Veronique had a very gradual onset of ME/CFS beginning in the 1990s when she was a family physician. Her symptoms worsened slowly over 10 years. At her worst activities such as sitting, standing, taking a shower, or talking exhausted her.
She changed careers and has since discovered and integrated research on how adverse life events (ALEs) affect health. The science dispels the out-of-date notions that such effects are psychological and that their influences on risk mean that chronic illnesses are psychosomatic.
Veronique has been researching the role of the nervous system and how it learns to perceive threat as an important and under-recognized contributor to chronic illnesses of all kinds. Not because chronic illness is psychosomatic or that being sick is our fault – but because life events shape our genes and biochemistry as well as how our nervous systems and physiology’s function.
Her work is informed by her background as an assistant professor of medicine; published research; an MA in somatic psychology with specialties in traumatic stress and body based psychotherapies; work with clients with chronic illness; as well as her own experiences with debilitating chronic illness. Check out Veronique’s website here.
Over the past 15 years I have come to a different way of thinking about chronic illness as a result of findings I never heard of in my training as a physician. These come from a large body of scientific studies in medicine, epigenetics, brain plasticity, embryology and early development, neurophysiology, epidemiology as well as research in different types of chronic illnesses. We’re learning now that life experiences affect health. This is not because our diseases are psychosomatic as has long been believed and used to judge many who are sick. It’s because the new science of epigenetics is showing us that life events interact with our genes to affect our physiology and long-term health. This includes physical health and chronic illness as well as mental health.
In this post I start with what I discovered about type 1 diabetes, which has helped me make sense of my own long-standing experience of ME/CFS, asthma and other symptoms. I’ve had debilitating fatigue for 20 years that gradually worsened over a decade. At its most intense in 2009 my fatigue felt “death-like” and I had difficulty sitting, standing and talking for almost a year.
The perspectives I learned about have helped me make strides since then, and I have been slowly improving to the point where I can run errands and walk 40 to 60 minutes most days among other things. These views have also given me a context from which to understand the evolution, course and gradual resolution of my disease.
I’m still limited by my health and I offer no quick fixes. The research, however, provides a different way to work with and begin to make sense of the symptoms present in ME/CFS and other chronic illnesses, recognize triggers, understand why treatments can work at first and but then decline over time or even stimulate resistance and more. It also offers some new tools to add to the few that do work (for some – some of the time) in ME/CFS.
This first post is part of a series introducing the science that lead me to this new perspective. I have written a second post describing an unexpected treatment that heals asthma by addressing risk factors from pregnancy, birth and infancy described below. My third post presents the emerging understanding of mechanisms that explain these findings, starting with how early experiences alter genes. I’ve included a few references here and a little more detail in my original article. There are more posts to come.
My current view of chronic illness, including ME/CFS, is that it:
- evolves through adaptations in our brains and nervous systems – and how they learn to perceive threat,
- involves a process that begins long before onset or diagnosis,
- results from a similar process in diseases as different as type 1 diabetes and heart disease at one end of the spectrum, and asthma, Parkinson’s, and ME/CFS at another.
- occurs after exposure to multiple events or “hits”
- follows a different pathway for each person – even in the same disease
- may be caused by different mechanisms – even in the same disease
First Steps. A Look at Type 1 Diabetes (T1D)
I began my explorations with type 1 diabetes (T1D). Unlike ME/CFS, fibromyalgia and some other diseases, T1D has clear diagnostic criteria which consist of high glucose levels in the presence of low to zero levels of insulin. These criteria make TID easy to identify and study.
T1D is the less common form of diabetes and is most commonly caused by an autoimmune process. In T1D survival depends on treatment with insulin. This contrasts with the more well-known type 2 diabetes (T2D), which can be associated with obesity (though not always), and can sometimes be managed through diet, activity levels, and weight loss or through oral medications or sometimes insulin shots. The lines between these two diseases are becoming increasing blurred and an epidemic of both is on the rise.
