Despite observed links between stress, trauma and type 1 diabetes (T1D) for over 2000 years, most doctors don’t know about the research. Despite 40 years of more specific, recent research showing that serious life events and trauma increase risk for T1D, the idea is still dismissed.
This means that people who suspect that trauma plays a role – such as because an accident or other difficult event triggered the onset of T1D, or because symptoms or other adverse events happened long before T1D ever developed – have trouble finding the evidence.
Today’s post introduces 7 myths that are still often used to dismiss the evidence showing links between stress, trauma and type 1 diabetes.
Table of Contents
- My Chronic Illness Guided My Interest in Diabetes Research
- I. Stress, Trauma and Type 1 Diabetes: 200 A.D. to the 1940s
- II. Psychosomatic Medicine: The Biggest Reason We Dismiss Trauma?
- III. Symptoms May Reflect an Intelligent Process Gone Awry
While writing this post, I received an email from Teri in Illinois describing this very problem:
I just read your post [about how trauma is making sense of your chronic illness]. I do not know how I found you, but am so grateful. My Son was diagnosed with Type 1 Diabetes in 2011 at 13 years old. Previous to his diagnosis he had a few situations which made me question over the years, what in the world was going on with him. He also was diagnosed with anxiety at age 4 and I was given information on ADHD/ADD and needed to bring him for testing at that time for an early intervention program, which he did not test “low” enough for.
At the time he was diagnosed, I looked directly at the endocrinologist and asked if this diagnosis could have had anything to do with stress. She said no. Every endo since this time has said no, even though we know full well cortisol levels and stress have affected his blood sugar levels all along and certainly do to this day.
Thank you for confirming there are studies out there for one. But even more so, thank you for sharing your story and putting it in black and white for us. We have known this for years, but it is hard to feel as if you are the only ones who do.
Research in T1D and disciplines as diverse as neurophysiology, nervous system development, brain plasticity, epigenetics, child development, attachment, and traumatic stress suggest the answers to Teri’s second question are Yes, trauma can trigger onset of T1D and Yes, trauma contributes to the cause and development of T1D.
This article is part of my discovery series presenting research I never knew as an MD. It draws from the increasing understanding that life experiences shape long-term health (post #1 and #2) and influence how genes function (post #3).
It’s not because it’s psychological.
Here I introduce a history of the links between stress, trauma and type 1 diabetes. I also present the top reasons why the belief has been dismissed, starting in the 1940s.
The same reasons are still often given today despite the research showing that serious life events actually do increase risk. In fact, recent studies show that kids and teens who develop type 1 diabetes have experienced three times more serious life events than their peers who have not.
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There is also little or no information on stress or trauma as risk factors for type 1 diabetes when searching websites of organizations such as the American Diabetes Association (ADA), the Juvenile Diabetes Research Foundation (JDRF), the International Diabetes Foundation (IDF), Diabetes Forecast, or the Mayo Clinic. Either it’s not mentioned at all, or it is discussed only with respect to the effects of stress on blood sugar levels or the trauma of being diagnosed with T1D (which are also clearly important to recognize).
Knowing about the links between stress, trauma and type 1 diabetes suggests that addressing the effects of serious life events, which happen outside of our control, may be helpful.
For example, some of these studies address Teri’s other question regarding whether her son might have been expressing symptoms well before the onset of T1D. Research findings offer insights about whether it might be possible to work with symptoms or with events she was concerned about so they aren’t missed opportunities for prevention, for delaying the onset or in potentially reducing severity.
As I will show in other posts, studies also find that serious life events affect risk for many other chronic diseases, where these questions about whether serious life events can cause chronic illness or trigger onset are just as common – illnesses such as rheumatoid arthritis, asthma and chronic lung disease, type 2 diabetes, heart disease, multiple sclerosis, Parkinson’s, depression, autism, fibromyalgia, and my own, which is ME/CFS (myalgic encephalitis / chronic fatigue syndrome) and many more.
I found my way to the research in type 1 diabetes because I developed a chronic illness myself. This is also how I learned about the effects of life events. That’s what I’ll introduce next. And if you already follow my blog and know my story feel free to skip to the next section on Stress, Trauma and Type 1 Diabetes.
