This series describes research for links between trauma and autoimmune disease that also apply to other chronic illnesses such as type 2 diabetes and obesity, heart disease and other characteristics of insulin resistance and the metabolic syndrome, asthma, and more.
This post identifies risk factors from pregnancy, birth and infancy, which I’ve coined as adverse babyhood experiences (ABEs) because the science builds on what we already know from the adverse childhood experiences (ACEs) research. It’s helpful to understand because addressing and healing effects of trauma and adversity that happens very early in life is possible, supports improved health and can occur even if you work with trauma decades after the event(s).
A prefacing post introduces the series and provides a list of diseases affected by trauma before and around birth as well as in childhood.
I had never heard of these kinds of studies as a medical doctor. These posts describe what everyone – health care professionals, people with chronic illness, parents and beyond – needs to know about the large numbers of well accepted but as-yet poorly known studies from across the globe that offer a new way of understanding disease.
The research I introduce in this series begins to show you how adverse events increase risk for long-term health conditions and why it’s not psychological or “all in your head.” It also sheds light on why it’s not a mother’s fault either. Research on father’s is slowly starting to happen and explains, here too, how it’s not a parents’ fault but due to adverse experiences that happen to them when they are trying to get pregnant, or during pregnancy and birth and early in their childrens’ lives.
It will also show you what we can do – as individuals, as a society, and in medical care – to prevent and better treat chronic diseases of all kinds.
I’ve shared a version of this and the previous post on Health Rising, a blog about chronic fatigue, also known as ME/CFS or “myalgic encephalitis/ chronic fatigue syndrome,” which is the chronic illness I have. My guest post on Cort Johnson’s blog appears with the title “What if ME/CFS is an Intelligent Process Gone Awry?”
Free eBook of this Post
Get the free PDF of this post. The form will appear momentarily.
I began my explorations wondering whether trauma might be a risk factor for chronic illness with a look at studies in type 1 diabetes (T1D). This is the autoimmune form of diabetes.
At first, I studied T1D out of curiosity. And because, unlike illnesses such as ME/CFS (chronic fatigue syndrome, which is the chronic illness I have), T1D has clear diagnostic criteria, which include high glucose (sugar) levels in the presence of low to no insulin. This makes it easy to identify and study.
The presence of antibodies, which are found in most people with T1D, is an additional biomarker that makes this disease especially amenable to study.
I also initially focused on studies in T1D because of the judgmental tone and blame so frequently found in ME/CFS research.
Because blood tests can be used to definitively diagnose diabetes, T1D is not a disease that doctors consider to be psychosomatic or believe to be “all in their patients’ heads.”
Unlike with chronic fatigue, doctors also don’t expect a person with T1D to be able to reverse their disease, not even if they meditate, decrease their stress levels, exercise, do cognitive behavioral therapy, develop better health habits or “try harder” (see my recent post on the limits of mind body medicine).
What I found in the T1D research turned out to apply to other diseases (see the list of diseases in the introductory post for an idea).
1. Differences Between Type 1 & Type 2 Diabetes
T1D is the more rare form of diabetes and is most commonly caused by an autoimmune process.
The autoimmune process is associated with the destruction of insulin-producing cells that lead to a lack of insulin. The cause of T1D has been found by researchers around the world to be due to interactions between genes and environmental factors but the specific risk factors remain unknown. Survival in T1D requires injection of insulin.
This contrasts with the more common and well-known type 2 diabetes (T2D), which can be associated with obesity (though not always) and sometimes managed or even reversed with diet, activity levels, and weight loss. It is often treated with oral medications (pills) and sometimes also with insulin. People with T2D have difficulty utilizing insulin and their cells are “resistant” to it. In contrast with T1D, there are often high levels of insulin in type 2 diabetes.
We are in the midst of an epidemic of both T1D and T2D.
Other forms of diabetes exist, including the recently discovered type 3c diabetes, which results from inflammation or direct injury to the pancreas.
People with type 2 diabetes have been found to have increased risk for dementia and Alzheimer’s. Insulin resistance and dysregulation of blood sugar levels appear to be a common factors for all of these diseases.
As seen in the lists in the earlier post, trauma and adversity in pregnancy, birth, infancy and childhood are risk factors for both types of diabetes as well as other diseases of insulin resistance, Alzheimer’s, other autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and lupus among others, as well as other chronic illnesses such as asthma, fibromyalgia, heart disease, and more.
As you’ll see from the research I discovered and present throughout this series, the effects of adversity are not psychological but are deeply physiological and very real.
These are just a few of the reasons why it’s helpful to understand how adversity affects our health – and what you can do about it (see links to more info and treatment recommends below in #3).
2. Chronic illness: An Intelligent Survival Mechanism With Long-Term Side-Effects?
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 our bodies are attacking themselves at random.
I wondered whether the patterns of blood sugar increases seen in T1D could also be found in any states of normal, healthy functioning.
