I started this blog on July 2, 2016 in the hopes of documenting our experiment with oxytocin. I had no idea I would become so enamoured with learning about oxytocin and with sharing my discoveries with others... I am so grateful for the relative success we have found with oxytocin treatment, for the opportunity to share our experiences with others who are similarly impacted, and for the chance to educate readers about the existing research on oxytocin and its potential effectiveness as a treatment for PHP, hypothalamic obesity, and their related conditions.
Although there is research that suggests oxytocin may be helpful in improving metabolic health, social behavior, compulsive behaviors, etc., research in its application as a treatment modality is still lacking; more research is needed to understand whether/how it is effective for specific clinical populations and how the application can be translated into medical treatment (best practices, dosing, side effects, drug interactions, contraindications, etc.). I have been very encouraged by some recent correspondence with oxytocin researchers (both in basic science and medical science) who also shared their excitement about studying more about oxytocin in order to learn about its potential to provide relief for the sufferers of these pituitary/hypothalamic conditions.
From my correspondence with other sufferers/caregivers of pituitary disease, it is apparent that oxytocin is not on the radar of the majority of practicing endocrinologists as a necessary hormone to replace. However, from my reading of the literature and first hand witnessing the difference it makes in my son's life, I believe very strongly that it is an essential hormone in need of replacement. I hope that readers share our experiences (albeit anecdotal) widely among those who may be affected and their physicians. Given that the research on the clinical applications of oxytocin is still nascent, I can only hope that whatever interest is piqued by readers of this blog may be a catalyst for more oxytocin-related interest/application in clinics and labs.
If you care to participate in a questionnaire, I will survey readers to learn about symptoms are co-morbid with panhypopituitarism. My plan is to construct a survey that inquires into common symptoms known to exist in people with PHP and HO across various hormone-deficient diagnostic groups. I believe that many may be oxytocin-deficiency/receptor related but not all physicians are necessarily aware that they may be related to oxytocin deficiency. Perhaps data (including what we learn from this type of survey) demonstrating the prevalence of these co-existing symptoms will help educate us all across diagnoses (whether PWS, Central Diabetes Insipidus, or Hypothalamic Obesity). Could oxytocin deficiency explain the cluster of certain untreated symptoms shared by patients who suffer from pituitary and hypothalamic disease? Let's find out...
If you are a pituitary patient or caregiver of a pituitary patient and would be interested in participating in an anonymous survey on the common symptoms shared by people with missing hormones, please take the poll indicating your interest so I know whether or not to design and send out a survey. If I see that there is substantial interest from readers and believe I could get a large enough sample, I may design a survey. What I learn will be shared on my blog with readers (including oxytocin researchers) so that we can learn more about the common symptoms of these hormone-related disorders. My intention for this potential survey is shed more light onto possible oxytocin-deficiency disorders and prompt further research in this important area of medicine.
Sunday, February 26, 2017
Monday, February 20, 2017
73) The vicious metabolic cycles of HO and what can be done about it?
Please bear with me- this is a detailed and somewhat technical post but I promise it will be worth reading if you want to understand how hyperinsulinemia and leptin resistance play a large role in HO and how oxytocin may mitigate this vicious cycle. In observing Sasha’s metabolic health over the last several years, I have become fascinated by the workings of the brain and body’s ability to achieve health and homeostasis. As a beginner and informal student of neuro-endocrinology, I know my understanding is basic and that I am painting very broad brush strokes in my description. For what it’s worth, here is my attempt at describing the relationships between some of these hormones important to metabolic health.
For the normal (non-HO) person:
1. Low blood sugar (hypoglycemia) triggers the hypothalamus to signal the sense of hunger.
2. When food (let’s say, a slice of pizza) is available, the hungry person eats it and this raises blood sugar, satisfying the person and making energy available for the person.
3. The pancreas produces and sends out insulin to facilitate blood glucose uptake into the cells to be immediately used for energy. Excess glucose is stored in fat cells as free fatty acids for later use.
4. In the absence of food, hunger triggers the person to secrete corticosteroids to convert stored glucose (glycogen), proteins, fats and carbs to raise blood glucose.
5. Corticosteroids also act like a traffic cop for glucose, slowing the flow of glucose into the cell, and preventing blood glucose from dropping too quickly.