When I first started exploring the T1D literature, I was experiencing symptoms of fatigue but did not yet realize I was in the initial phases of a debilitating chronic illness that would last for more than 20 years. I was in my early 30s and, after a lifetime of excellent health, I assumed my decreasing capacity to work, exercise and play was simply due to stress.
I had had a busy schedule as an assistant professor of family medicine at the time, and found the hours, responsibilities and demands stressful. I also felt increasing anguish about the limits of what I could offer my patients, especially those who were coming to me for help with their chronic diseases.
When my symptoms worsened despite decreasing my work hours for a year and then taking a 15-month-long sabbatical, it seemed that something much more serious than stress had to be causing my symptoms.
In my time off I had slowed down, started Tai Chi, changed my diet, and also practiced mindfulness and “being in the present moment.” Even though I’d felt much better emotionally, the common perspective that stress affects physical health hadn’t seemed to hold much water in my case.
At the end of my year off I left medicine for good and entered a new field of study, where I was introduced to a completely different way of understanding how life events can affect long-term health.
It changed my world view.
I developed a profound curiosity about whether life experiences could affect risk for chronic illness by altering our physiology, rather than because they influenced our psychology. Perhaps this was why my own health had not improved despite making changes and getting out of the fast lane.
I wondered if chronic illness could be the result of an innate, intelligent process that had somehow gotten “stuck” in the wrong gear.
I started exploring whether links existed between stress, trauma and type 1 diabetes (T1D).
What I learned eventually made sense of why reducing stress was not enough for me to recover. Healing and gradual improvement have instead come from addressing the more complex effects of serious life events and trauma that I never realized I had experienced. That’s part of what I share in my story that Teri referred to when she first emailed me.
My Chronic Illness Guided My Interest in Diabetes Research
All forms of diabetes are characterized by high levels of sugar in the blood but the mechanisms differ.
Type 1 diabetes is the less common, autoimmune form of diabetes. Although it can develop at any age T1D is frequently diagnosed in childhood. Symptoms are caused by the loss of insulin-producing cells in the pancreas and a lack of insulin.
Type 2 diabetes (T2D) results from a decreased ability of the body to utilize insulin, which may be present in large or small quantities. While onset of T2D usually occurs in adulthood, it has become much more common in children. T2D comprises 90% to 95% of all diabetes.
Both types of diabetes have been increasing around the world since the 1950s.
When I was first drawn to learn more about T1D, I didn’t yet have a name for my own symptoms.
I was eventually diagnosed with ME/CFS, which is associated with exhaustion that can be disabling (I eventually became nearly bedridden for 9 months) and linked to an inability to recover following exercise and activity. At one point, even speaking was difficult for me because it left me empty and tired. ME/CFS is also associated with other symptoms such as cognitive difficulties and remains a poorly understood disease for which no diagnostic tests exist.
What little research I could find in the early days of ME/CFS often proposed it was of psychological in origin.
Beyond the fact that this common view was limited, judgmental, and shaming, however, it didn’t feel accurate.
And so I continued with the vastly more abundant research in T1D, motivated by the fact that I kept making discoveries I had never heard of as a doctor.
For example, I had always thought T1D was a genetic disease. As I’ll describe with an example later in this post, this is a common reason links between stress, trauma and type 1 diabetes are dismissed.
But if one identical twin develops T1D the co-twin, who has the same genes, develops T1D less than half the time. And while having a family member with T1D (parent, sibling or relative) increases risk, rates of T1D have been increasing in genetically similar populations. These findings are all characteristics of nongenetic risk factors.
It turns out that at least half of the contribution to risk for T1D comes from the environment.
The reason to be interested in nongenetic risk factors is that, unlike genes, we may have some control over them or be able to treat or prevent or address them.
The environmental factors thought to confer greatest risk for T1D include having older parents and being breastfed for shorter periods.
Other risk factors are less clear, including the role of
- cow’s milk
- lack of sufficient exposure to everyday microbes during immune system development (the hygiene hypothesis)
- and trauma
Risk factors for T1D involve genes only 50% of the time. They include having older parents an being breastfed for shorter periods. The role of infections, cow’s milk, vaccines, toxins and trauma seem to be less clear.