I thought about how levels of glucose and insulin are influenced by the physiological states of our bodies.
Insulin maintains levels of sugar in the blood at remarkably constant levels. This is supported during states of “rest and digest,” which are regulated by the parasympathetic branch of the autonomic nervous system.
One of the characteristics of the fight or flight response, on the other hand, is a decrease in insulin.
Together with other hormones, these mobilizing states manipulate insulin and glucose levels to make sugar available as a source of fuel to be utilized by muscles for running or fighting.
Fight and flight are mediated by the sympathetic branch of the autonomic nervous system.
In fight or flight, decreases in insulin levels allow for a rise in blood sugar levels.
I realized that this was also a snapshot of T1D.
Brain states of fight and flight increase blood sugar levels and decrease insulin levels.
This is also a snapshot of type 1 diabetes.
I wondered if anything could lead to prolonged states of such specific phases of autonomic nervous system arousal of high blood sugar in the face of low insulin.
Not as a psychological response or a stress response, but as a new state. As an altered way of being in the world.
I also wondered whether such states were reversible.
These are the questions that launched me into new explorations. This is what I present in this series. It’s not yet what’s being taught in medical school even as there is powerful new research documenting this process at the metabolic level through what is called “the cell danger response.” I talk about this in a recent blog post.
II. Lessons from Type 1 Diabetes (T1D)
1. Most People at Risk Do Not Develop T1D
When I first started learning about T1D after I had left my career as a family physician, I made a series of discoveries that I had not learned in my medical training:
- Only about 50% of risk for T1D is genetic.
- If an identical twin develops T1D, for example, the co-twin develops T1D less than half of the time (1)Diabetes Epidemiology Research International (1987). “Preventing insulin dependent diabetes mellitus: the environmental challenge.” BMJ 295(6596): 479-481 – more recent research has not changed this view, (2)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.
- Many other chronic illnesses show similar patterns in which genetic influences affect risk less than 50% of the time.
- Only 10% of people at genetic risk for T1D ever develop the disease (3)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, (4)Dahlquist, G. (1998). “The aetiology of type 1 diabetes: an epidemiological perspective.” Acta Paediatr Suppl 425: 5-10.
- Although people at high genetic risk are more likely to have a family member with T1D, 90% of people 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 (or other chronic illness) 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 influenced by genes but didn’t come from family members with a similar disease, it suggested a different set of risk factors.
2. 50% of Risk for Autoimmune Disease is “Environmental” (Not Genetic)
Environmental factors involve what we experience and what we do.
Researchers studying such risk factors look at things like diet and nutrition; place of birth; parental socioeconomic status; birth order or number of siblings; effects of smoking; exposures to vaccines, toxins and the like.
Trauma and adverse life events are also examples of environmental factors that can affect risk.
Unlike our genes, environmental factors that affect health are sometimes in our power to choose (such as smoking or diet) or to change such as through altering diet, quitting smoking, starting or increasing exercise, or healing the effects of trauma.
Environmental risk factors therefore offer potentially powerful tools for prevention and treatment.
In his book “Diabetes Rising,” journalist Dan Hurley introduces research he never heard of despite having had type 1 diabetes for over 30 years, being a science writer, and having regular contact with health care professionals for his medical care.
Even though I didn’t specialize in T1D as a physician, I had never heard of these theories either until I started delving into the research.
Environmental factors that have been explored include the following. Findings have either been conflicting or inconclusive (5)Rewers, M. and J. Ludvigsson (2016). “Environmental risk factors for type 1 diabetes.” Lancet 387(10035): 2340-2348:
- early exposure to cow’s milk
- insufficient levels of vitamin D
- the hygiene hypothesis, which looks at the role of our cleaner environments and decreased exposures to infections as one way our immune systems get trained, and as a possible risk factor for many types of diseases including T1D, multiple sclerosis and asthma
- the accelerator hypothesis, which looks at factors that increase stress on insulin-producing cells that are already suffering and losing capacity, thus making them work so hard that their loss of function becomes overt and creates the symptoms of T1D
- and more
These studies, however, were another indication of just how important non-genetic risk factors are for chronic disease.
I kept looking and delving into the research, holding my question about a possible intelligent process that might underlie type 1 diabetes.
And I was curious about the role of adversity and trauma, which can alter the nervous system, the immune system, gut function and flora and more.
When I came across studies looking at antibodies, I stumbled across a gold mine.
3. Insights from Antibodies
Many people with T1D have one or more types of detectable antibodies at the time of diagnosis.
I was surprised by the many intriguing characteristics I hadn’t known about antibodies (and that we only started to learn about after the late 1970s when antibodies were first discovered):
- The presence of one antibody associated with risk for T1D is common in the general population (6)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.
- Only a small number of people with insulin-related antibodies ever develop T1D.
