs. But since they increasingly lived in places without any vegetation on the surface, they had to stretch out their neck and forelimbs to pick leaves to eat, resulting in a slight elongation of these parts. Those beneficial characteristics passed over time from generation to generation and ultimately resulted in a species with long necks and forelimbs. Like a giraffe, Lamarck argued, a blacksmith, through his work, strengthened the muscles in his arms. And this phenotype would be observable in the first filial generation. Essentially, traits that an individual organism acquired through use or disuse could be passed on to its offspring. 

The pitting of Darwin versus Lamarck has been vastly over-dramatized as Darwin’s pangenesis theory of 1868 did allow for the transferal of altered characteristics to offspring. While both Darwin and Lamarck hypothesized around the mechanisms for this process, neither really understood the mode of action.  

Darwin's theories underwent their own ideological evolution over the course of the 20th century. Neo-Darwinists denied that acquired characteristics could be inherited and painted Lamarck as a charlatan. While bulging biceps may not be transferred directly from a weightlifter to his progeny, the 21st century has begun to redeem the erstwhile discredited Lamarck through the emerging science of epigenetics. 

Mother Nurture

I’ve always said that my daughters never listen to me, but they never fail to imitate me. The fact that children often mimic their parents seems completely instinctual. As a father to three daughters, I can easily point to how my behavior influences them – how both my strengths and unresolved trauma impacts them for the better and worse. It’s fairly easy to understand the ramifications of nurture. For example, studies show that children of alcoholics are four times more likely than the general population to develop alcohol problems irrespective of their underlying genetics.

From time to time, we notice how much we become like our parents – sometimes even adopting their less desirable traits. I repeat the same old limp jokes over and over to my girls and, in rare moments of self-awareness, I realize I’ve become my father. 

Beyond the impacts of “nurture,” we are beginning to comprehend how stress can impact unborn children in utero. In 1998, there was a monumental ice storm in Montreal that knocked out electricity in parts of the city for weeks. Suzanne King, a researcher at the Douglas Mental Health University Institute, studied the health profiles of 100 pregnant women and their children born during this period. The duration of how long pregnant women went without electricity made a difference in children's IQ, body mass index, immune functions, insulin secretion and risk of diabetes. The study demonstrated that a prenatal elevation of stress hormones in the mother can cross the placenta and influence infant development. 

But generational inheritance of acquired traits goes even further. It appears there are mechanisms that pass down acquired behavioral characteristics in a single generation irrespective of the underlying fixed genes. 

Trauma & Transgenerational Inheritance

Dr. Rachel Yehuda is a professor of Psychiatry and Neuroscience and the director of the Traumatic Stress Studies Division at the Mount Sinai School of Medicine in New York City. Yehuda has conducted numerous studies on the neurobiological and psychological aspects of PTSD, including research on cortisol and glucocorticoid receptor functioning. Specifically, Yehuda has studied traumatized groups including combat veterans, survivors of the 9/11 attack on the World Trade Center and the community of Holocaust survivors in her hometown of Cleveland, Ohio. 

Yehuda found a consilience across all of these disparate groups. They had a prevalence of PTSD, high levels of adrenaline and low cortisol levels. Initially, these findings were not instinctual. Because trauma usually causes stress hormones, including cortisol, to rise, chronic low cortisol rates among traumatized groups was surprising. Upon further examination, though, it appears that prolonged activation of the stress response can result in a protective measure that leads to a reverse cortisol curve over time. 

Dr. Isabella Wentz’s work also points to how stress over time leads to dysregulation of the adrenals and low cortisol secretion. Additionally, Yehuda observed reduced (hypo)methylation in an important region of NR3C1, a gene that encodes the glucocorticoid receptor, increasing the sensitivity of these receptors.

When the glucocorticoid receptor becomes more sensitive, a smaller amount of cortisol is needed to activate the receptor. In other words, the receptor can respond more strongly or more quickly to the same levels of cortisol. This modifies the normal functioning of the HPA (hypothalamic-pituitary-adrenal) axis. This phenomenon can alter the body’s stress response and contribute to depression and anxiety disorders. 

While studying survivors of the Holocaust, Yehuda began to collect anecdotal evidence that demonstrated that the offspring of Holocaust survivors in Cleveland, Ohio, were also suffering from disproportionate rates of depression and PTSD. This group’s parents had endured the unspeakable horrors of the Holocaust, but the offspring predominantly grew up in Cleveland long after the end of World War II.

The flood of anecdotes prompted Yehuda and five of her colleagues to go to Cleveland to study the offspring of survivors. They conducted interviews and collected urine and blood samples. Indeed, they found abnormally high levels of PTSD and low cortisol levels in the offspring of female survivors with PTSD. Further, they discovered lower methylation within the glucocorticoid receptor gene, NR3C1, in Holocaust offspring whose mothers, or both parents, had PTSD. The epigenetic marker had been passed down transgenerationally. 

Methylation may be the mechanism that explains multi-generational trauma. And the link between trauma and physiological and psychological disease is well established. This means trauma suffered by one generation can contribute to physiological disorders in future generations. In other words, the trauma of one generation can present as diabetes, for example, in the next. 

(I went to methylation in more depth in last week’s essay here.)

Opening Up a Can of Worms

Dr. Oded Rechavi is a research scientist studying epigenetics. His experiments use model organisms, primarily C. Elegans nematodes – known to you and me as worms. C. Elegans are marvelous subjects for studies on epigenetics as their lifespan is a mere three days. This abbreviated life expectancy produces data that can be quickly harvested and interpreted. 

Rechavi set out to test whether or not C. Elegans could produce transgenerational resistance to specific viruses. The worms do not have an immune system per se. They don’t possess immune cells like B-cells and T-cells, nor do they generate antibodies the way humans do. That said, these nematodes can defend themselves using RNA. In fact, when Rechavi infected the worms, they detected the virus and their genome responded by producing small RNA molecules that silenced the RNA in the virus.

Then Rechavi collected the progeny of these worms and removed the gene that coded for the virus-neutralizing RNA. Rechavi proceeded to infect this F-1 generation with the same (fluorescent) virus. If the worms turned bright green then the virus would have taken hold. But they didn’t.

The worms transferred the virus-fighting RNA between generations despite Rechavi removing the underlying genetic machinery to make it.

Does this same phenomenon apply to humans? We don’t know. But Rechavi’s findings suggest that acquired traits are heritable, at least in in C. Elegans, and RNA may be the molecule to potentially transmit these acquired traits between generations. 

Recent papers published in Nature suggest that sperm RNA may be the mediator of intergenerational transmission of paternally acquired phenotypes such as diet-induced metabolic disorders and mental stress phenotypes. The basic idea is that sperm RNAs respond to environmental inputs and changes and then encode the acquired traits, subsequently shaping early embryonic development.

Of course, this notion of acquired heritable traits flies in the face of what we thought we knew about genetics – that genetic phenotypes evolve over long periods of time through pressure and random mutation. 

While our DNA may be static, their expression is patently not fixed. This idea of being unfixed is both empowering and a little scary. Empowering because you have agency. Scary because your life is not just your own. Like the Buddha suggested, we are all caught up in a mutually interdependent net of humanity – in constant relationship with everything and everyone around us. 

The field of epigenetics is still in its infancy. There is so much yet to discover. 

I hope this series of articles provided a helpful initial primer. Remember – you have agency over your health. We are not simply pushed around by our genes. By adopting health-conferring protocols, we can wrest back control over our own well-being.