#6 Trauma Triggers Type 1 Diabetes and Other Diseases (Buffers, ACEs, Delayed Onset after Trauma+)

In this 6th post of my discovery series, I review 25 years of studies examining links between stress, serious life events such as trauma, and type 1 diabetes (T1D). This first series of studies, which were done in the 1980s and 1990s, validate the long-held suspicion that trauma triggers type 1 diabetes.

Whether you have T1D or a different chronic illness, the research can help you make sense of why and how you developed a chronic disease. I share some of my personal discoveries and events I never considered could possibly be trauma-related, and how I began to recognize that they had had an impact on my health. I introduce the role of support and safety as experiences that help counteract or “buffer” the effects of trauma and more.

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In the first four articles of this series I introduced research showing how trauma increases risk for type 1 diabetes and other diseases, beginning in pregnancy, birth and infancy. This is not because these diseases are psychological, but because environmental stressors such as infections, toxins and both physical and psychological trauma can trigger and prolong the cell danger response as well as nervous system perceptions of threat.

The emerging science shows how  life experiences shape nervous systems patterns of regulation early in life and influence long-term health. Early experiences, which I refer to as adverse babyhood experiences or “ABEs” also alter genes to influence how they are expressed.

In the most recent post, I described the 2000 year history of suspected links between stress, trauma and type 1 diabetes and 7 myths explaining why trauma was (and still is) often dismissed.

These same reasons are used to negate the role of trauma and adversity as risk factors for many other chronic illnesses, including my own, which is chronic fatigue syndrome (ME/CFS).

Some of the reasons trauma gets dismissed were addressed in last post.

Today’s post begins to address the myths in more detail, offer more insights into symptoms seen in disease, and to present the research showing that trauma triggers type 1 diabetes.

Top Reasons Trauma Research in Type 1 Diabetes is Dismissed

1. Myth: T1D is purely genetic. The Research: Genes that predispose us to risk of developing T1D do not express themselves in isolation. They must interact with the environment over time in order to manifest the disease ⁽¹⁾Pociot, F. and A. Lernmark (2016). “Genetic risk factors for type 1 diabetes.” Lancet387(10035): 2331-2339, ⁽²⁾Knip, M., et al. (2005). “Environmental triggers and determinants of type 1 diabetes.” Diabetes 54 Suppl 2: S125-136.
2. Myth All effects of trauma are psychological, so it cannot be a risk factor for T1D. The Research: This view of out of date ⁽³⁾McFarlane, A. C., et al. (2017). “The Need to Take a Staging Approach to the Biological Mechanisms of PTSD and its Treatment.” Curr Psychiatry Rep 19(2): 10, ⁽⁴⁾McFarlane, A. C. (2017). “Post-traumatic stress disorder is a systemic illness, not a mental disorder: is Cartesian dualism dead?” Med J Aust 206(6): 248-249, ⁽⁵⁾Baldwin, D. V. (2013). “Primitive mechanisms of trauma response: an evolutionary perspective on trauma-related disorders.” Neurosci Biobehav Rev 37(8): 1549-1566. Trauma has many effects, including on physiology, biology, the HPA (hypothalamic-pituitary-adrenal) axis, and nervous system regulation, among others ⁽⁶⁾Yehuda, R., et al. (2015). “Post-traumatic stress disorder.” Nature Reviews Disease Primers October: 150-157, ⁽⁷⁾Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246.

The following are also mistaken and out of date beliefs about trauma as a risk factor for T1D that I will address in today’s post:

1. War did not increase rates of diabetes, so trauma cannot be a risk factor.
2. Adverse events are common. Since most people do not develop T1D after trauma, it must not be a risk factor.
3. Worker’s compensation may incite false or exaggerated links to trauma.
4. Cause of T1D involves only the specific organ of the pancreas.
5. The role of trauma makes no sense if diabetes begins too long after exposure.

Below I share some of the first studies I discovered when I started asking the question of whether trauma increases type 1 diabetes. I have since uncovered similar kinds of studies (and findings) for many other chronic illnesses.

Just as it took me a while to recognize my own risk factors among the subtle adverse experiences in my own prenatal life, birth and infancy (introduced in Post #1 and #2 of this series), I didn’t initially connect the dots with the types of serious life events I introduce here either. I’ve been through events similar to those I will describe below, but, like so many of us, I was slow to realize that these seemingly “ordinary” events had 1) happened to me and 2) could have in fact influenced my health.

We have our notions of what serious life events consist of – and it can take time, introspection and validation from others as well as from seeing the links to our own symptoms to change these views.

What are Serious Life Events (SLEs)?

Researchers in T1D and other chronic diseases have commonly used questionnaires to identify significant life events, whether negative or positive. These questionnaires cover a broad range of events that can be stressful or difficult to cope with or adapt to.