- Antibodies can arise and they can also resolve (ie: antibodies are not always permanent) (7)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, (8)Vehik, K., et al. (2016). “Reversion of beta-Cell Autoimmunity Changes Risk of Type 1 Diabetes: TEDDY Study.” Diabetes Care 39(9): 1535-1542
- Risk for developing T1D is associated with increasing levels and types of antibodies, and longer persistence in the body.
- Antibodies may not actually destroy insulin-producing beta-cells and may only serve as a marker of destruction (9)Knip, M., et al. (2016). “Role of humoral beta-cell autoimmunity in type 1 diabetes.” Pediatric Diabetes 17 Suppl 22: 17-24.
I hadn’t known that a lot of us carry risk factors for T1D but never develop the disease.
And I hadn’t realized that the existence of antibodies is not always permanent. And that their presence is not a clear indication of a direct path to disease.
The existence of antibodies, and the patterns that were being discovered in T1D, offered a way of potentially tracking the effects of environmental factors to see which ones make people more susceptible.
I have relatives who have been disabled by ME/CFS on both sides of my family tree and wondered whether I had a genetic predisposition for my chronic illness.
On learning of the 50% contribution from the environment, however, I was curious as to whether my getting sick was the result of exposure to risk factors that were not genetic.
And whether I might have some control over what I might do to recover.
The presence of antibodies does not always lead to a specific chronic disease.
Antibodies can come and go and can even resolve completely.
4. Risk Begins Long Before Onset
Another discovery I made was that risk for many chronic illnesses begins years or decades before onset and not just in the days or weeks just before symptoms suddenly manifest.
- Antibodies in people who develop T1D arise over a period of time (10)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, (11)Steck, A. K., et al. (2015). “Predictors of Progression From the Appearance of Islet Autoantibodies to Early Childhood Diabetes: The Environmental Determinants of Diabetes in the Young (TEDDY).” Diabetes Care 38(5): 808-813.
- These antibodies can appear up to 13 years (12)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, or longer before onset (13)Ziegler, A. G., et al. (2013). “Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children.” JAMA 309(23): 2473-2479.
- Antibodies associated with lupus (systemic lupus erythematosis or SLE), another autoimmune disease, have been found to occur up to 9 years before the onset of clinical symptoms (14)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.
- As in T1D, not everyone with these antibodies develops lupus and a greater number.
- Also as in T1D, persistence of these antibodies also predicts greater risk (15)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.
- Rheumatoid factor and other antibodies have also been found to arise more than 10 years before the onset of rheumatoid arthritis (16)Edwards, C. J. and C. Cooper (2006). “Early environmental factors and rheumatoid arthritis.” Clin Exp Immunol 143(1): 1-5.
The existence of markers years prior to the onset of clinical symptoms showed that there is a process that takes place under the radar, that it occurs over a long period of time, and that it does not always lead to disease.
In this way, antibodies offer important clues in determining risk factors and causes of type 1 diabetes.
Putting all this data together, researchers in T1D proposed that environmental factors initiate risk or accelerate an underlying autoimmune process that is linked to risk for T1D.
They suspect that environmental factors are also what precipitates or triggers the onset of T1D. They do so by unmasking a process that has been developing out of sight and outside of our awareness (17)Dahlquist, G. (1998). “The aetiology of type 1 diabetes: an epidemiological perspective.” Acta Paediatr Suppl 425: 5-10, (18)Ziegler, A. G., et al. (2013). “Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children.” JAMA 309(23): 2473-2479.
With this information I recalled that I had experienced two brief periods of inexplicable fatigue long before the onset of my own ME/CFS. These had both been in response to exercise. One period had occurred in childhood and the other in college when I was in my 20s. My symptoms of ME/CFS didn’t start until years later when I was in my 30s.
I wondered if there was a link between these seemingly random events from my past and my current illness.
I would eventually learn that many people with the onset of a chronic disease in adulthood had brief periods of symptoms years and often decades before actual onset.
The development of T1D begins years or decades before symptoms become detectable or stable.
Other chronic illnesses also begin long before the onset of overt or recognizable symptoms.
5. Risk for T1D Begins Before Birth
Because T1D most commonly begins in childhood and antibodies can arise a long time before clinical symptoms ever begin, scientists looked for risk factors occurring very early in life, including during pregnancy and birth.
Gisela Dahlquist is a Swedish diabetes researcher who has looked into such non-genetic risk factors.
Sweden collects data from pregnancy and birth in population-wide registries and also tracks diagnoses of T1D and other health conditions later in life.
The statistics include information from the time of pregnancy such as maternal age and marital status, work outside the home, smoking habits; as well data from labor and birth, including the use of pain medications and anesthesia for delivery, type of delivery (such as vaginal vs cesarean etc), birth weight, diagnoses in mother and fetus/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 (19)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 found that, in addition to maternal diabetes and increasing maternal age, risk factors for T1D in kids included:
- being born prematurely,
- maternal illness such as pre-eclampsia (toxemia),
- delivery by cesarean section,
- respiratory illnesses in the newborn,
- and blood-group incompatibility.