Over the years, the exquisite series of links in the research I unearthed began to make sense of a connection between stress, trauma and type 1 diabetes.
Many of the perspectives I gained also helped make sense of my own experiences leading up to and following the onset of ME/CFS, as well as for asthma I developed in childhood.
I. Stress, Trauma and Type 1 Diabetes: 200 A.D. to the 1940s
The two different types of diabetes have been noted throughout the history of diabetes although a clear distinction was not made until the 1970s. As a result, early views reflect risk for both kinds of diabetes.
In 200 A.D. the Greek physician Aretaeus, who coined the name for diabetes, observed that the illness often began following “injury, moral shock or acute disease” such as influenza.
In 1679 Dr. Thomas Willis a British physician who added the term “mellitus” to the name because the urine of people with diabetes tasted of honey, stated that “a prolonged sorrow” was an important cause.
In 1948, Harvard trained physician George Daniels wrote about emerging beliefs that there were no links between stress, trauma and type 1 diabetes. He described how this seemed unwarranted, given the large collection of stories:
references to the sudden appearance of diabetes associated with dramatic stress (for example, in a prisoner whose brother, also a prisoner, was shot in his sleep; or in a child after being rescued from drowning; or in a person after begin frightened at the parting of the steering gear of his car in heavy traffic) are scattered through the literature of the last fifty years.
Dr. William Menninger, a psychiatrist and co-founder of The Menninger Clinic, and Harold Wolff, a neurologist, were among the many who agreed with Daniels that trauma was a common trigger for the onset of diabetes (1)Treuting, T. F. (1962). “The role of emotional factors in the etiology and course of diabetes mellitus: a review of the recent literature.” Am J Med Sci: 131/193-147/109, (2)Wolff, H., G. (1959). “Brain and diabetes: the role of the highest integrative functions in disease.” Diabetes 8(5): 358, (3)Robinson, N. and J. H. Fuller (1985). “Role of life events and difficulties in the onset of diabetes mellitus.” J Psychosom Res 29(6): 583-591.
7 Myths About Stress, Trauma and Type 1 Diabetes
Dr. Elliott Joslin initially supported the idea that serious life events might be risk factors for T1D.
He was the first medical doctor to specialize in diabetes in the United States and got interested in T1D when his aunt developed the disease. His mother developed type 2 diabetes after he started practice and his approach (low carbs, exercise, good self care) helped her live another 10 years, which was unheard of at the time.
Joslin was a pioneer in the support of patients learning to care for their own diabetes and maintaining tight blood sugar levels as a way to minimize severity and number of long-term complications. He founded the Joslin Center, which still focuses on diabetes research, care and education; created the first diabetes database with the thousands of cases he saw in his 70 years of medical practice; and became the world’s spokesman for diabetes in the mid 1920s.
Myth 1. No Increase of T1D in WWII Means Trauma is Not a Risk Factor. In his 1943 paper (4)Joslin, E. P. (1943). “The Relation of Trauma to Diabetes.” Ann Surg 117(4): 607-622, Joslin abandoned the theory that trauma could cause diabetes when the severe traumas of war did not increase rates of the illness. His writings echoed the views of many physicians:
“the World War presented an ideal opportunity for the physical and psychic traumatic origin of diabetes both in the combatants and noncombatants and that the disease did not materialize is most significant.
Despite seeing over 50,000 patients with diabetes over the course of his career, Joslin did not believe he ever saw a case where stress or trauma had been the cause except when a patient had experienced a direct blow to the pancreas.
Myth 2. People With the Same Traumatic Experiences Do Not All Develop Diabetes Therefore Trauma is Not a Risk Factor. When Joslin heard the case of a child who had developed diabetes after nearly drowning in a pond, trapped under the ice, and who had then been saved by his dog, Joslin stated that he’d had the very same experience as a child. He, too, had nearly drowned beneath the ice and been rescued by his dog. His contention was that neither he – nor his dog – had ever developed diabetes (5)Vague, J., et al. (1969). “[Sugar diabetes and trauma].” Mars Med 106(10): 755-764.