Examples of serious or severe life events (SLEs) evaluated in many of these studies include:

• loss of a parent, such as from death or divorce
• family chaos, disturbance or conflict
• having a parent with a serious mental or physical illness
• hospitalization for reasons not related to T1D
• accidents
• being adopted or having been in foster care
• having a parent in jail
• death of a parent, friend, sibling, or grandparent
• serious parental physical or mental illness
• new beginnings, such as starting at a new school or beginning a new school year, changing schools, parent beginning work, arrival of a new sibling
• indicators of stress or trauma such as problems in school or in maintaining friendships, difficulty going to sleep, behavioral changes, or frequent occurrence of nightmares

Is it True That Trauma Triggers Type 1 Diabetes?

In 1976, the discovery ⁽⁸⁾Gale, E. A. (2001). “The discovery of type 1 diabetes.” Diabetes 50(2): 217-226 that our immune systems can attack our own cells to cause autoimmune diseases provided new opportunities for diabetes research.

It made it easier to differentiate between type 1 diabetes, the less common autoimmune form of the disease, which requires insulin and often begins in childhood; and type 2 diabetes, which is often associated with weight gain but not always, and which is increasingly common in children as well.

Studies began to look at whether trauma increases type 1 diabetes.

Investigators examined nitty gritty details that can be so tricky to identify when measuring whether someone has experienced trauma and whether it has played a role in long-term health. These included whether severity of stressful events, number of exposures, or supportive experiences made a difference in risk.

The focus on type 1 diabetes took many forms.

Some studies involved country-wide assessments, such as the Swedish Childhood Diabetes Study, which documented all cases of T1D in children aged 0-14 through a national registry. Most involved questionnaires, sometimes sent to individuals newly diagnosed in clinics, other times conducted through interviews by phone or in person. Studies also looked for patterns in antibody expression.

Most of the studies I present below used control groups, which involves selecting both participants with T1D and others who are similar, such as by age but who do not have T1D. Cohorts offer a means of comparison.

Can Trauma Trigger the Onset of T1D?

Observations in 200 A.D., in the late 1600s, and through the early 1900s suggested that stress and trauma could trigger the onset of T1D. Many of the studies first examining whether serious life events increase risk for type 1 diabetes in the period before onset reached similar conclusions.

Researchers found a greater number of SLEs in the year before onset of T1D in 5-9 year olds in Sweden ⁽⁹⁾Hagglof, B., et al. (1991). “The Swedish childhood diabetes study: indications of severe psychological stress as a risk factor for type 1 (insulin-dependent) diabetes mellitus in childhood.” Diabetologia 34(8): 579-583, 10-14 year olds in Hungary ⁽¹⁰⁾Soltesz, G., et al. (1994). “Non-genetic risk determinants for type 1 (insulin-dependent) diabetes mellitus in childhood. Hungarian Childhood Diabetes Epidemiology Study Group.” Acta Paediatr 83(7): 730-735, and in kids under 17 years of age in Montreal, Quebec in Canada ⁽¹¹⁾Siemiatycki, J., et al. (1989). “Case-control study of IDDM.” Diabetes Care 12(3): 209-216. Individuals diagnosed with T1D at older ages also experienced more SLEs in the 12 months before onset in a study in France ⁽¹²⁾Vialettes, B., et al. (1989). “Stress antecedents and immune status in recently diagnosed type I (insulindependent) diabetes mellitus.” Diabete Metab 15(1): 45-50 and in the three years before onset in the UK ⁽¹³⁾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. Participants in the UK study who were diagnosed after age 21 had more total numbers of SLEs than younger individuals.

One particular study, begun in 1992 and 1993, that found no differences in number of SLEs was The Diabetes Incidence Study in Sweden (DISS). Interestingly, the results suggest the opposite of their statement of no link presented in their abstract ⁽¹⁴⁾Littorin, B., et al. (2001). “Family characteristics and life events before the onset of autoimmune type 1 diabetes in young adults: a nationwide study.” Diabetes Care 24(6): 1033-1037.

DISS sent questionnaires to all individuals 15-34 years of age recently diagnosed with T1D in Sweden. Like the Swedish Childhood Study ⁽¹⁵⁾Hagglof, B., et al. (1991). “The Swedish childhood diabetes study: indications of severe psychological stress as a risk factor for type 1 (insulin-dependent) diabetes mellitus in childhood.” Diabetologia 34(8): 579-583, 2 nondiabetic controls were selected for each child with T1D and matched for age and gender. The authors examined whether serious life events increase risk for type 1 diabetes in the 12 months before onset.

Despite stating that no differences existed, DISS results showed that individuals with T1D had much higher rates of serious illnesses, had been more frequently hospitalized for more than a week, and had more often lost one or both grandparents in the year before onset. The participants with T1D had 6 additional SLEs in the 26-question survey that occurred more frequently than in controls. All 9 findings were statistically significant. These included having less success and more unresolved conflicts with spouses. They had difficulty understanding why the remaining SLEs caused or could reflect problems, and this may be part of why the SLEs were not included as risk factors in their conclusions.