Dahlquist et al wondered whether the common element for many of the prenatal risk factors they had identified was that they each represented some form of prenatal stress. It was a whole new way of looking potential causes of type 1 diabetes.
The fact that prenatal events could affect risk for a chronic illness was news to me too.
Risk factors for T1D include events before and around the time of birth.
6. Prenatal and Birth Events Affect Risk for Other Chronic Illnesses
When I was a family doctor I followed women during pregnancy and helped them deliver their babies.
I knew first-hand how difficult, long and complicated labor could be, how many interventions we performed as medical doctors even when they weren’t always necessary, and how blue and limp babies could be in their first minutes or hours after a difficult birth.
These events were all considered pretty common on the labor and delivery floor of the hospitals I worked in, but nurses and other doctors and family members were always a little uncomfortable and concerned until we knew that everything had turned out okay.
Even though most babies seemed to recover fully with a little time, I always wondered whether there were any long-term consequences we were overlooking.
So I was really curious whether there was any research on this topic once I started learning there were studies.
I found many important bodies of research examining the role of prenatal events in risk for chronic illness.
The fetal origins of adult disease (FOAD) (20)Calkins, K. and S. U. Devaskar (2011). “Fetal origins of adult disease.” Curr Probl Pediatr Adolesc Health Care 41(6): 158-176. is one such area. The 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 have shown that lack of food during pregnancy is strongly linked to an increased risk for the metabolic syndrome (also known as Syndrome X). The metabolic syndrome includes having 3 or more symptoms such as type 2 diabetes, heart disease, high blood pressure, high cholesterol, and/or obesity. Their findings have been widely replicated and show that different types of prenatal stress can all result in the metabolic syndrome and other chronic illnesses.
FOAD increases risk for diseases such as (see summary of the research Table 1):
- Alzheimer’s Disease
- Blood Pressure (high)
- Diabetes, type 2
- Fat metabolism / lipid metabolism
- Heart disease (coronary artery disease)
- Kidney disease
- Liver disease
- Mental Illness such as Depression, Anxiety, Bipolar Disorder, Schizophrenia
- Osteoporosis and reduced bone mass
Additional research shows that many kinds of stressful events in early life also increase risk for autoimmune and other chronic diseases.
These include adverse prenatal events such as:
- 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, cesarean, use of certain medications),
- breech birth,
- distress in the baby after birth (such as when a baby needs resuscitation or has low apgar scores).
Prenatal and birth events have been associated with risk for chronic illnesses such as:
- type 1 diabetes (21)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, (22)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, (23)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)., (24)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.
- inflammatory bowel disease (Crohn’s, Ulcerative Colitis) (25)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, (26)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,
- multiple sclerosis (27)Maser, C. (1969). “[The perinatal period of multiple sclerosis patients].” Schweiz Med Wochenschr 99(50): 1824-1826, (28)Maghzi, A. H., et al. (2012). “Cesarean delivery may increase the risk of multiple sclerosis.” Mult Scler 18(4): 468-471
- asthma (29)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, (30)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, (31) Xu, B., J. Pekkanen and M. R. Jarvelin (2000). “Obstetric complications and asthma in childhood.” J Asthma 37(7): 589-594, (32)Madrid, A. (2005). “Helping children with asthma by repairing maternal-infant bonding problems.” Am J Clin Hypn 48(3-4): 199-211, (33)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).
It has also been suggested that events occurring during the prenatal time frame are associated with risk for lupus (34)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, rheumatoid arthritis (35)Edwards, C. J. (2010). “Can the Events of Early Life Influence the Development of Rheumatoid Arthritis?” J Rheumatol 37(1): 1-2, and ME/CFS (36)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, among others.
Dietert, the author of the article proposing early risk factors for ME/CFS, thinks in similar ways to researchers in T1D. He describes how both genes and environmental experiences influence the incidence of ME/CFS and the fact that ME/CFS occurs in children and adolescents and is not limited to adults indicates that causative factors exist in early life. With the long history of immune system dysfunction identified in ME/CFS he proposes that prenatal stress and other early exposures alter the regulation of the immune system later in life and also influence function in neurological, endocrine and reproductive tissues.
7. Unanswered Questions about Trauma and Autoimmune Disease
There was a certain level of complexity and confusion in results from studies in prenatal events, however, that didn’t seem easily explained:
- Not everyone exposed to difficult prenatal or birth events develops a chronic illness.
- Specific risk factors increase the chances of chronic illness in many studies but not in all of them. Risk for T1D increased with cesareans and decreased with breastfeeding in some studies, for example, but not in others. The same was true for most risk factors, in which there were almost always a few studies that showed no changes in risk.
- None of these issues seemed to fit my own history. My mother had had a normal pregnancy. She had not experienced starvation or illnesses or problems in delivering me, for example.
