What One Short Night’s Sleep does to your Glucose Metabolism

11 05 2010

ResearchBlogging.orgAs a blogger I regularly sleep 3-5 hours just to finish a post. I know that this has its effects on how I feel the next day. I also know short nights don’t promote my clear-headedness and I also recognize short-term effects on  memory, cognitive functions, reaction time and mood (irritability), as depicted in the picture below. But I had no idea of any effect on heart disease, obesity and risk of diabetes type 2.

Indeed, short sleep duration is consistently associated with the development of obesity and diabetes in observational studies (see several recent systematic reviews, 3-5). However, as explained before, an observational design cannot establish causality. For instance, diabetes type 2 may be the consequence of other lifestyle aspects of people who spend little time sleeping, or sleep problems might be a consequence rather than a cause of diabetogenic changes.

Diabetes is basically a condition characterized by difficulties processing carbohydrates (sugars, glucose). Type 2 diabetes has a slow onset. First there is a gradual defect in the body’s ability to use insulin. This is called insulin resistance. Insulin is a pancreatic hormone that increases glucose utilization in skeletal muscle and fat tissue and suppresses glucose production by the liver, thereby lowering blood glucose levels.  Over time, damage may occur to the insulin-producing cells in the pancreas (type 2 diabetes),  which may ultimately progress to the point where the pancreas doesn’t make enough insulin and injections are needed. (source: about.com).

Since it is such a slow process one would not expect insulin resistance to change overnight. And certainly not by just partial sleep deprivation of 4-5 hrs of sleep.

Still, this is the outcome of a study, performed by the PhD student Esther Donga. Esther belongs to the study group of Romijn who also studied the previously summarized effects of previous cortisol excess on cognitive functions in Cushing’s disease .

Donga et al. have studied the effects of one night of sleep restriction on insulin sensitivity in 9 healthy lean individuals [1] and in 7 patients with type 1 diabetes [2]. The outcomes were practically the same, but since the results in healthy individuals (having no problems with glucose metabolism, weight or sleep) are most remarkable, I will confine myself to the study in healthy people.

The study design is relatively simple. Five men and four healthy women (mean age 45 years) with a lean body weight and normal  sleep pattern participated in the study. They were not using medication affecting sleep or glucose metabolism and were asked to adhere to their normal lifestyle pattern during the study.

There were 3 study days, separated by intervals of at least 3 weeks. The volunteers were admitted to the clinical research center the night before each study day to become accustomed to sleeping there. They fasted throughout these nights and spent 8.5 h in bed.  The subjects were randomly assigned to sleep deprivation on either the second or third occasion. Then they were only allowed to sleep from 1 am to 4 am to secure equal compression of both non-REM and REM sleep stages.

(skip blue paragraphs if you are not interested in the details)

Effects on insulin sensitivity were determined on the day after the second and third night (one normal and one short night sleep) by the gold standard for quantifying insulin resistance: the hyperinsulinemic euglycemic clamp method. This method uses catheters to infuse insulin and glucose into the bloodstream. Insulin is infused to get a steady state of insulin in the blood and the insulin sensitivity is determined by measuring the amount of glucose necessary to compensate for an increased insulin level without causing hypoglycemia (low blood sugar). (see Figure below, and a more elaborate description at Diabetesmanager (pbworks).

Prior to beginning the hyperinsulinemic period, basal blood samples were taken and labeled [6,6-2H2]glucose was infused  for assessment of glucose kinetics in the basal state. At different time-points concentrations of glucose, insulin, and plasma nonesterified fatty acids (NEFA) were measured.

The sleep stages were differently affected  by the curtailed sleep duration: the proportion of the stage III and stage II sleep were greater (P < 0.007), respectively smaller (P < 0.006) in the sleep deprived night.

Partial sleep deprivation did not alter basal levels of glucose, nonesterified fatty acids (NEFA), insulin, glucagon, or cortisol measured the following morning, nor did it affect basal endogenous glucose production.