I also initially focused on studies in T1D because of the judgmental tone and blame so frequently encountered in the ME/CFS community and promulgated by some types of ME/CFS. No one would ever tell a person with T1D that their disease is all in their heads or psychosomatic, or that all they have to do to recover is to meditate, decrease their stress levels, exercise, do cognitive behavioral therapy, develop better health habits or to just “try harder.”
What I found in the T1D research, though, turned out to apply to other diseases – including my own. I’ll come back later in this series to describe these similarities.
What if chronic illness reflects an intelligent mechanism gone awry?
When I first started out to better understand chronic illness, I wondered whether the underlying drivers of disease might reflect an intelligent, natural process rather than one in which something is broken or in which our bodies are mistakenly attacking themselves.
I wondered whether the state of glucose dysregulation seen in T1D could also be found in normal, healthy functioning.
I thought about how levels of glucose and insulin vary according to the physiological states of our bodies. In states of parasympathetic nervous system (PNS) dominance where “rest and digest” processes prevail, for example, increased insulin availability enables glucose to enter cells. It also maintains blood sugar at remarkably constant levels.
In contrast, a sympathetic nervous system (SNS) response that occurs during jogging or a fight and flight type situation – results in a decrease in insulin and a concomitant rise in the availability of blood sugar. Together with other hormones, SNS states manipulate insulin and glucose levels to make sugar available as a source of fuel to be utilized by muscles when running, fleeing or fighting.
I realized that this SNS state is also a snapshot of T1D.
I wondered if something could lead to prolonged states of autonomic nervous system (ANS) arousal and high glucose levels in the face of low insulin. ????
And I wondered whether such states, like shifts into and out of fight and flight, were reversible.
Risk for most chronic illnesses is only partly genetic
In learning more about T1D, I made a series of unexpected discoveries my medical training had not prepared me for:
- Only about 50% of the risk for T1D is genetic. If an identical twin develops T1D, for example, the co-twin develops T1D less than half of the time (Diabetes Epidemiology Research International, 1987; Nistico, 2012; wikipedia). (The risk for many other chronic illnesses is also less than 50% genetic.)
- Only 10% of people at genetic risk for T1D ever develop the disease (Knip, 2005; Dahlquist, 1989).
- Although people at high genetic risk are more likely to have a family member with T1D, 90% have no close relatives with T1D at the time they are diagnosed.
These findings suggested that even when there was a genetic predisposition, development of T1D and other chronic illnesses was not a foregone conclusion. It showed that even people at risk had a remarkably low chance of developing the disease. And if T1D was genetic but didn’t come from family members with a similar disease, it suggested a very different set of risk factors.
Studies indicated that fifty percent of major risk factors T1D – and for many other chronic illnesses – are not genetic, but environmental factors that derive from what we experience and do. This includes exposures, such as to vaccines, toxins, or infections or to low levels of vitamin D; smoking; diet and nutrition; place of birth; parental socioeconomic status; birth order or number of siblings and the like.
Unlike our genes, environmental factors are sometimes within our power to choose or change (diet, smoking, supplements, exercise, etc).
Because relatives disabled by ME/CFS are present on both sides of my family tree, I wondered whether genetic predisposition existed for me but, like T1D had simply failed to manifest in everyone.
Antibody patterns show that risk for T1D is not set in stone
Many people with T1D have one or more types of antibodies at the time of diagnosis. Another discovery I made was that these antibodies have many intriguing characteristics:
- The presence of one antibody associated with risk for T1D is common in the general population (Knip, 2005)
- Only a small number of people with insulin-related antibodies ever develop T1D
- The existence of antibodies remits in up to 78% of people (ie: antibodies are not always permanent) (Bennet, 1997)
- The higher the levels and types of antibodies and the longer they persist, the greater the risk of developing T1D
I hadn’t known that a lot of us carry risk factors for T1D but never develop the disease. Nor did I realize that the existence of antibodies is not always permanent, and therefore does not imply a clear or direct path to disease. My own antinuclear antibody (ANA) levels, a fairly general antibody not specific for ME/CFS, were abnormal in 2009, rose slightly over a few years, and then went back to normal around 2015.