Another big question was, “Why care about such risk factors if you can’t change them?”
Delving further into Dahlquist’s study, I was curious about her second finding, which was that blood-group incompatibility was the factor associated with greatest risk for T1D.
8. The Greatest Prenatal Risk Factor for T1D (and Other Autoimmune Diseases?)
The process associated with blood-group incompatibility involves an interaction between a mother’s and fetus’ different blood types, which can cause symptoms for the baby that range from mild to life-threatening. It is also one of the causes of jaundice in newborns. Dahlquist couldn’t tell what the risk was specifically associated with.
In standard treatment for jaundice at the time of Dahlquist’s study (as well as today), newborns often needed to be placed in incubators for symptom reduction using phototherapy.
Dahlquist replicated this in a study with T1D-prone mice by removing the pups from their cages for two 4-hour periods a day for 5 days in their first few days of life (37)Dahlquist, G. and B. Kallen (1997). “Early neonatal events and the disease incidence in nonobese diabetic mice.” Pediatr Res 42(4): 489-491. She had a control group that stayed with their dams and two treatment groups: one treated with light therapy and the other with a sham 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. To her surprise, it was the separation of mice pups from their mothers that influenced risk for T1D.
I’d never heard of this as a risk factor for chronic illness either.
Separation at the time of birth was the biggest risk factor for type 1 diabetes.
III. Effects of Mother-Infant Separation At Birth
Some of the first research I discovered regarding the role of separation between mothers and their babies was conducted by Columbia University professor and physician Myron Hofer (38)Hofer, M. A. (1994). “Early relationships as regulators of infant physiology and behavior.” Acta Paediatr Suppl 397: 9-18. 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 learned 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, pheremones, physical activities such as suckling, and other unconscious, ANS (autonomic nervous system) driven processes and behaviors.
As Dahlquist found in 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 mother or baby, the need for treatment, prematurity and more etc. This was another potential clue about causes of type 1 diabetes.
Maternal-infant separation a source of altered physiology and health in animals and humans.
1. Mothers’ Closeness Regulates Baby’s Temp, Blood Pressure and Physiology
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 of the autonomic nervous system 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 (39)Klaus, M. H. and J. H. Kennell (1976). Maternal-infant bonding. St. Louis, Mosby, (40)Schore, A. N. (1994). Affect regulation and the origin of the self: the neurobiology of emotional development. Hillsdale, NJ, Lawrence Erlbaum, (41)Sandman, C. A. (2015). “Mysteries of the Human Fetus Revealed.” Monogr Soc Res Child Dev 80(3): 124-137.
This body of research has lead to the use of practices such as Kangaroo Care in neonatal intensive care units, in which premature and other babies are held in skin to skin contact by their parents. 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, has cofounded The Family Nurture Intervention at Columbia University Medical Center. Her treatment approach is part of a research study and 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.
2. Early Separation Affects Risk for Chronic Illness
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.
3. How Early Separation Affects Risk for Chronic Disease and Why There’s Hope
Risk for chronic illnesses such as type 2 diabetes and other symptoms of the metabolic syndrome is higher in at least two generations of people whose mothers experienced the Dutch Hunger Winter.
The NOVA documentary “The Ghost in Your Genes,” (here’s a transcript) describes the effects of environmental factors, including prenatal events, on health.
The influence of nongenetic factors is increasingly understood to be affected by epigenetics. This is also the process by which experiences of prenatal stress influence multiple generations.
Prenatal stress and early separation are two factors that affect health for multiple generations.
Epigenetics is the process by which small chemicals attach to the surfaces of genes to alter their behavior by turning them on and off.
Epigenetic changes are influenced by environmental factors.
Remember that environmental factors affect at least 50% – or more – of risk for type 1 diabetes.
Unlike inherited genes that exist in all of our cells, environmental factors often CAN be changed. Epigenetic changes can sometimes be reversed through changes in behavior, such as exercise and diet, as well as through medications and other forms of treatment (including types of psychotherapy used to heal the nervous system, perceptions of threat and effects trauma (42)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, which I describe in my introductory post on epigenetics).
Chemical attachments that alter how our genes function can be transmitted from one generation to the next.
You’ll find a wonderful overview and indepth article about this epigenetic process by Dan Hurley (who wrote “Diabetes Rising,” mentioned earlier) in Discover magazine. This article is about discoveries made by researchers at McGill in Montreal, Quebec and how early life experiences alter our genes to contribute to longterm health.
From what I’ve learned over the past 15 years, the epigenetic process described in Dan’s article appears to be one of the mechanisms explaining the role of early events in risk for T1D and other chronic diseases. I describe what I learned in more detail in the next two blog posts of this series.
The new knowledge that we are gaining allows for the development of different ways of understanding and looking at chronic illness. It also suggests considerations for treatment as well as approaches for prevention.