However, during the CLAMP-procedure there were significant alterations on the following parameters:

  • Endogenous glucose production – increase of approximately 22% (p< 0.017), indicating hepatic insulin resistance.
  • Rate of Glucose Disposal – decrease by approximately 20% (p< 0.009), indicating decreased peripheral insulin sensitivity.
  • Glucose infusion rate – approximately 25% lower after the night of reduced sleep duration (p< 0.001). This is in agreement with the above findings: less extra glucose needed to maintain plasma glucose levels.
  • NEFA – increased by 19% (p< 0.005), indicating decreased insulin sensitivity of lipolysis (breakdown of triglyceride lipids– into free fatty acids).

The main novelty of the present study is the finding that one single night of shortened sleep is sufficient to reduce insulin sensitivity (of different metabolic pathways) in healthy men and women.

This is in agreement with the evidence of observational studies showing an association between sleep deprivation and obesity/insulin resistance/diabetes (3-5). It also extends results from previous experimental studies (summarized in the paper), that document the effects on glucose-resistance after multiple nights of sleep reduction (of 4h) or total sleep deprivation.

The authors speculate that the negative effects of multiple nights of partial sleep restriction on glucose tolerance can be reproduced, at least in part, by only a single night of sleep deprivation.

And the media conclude:

  • just one night of short sleep duration can induce insulin resistance, a component of type 2 diabetes (Science Daily)
  • healthy people who had just one night of short sleep can show signs of insulin resistance, a condition that often precedes Type 2 diabetes. (Medical News Today)
  • even a single of night of sleep deprivation can cause the body to show signs of insulin resistance, a warning sign of diabetes (CBS-news)
  • And this was of course the message that catched my eye in the first place: “Gee, one night of bad sleep, can already disturb your glucose metabolism in such a way that you arrive at the first stage of diabetes: insulin resistance!…Help!”

    First “insulin resistance” calls up another association than “partial insulin resistance” or a “somewhat lower insulin sensitivity” (as demonstrated in this study).  We interpret insulin resistance as a disorder that will eventually lead to diabetes, but perhaps adaptations in insulin sensitivity are just a normal phenomenon, a way to cope with normal fluctuations in exercise, diet and sleep. Or a consequence of other adaptive processes, like changes  in the activity of the autonomous nervous system in response to a short sleep duration.

    Just as blood lipids will be high after a lavish dinner, or even after a piece of chocolate. And just as blood-cortisol will raise in case of exercise, inflammation or stress. That is normal homeostasis. In this way the body adapts to changing conditions.

    Similarly -and it is a mere coincidence that I saw the post of Neuroskeptic about this study today- an increase of blood cortisol levels in children when ‘dropped’ at daycare, doesn’t mean that this small increase in cortisol is bad for them. And it certainly doesn’t mean that you should avoid putting toddlers in daycare as Oliver James concludes, because “high cortisol has been shown many times to be a correlate of all manner of problems”. As neuroskeptic explains:

    Our bodies release cortisol to mobilize us for pretty much any kind of action. Physical exercise, which of course is good for you in pretty much every possible way, cause cortisol release. This is why cortisol spikes every day when you wake up: it helps give you the energy to get out of bed and brush your teeth. Maybe the kids in daycare were just more likely to be doing stuff than before they enrolled.

    Extremely high levels of cortisol over a long period certainly do cause plenty of symptoms including memory and mood problems, probably linked to changes in the hippocampus. And moderately elevated levels are correlated with depression etc, although it’s not clear that they cause it. But a rise from 0.3 to 0.4 is much lower than the kind of values we’re talking about there.

    So the same may be true for a small temporary decrease in glucose sensitivity. Of course insulin resistance can be a bad thing, if blood sugars stay elevated. And it is conceivable that bad sleep habits contribute to this (certainly when combined with the use of much alcohol and eating junk food).