As I researched further, I realized that the existence of antibodies, and the patterns being discovered in T1D, offered me a way of potentially understanding and tracking the effects of environmental factors that make some people more susceptible to coming down with a chronic illness.
Risk for Chronic Illness Begins Long Before Onset
Antibody markers that sometimes show up years prior to the onset of clinical symptoms indicated that a process can take place under the radar for years prior to a person becoming ill. Studies indicate that:
- Antibodies in people who develop T1D arise over a period of time (Yu, 1996)
- These antibodies can appear up to 13 years (and possibly longer) before onset (Johnston, 1989)
- Antibodies associated with lupus (systemic lupus erythematosus or SLE), another autoimmune disease, have been found to occur up to 9 years before the onset of clinical symptoms (Arbuckle, 2001). As in T1D a greater number and persistence of these antibodies predicts greater risk although not everyone with these antibodies develops lupus (Arbuckle, 2003) .
Pic 2: Type 1 Diabetes 10 facts I didn’t know as an MD
Researchers in T1D proposed that environmental factors initiate or accelerate an underlying autoimmune process that triggers TID. They suspect that the environmental factors which precipitate or trigger the onset of T1D may be unmasking a process that has been developing out of sight and outside of our awareness (Dahlquist, 1998).
This information prompted me to recall two brief periods of inexplicable fatigue I’d experienced long before the onset of my ME/CFS. Both had been in response to exercise. One period had occurred in childhood and the other in college more than 10 years before the onset of my ME/CFS symptoms, which started in my 30s.
Events Occurring Before and Around Birth Can Increase the Risk of Coming Down with T1D
Because T1D commonly begins in childhood and antibodies can arise a long time before clinical symptoms ever begin, researchers began looking for risk factors occurring very early in life, including during pregnancy and birth.
Gisela Dahlquist is a Swedish diabetes researcher who has looked into non-genetic risk factors for the disease. She’s enabled in her search by Sweden’s penchant for tracking data from pregnancy and birth in population-wide registries and diagnoses of T1D and other health conditions later in life. The pregnancy data includes information on the mother’s age and marital status, work outside the home, smoking habits; her labor and birth (use of pain medications and anesthesia), type of delivery (vaginal or caesarean, etc.), birth weight, diagnoses in mother and baby during and after pregnancy (such as infections and illnesses), as well as the need for resuscitation etc. These are all examples of environmental factors.
Dahlquist and her group (1992) found that, in addition to the presence of diabetes and/or the increased age of the mother, the early childhood factors that increased one’s risk of coming down with T1D later included:
- being born prematurely
- a maternal illness such as pre-eclampsia (toxemia)
- delivery by caesarean section
- a neonatal respiratory illnesses
- and blood-group incompatibility
Dahlquist et al wondered whether the common element for many of the prenatal risk factors they’d uncovered was simply that they each represented some form of prenatal stress.
The fact that prenatal and birth events could affect risk for a chronic illness was news to me.
Prenatal and Birth Events Also Increase the Risk for Other Chronic Illnesses
The fetal origins of adult disease (FOAD) hypothesis comes from a large series of prospective and now multigenerational studies showing links between prenatal events and adult health.
The original study followed babies whose mothers experienced starvation during a siege in World War II known as the Dutch Hunger Winter. These studies indicated that nutritional stress is strongly linked to an increased risk for metabolic syndrome (heart disease, high blood pressure, elevated cholesterol, type 2 diabetes and/or obesity) and other chronic illnesses. The study findings have been widely replicated. They show that prenatal stressors such as nutritional deficiencies and emotional distress can increase the risk for metabolic syndrome and other chronic illnesses.