Joslin and others argued that these types of traumas are a normal part of everyday life. Since most people experience similar events but never develop diabetes, they reasoned, such experiences couldn’t really be factors of relevance.
Myth 3. Type 1 Diabetes is Due Solely to a Problem with the Pancreas and Anatomy. A third reason Joslin and others dismissed the links between stress, trauma and type 1 diabetes stemmed from the finding in 1889 that diabetes could be induced by removing the pancreas. The emerging idea that the nervous system played a role in diabetes through it’s effects on sugar and insulin levels was essentially set aside. The focus on causes of diabetes turned to the specific organ and the insulin-producing cells within.
“This anatomic fact [of the pancreas’ role], in itself, shows how futile the attempt must be to connect bodily trauma with diabetes Joslin (1943).
Myth 4. Variation in Time of Onset After Traumatic Events Means Trauma Has No Role if Too Far in the Past. Another concern about trauma as a risk factor was that diabetes sometimes occurred within hours or days of a stressful event but could also arise weeks, months or even years later. Joslin and others stipulated that if stress and trauma were risk factors, diabetes must begin within a “reasonable” amount of time after such events. Although the reasons for this varying period of delay were not known, the time frame was eventually limited to 1 year between a traumatic event and onset of diabetes for the link to be deemed relevant.
Myth 5. Disability Insurance Means People Will Manufacture a Trauma History or Malinger. The advent of disability insurance in Europe was a final issue for Joslin, who worried that people would take advantage of it to falsely or excessively claim that a traumatic event had caused their diabetes in order to receive compensation.
Ultimately, Joslin was among a number of physicians who agreed that trauma might activate or accelerate an underlying process of diabetes in those already predisposed (such as due to genetic factors), but that trauma was not a cause.
During this period in the mid 1900s, physicians in other specialties were also considering trauma to be a potential risk factor for multiple sclerosis and ALS (6)Harris, W. (1933). “The traumatic factor in organic nervous disease.” British Medical Journal 2: 955-960. Like Joslin, however, many began to dismiss the link. Grimberg, a neurologist in New York, documented the same phenomenon in Parkinson’s disease (7)Grimberg, L. (1934). “Paralysis agitans and trauma.” J Nerv & Ment Dis 79: 14-43.
7 Reasons Links Between Stress, Trauma and Type 1 Diabetes Were Dismissed
To summarize, Joslin gave 5 reasons stress and trauma were dismissed as potential causes of diabetes (as well as potential causes of MS, ALS and Parkinson’s), in the mid 1900s (1943):
- even the most serious traumatic events such as war do not seem to increase rates of diabetes
- stressful & traumatic events are common and most people do not develop diabetes afterwards
- causes of diabetes most likely involve a specific organ (the pancreas)
- the role of trauma only makes sense if diabetes begins in a limited window of time after exposure
- the arrival of worker’s comp may incite more and exaggerated stories and links to trauma
The Joslin Center’s website response to the question of whether trauma can cause diabetes cites views from his 1943 publication. They include a statement that “the thesis that trauma de novo can cause diabetes has steadily lost support.”
Many individuals with T1D and other chronic diseases have similar reasons for dismissing potential links between stress, trauma and type 1 diabetes today.
It’s also still an issue that’s been recently investigated for insurance companies.
Myth 6. Type 1 Diabetes Is Purely Genetic. This last concern was highlighted by another email I received while working on this post. This one was from a parent who has two sons with type 1 diabetes. Both were diagnosed after serving in the marines. The first received full service related disability. The second did not, the reason being that since his older brother had T1D, his own disease had to be genetic.
Having two of your children be diagnosed with an incurable illness can be painful and stressful for a parent. Having both develop the disease under similar circumstances while only one receives support for a complex, lifelong illness that requires close daily management can be devastating.
The fact that veterans with T1D can be awarded disability support acknowledges the role of trauma and suggests that new research (which I’ll present in future posts of this series) is being recognized.
The lack of similar benefits for his brother, however, may reflect challenges. Whether in keeping up with the research, hanging on to outdated beliefs or simply due to our inability to know what truly causes a chronic disease. It may also represent the 6th reason why links between stress, trauma and type 1 diabetes are dismissed: the belief that genetics are more important than environmental risk factors and that family history implies a purely hereditary cause.