IV. The Cell Danger Response Adds Further Support to This View
Some of the most recent support for this unifying point of view comes from a metabolomics research lab at UC San Diego run by Dr. Robert Naviaux, MD, PhD. He has recognized that environmental risk factors fall into a small set of common stressors. These environmental stressors all trigger cell danger responses, which are survival reactions to threat that happen at the biochemical level in mitochondria.
As Naviaux describes, the cell danger response (CDR) is a healthy way in which the body addresses threats of all kinds by releasing adenosine triphosphate (ATP) outside of the cell to address threat (this is mentioned in the video link beginning at about 1:38).
The CDR, however, can get stuck in danger response signaling and unable to return to baseline functioning as it is designed to do during periods of safety. As Dahlquist and Hofer and others have discovered, it is not the environmental stressors that cause disease, but their effects on the body.
Naviaux’ research helps identify that the process that gets activated to lead to diseases is the cell danger response.
Environmental stressors that can trigger the CDR to cause disease include:
- Microbial threats such as viruses, bacteria, fungi, and parasites
- Physical threats such as UV, ionizing radiation, low oxygen levels, surgery, accidents; As we are seeing with perinatal research studies, these also include early mother-infant separation, low oxygen from prematurity, infections that require hospitalization or incubator care, which separates mothers and babies
- Chemical forms of danger such as heavy and trace metals and flame retardants, but possibly antibiotics and other medications when used in large amounts in tiny, immature baby’s bodies
- Psychological trauma, which include neglect, abuse, work and financial stress, loss of a loved one but that in very early life can also include separation and bonding disruptions
Naviaux explains that the effects of environmental stressors add up and can have “synergistic effects.” (43)Naviaux, R. K. (2014). “Metabolic features of the cell danger response.” Mitochondrion 16: 7-17, p. 7.
Infections during pregnancy, immediately after birth or in infancy are an example of how environmental stressors can interact with one another to increase threat, and therefore risk.
Babies who need treatment immediately after birth, for example, may require incubator care, which separates them from their mothers. This has multiple effects:
1) It reduces psychobiological regulation of temperature, heart rate, respiration and other basic functions that contribute to health and healing and that can increase perceptions of threat and thereby intensify the difficulty of recovery; and
2) can disrupt bonding and long-term attachment.
Babies who need hospitalization after being discharged home are also separated from their mothers and other caregivers, leading to similar compounding effects of threat that trigger that CDR.
V. Conclusion to Trauma and Autoimmune Disease Post #1
One of the things I learned about chronic illness is that non-genetic risk factors such as early life events shape our physiologies.
They also affect our biochemical pathways, our biologies, and influence long-term health.
This is because our brains, nervous systems and other organ systems are genetically programmed to develop through interaction with our environments.
These interactions shape the directions in which our autonomic nervous systems learn to prepare for and respond to their unique environments as they grow and develop (44)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, (45)Sandman, C. A. (2015). “Mysteries of the Human Fetus Revealed.” Monogr Soc Res Child Dev 80(3): 124-137, (46)Schore, A. N. (1994). Affect regulation and the origin of the self: the neurobiology of emotional development. Hillsdale, NJ, Lawrence Erlbaum, (47)Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246, (48)Shonkoff, J. P. (2016). “Capitalizing on Advances in Science to Reduce the Health Consequences of Early Childhood Adversity.” JAMA Pediatr 170(10): 1003-1007.
Most children and adults today have experienced periods of early separation in the hours and days following birth.
Separating moms and babies has become a routine part of healthy newborn care. With discovering this research I wondered if changes in how women are assisted in giving birth, with increasing hospital births starting around the 1930s in the United States, have been a contributing factor.
There have been epidemic rises in rates of type 1 diabetes and other autoimmune and chronic diseases around the world since World War II,
Babies who are sick, premature, are delivered by cesarean, require treatment or whose mothers are ill experience longer periods of separation.
As I’ll describe in the next post of this series, maternal-infant separation after birth is a risk factor for chronic illness (among other health problems). And I’ll show you what you can do about it.
Ultimately, the effects of early separation have been greatly underestimated.
While they were just one risk factor among a number of others that I discovered in my research – they appeared to be important events that might initiate or increase risk for chronic illness.
Prenatal and birth events affect risk for type 1 and type 2 diabetes and other chronic illnesses.
VI. The Next Post on Trauma and Chronic Illness
In the next post of the series I’ll tell you about Dr. Antonio Madrid, a psychologist who accidentally cured an 8-year-old girl of her asthma.
He had inadvertently treated the mother for the effects that early separation had had on her.
Tony has since reproduced these findings in multiple studies.
Tony’s work showed me how to recognize the subtle stressful events my own mother had experienced when pregnant with me and to begin to make sense of this new information with regards to my illness.
It added more support for my question about whether chronic illness might be the result of an intelligent process that leads to symptoms when it remains unresolved.