Additional research links a wide variety of prenatal events to risk for other chronic illnesses. Such risk factors include:
- infections and illnesses in mothers or babies during pregnancy
- infections and illnesses in mothers or babies in the first days after birth
- premature birth
- complications during delivery (forceps, caesarean delivery, use of certain medications)
- breech birth
- distress in the baby after birth (such as evidenced by the need for neonatal resuscitation or low apgar scores)
Prenatal and birth events have been associated with risk for chronic illnesses such as:
- inflammatory bowel disease (Crohn’s, Ulcerative Colitis) (Ekbom, 1990 & 1991)
- multiple sclerosis (Maser, 1969; Maghzi, 2012)
- asthma (Lewis, 1995; Oliveti, 1996; Xu, 2000; Madrid, 2005-2012)
- type 1 diabetes (McKinney, 1997; Patterson, 1994; Sepa, 2005; Stene, 2004)
It has also been suggested that events occurring during the prenatal time frame are associated with risk for lupus (Edwards, 2006) as well as ME/CFS (Dietert, 2008), among others.
A certain level of complexity and confusion in the results from prenatal event studies, however, wasn’t easily explained:
- Not everyone exposed to difficult prenatal events develops a chronic illness.
- Specific risk factors increased the chances of chronic illness in many studies, but not in all of them. The risk for T1D was higher with caesarean births in some studies, for example, but not in others. The same was true for most risk factors.
- None of these issues seemed to fit my own history. My mother had had a normal pregnancy. She had not experienced starvation, illness or problems in delivering me, for example.
Another big question for me was, “Why care about such risk factors if you can’t change them?”
Delving further into Dahlquist’s study, I became curious about her second finding, which was that blood-group incompatibility was the greatest risk factor for T1D.
The Greatest Risk Factor for T1D
Blood-group incompatibility occurs when a mother and her fetus have different blood types. It can cause symptoms ranging from mild to life-threatening. It’s also one of the most common causes of jaundice in newborns. Dahlquist couldn’t tell what the risk was specifically associated with. The standard treatment for jaundice at the time (as well as today) involved the newborns being placed in incubators where they were given phototherapy.
Dahlquist replicated this protocol in a study with T1D-prone mice by exposing one set of mice to isolation. She removed one set of pups from their cages for two 4-hour periods a day for 5 days during their first few days of life (1997). Another group which stayed with their dams was either treated with light therapy or a treatment.
A whopping 30% of the little guys who were separated from their mothers died compared to very few in the control group. A significant percentage of the treated group who survived developed T1D.
Dalhquist discovered that the risk factor for T1D was not the treatment, the jaundice, nor the blood group incompatibility – it was the separation of mice pups from their mothers.
I’d never heard of this as a risk factor for chronic illness either.
III. Maternal-Infant Separation Affects Health
Some of the first research I discovered regarding the role of maternal-infant separation was conducted by Columbia University professor and physician Myron Hofer (1994). He came to work one morning in 1968 to find that a mother rat had escaped her cage and that her pups’ heart rates were 40% below normal.
Over the years he discovered that close physical proximity between adult animals and their offspring regulates multiple autonomic nervous system processes that babies are not fully able to control on their own. This is due to the immaturity of their nervous and immune and other organ systems at birth.
The process by which close proximity enables offspring to regulate their physiologies involves what Hofer calls “hidden regulators.” He’s discovered that such subtle regulators include smells, pheromones, physical activities such as suckling, and other unconscious, ANS-driven processes and behaviors.
As Dahlquist found while looking at risk factors for T1D, human physiologies are affected by separation and proximity too. She noted that separation was a common result of many of the prenatal stressors that had been identified in her study – including infection and illness in the mother or baby, premature births, the need for treatment and more etc.
Prenatal stress is a well established but as yet still poorly recognized example of an environmental (nongenetic) risk factor for chronic illness.