Being diagnosed with a serious illness such as T1D can be life-threatening and traumatic. Hospitalization can be as well, and can also trigger intense states of helplessness and despair, especially in children.

Hagglof and colleagues ⁽¹⁶⁾Hagglof, B., et al. (1991). “The Swedish childhood diabetes study: indications of severe psychological stress as a risk factor for type 1 (insulin-dependent) diabetes mellitus in childhood.” Diabetologia 34(8): 579-583 removed serious illness and hospitalizations from their Swedish Diabetes Childhood Study questionnaire on discovering that these events were often cited by parents in relation to the diagnosis of T1D. Littorin’s group did not know whether these events were linked to T1D or other illness. The loss of grandparents was a separate, additional SLE found to be more common in the T1D group than in controls.

The conflict between the DISS findings and their statement that there are no links is a problem with this study rather than lack of support for SLEs as risk factors.

Serious Life Events (SLEs) and Age of Onset

Hagglof’s study was part of a larger Swedish Childhood Study ⁽¹⁷⁾Dahlquist, G., et al. (1991). “The Swedish Childhood Diabetes Study: a multivariate analysis of risk determinants for diabetes in different age groups.” Diabetologia 34(10): 757-762 looking at multiple additional environmental risk factors for T1D such as diet, infections and vaccines. Each of these factors independently increased risk. Dahlquist and her colleagues summarized their findings

Of all the environmental risk factors examined (diet, vaccine status, infections, stress), psychological stress in the year before diagnosis was the only factor to influence age of onset of T1D, suggesting that it triggered onset.

The early studies in T1D had some problems, including differences in defining SLEs; differences in questions, number of questions, and questionnaires; and because of relatively small numbers. Their findings were supportive, however, of the long-held belief that SLEs could trigger onset of T1D with the added discovery that SLEs could also decrease the age of onset.

The variations in results suggested that the effects of SLE’s were nuanced.

Characteristics of Serious Life Events Informed by Trauma Research

Some of the findings in the studies mentioned above were of particular interest to me. This was because of what I was learning from research in traumatic stress.

Actual or Threatened SLEs

The Swedish Childhood Study by Hagglof et al ⁽¹⁸⁾Hagglof, B., et al. (1991). “The Swedish childhood diabetes study: indications of severe psychological stress as a risk factor for type 1 (insulin-dependent) diabetes mellitus in childhood.” Diabetologia 34(8): 579-583 noted that the number of SLEs was only significant when both ACTUAL and THREATENED losses were included. In other words, events did not have to be overt, severe, or actually life-threatening to have an impact on health and risk for T1D. Furthermore, these were events that had happened within the family, and not independently to the child. The authors surmised that such SLEs would inevitably be highly stressful for children.

This finding was also consistent with what I was learning about traumatic stress ⁽¹⁹⁾Scaer, R. C. (2001). The body bears the burden: trauma, dissociation, and disease. New York, Haworth Medical, ⁽²⁰⁾Levine, P. (1997). Waking the Tiger: Healing Trauma. Berkeley, North Atlantic Books, ⁽²¹⁾Yehuda, R., et al. (2015). “Post-traumatic stress disorder.” Nature Reviews Disease Primers October: 150-157.

From our understanding of trauma, the effects of SLEs are not so much about specific types of events as much as about how these events are perceived and experienced by an individual. A car accident might feel life-threatening or like a complete shock to one person, for example, but not a big deal for another. Same event, different experiences and effects.

Effect of SLEs and Trauma Add Up

Robinson and Fuller, who conducted the UK study in 1985 ⁽²²⁾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, found that participants more often experienced one or more SLEs (77%) compared with the controls, who consisted of their non-diabetic siblings (31%) and neighbours (15%). They lived through more SLEs in the 3 years before onset as well as more SLEs in the 6 months before onset. In other words, it wasn’t just SLEs in family life or an occasional SLE that triggered onset but an overall greater number of events experienced by each individual.

Research in traumatic stress shows similar results. Soldiers are at greater risk of developing PTSD (post-traumatic stress disorder) if they’ve experienced other events prior to the recognizable event that triggers the onset of symptoms. This includes events from childhood ⁽²³⁾Yehuda, R., et al. (2015). “Post-traumatic stress disorder.” Nature Reviews Disease Primers October: 150-157.

The effects of SLEs, in other words, add up over time.

Mistakenly Dismissing Trauma as a Risk Factor?

In 2004, an occupational physician named Martin Cosgrove reviewed many of the studies mentioned above ⁽²⁴⁾Cosgrove, M. (2004). “Do stressful life events cause type 1 diabetes?” Occup. Med. 54(4 %U http://occmed.oxfordjournals.org/cgi/content/abstract/54/4/250 %8 June 1, 2004. His review stemmed from the question of whether pensions for injuries should include work-related stress as a potential trigger for T1D. This question has been raised since the advent of worker’s compensation and was a concern of the first world diabetes specialist, Dr. Elliot Joslin and many of his colleagues.