    What is remarkable (and not discussed by the authors) is that the changes in sensitivity were only “obvious” (by eyeballing) in 3-4 volunteers in all 4 tests. Was the insulin resistance unaffected in the same persons in all 4 tests or was the variation just randomly distributed? This could mean that not all persons are equally sensitive.

    It should be noted that the authors themselves remain rather reserved about the consequences of their findings for normal individuals. They conclude “This physiological observation may be of relevance for variations in glucoregulation in patients with type 1 and type 2 diabetes” and suggest that  “interventions aimed at optimization of sleep duration may be beneficial in stabilizing glucose levels in patients with diabetes.”
    Of course, their second article in diabetic persons[2], rather warrants this conclusion. Their specific advise is not directly relevant to healthy individuals.



    1. Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, & Romijn JA (2010). A Single Night of Partial Sleep Deprivation Induces Insulin Resistance in Multiple Metabolic Pathways in Healthy Subjects. The Journal of clinical endocrinology and metabolism PMID: 20371664
    2. Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen K, Hoogma RP, Corssmit EP, & Romijn JA (2010). Partial sleep restriction decreases insulin sensitivity in type 1 diabetes. Diabetes care PMID: 2035738
    3. Nielsen LS, Danielsen KV, & Sørensen TI (2010). Short sleep duration as a possible cause of obesity: critical analysis of the epidemiological evidence. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 20345429
    4. Monasta L, Batty GD, Cattaneo A, Lutje V, Ronfani L, van Lenthe FJ, & Brug J (2010). Early-life determinants of overweight and obesity: a review of systematic reviews. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 20331509
    5. Cappuccio FP, D’Elia L, Strazzullo P, & Miller MA (2010). Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Diabetes care, 33 (2), 414-20 PMID: 19910503
    The subjects were studied on 3 d, separated by intervals of at
    least 3 wk. Subjects kept a detailed diary of their diet and physical
    activity for 3 d before each study day and were asked to maintain
    a standardized schedule of bedtimes and mealtimes in accordance
    with their usual habits. They were admitted to our clinical
    research center the night before each study day, and spent 8.5 h
    in bed from 2300 to 0730 h on all three occasions. Subjects fasted
    throughout these nights from 2200 h. The first study day was
    included to let the subjects become accustomed to sleeping in our
    clinical research center. Subjects were randomly assigned to sleep
    deprivation on either the second (n4) or third (n5) occasion.
    During the night of sleep restriction, subjects spent 8.5 h in
    bed but were only allowed to sleep from 0100 to 0500 h. They
    were allowed to read or watch movies in an upward position
    during the awake hours, and their wakefulness was monitored
    and assured if necessary.
    The rationale for essentially broken sleep deprivation from
    2300 to 0100 h and from 0500 to 0730 h, as opposed to sleep
    deprivation from 2300 to 0300 h or from 0300 to 0730 h, was
    that in both conditions, the time in bed was centered at the same
    time, i.e. approximately 0300 h. Slow-wave sleep (i.e. stage III of
    non-REM sleep) is thought to play the most important role in
    metabolic, hormonal, and neurophysiological changes during
    sleep. Slow-wave sleep mainly occurs during the first part of the
    night, whereas REM sleep predominantly occurs during the latter
    part of the night (12). We used broken sleep deprivation to
    achieve a more equal compression of both non-REM and REM
    sleep stages. Moreover, we used the same experimental conditions
    for partial sleep deprivation as previously used in other
    studies (7, 13) to enable comparison of the results.

    Irreversible Effects of Previous Cortisol Excess on Cognitive Functions in Cushing’s Disease

    10 04 2010

    ResearchBlogging.orgApril 8th is Cushing’s Awareness Day. This day has been chosen as a day of awareness as it is the birthday of Dr. Harvey Cushing, a neurosurgeon, who discovered this illness.