New Research Findings and Insights
Genes Account for less than 50% of Risk. As mentioned earlier, the scientific consensus is that 50% or less of risk for type 1 diabetes is caused by genes. And if one family member develops T1D his or her sibling develops T1D only 8% of the time. Other chronic diseases also show the same statistics in which genes account for less than half the risk while environmental exposures explain the rest.
Environmental Stressors act as Triggers. Only 10% of people at genetic risk for T1D ever develop the disease and environmental triggers appear to be necessary for individuals to actually develop T1D (8)Knip, M., et al. (2005). “Environmental triggers and determinants of type 1 diabetes.” Diabetes 54 Suppl 2: S125-136 even if they have a genetic predisposition (9)Pociot, F. and A. Lernmark (2016). “Genetic risk factors for type 1 diabetes.” Lancet 387(10035): 2331-2339. The effects of exposures to triggers accumulates over time when a person does not have sufficient counterbalancing experiences of time, support, and safety to enable the body to heal. As a result, some people develop a chronic illness after a last straw event when others, who have had more “buffers” and supportive experiences or time to heal, do not.
Environmental Stressors Trigger the Cell Danger Response. Environmental stressors can trigger the onset of chronic diseases of all kinds, regardless of whether exposures are infections, toxins, or physical or psychological trauma. This is because environmental stressors trigger the cell danger response (CDR), which occurs in all cells when faced with threat. If this cell danger response becomes prolonged and stuck in the “on” position it can lead to disease. Each disease is caused by different variations of individual types of cell danger responses or a mixture of these CDRs. These may look like variations of an organism caught in states of prolonged fight and flight, or prolonged freeze such as in chronic fatigue syndrome (ME/CFS). See a list of over 100 diseases in Table 1 of Dr. Robert Naviaux 2018 article proposing the cell danger response as a unifying new paradigm for understanding disease (10)Naviaux, R. (2018 (epub ahead of print. “Metabolic features and regulation of the healing cycle—A new model for chronic disease pathogenesis and treatment.” Mitochondrian)), (11)Naviaux, R. K. (2014). “Metabolic features of the cell danger response.” Mitochondrion 16: 7-17. This supports Joslin’s view that trauma does not actually cause T1D, but explains that trauma is indeed an important risk factor.
Trauma Increases Risk for T1D and Triggers Onset. What’s helpful for individuals like us to know is that research starting in the 1980s has established links between stress, trauma and type 1 diabetes. Studies have found that children exposed to trauma are at three times higher risk for T1D than kids who are not (12)Nygren, M., et al. (2015). “Experience of a serious life event increases the risk for childhood type 1 diabetes: the ABIS population-based prospective cohort study.” Diabetologia 58(6): 1188-1197, and trauma is an important trigger for T1D and other chronic diseases of all kinds.
Studies in T1D and from other areas of science also show that the role of serious life events is much more important than we’ve recognized.
This is not just about risk for T1D but includes other autoimmune as well as many other kinds of chronic diseases.
Myth 7. The Effects of Trauma Are Only Psychological and Do Not Include Physical Disease. Before going any further into the research, I will end today’s post with the 7th reason stress and trauma are commonly dismissed. The belief that trauma’s effects are entirely and only psychological may be one of the biggest reasons that we fail to recognize the links between serious life events and risk for chronic diseases such as T1D.
II. Psychosomatic Medicine: The Biggest Reason We Dismiss Trauma?
The earliest theories linking stress, trauma and type 1 diabetes arose before mind and body became separate fields of study. This may be one of the most important reasons that we struggle – as a society, as a culture, in medical care and training, and as individuals – with the concept of potential links between stress, trauma and type 1 diabetes.
The effects of stress and trauma have long been assigned to the field of mental health.
Symptoms resulting from severe or serious life events (SLEs) are currently viewed as distinctly separate from what are often considered to be “more legitimate” risk factors for physical diseases, which are commonly assigned to faulty physical and biological processes (genes and mutations, missing enzymes, altered proteins, etc).