Separation affects physiology in newborns
Human babies’ nervous systems and brains, immune systems, guts and other organ systems are immature and still developing at the time of birth. Progress in our understanding of early development has shown that basic functions such as body temperature, heart rate, blood pressure, cortisol levels, the functioning of the HPA axis, and levels of activation or arousal, among others, respond to proximity and separation in mammals. The same is seen in humans (Klaus, 1976; Schore, 1994; Sandman, 2015).
This body of research has lead to the use of practices such as Kangaroo Care in neonatal intensive care units (NICUs), in which premature and other babies are held in skin to skin contact by their parents in their first days and weeks of life. These neonates make more rapid health gains than when they are cared for solely in incubators.
Dr. Martha Welch, a former mentee of Dr. Myron Hofer’s, cofounded The Family Nurture Intervention at Columbia University Medical Center. Her treatment approach is part of a research study which is demonstrating that support for connection and calming early contact between mothers and their premature babies in the NICU improves neurodevelopment, cognition, behavior and other risks associated with early separation (2015). Her program was presented on PBS in May, 2017.
Early Separation Affects Risk Across Multiple Generations
Another striking finding in Hofer’s research was that experiences of early separation in rats influenced their risk for and susceptibility to disease such as high blood pressure in the teen years and adulthood. As studies in the role of prenatal stressors have also found, these effects can persist for multiple generations.
The same patterns are seen in humans.
How Early Separation Can Cause Chronic Illness and Why it Offers Hope
Risk for chronic illnesses such as the metabolic syndrome are higher in at least two generations of descendants whose mothers experienced the Dutch Hunger Winter.
The influence of nongenetic factors is increasingly understood to be affected by epigenetics. Epigenetics is also the process by which experiences of prenatal stress influence multiple generations.
Epigenetics is the process by which small chemicals attach to the surfaces of genes and alter their behavior by turning them on and off. Epigenetic changes are influenced by environmental factors and can be transmitted from one generation to another. Exercise and diet, medications, as well as some types of psychotherapy that work with the nervous system to reduce perceptions of threat and effects of trauma can sometimes reverse epigenetic changes as well (Yehuda, 2013).
The new knowledge that we are gaining allows for the development of different ways of understanding chronic illness. The current paradigm which asserts that psychological events – such as life experiences – cause psychological illnesses while physical events – such as infections, genetic mutations etc. – cause physical conditions, is incorrect (Baldwin, 2013). The emerging science also suggests new possibilities for treatment as well as approaches for prevention.
Conclusion to Part I
One of the things I learned about chronic illness is that non-genetic risk factors such as early life events can affect biochemical pathways that influence our long-term health.
This is because our brains, nervous systems and other organ systems are genetically programmed to develop through interactions with our environments, including our mothers during pregnancy, birth and infancy (National Research Council and Institute of Medicine, 2000; Sandman, 2015; Schore, 1994; Shonkoff, 2012 & 2016).
Most children and adults today have experienced periods of early separation in the hours and days following birth. This was, and often still is, a routine part of healthy newborn care in hospital-based birthing settings. Babies who are sick, are delivered by caesarean, require treatment or whose mothers are ill experience longer periods of separation. Such practices are one risk factor among many that either predispose us to risk for chronic illness (among other health problems) or which accumulate over time with other non-genetic factors to gradually increase risk. I share more about this finding in the next post of the series.
Ultimately, the effects of early separation have been greatly underestimated. They are, however, just one risk factor among a number of others that may play important roles in many different kinds of chronic illness.
In the second post of the series I write about meeting a researcher who accidentally cured an 8-year-old girl of asthma, after inadvertently treating the mother for the effects that early separation had had on her. He has since reproduced these findings in multiple studies and continues to have success in helping kids recover from asthma by treating their mothers. His work showed me how to recognize the subtle events my own mother had experienced when pregnant with me and helped me make sense of my asthma and possibly my ME/CFS as well. It also provided a glimpse of some unexpected approaches that might offer new tools to support and even treat chronic illnesses.