    Cushing’s disease is a rare hormone disease caused by prolonged exposure to high levels of the stress hormone cortisol in the blood, whereas Addison’s disease is caused by the opposite: the lack of cortisol. For more background information on both see this previous post. Ramona Bates MD, of Suture for a Living, has written an excellent review (in plain language) about Cushing’s Disease on occasion of Cushing Awareness Day at EmaxHealth.

    From this you can learn that Cushing’s disease can be due to the patient taking cortisol-like glucocorticoids, such as prednisone for asthma (exogenous cause), but can also arise because people’s bodies make too much of cortisol itself.  This may be due to a tumor on the pituitary gland, the adrenal gland, or elsewhere in the body.

    Symptoms of Cushing’s disease are related to the effects of high levels of cortisol or other glucocorticoids on the immune system, the metabolism and  the brain. Symptoms include rapid weight gain, particularly of the trunk and face (central obesity, “moon face” and buffalo neck), thinning of the skin and easy bruising, excessive hair growth, opportunistic infections, osteoporosis and high blood pressure.

    Less emphasized than the clinical features are the often very disabling cognitive deficits and emotional symptoms that accompany Cushing’s disease. Cushing patients may suffer from various psychological disturbances, like insomnia, mood swings, depression and manic depression, and from cognitive decline. Several studies have shown that these glucocorticoid induced changes are accompanied by atrophy of the brain, and in particular of the  hippocampal region, leading to hippocampal volume loss and a profound loss of synapses [2]. This hippocampal loss seems reversible [2], but are neurological and psychological defects also restored? This is far more important to the patient than anatomic changes.

    If we listen to Cushing patients, who are “cured” and have traded Cushing’s disease for Addison’s disease, we notice that they feel better after their high levels of cortisol have normalized, but not fully cured (see two examples of ex-Cushing patients with longlasting if not irreversible health) problems in my previous post here. [added 2010-04-17)
    To realize how this affects daily life, I recommend to read the photo-blog 365 days with Cushing by Robin (also author of Survive the Journey). Quite a few of her posts deal with the continuous weakness (tag muscle atrophy), tiredness (tag fatigue), problems with (short-term) memory (see tag memory)  or both (like here and here).

    Scientifically the question is to which extent ex-Cushing patients score worse than other healthy individuals or chronically ill people and, if so, whether this can be attributed to the previous high levels of glucocorticoids.

    A recent study by endocrinologists (and one neurologists) from the Leiden University Medical Center assessed the cognitive functioning of patients  after long-term cure of their Cushing’s disease (caused by a ACTH producing pituitary adenoma, that induces overproduction of cortisol (hypercortisolism) by the adrenals [1]. Previous studies had contradictory outcomes and/or were too small to draw conclusions.

    The authors first compared a group of 74 Cushing patients (with a previous pituitary tumor) with matched healthy controls (selected by the patients themselves). Matched means that these controls had the same characteristics as the Cushing patients with respect to gender (male/female: 13/61), age (52 yr) and education.
    Cushing patients were on average 13 years in remission and were followed for another 3 years (total 16 yrs follow-up). Cushing’s disease  had been established by clinical signs and symptoms and by appropriate biochemical tests. All patients were treated by transsphenoidal surgery (surgery via the nostrils), if necessary followed by repeat surgery and/or radiotherapy (27%). Cure of Cushing’s disease was defined by normal overnight suppression of plasma cortisol levels after administration of dexamethasone and normal 24-h urinary excretion rates of cortisol. 58% of the patients had at least one form of hypopituitarism (deficiency of one or more hormones) and half of the patients needed hydrocortisone replacement therapy.

    Long after their cure, 62% of the Cushing patients reported memory problems, and 47% reported problems in executive functioning. The Hospital Anxiety and Depression Scale (HADS)-score (10.5)  indicated no clinical depression or anxiety. Patients with long-term cure of Cushing’s disease did not perform worse on measures of global cognitive functioning. However, these patients had several other cognitive impairments, mainly in the memory domain.
    Only a single test result (FAS, measures verbal mental flexibility and fluency) was significantly different between patients with short and long-term remission.