Cosgrove’s conclusion was,

“Given the progress in understanding the molecular biology of diabetes, the concept that stress causes type 1 diabetes is no longer plausible.”

In his review, Cosgrove discounted results from many of the studies for having small sample sizes and problems with selection of control groups. While some sample sizes were small, it’s relevant to note that many controls were well selected and findings were statistically significant. In addition, results showing increased SLEs were similar across different populations. Even though Sweden and Finland have the highest rates of T1D in the world, for example, SLEs were also found to be triggers for onset in countries with much lower incidence and where different environmental exposures might also be contributing to risk.

Cosgrove’s favorite study was Littorin’s DISS study because of its prospective nature (sending questionnaires very soon after diagnosis) and quality of controls that were selected. Cosgrove favored the negative conclusions made by DISS despite the 9 statistically significant SLEs that were not acknowledged as being more common in T1D

Review articles such as Cosgrove’s can carry a lot of weight. They can also compound misperceptions.

Cosgrove’s paper, for example, was cited in a 2004 review of the literature in Diabetes Spectrum, a journal of the American Diabetes Association. The authors referenced only Cosgrove’s study when looking at whether SLEs are a risk factor for T1D ⁽²⁵⁾Lloyd, C., et al. (2005). “Stress and Diabetes: A Review of the Links.” Diabetes Spectrum 18(2): 121-127.

Overall, early studies supported the 2000 year-old perception that SLEs could be a trigger for the onset of T1D.

Investigators were also curious about whether serious life events increase risk for type 1 diabetes with respect to causation.

Can Stress, Trauma or Serious Life Events CAUSE T1D?

Individuals with T1D have long wondered whether serious life events increase risk for type 1 diabetes by serving as a trigger for onset.

They have also been curious about whether SLEs can CAUSE T1D.

Researchers dug into this question by looking at the role of SLEs throughout the lifetime instead of specifically in the period before onset.

Do Lifetime Exposures to Serious Life Events Increase Risk for Type 1 Diabetes?

A 1980 study in northern California by Leaverton and colleagues found that kids with T1D had more lifetime exposures to SLEs and more family conflict than their healthy counterparts ⁽²⁶⁾Leaverton, D. R., et al. (1980). “Parental loss antecedent to childhood diabetes mellitus.” J Am Acad Child Psychiatry 19(4): 678-689.

Twice the number of children who developed T1D had lost a parent through divorce, emotional or physical separation, adoption, foster care, or death compared to healthy kids. They had also experienced more disturbances in their families, such as conflict and chronic physical or mental illnesses in one or both parents. In addition, diabetic kids with parental loss and family chaos were hospitalized much more often for complications of their diabetes (severe acidosis, dehydration, and coma) than the other children with T1D in the study.

These findings supported the possibility that SLEs contributed to cause and were more than triggers for onset.

The 1989 Canadian study cited earlier looked at lifetime exposures and found only that SLEs were increased in the year before onset ⁽²⁷⁾Siemiatycki, J., et al. (1989). “Case-control study of IDDM.” Diabetes Care 12(3): 209-216. In their study, no increased risk was linked to loss of a parent through separation or divorce. It’s not clear whether other forms of parental loss as detailed in the California study were evaluated. This is one of the few studies finding no increase in risk other than the period before onset.

In 1995, a thoughtful Swedish study by Thernlund and colleagues evaluated children and teens aged 0-14 years from five pediatric clinics who were newly diagnosed ⁽²⁸⁾Thernlund, G. M., et al. (1995). “Psychological stress and the onset of IDDM in children.” Diabetes Care 18(10): 1323-1329. Like Leaverton, they, too, noted a higher rate of family chaos in children who eventually developed T1D. In their study of lifetime exposures, SLEs were almost  twice as common in the first 2 years of life. What they also found was that children who developed T1D also had more events that were difficult for them to adapt to throughout their lives. A third finding was that behavior problems such as acting out, which often reflect exposure to SLEs, were higher in all age groups.

Investigators also explored this question by looking even earlier in life.

Serious or Adverse Events During Pregnancy, Birth and Infancy

The large body of research exploring whether serious life events increase risk for type 1 diabetes included a look at adverse babyhood experiences (ABEs) occurring during pregnancy, birth and infancy.