Veronique writes about the large body of research linking subtle and overt adverse life events to risk for chronic illness on her blog Chronic Illness Trauma Studies. She draws from the science of epigenetics, traumatic stress, neurophysiology and research in different chronic illnesses. These offer a view much different from the current “psychosomatic” perspectives that link a history of trauma to implications that such diseases are “all in our heads.”
Arbuckle, M. R., J. A. James, K. F. Kohlhase, M. V. Rubertone, G. J. Dennis and J. B. Harley (2001). “Development of anti-dsDNA autoantibodies prior to clinical diagnosis of systemic lupus erythematosus.” Scand J Immunol 54(1-2): 211-219.
Arbuckle, M. R., M. T. McClain, M. V. Rubertone, R. H. Scofield, G. J. Dennis, J. A. James and J. B. Harley (2003). “Development of autoantibodies before the clinical onset of systemic lupus erythematosus.” N Engl J Med 349(16): 1526-1533.
Baldwin, D. V. (2013). “Primitive mechanisms of trauma response: an evolutionary perspective on trauma-related disorders.” Neurosci Biobehav Rev 37(8): 1549-1566.
Bennet, P., M. Rewers and W. Knowler (1997). Epidemiology of diabetes mellitus. Ellenberg and Rifkin’s diabetes mellitus. D. Porte and R. Sherwin. Stamford, CT, Appleton and Lange: 373-400.
Calkins, K. and S. U. Devaskar (2011). “Fetal origins of adult disease.” Curr Probl Pediatr Adolesc Health Care 41(6): 158-176.
Dahlquist, G. (1998). “The aetiology of type 1 diabetes: an epidemiological perspective.” Acta Paediatr Suppl 425: 5-10.
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.
Dahlquist, G. and B. Kallen (1997). “Early neonatal events and the disease incidence in nonobese diabetic mice.” Pediatr Res 42(4): 489-491.
Diabetes Epidemiology Research International (1987). “Preventing insulin dependent diabetes mellitus: the environmental challenge.” BMJ 295(6596): 479-481.
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.
Edwards, C. J. and J. A. James (2006). “Making lupus: a complex blend of genes and environmental factors is required to cross the disease threshold.” Lupus 15(11): 713-714.
Ekbom, A., H. O. Adami, C. G. Helmick, A. Jonzon and M. M. Zack (1990). “Perinatal risk factors for inflammatory bowel disease: a case-control study.” Am J Epidemiol 132(6): 1111-1119.
Ekbom, A., C. Helmick, M. Zack and H. O. Adami (1991). “The epidemiology of inflammatory bowel disease: a large, population- based study in Sweden.” Gastroenterology 100(2): 350-358.
Hofer, M. A. (1994). “Early relationships as regulators of infant physiology and behavior.” Acta Paediatr Suppl 397: 9-18.
Johnston, C., B. A. Milward, P. Hoskins, R. D. G. Leslie, G. F. Bottazzo and D. A. Pyke (1989). “Islet-cell antibodies as predictors of the later development of type 1 (insulin-dependent) diabetes. A study in identical twins.” Diabetologia 32: 382-386.
Klaus, M. H. and J. H. Kennell (1976). Maternal-infant bonding. St. Louis, Mosby.
Knip, M., R. Veijola, S. M. Virtanen, H. Hyoty, O. Vaarala and H. K. Akerblom (2005). “Environmental triggers and determinants of type 1 diabetes.” Diabetes 54 Suppl 2: S125-136.
Lewis, S., D. Richards, J. Bynner, N. Butler and J. Britton (1995). “Prospective study of risk factors for early and persistent wheezing in childhood.” Eur Respir J 8(3): 349-356.