    From direct comparison with healthy controls it is not clear what causes these cognitive alterations in Cushing patients.

    Therefore the cognitive function of Cushing patients was compared to that of patients previously treated for non-functioning pituitary macroadenomas (NFMA).
    NFMA patients were chosen, because they have undergone similar treatments (transsphenoidal surgery (100%), with repeat surgery and/or radiotherapy (44%) as the Cushing patients. They also shared hypopituitarism and the need for hydrocortisone substitution in half of the cases. NFMA patients, however, have never been exposed to prolonged excess of cortisol.

    Cushing patients could not be directly compared to NFMA-patients, because these patient groups differed with regard to age and gender.

    Thus Cushing patients were compared to matched healthy controls and NFMA to another set of healthy controls, matched to these NFMA patients (Male/Female: 30/24  and mean age: 61 yr).

    To compare Cushing patients with NFMA patients the Z-scores* were calculated for each patient group in relation to their appropriate control group. A general linear model was used to compare the Z-scores.

    Overall Cushing patients performed worse than NFMA patients. In the memory domain, patients cured from Cushing’s disease had a significantly lower MQ measured with the Wechsler Memory Scale compared with patients with NFMA in the subscales concentration and visual memory. On the Verbal Learning Test of Rey, patients cured from Cushing’s disease recalled fewer words in the imprinting, the immediate and delayed recall trials. Furthermore, on the Rey Complex Figure, patients with cured Cushing’s disease scored worse on both trials when compared with NFMA patients. In tests measuring executive function, patients cured from Cushing’s disease made fewer correct substitutions on the Letter-Digit Substitution Test and came up with fewer correct patterns on the Figure Fluency Test compared with treated NFMA patients.

    These impairments were not merely related to pituitary disease in general and/or its treatment, because these patients with long-term cure of Cushing’s disease also revealed subtle impairments in cognitive function compared with patients previously treated for NFMA. These are most likely caused by the irreversible effects of previous glucocorticoid excess on the central nervous system (because this is the main difference between the two).

    Sub-analysis indicated that hypopituitarism was associated with mildly impaired executive functioning** and hydrocortisone dependency** and additional radiotherapy were negatively associated with memory and executive functioning, whereas the duration of remission positively influenced memory and executive functioning.

    The main point of criticism, apparently raised during the review process and discussed by the authors, is the presentation of the data without adjustments for multiple comparisons. When more than one test is used, the chance of finding at least one test statistically significant due to chance increases. As the authors point out, however, the positive significant results were not randomly distributed among the different variables. Furthermore, the findings are plausible given the irreversible effects of cortisol excess on the central nervous system in experimental animal and clinical studies.

    Although not addressed in this study, similar cognitive impairments would be expected in patients having continuous overexposure to exogenous glucocorticosteroids, like prednison.

    * Z-scores: The z score for an item, indicates how far and in what direction, that item deviates from its distribution’s mean, expressed in units of its distribution’s standard deviation. The z score transformation is especially useful when seeking to compare the relative standings of items from distributions with different means and/or different standard deviations (see: http://sysurvey.com/tips/statistics/zscore.htm).

    ** This makes me wonder whether Addison patients with panhypopituitarism have lower cognitive functions compared to healthy controls as well.