SLEs in early life that have been found to increase risk for T1D include ⁽²⁹⁾Dahlquist, G. and B. Kallen (1992). “Maternal-child blood group incompatability and other perinatal events increase the risk for early-onset type 1 (insulin-dependent) diabetes mellitus.” Diabetologia 35(7): 671-675, ⁽³⁰⁾McKinney, P. A., et al. (1997). “Antenatal risk factors for childhood diabetes mellitus: a case control study of medical record data in Yorkshire, UK.” Diabetologia 40: 933-939, ⁽³¹⁾Cardwell, C. R., et al. (2008). “Caesarean section is associated with an increased risk of childhood-onset type 1 diabetes mellitus: a meta-analysis of observational studies.” Diabetologia 51(5): 726-735,⁽³²⁾Stene, L. C., et al. (2004). “Perinatal factors and development of islet autoimmunity in early childhood: the diabetes autoimmunity study in the young.” Am J Epidemiol 160(1): 3-10:

• being born prematurely,
• maternal illness such as pre-eclampsia (toxemia),
• delivery by cesarean section (20% increased risk by meta-analysis),
• respiratory illnesses in the newborn,
• blood-group incompatibility
• amniocentesis
• birth complications, including breech birth, assistance with vacuum extraction or forceps

Because of these findings, Swedish researcher Gisela Dahlquist and others wondered whether such early events might initiate risk, induce or trigger predisposition to risk, or otherwise play a role in causing T1D ⁽³³⁾Dahlquist, G. and B. Kallen (1992). “Maternal-child blood group incompatability and other perinatal events increase the risk for early-onset type 1 (insulin-dependent) diabetes mellitus.” Diabetologia 35(7): 671-675.

Learn more in the first post on T1D and adverse babyhood events.

T1D: Pancreas, Genes and the Nervous System

Dahlquist proposed that a common denominator among the very earliest risk factors, which occurred well before the onset of T1D, was that they are all stressful ⁽³⁴⁾Dahlquist, G. and B. Kallen (1992). “Maternal-child blood group incompatibility and other perinatal events increase the risk for early-onset type 1 (insulin-dependent) diabetes mellitus.” Diabetologia 35(7): 671-675. Another common link she and her colleagues identified was that they lead to separation between mothers and babies ⁽³⁵⁾Dahlquist, G. and B. Kallen (1997). “Early neonatal events and the disease incidence in nonobese diabetic mice.” Pediatr Res 42(4): 489-491.

My first and second post describe the research explaining how maternal-infant separation can influence nervous system patterns of regulation and physiology to affect long-term health. My third post introduces one of the mechanisms by which this happens, showing how life experiences interact with and alter genes. Studies of the cell danger response further validate Dahlquist’s observations. They propose a unifying theory of disease based on the finding that environmental stressors of all different kinds act as environmental stressors that trigger different diseases because they elicit different cell danger responses. Disease arises when the cel danger response gets prolonged ⁽³⁶⁾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)).

t turns out that the pancreas is not the sole problem in T1D or the direct cause, and that insulin-producing cells do not operate in isolation. The nervous system, which directs blood sugar and insulin levels to influence pancreatic functioning, and genes, are also mechanisms involved in the pathophysiology of T1D. The nervous system and genes are also players in the pathophysiology of other chronic illnesses.

Reasons Trauma is Dismissed Do Not Hold

Conflicting findings such as those concerning age of exposure, risk factors such as the loss of a parent, and more SLEs throughout the lifetime in some studies and not in others, are examples of why uncertainty long persisted in the field of T1D research as well as in similar studies of other chronic illnesses.

Overall, however, the evidence supports a role for SLEs as both potential triggers for the onset of T1D as well as contributors to cause, beginning before birth and continuing through childhood and into adulthood.

The first 20 years of studies in T1D provide arguments against Boston diabetes specialist Elliott Joslin’s perspectives (1943), Cosgrove’s review (2004) and others’ reasons for dismissing trauma as a risk factor for T1D.

The findings provide evidence against the concept that trauma is too common and T1D too rare for there to be a link. They also negate the belief that trauma cannot be a risk factor since there were no (known) increases in T1D as a result of WWI.

Because most study participants in these earliest studies were children, the findings also begin to alleviate concerns that worker’s compensation laws would lead to false links between trauma and T1D from people seeking financial gain.

The question raised in Joslin’s 1943 paper regarding variable length of delays between exposure to SLEs and onset, however, remained ⁽³⁷⁾Joslin, E. P. (1943). “The Relation of Trauma to Diabetes.” Ann Surg 117(4): 607-622.

Antibody research in T1D helped address this question.

Life Events Influence Antibody Levels

Serious Life Events Increase Risk for Type 1 Diabetes Related Antibodies

When studies of antibodies became possible in the late 1970s, it was found that these markers of immune system activation can be present for a decade or more before the onset of T1D ⁽³⁸⁾Spencer, K. M., et al. (1984). “Fluctuating  islet-cell autoimmunity in unaffected relatives of patients with insulin-dependent diabetes.” Lancet 1: 764-766.

Antibodies can also resolve completely, fluctuate without the disease ever developing, or increase steadily until T1D begins ⁽³⁹⁾Millward, B. A., et al. (1986). “Immune changes associated with insulin-dependent diabetes may remit without causing diabetes: a study in identical twins.” British Medical Journal 292: 793-796, ⁽⁴⁰⁾Yu, J., et al. (2000). “Transient antiislet autoantibodies: infrequent occurrence and lack of association with “genetic” risk factors.” J Clin Endocrinol Metab 85(7): 2421-2428. Risk increases as the number and type of antibodies accumulate ⁽⁴¹⁾Orban, T., et al. (2009). “Pancreatic islet autoantibodies as predictors of type 1 diabetes in the Diabetes Prevention Trial-Type 1.” Diabetes Care 32(12): 2269-2274.