Madrid, A. (2005). “Helping children with asthma by repairing maternal-infant bonding problems.” Am J Clin Hypn 48(3-4): 199-211.
Madrid, A., et al. (2012). “The Mother and Child Reunion Bonding Therapy: The Four Part Repair.” Journal of Prenatal and Perinatal Psychology and Health 26(3).
Maghzi, A. H., et al. (2012). “Cesarean delivery may increase the risk of multiple sclerosis.” Mult Scler 18(4): 468-471.
Maser, C. (1969). “[The perinatal period of multiple sclerosis patients].” Schweiz Med Wochenschr 99(50): 1824-1826.
McKinney, P. A., R. Parslow, K. Gurney, G. Law, H. J. Bodansky and D. R. R. Williams (1997). “Antenatal risk factors for childhood diabetes mellitus: a case control study of medical record data in Yorkshire, UK.” Diabetologia 40: 933-939.
Mead, V. P. (2004). “A new model for understanding the role of environmental factors in the origins of chronic illness: a case study of type 1 diabetes mellitus.” Med Hypotheses 63(6): 1035-1046.
National Research Council and Institute of Medicine (2000). From Neurons to Neighborhoods: the science of early childhood development. Committee on integrating the science of early childhood development. Board on children, youth, and families, Commission on behavioral and social sciences and education. Washington, D.C., National Academy Press.
Nistico, L., et al. (2012). “Emerging effects of early environmental factors over genetic background for type 1 diabetes susceptibility: evidence from a Nationwide Italian Twin Study.” J Clin Endocrinol Metab 97(8): E1483-1491.
Oliveti, J. F., C. M. Kercsmar and S. Redline (1996). “Pre- and perinatal risk factors for asthma in inner city African- American children.” Am J Epidemiol 143(6): 570-577.
Patterson, C. C., D. J. Carson, D. R. Hadden, N. R. Waugh and S. K. Cole (1994). “A case-control investigation of perinatal risk factors for childhood IDDM in northern Ireland and Scotland.” Diabetes Care 17(5): 376-381.
Sandman, C. A. (2015). “Mysteries of the Human Fetus Revealed.” Monogr Soc Res Child Dev 80(3): 124-137.
Schore, A. N. (1994). Affect regulation and the origin of the self: the neurobiology of emotional development. Hillsdale, NJ, Lawrence Erlbaum.
Sepa, A., et al. (2005). “Mothers’ experiences of serious life events increase the risk of diabetes-related autoimmunity in their children.” Diabetes Care 28(2394-2399).
Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246.
Shonkoff, J. P. (2016). “Capitalizing on Advances in Science to Reduce the Health Consequences of Early Childhood Adversity.” JAMA Pediatr 170(10): 1003-1007.
Stene, L. C., K. Barriga, J. M. Norris, M. Hoffman, H. A. Erlich, G. S. Eisenbarth, R. S. McDuffie and M. Rewers (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.
Welch, M. G., et al. (2015). “Family Nurture Intervention in the Neonatal Intensive Care Unit improves social-relatedness, attention, and neurodevelopment of preterm infants at 18 months in a randomized controlled trial.” J Child Psychol Psychiatry 56(11): 1202-1211.
Xu, B., J. Pekkanen and M. R. Jarvelin (2000). “Obstetric complications and asthma in childhood.” J Asthma 37(7): 589-594.
Yehuda, R., et al. (2013). “Epigenetic Biomarkers as Predictors and Correlates of Symptom Improvement Following Psychotherapy in Combat Veterans with PTSD.” Front Psychiatry 4: 118.
Yu, L., M. Rewers, R. Gianani, E. Kawasaki, Y. Zhang, C. Verge, P. Chase, G. Klingensmith, H. Erlich, J. Norris and G. S. Eisenbarth (1996). “Antiislet autoantibodies usually develop sequentially rather than simultaneously.” J Clin Endocrinol Metab 81(12): 4264-4267.
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