    Hattip: Hersenschade door stresshormoon lijkt onomkeerbaar (2010/04/08/) (medicalfacts.nl/)


    1. Tiemensma J, Kokshoorn NE, Biermasz NR, Keijser BJ, Wassenaar MJ, Middelkoop HA, Pereira AM, & Romijn JA (2010). Subtle Cognitive Impairments in Patients with Long-Term Cure of Cushing’s Disease. The Journal of clinical endocrinology and metabolism PMID: 20371667
    2. Patil CG, Lad SP, Katznelson L, & Laws ER Jr (2007). Brain atrophy and cognitive deficits in Cushing’s disease. Neurosurgical focus, 23 (3) PMID: 17961025 Freely available PDF, also published at Medscape

    Invisible Chronic Illness: Addison’s Disease

    17 08 2009

    This week the Grand Round will be hosted by Invisible Illness Week, a blog dedicated to the National Invisible  Ilness Week, which runs September 14 -20, 2009. The purpose:

    National Invisible Chronic Illness Awareness Week  (..) is a worldwide effort to bring together people who live with invisible chronic illness and those who love them. Organizations are encouraged to educate the general public, churches, healthcare professionals and government officials about the impact of living with a chronic illness that is not visually apparent.

    The theme of the Grand Round is, not very surprisingly: Invisible chronic Illness.

    I won’t write about this professionally -being a librarian-, but I will speak from my own experience.

    As many of you know, I’ve the chronic illness Addison’s Disease. Not that I feel ill. It doesn’t affect me, really… Not anymore.. I think.

    But many people with Addison’s disease suffer silently from this disease. And like many other diseases this disease is seldomly understood by partners, colleagues, friends ….. and doctors.

    Before I explain more about Addison’s disease, first let me say that almost every disease is “invisible” to others. People can never fully understand what an illness means to someone suffering from it.

    Ball-and-stick model of the cortisol (hydrocor...

    Cortisol, Image via Wikipedia

    Patients with Addison’s disease make no or too small amounts of cortisol, a hormone made by the adrenal cortex. Cortisol has a bad reputation as the stress hormone among many people. It doesn’t deserve this reputation as this hormone is vital to life. Corticosteroids are involved in a wide range of physiologic systems such as stress response, immune response and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior (Wikipedia)

    Too much of this hormone causes Cushing’s disease, too little causes Addison’s disease. If you want to know what Cushing does to your body and mind, then please read the letter of Kate when she was first diagnosed with Cushing’s, at Robin’s “Survive the Journey”.

    Here, I will confine myself to Addison’s disease. It is a very good example of an invisible yet serious disease.

    There are 3 forms of Addison: primary (defect in the adrenal cortex itself, often also leading to a defect in aldosteron production), secondary Addison (by a defect in the hypophysis or hypothalamus) and iatrogenic Addison (caused by overtreatment with corticosteroids)

    Here some reasons why the illness, although “invisible”, can have great impact on your live.

    1. Diagnosis.


    Diagnosis is often a challenge, especially in patients with primary Addison, most of whom look healthy because of their pigmented skin. Nowadays, the main cause of primary Addison’s disease is immune destruction of the adrenal cortex. This has often a slow onset and in 50% of the patients the diagnosis takes more than 2, sometimes even more than 10 years [1]. 38% of the patients even experience vague complaints, that can later be attributed to Addison, during 11->30 years before diagnosis [1].

    Before the diagnosis is made, people with Addison’s Disease often feel extremely tired and miserable. Even when the disease fully manifests itself the symptoms are largely vague and aspecific. The most common symptoms are fatigue, dizziness, muscle weakness, weight loss, difficulty in standing up, vomiting, anxiety, diarrhea, headache, sweating, changes in mood and personality, and joint and muscle pains. Often the symptoms aren’t taken seriously (enough) or the illness is mistaken for anorexia or depression.

    My secondary Addison was the consequence of an injury to the pituitary gland as result of heavy blood loss during complicated childbirth (see previous post). The week between the cause and the diagnosis of the disease, was the most terrible week of my life. I felt awful, weak, (well I lost >3 liters of blood to start with), couldn’t give breast milk (no prolactin), and I disgusted food so much, you can’t imagine. I couldn’t get anything down my throat, only the look of it made me vomit. And I felt so bad not being able to care for the baby, but I just couldn’t. I couldn’t even stand for more then a few minutes, couldn’t walk.  And then there was unstoppable diarrhea, dizzyness, and speaking with double tongue. And practically no one took it seriously, not the gynaecologists, not the nurses, not the paediatricians, nor my friends or family.