The rate at which antibodies develop also links to age of onset, with diagnosis occurring at younger ages when antibodies develop more rapidly ⁽⁴²⁾Steck, A. K., et al. (2016). “Predictors of slow progression to diabetes in children with multiple islet autoantibodies.” J Autoimmun 72: 113-117.

Some Experiences & Life Events Decrease (Buffer) Risk for T1D

Robinson and Fuller, who conducted the UK study with 17 to 34 year olds showing increased risk with more SLEs in the 3 years before onset, did a small and very interesting follow-up to assess wether SLEs affected antibodies ⁽⁴³⁾Robinson, N., et al. (1989). “Psychosocial factors and the onset of Type 1 diabetes.” Diabet Med 6: 53-58. They tested family members of individuals with T1D for antibodies and followed them for 5 years.

During the 5-year study the second family member who developed T1D experienced more SLEs than antibody-positive family members who did not progress to the illness ⁽⁴⁴⁾Robinson, N., et al. (1989). “Psychosocial factors and the onset of Type 1 diabetes.” Diabet Med 6: 53-58.

In addition, family members who were antibody positive but who did not go on to develop T1D also had more supportive relationships in their lives such as friends and more frequent direct contact and connection with others. The authors proposed that these protective factors acted as “buffers” and counteracted negative effects of SLEs.

Antibody studies and patterns enabled researchers to begin to see that risk for T1D could begin many years before onset, that SLEs could affect progression to overt diabetes, and that resources could buffer the effects of adverse life events to delay onset or possibly even prevent the development of T1D.

Another potential buffer is breast feeding (BF). This topic is so large that it requires at least an entire blog post. In short, though, I discovered that breast feeding acts through multiple mechanisms that can influence health.

While the nutritional contributions from breast milk very probably play an important role in long-term health, additional research suggests the effects are more complex and subtle.

Studies on the influence of SLEs on maternal-infant interactions, for example, show that prenatal stress and other adverse events can interfere with breast feeding just as they interrupt skin to skin contact and bonding ⁽⁴⁵⁾Klaus, M. H. and J. H. Kennell (1976). Maternal-infant bonding. St. Louis, Mosby, ⁽⁴⁶⁾DiMatteo, M. R., et al. (1996). “Cesarean childbirth and psychosocial outcomes: a meta-analysis.” Health Psychol 15(4): 303-314. Rates of breast feeding may sometimes serve as markers that reflect potential maternal exposure to SLEs during pregnancy and birth.

And here I’ll give you just one more item as food for thought, even as I will not explore it in-depth here. BF also has an impact on a mother – and consequently on her infant’s – states of nervous system regulation ⁽⁴⁷⁾Walker, C. D., et al. (2004). “Mother to infant or infant to mother? Reciprocal regulation of responsiveness to stress in rodents and the implications for humans.” J Psychiatry Neurosci 29(5): 364-382, ⁽⁴⁸⁾Tu, M. T., et al. (2005). “Measuring stress responses in postpartum mothers: perspectives from studies in human and animal populations.” Stress 8(1): 19-34. This suggests one more potential area of contribution between early interactions and life experiences that influence long-term nervous system patterns of regulation.

Like so much of the research I had never heard of in my training as a physician, the studies introduced a wealth of new perspectives for me to ponder.

Studies of traumatic stress provided additional insights into the role of buffers.

The Delay Between Exposure and Onset

Preclinical or “Latency” Periods in Type 1 Diabetes

The variable window of time between exposure to trauma and the onset of T1D has long been confounding to physicians, people with chronic illness and researchers. The period of delay between exposure to as yet unclear environmental risk factors, development of antibodies and onset of symptoms is referred to as a preclinical or latent period in type 1 diabetes ⁽⁴⁹⁾Knip, M. (2002). “Natural course of preclinical type 1 diabetes.” Horm Res 57 Suppl 1: 6-11. Latency periods during which the disease process begins before the onset of symptoms are also seen in many other chronic illnesses, such as MS ⁽⁵⁰⁾Wolfson, C. and D. B. Wolfson (1995). “Studies of the latency period in multiple sclerosis.” Acta Neurol Scand Suppl 161: 89-92, ⁽⁵¹⁾Currier, R. D., et al. (1974). “Prior events in multiple sclerosis.” Neurology 24(8): 748-754, rheumatoid arthritis / disease ⁽⁵²⁾Majka, D. S. and V. M. Holers (2003). “Can we accurately predict the development of rheumatoid arthritis in the preclinical phase?” Arthritis Rheum 48(10): 2701-2705, lupus ⁽⁵³⁾Arbuckle, M. R., et al. (2003). “Development of autoantibodies before the clinical onset of systemic lupus erythematosus.” N Engl J Med 349(16): 1526-1533, and others. The process is suspected in ME/CFS too ⁽⁵⁴⁾Dietert, R. R. and J. M. Dietert (2008). “Possible role for early-life immune insult including developmental immunotoxicity in chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME).” Toxicology 247(1): 61-72.