Tony’s findings also provided a glimpse at possible approaches to consider for the treatment – and maybe also the prevention – of chronic illness, including my own.
Continue with the Making Sense of Chronic Illness Discovery Series
Want to learn more? The next post describes research in asthma to explain how similarly stressful events in pregnancy, birth and infancy affect risk (post #2). I’ve learned over the years that these are risk factors for many other chronic diseases as well, including my own (asthma and ME/CFS). The studies’ findings helped me recognize contributions from events in my own birth and infancy that I had never thought were other than normal. A mechanism by which life experiences affect long-term health is that they alter gene expression (#3). Post #4 is a recap of how early events increase risk for chronic disease. Epigenetic changes are also seen in PTSD and have been shown to be reversible when PTSD symptoms are treated and healed with trauma therapy. Links between stress, trauma and chronic illness have long been mistakenly dismissed (#5), in part because psychosomatic medicine promotes the inaccurate and outdated view that all effects of trauma are psychological. Therapies for working with the effects of adverse life events help regain nervous system regulation. New science is also helping me make sense of how life experiences affect risk for chronic fatigue syndrome and as well as recover from ME/CFS and asthma.
Adverse Babyhood Experiences and Chronic Illness 1.0: A Subset of ACEs (Free ABE Fact Sheets & Checklist)
You can learn about more of the research and this view in these and in my other free downloadable ebooks:
|↑1||Diabetes Epidemiology Research International (1987). “Preventing insulin dependent diabetes mellitus: the environmental challenge.” BMJ 295(6596): 479-481 – more recent research has not changed this view|
|↑2||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|
|↑3, ↑6||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|
|↑4, ↑17||Dahlquist, G. (1998). “The aetiology of type 1 diabetes: an epidemiological perspective.” Acta Paediatr Suppl 425: 5-10|
|↑5||Rewers, M. and J. Ludvigsson (2016). “Environmental risk factors for type 1 diabetes.” Lancet 387(10035): 2340-2348|
|↑7||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|
|↑8||Vehik, K., et al. (2016). “Reversion of beta-Cell Autoimmunity Changes Risk of Type 1 Diabetes: TEDDY Study.” Diabetes Care 39(9): 1535-1542|
|↑9||Knip, M., et al. (2016). “Role of humoral beta-cell autoimmunity in type 1 diabetes.” Pediatric Diabetes 17 Suppl 22: 17-24|
|↑10||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|
|↑11||Steck, A. K., et al. (2015). “Predictors of Progression From the Appearance of Islet Autoantibodies to Early Childhood Diabetes: The Environmental Determinants of Diabetes in the Young (TEDDY).” Diabetes Care 38(5): 808-813|
|↑12||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|
|↑13, ↑18||Ziegler, A. G., et al. (2013). “Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children.” JAMA 309(23): 2473-2479|
|↑14||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|
|↑15||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|
|↑16||Edwards, C. J. and C. Cooper (2006). “Early environmental factors and rheumatoid arthritis.” Clin Exp Immunol 143(1): 1-5|
|↑19||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|
|↑20||Calkins, K. and S. U. Devaskar (2011). “Fetal origins of adult disease.” Curr Probl Pediatr Adolesc Health Care 41(6): 158-176.|
|↑21||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|
|↑22||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|
|↑23||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).|
|↑24||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|
|↑25||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|
|↑26||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|
|↑27||Maser, C. (1969). “[The perinatal period of multiple sclerosis patients].” Schweiz Med Wochenschr 99(50): 1824-1826|
|↑28||Maghzi, A. H., et al. (2012). “Cesarean delivery may increase the risk of multiple sclerosis.” Mult Scler 18(4): 468-471|
|↑29||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|
|↑30||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|
|↑31||Xu, B., J. Pekkanen and M. R. Jarvelin (2000). “Obstetric complications and asthma in childhood.” J Asthma 37(7): 589-594|
|↑32||Madrid, A. (2005). “Helping children with asthma by repairing maternal-infant bonding problems.” Am J Clin Hypn 48(3-4): 199-211|
|↑33||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).|
|↑34||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|
|↑35||Edwards, C. J. (2010). “Can the Events of Early Life Influence the Development of Rheumatoid Arthritis?” J Rheumatol 37(1): 1-2|
|↑36||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|
|↑37||Dahlquist, G. and B. Kallen (1997). “Early neonatal events and the disease incidence in nonobese diabetic mice.” Pediatr Res 42(4): 489-491|
|↑38||Hofer, M. A. (1994). “Early relationships as regulators of infant physiology and behavior.” Acta Paediatr Suppl 397: 9-18|
|↑39||Klaus, M. H. and J. H. Kennell (1976). Maternal-infant bonding. St. Louis, Mosby|
|↑40, ↑46||Schore, A. N. (1994). Affect regulation and the origin of the self: the neurobiology of emotional development. Hillsdale, NJ, Lawrence Erlbaum|
|↑41, ↑45||Sandman, C. A. (2015). “Mysteries of the Human Fetus Revealed.” Monogr Soc Res Child Dev 80(3): 124-137|
|↑42||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|
|↑43||Naviaux, R. K. (2014). “Metabolic features of the cell danger response.” Mitochondrion 16: 7-17, p. 7|
|↑44||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|
|↑47||Shonkoff, J. P., et al. (2012). “The lifelong effects of early childhood adversity and toxic stress.” Pediatrics 129(1): e232-246|
|↑48||Shonkoff, J. P. (2016). “Capitalizing on Advances in Science to Reduce the Health Consequences of Early Childhood Adversity.” JAMA Pediatr 170(10): 1003-1007|
A Mom says
My son developed Type 1 at the age of 28…
he has developmental PTSD but I don’t bother talking about it since he’s too well defended for it to be a helpful conversation for either of us. He is a courageous person but info from momma just isn’t helpful.