    But this was only one week. How would it have been if it durated 5 or 10 years?

    2. Grieve and adaptation.

    Once the disease is diagnosed you have to learn to live with a body that has let you down (grieve) and you have to learn to become confident again (adapt). You also have to find a new balance. I’ve lost a few hormones overnight (ACTH, cortisol, thyroid hormone, growth hormone, prolactin, gonadotrope hormones) and believe me, it took me a few years to feel reasonable normal again. It is quite surprising how badly I was informed. Very little information about the risk of an Addisonian crises, the dosing of cortisol under various conditions.
    It was also confronting how little people wanted to know about the disease or what I had been through. Visitors after the birth wanted me to be euphoric and didn’t want me to go into any detail of what had happened. They cut me short by saying: “But you have a lovely baby”. Somebody cried that she didn’t want to hear it. So I stopped trying to speak about it.

    I took no sick leave, immediately went back to work. My boss – a nephrologist, never asked after my health, not once.

    As I said it took a few years before my “come-back”. I didn’t feel myself. It was as if I couldn’t think, as if my head was filled with cottonwool. Afterwards I think the main reason for improval was the reduction of the cortisol from 30 mg to 12.5 per day and the use of DHEAs plus that I regained confidence in myself.

    3. Comorbidity

    With cortisol I lost some other hormones which are also essential. Patients with primary Addison often miss aldosteron as well, which makes them more liable for an Addisonian crisis. Primary Addisonians may also have other immune diseases, like autoimmune thyroid disease, gonadal failure, type 1 diabetes and vitiligo.

    4. Addisonian crisis

    An addisonian crisis is an emergency situation, with possible fatal outcome, associated mainly with an acute deficiency of the glucocorticoid cortisol. This occurs in (extremely) stressful situations. Some Addisonpatients are more prone to it than others. You can -and should – take precautions, like wearing alert bracelets or necklaces, so that emergency personnel can identify adrenal insufficiency and provide stress doses of steroids in the event of trauma, surgery, or hospitalization.

    Some Addisonians fear these crises so much that they dear not walk or run alone. Many Addison patients don’t go to a country far away, some don’t even pass the border (and you know the Netherlands aren’t that big).

    5. Addison’s disease can be treated but not cured.

    Addison patients are treated with corticosteroids like hydrocortisone and are substituted with other hormones that they may lack. Without treatment, the disease is lethal, with treatment the disease is not cured. I do feel all right now, but many of my fellow patients don’t. I think that the following excerpt from a Seminar of Wiebke Arlt and Bruno Allolio about adrenal insufficiency [2] makes this very clear.

    Despite adequate glucocorticoid and mineralocorticoid replacement, health-related quality of life is greatly impaired in patients with primary and secondary adrenal insufficiency. Predominant complaints are fatigue, lack of energy, depression, and anxiety. In addition, affected women frequently complain about impaired libido. In a survey of 91 individuals, 50% of patients with primary adrenal insufficiency considered themselves unfit to work and 30% needed household help. In another survey of 88 individuals the number of patients who received disablility pensions was two to three times higher than in the general population. The adverse effect of chronic adrenal insufficiency on health-related quality of life is comparable to that of congestive heart failure. However, fine-tuning of glucocorticoid replacement leaves only a narrow margin for improvement, and changes in timing or dose do not result in improved wellbeing.


    1. Zelissen PM. Addison patients in the Netherlands: medical report of the survey. The Hague: Dutch Addison Society, 1994.
    2. Wiebke Arlt, Bruno Allolio. Adrenal Insufficiency, Lancet 2003; 361: 1881–93 , full text on http://www.addisonssupport.com/Documentation/adrenal-insufficiency-2003.pdf

    Earlier posts on the subject:

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