The latency period is also a characteristic of trauma ⁽⁵⁵⁾McFarlane, A. C. (2010). “The long-term costs of traumatic stress: intertwined physical and psychological consequences.” World Psychiatry 9(1): 3-10

Delayed Onset of PTSD Also Occurs After Trauma

Symptoms of trauma such as PTSD, depression and anxiety develop at varying rates after traumatic events. Symptoms may begin within days or weeks, or a year or more later. The experience of more support, connection and resources act as buffers that can delay onset of PTSD and other symptoms. It can prevent the development of PTSD, or slow development of symptoms ⁽⁵⁶⁾Lehrner, A., et al. (2016). Chapter 11: Cortisol and the Hypothalamc-Pituitary-Adrenal Axis in PTSD [uncorrected proof]. Posttraumatic Stress Disorder: From Neurobiology to Treatment, John Wiley & Sons, Inc: 265-290. The mechanisms include another process by which patterns of nervous system regulation are affected. Following traumatic events, certain nerve pathways become more interconnected and wired together. With time and additional “hits” from more stress or SLEs, these pathways become more easily activated with smaller and smaller cues or reminders of a past traumatic event. The process is referred to as kindling ⁽⁵⁷⁾Yehuda, R., et al. (2015). “Post-traumatic stress disorder.” Nature Reviews Disease Primers October: 150-157.

The research in the neurobiology of PTSD made sense of the variable rates at which antibodies or symptoms  of T1D developed after SLEs.

The more I learned through perusing the library stacks, the more I found that research was beginning to address the common questions that lead many to dismiss the links between stress, trauma and type 1 diabetes.

In type 1 diabetes, the varying delays between exposure to SLEs appeared to be influenced by the balance between the number of buffers individuals had in their lives and the number of SLEs they experienced.

There was one more eye-opening study to peak my interest and entice me to think about chronic illness in new ways.

The Adverse Childhood Experiences (ACE) Study

At one point in my early forays into the literature about traumatic stress, a paper called the  The Adverse Childhood Experiences (ACE) Study caught my eye ⁽⁵⁸⁾Felitti, V. J., et al. (1998). “Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study [see comments].” Am J Prev Med 14(4): 245-258. The full title was,”Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults.”

Diabetes (both type 1 and type 2) was – and still is – one of the top 10 causes of death in the United Sates.

Dr. Vincent Felitti, an internist at Kaiser Permanente, and medical epidemiologist Dr. Robert Anda from the Centers for Disease Control, collaborated in the ACE study. After detailed research, Anda chose 10 specific areas of childhood trauma to examine, drawing from problems for which national programs were being created in the 1990s (he started with 7 in the first study and added another 3 soon after). Questionnaires were sent in two waves to 17,337 adult Kaiser patients.

The 10 ACEs are:

1. sexual abuse
2. physical abuse
3. emotional abuse
4. having a parent with a mental illness or who had committed suicide
5. having a mother who had been treated violently
6. living with an adult in the household who had been in jail
7. living with an adult in the household who was a problem drinker, alcoholic or used street drugs
8. physical neglect
9. emotional neglect
10. losing a parent through divorce or separation

Felitti and Anda were staggered to find that almost two thirds (64%) of their white, middle and upper class participants, nearly half of whom were also college-educated with good health insurance, had experienced at least 1 ACE.

37% had experienced 2 or more ACEs.

They also discovered that chronic health conditions and risk behaviors increased as the number of ACEs rose, and that the effect wasn’t subtle.

“When the first results of the survey were due to come in, Anda was at home in Atlanta. Late in the evening, he logged into his computer to look at the findings. He was stunned. “I wept,” he says. “I saw how much people had suffered and I wept.”

The 10 ACEs played an extraordinarily important role in increasing risk for physical diseases such as chronic lung disease, heart disease, diabetes, obesity and fractures. They also increased rates of mental illness such as depression; cancer, substance abuse, violence, suicide, early death and more.

I Didn’t Think The ACE or T1D Studies Applied to Me

Like Anda and Felitti, I found the results striking too.

I would later discover many more follow-up studies that convinced me of the link, especially in a 2009 publication showing that ACEs increased risk for autoimmune diseases. T1D was the most common autoimmune disease associated with ACEs in that study.

This body of research would provide striking evidence to address the argument dismissing trauma as a risk factor because SLEs are common while T1D is not.

The ACE studies have since repeatedly shown that the effects of adverse events in childhood are associated with risk for many different kinds of chronic diseases, of which T1D is only one.