I sent him the link to your essay, though.
I’d relate my own many “psychosomatic” illnesses but it would fatigue me to list them all. Not to mention the triggering it would cause. I’m surprised I’ve managed to live as long as I have.
Exploring epigenetics gives me hope for the generations to follow.
Another son has lung problems. “Reactive airways disease”…he’s working on it.
Any way you can omit my name and email?
Veronique Mead, MD, MA says
Dear A Mom,
I’m so glad that our understanding of epigenetics is offering you hope even as you are not able to help your son(s) more directly.
It takes courage to witness a loved one’s suffering and to acknowledge their pain rather than to deny or pretend that it is not there. It takes love to respect who they are and the boundaries they give us.
If it helps, know that working on our own trauma / histories / symptoms linked to our personal experiences of trauma can be a way of not only helping ourselves to heal (even if our trauma occurred decades ago). It also supports future and past generations. You’ll find more about this in the second post of this series if you haven’t read it yet. It talks about asthma, which is also often referred to as reactive airways disease (RAD). It’s not as quick or direct when kids are older, but I still think it can make a significant difference. This is even true for parents of kids who were adopted (you’ll find a link to such a story in the sequels to this first post).
If it helps, here’s a link to a page with different approaches to healing developmental trauma.
Thank you for sharing here. I wish you all the best on this journey.
moira mccaskill says
I am thrilled to have discovered your site Veronique and very grateful for the way you are sharing all your work freely. I am working my way through the content slowly. Everything you say makes sense to me and makes something deep in me relax.
I’m 65 and got sick when I was 30 with CFS. For most of these years I had some good days and managed daily life. The last couple of years I have been getting worse and feel quite sick constantly.
The amount of advice that comes at me from the perspective that my thoughts are responsible or could change my situation has always irritated me and yet I know there is a way how I feel changes with stress, and events that affect my mental state. You are untangling this mystery in a vey helpful way that doesn’t add to my guilt but makes so much sense.
I just added a new anti depressant to the low dose one I have taken forever and have very mixed feelings about this even as it seems to be helping. Have you looked at anti- depressants?
Many thanks for your work
Veronique Mead, MD, MA says
First let me say that I’m very glad to hear that this information is helpful and also that it is both supporting something in you to relax and that it is not adding to any guilt. Those are among my highest intentions.
Re anti-depressants. We are on leading edge re explorations about how to work with our symptoms while considering the paradigm that I share here. I think it’s about testing it out with your own system and symptoms and seeing what happens. Maybe you’ll end up wanting to adjust the dose (up OR down). Maybe it will make some things easier to do or try. Maybe it is temporary while you find other avenues to try and that are helpful and address underlying contributing factors more effectively. Or maybe it will make a difference that’s worth continuing.
I also voice another view in my story in which I wonder if taking an antidepressant could have contributed / been one of many triggers to the onset of my ME/CFS by blocking underlying survival responses as I headed down into freeze and altered patterns of nervous system regulation. I’m not sure if that’s the case and I think that being mindful and tracking and holding these perspectives in mind can be helpful and don’t mean a treatment is going to cause problems. I suspect it’s all fairly complex and that it’s good to remember that sometimes easy / quick things can be really helpful.
I’d love to hear what you discover over time and it may be helpful for others too.
Thanks for commenting and I wish you well on this journey!
How exciting to learn about your site and the immense body of information you are offering to readers. I appreciate, also the comment section taking words out of my mouth, especially being an aging parent of adults.
Have passed along links that could be very useful to premie baby hoping that YOUR advice (professional) may be found useful, respectable and necessary (epigenetics and mysterious ‘whys’), for mothering her own children!
Immense insights here. (i.e. your feedback about respecting boundaries they have set – huge).
Veronique Mead, MD, MA says
So glad it’s helpful information and I so appreciate your willingness to share this with me and others here. I so want to support healing through the generations with as many boundaries as well as support as are helpful and needed!