Physical diseases that can be found to have emotional or psychological risk factors are still considered by many to be psychosomatic. They are then believed to be less “valid” than others.
Today, most people with a chronic disease will tell you that the term “psychosomatic” feels like a dirty word. As do the terms “stress” and “trauma.”
In recent decades, the implication that emotional factors and life experiences can affect physical health has often placed blame on patients.
The concept has been wielded, sometimes unconsciously often directly, to suggest that such a disease is their fault, is being faked, was caused by poor lifestyle choices, or is due to personality flaws, weakness, or laziness.
While it’s true that lifestyle and dietary changes can sometimes reverse type 2 diabetes and other chronic diseases for some people, it is not a widely effective cure for chronic illness. Furthermore, no one deliberately sets out to develop a chronic debilitating disease.
Hearing of potential links between stress, trauma and type 1 diabetes or other chronic diseases can feel to many as though they are being stuffed back down the old rabbit hole and judged once again. No matter how well-researched, well-intentioned, or non “psychological.”
That’s the dark side of trauma, mind body medicine and psychosomatics.
III. Symptoms May Reflect an Intelligent Process Gone Awry
On the intriguing, ever-evolving and brighter side, science is beginning to reveal how adverse life events can affect long-term physical health and risk for chronic disease as well as emotional and mental health.
Physicians such as Daniels, Menninger and Wolff had detailed theories about how the effects of trauma might result from the body’s attempt to adapt to a difficult situation only to later be expressed, when unresolved, as diseases like diabetes. They suggested the adaptations occurred through the brain and nervous system, the endocrine system, or changes in biology (13)Treuting, T. F. (1962). “The role of emotional factors in the etiology and course of diabetes mellitus: a review of the recent literature.” Am J Med Sci: 131/193-147/109, (14)Rabkin, J. G. and E. L. Struening (1976). “Life events, stress, and illness.” Science 194(4269): 1013-1020, (15)Calobrisi, A. (1983). “Biopsychosocial study of diabetes mellitus.” Psychother Psychosom 39(4): 193-200, (16)Evans, M. B. (1985). “Emotional stress and diabetic control: a postulated model for the effect of emotional distress upon intermediary metabolism in the diabetic.” Biofeedback Self Regul 10(3): 241-254.
These physicians were compassionate pioneers in the field of psychosomatic medicine, which originally saw mind and body as interactive and interdependent rather than separate.
The science of the day, however, could not make sense of these perspectives.
As anatomy and more easily measurable physical abnormalities were brought to light for T1D, multiple sclerosis, Parkinson’s and other diseases, medicine and the primacy of the body gradually took precedence over possible contributions of experience.
When I prepared to return to work after my sabbatical from medical practice, I was still overly tired but able to function, and I decided to retrain in a new profession.
I chose my new field because I’d worked with a therapist who showed me just how intelligent and helpful my body, my sensations, my symptoms and my impulses could be. I’d also been inspired by Dr. Rachel Remen, a clinical professor of family and community medicine at UCSF School of Medicine, as well as a pediatrician-turned-counselor with inflammatory bowel disease, who helped individuals with cancer find meaning and healing in their lives, just as she had experienced in her own.
It was also because I’d never felt so deeply heard, seen or supported as I had in my therapy work.
The field I retrained in is called somatic psychology and has roots in the paradigm of psychosomatic medicine. Instead of accusations and labels, however, it invites curiosity and nonjudgment. It supports the possibility that there is an intelligence that underlies symptoms. This is also an intelligence that can be accessed and supported by listening to the language of the body – which includes symptoms.
Although my new field of training was in the field of mental health, I had an aha moment that made me wonder whether life experiences that could shape mental health conditions might, in some cases, lead instead to physical diseases.
This was not because such diseases were psychological or psychosomatic.
It was because new science is revealing how the concept that psychological events cause only psychological symptoms is both inaccurate (17)Baldwin, D. V. (2013). “Primitive mechanisms of trauma response: an evolutionary perspective on trauma-related disorders.” Neurosci Biobehav Rev 37(8): 1549-1566 and out of date (18)McFarlane, A. C. (2015). “One hundred years of lessons about the impact of war on mental health; two steps forward, one step back.” Australas Psychiatry, (19)Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246.