Back in my early days of research, however, my reaction to the first ACE study was more complicated.

Even though I was initially excited by the ACEs study discoveries, I felt underwhelmed. My response was not unlike Dr. Elliott Joslin’s, the first physician to specialize in diabetes, who founded the Joslin Diabetes Center, and dismissed the links between SLEs and diabetes in the 1940s.

Like Joslin, the links between trauma and chronic illness in the ACE studies didn’t seem to fit what I was studying. And they didn’t seem to fit my personal experiences either.

Since the type of diabetes was not specified in the ACE study and was named along with obesity and heart disease as one of the chronic health conditions affected by risk, the effects seemed most likely related to the more common T2D. As a result, the first ACE study results didn’t seem relevant to my explorations of links to T1D even though many of the ACEs were similar to SLEs in the T1D studies I was finding.

I was also becoming debilitated by a chronic illness of my own at the time I was doing this research. And I did not think I had experienced any of the risk factors that had been identified in the ACE study.

In other words, I was pretty sure I had an ACE score of 0.

Like so many other physicians, including neurologists studying T1D, MS, ALS, and Parkinson’s 70 years before me who dismissed links between trauma and the illnesses they were studying, I didn’t quite understand the importance of the new data. I didn’t quite understand how so many seemingly ordinary stressors that happen in everyday life could affect risk for chronic illness either.

I had done the same thing on first discovering links between risk factors for T1D in pregnancy, birth and infancy. I had looked at my own past, thought it seemed remarkably normal, and wondered how the research could possibly relate to me or my illness. It took time, more evidence, a more refined understanding, and a closer look at my past and my symptoms before I began to recognize the links between my chronic fatigue (ME/CFS) and my own history.

At the time, I stashed the first ACE study deep into my archives and continued to dive into the book stacks and online databases for more information.

Why Care if Trauma Increases Risk?

As I’ve referenced in Post #2, the insights presented here offer potential new tools for early detection, prevention and even treatment of chronic illness such as T1D and many other diseases, including my own. This is why it’s so helpful to understand just how much research links trauma as a risk factor for chronic illness and how much evidence is emerging. I’ve created a list of books and therapies for healing the effects of trauma.

Summary

The first few decades of research in T1D supported the long-held suspicion that serious life events  (SLEs) increase risk for type 1 diabetes.

These studies found that SLEs trigger onset of T1D, just as so many people suspect.

Serious life events also contribute to the evolution and progression to overt T1D. Lifetime studies, studies of antibody patterns and of SLEs in pregnancy, labor and birth all supported this second assessment.

There were also limitations to these early studies.

As mentioned earlier, one was the small size of some studies even as others recruited over 300 individuals with T1D and compared their experiences with over 500 controls.

Yet the findings showed a remarkable consistency and results were statistically significant.

Early studies showed that

• SLEs are often more common in the period before onset of T1D
• SLEs are more numerous throughout the lifetime in those who develop T1D
• SLEs decrease the age of onset of T1D
• The effects of SLEs, like trauma, may be additive
• SLEs increase risk for progression to T1D in those who already have antibodies
• Risk is affected by how an event is experienced & perceived and not only the type of SLE
• Buffers such as experiences of support (friendships, for example) can lower risk
• Breast feeding may also buffer or lower risk through multiple mechanisms
• There is a preclinical period visible by the presence of antibodies
• Latency periods can last 13 years or longer before onset
• Latency periods are influenced by the balance between buffers and exposure to SLEs
• Not everyone who is at risk or who has antibodies goes on to develop T1D

Despite all of these growing findings, an important concern in the research community was that most of these early studies evaluated individuals who had already developed T1D.

Such retrospective approaches asked about the recollection of stressful or traumatic events from years before onset, and our memory is not always clear about the past.

The accuracy of memory for SLEs could also be suspect since the onset of a chronic illness such as T1D is stressful in and of itself and can skew perceptions of other events around the time of onset.

There was a need for information about risk factors for T1D to be collected starting well before onset and continuing up to the time of diagnosis.

Such a study looking at whether serious life events increase risk for type 1 diabetes was started in 1997. It started with over 10,000 healthy babies and followed them for 15 years.

I’ll tell you about the best studies so far in the next post of the discovery series.

Free Series Download (includes this post)

You can learn more about trauma and chronic illness in my free ebooks, or starting in post #1 about serious life events affecting risk for T1D in pregnancy, birth and infancy; in post #2 showing similar risk factors for asthma and an accidental cure that addresses these risk factors; in post #3 explaining how SLEs alter genes; and in post #4 which recaps the previous posts. You can also learn about the adverse childhood experiences (ACE) studies and risk for chronic illness, and find books and therapies for healing the effects of trauma. I describe how everything I learned about adverse life events and trauma helped me make sense of my own chronic illness and begin to recover. It also offers insights that help make sense of Dan’s story of onset with T1D and other symptoms he’s had.