And so I started integrating my background in medicine with what I was learning in psychology. Looking at the research from my eyes as both a physician and a somatic and trauma therapist.
It lead me to new questions. New ideas. And eye-opening studies.
In post #6 of this series I review 25 years of trauma research in diabetes showing that adverse events increase risk for and trigger onset of type 1 diabetes (and other chronic illnesses). It explains characteristics of trauma seen in T1D and other diseases that address the myths in more detail. It also gives a better understanding of why we cannot dismiss the role of physical and psychological trauma as a risk factor for T1D and other chronic diseases.
Free Series Download (includes this post)
Want to learn more? My first post of the series introduces the discovery that adverse events during pregnancy, birth and infancy increase risk for type 1 diabetes and other chronic diseases, and that addressing similar risk factors in asthma can cure it in many kids. This offers insights into potential for treatment and prevention. Post 3 describes how early life events affect genes and Post 4 is a recap. I’ve summarized the research I’ve integrated to make sense of disease over the past 15+ years in this post. Or you can download my free ebooks which include an overview of the research (see book 1). The trauma perspective offers insights into Dan’s story of onset with T1D. A recent metabolics study in ME/CFS and my personal story give you an idea of how trauma makes sense of my own chronic illness. If you’re thinking about working with symptoms from these perspectives here’s a list of books and therapies for addressing the effects of adverse life experiences from any time in life (prenatal & birth; infancy or childhood; multigenerational; current day etc) and a list of 10 tools that support healing nervous system perceptions of threat.
|↑1, ↑13||Treuting, T. F. (1962). “The role of emotional factors in the etiology and course of diabetes mellitus: a review of the recent literature.” Am J Med Sci: 131/193-147/109|
|↑2||Wolff, H., G. (1959). “Brain and diabetes: the role of the highest integrative functions in disease.” Diabetes 8(5): 358|
|↑3||Robinson, N. and J. H. Fuller (1985). “Role of life events and difficulties in the onset of diabetes mellitus.” J Psychosom Res 29(6): 583-591|
|↑4||Joslin, E. P. (1943). “The Relation of Trauma to Diabetes.” Ann Surg 117(4): 607-622|
|↑5||Vague, J., et al. (1969). “[Sugar diabetes and trauma].” Mars Med 106(10): 755-764|
|↑6||Harris, W. (1933). “The traumatic factor in organic nervous disease.” British Medical Journal 2: 955-960|
|↑7||Grimberg, L. (1934). “Paralysis agitans and trauma.” J Nerv & Ment Dis 79: 14-43|
|↑8||Knip, M., et al. (2005). “Environmental triggers and determinants of type 1 diabetes.” Diabetes 54 Suppl 2: S125-136|
|↑9||Pociot, F. and A. Lernmark (2016). “Genetic risk factors for type 1 diabetes.” Lancet 387(10035): 2331-2339|
|↑10||Naviaux, R. (2018 (epub ahead of print|
|↑11||Naviaux, R. K. (2014). “Metabolic features of the cell danger response.” Mitochondrion 16: 7-17|
|↑12||Nygren, M., et al. (2015). “Experience of a serious life event increases the risk for childhood type 1 diabetes: the ABIS population-based prospective cohort study.” Diabetologia 58(6): 1188-1197|
|↑14||Rabkin, J. G. and E. L. Struening (1976). “Life events, stress, and illness.” Science 194(4269): 1013-1020|
|↑15||Calobrisi, A. (1983). “Biopsychosocial study of diabetes mellitus.” Psychother Psychosom 39(4): 193-200|
|↑16||Evans, M. B. (1985). “Emotional stress and diabetic control: a postulated model for the effect of emotional distress upon intermediary metabolism in the diabetic.” Biofeedback Self Regul 10(3): 241-254|
|↑17||Baldwin, D. V. (2013). “Primitive mechanisms of trauma response: an evolutionary perspective on trauma-related disorders.” Neurosci Biobehav Rev 37(8): 1549-1566|
|↑18||McFarlane, A. C. (2015). “One hundred years of lessons about the impact of war on mental health; two steps forward, one step back.” Australas Psychiatry|
|↑19||Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246|