6. In sum, the normal person's hypothalamus behaves in a way to respond to the low blood sugars using the feedback loop between his/her corticosteroids and insulin, creating a balanced system: insulin makes it possible for glucose to be used for energy as needed and any extra glucose to be stored as free fatty acids to be saved for another time when energy is needed in the absence of food. This process makes if possible for a person’s weight to remain stable.
For the HO person with hyperinsulinemia (who also has AI, Adrenal Insufficiency):
1. Low blood sugar (hypoglycemia) triggers the hypothalamus to signal a sense of hunger.
2. When food is available (pizza), the HO/AI hungry person eats it and this raises blood sugar (same as above).
3. Insulin does its job by sending glucose into the working cells and fat storage cells. However, in the case of the HO person, there is an oversecretion of insulin in response to the amount of glucose in the blood. See* below #5 for the explanation why HO person may hypersecrete insulin.
3. Glucose leaves the blood quickly as soon as insulin arrives but insulin takes longer to clear from the blood. As long as insulin is still in the blood, free fatty acids (stored in fat cells) cannot be accessed or released in the blood for later use.
4. The HO/AI person feels hungry (again), eats in response to the hunger, and the cycle continues with the insulin never being cleared from the body and more fatty acids being stored/trapped in the fat cells (making the person fatter).
5. In the absence of food, corticosteroids are not available to convert stored glucose, proteins, fats, and carbs to raise blood glucose. Unlike the normal person who can utilize corticosteroids to raise the blood glucose levels under the stressful conditions of hunger, the HO/AI person’s blood glucose drops further. *This state of low blood glucose is physically stressful and it causes insulin to increase because demand for energy in cells is greater.
6. In this low blood sugar state, the HO/AI person feels hungrier and is driven to eat. If s/he eats (esp carbs), glucose spikes, insulin rises in response and stays elevated, glucose drops again, fatty acids cannot be accessed for energy and the person becomes fatter. This becomes the vicious cycle familiar to HO sufferers.
Role of Leptin:
Known as the “satiety hormone”, leptin, a hormone released from the fat cells located in adipose (fat) tissues, sends signals to the hypothalamus in the brain. This particular hormone helps regulate and alter long-term food intake and energy expenditure, not just from one meal to the next like insulin. The primary design of leptin is to help the body maintain its weight.
Because it comes from fat cells, leptin amounts are directly connected to an individual’s amount of body fat. When the body is functioning properly, excess fat cells will produce leptin, which will trigger the hypothalamus to lower the appetite, allowing the body to dip into the fat stores to feed itself which keeps the person at a normal, stable weight. Unfortunately, when someone is obese, that individual will have too much leptin in the blood. This can cause a lack of sensitivity to the hormone, a condition known as leptin resistance and the person’s appetite does not get lowered. Because the individual keeps eating, the fat cells produce more leptin to signal the feeling of satiety, leading to increased leptin levels, more leptin resistance, more weight gain, etc. Similarly, if a person decreases fat/calories (by dieting, for example), leptin will also decrease and appetite will increase. Leptin may be the reason why it is impossible to keep weight off in the long run after initially losing weight from a diet. Dieting may in fact, drive down leptin and drive UP appetite.
Between the vicious cycle of glucose, hyperinsulin secretion, overeating and weight gain, the weight maintaining function of leptin, and weight gaining effects of leptin resistance, it is not looking good for the sufferer of HO.
WHAT TO DO?
When it comes to an eating regimen, the low carbohydrate diet is known as one of the best choices for people with HO. By keeping the sugar levels from precipitously rising (and falling and this prevents the triggering of the glucose/insulin roller coaster), rapid weight gain can be stopped or slowed. Maintaining a more stable weight also prevents the overproduction of leptin and the development of leptin resistance.
Bariatric surgery and many drugs have been tried to find a cure and stop the scourge of HO but still, to my knowledge, this is still a work in progress.
So, where does oxytocin fit in as a possible therapeutic agent for HO, and in particular, hyperinsulinemia and leptin resistance?
1. Oxytocin may be an effective treatment against impaired leptin signaling or leptin resistance.
http://journal.frontiersin.org/article/10.3389/fendo.2015.00119/full
2. Oxytocin may cause increased sensitivity to satiety signals:
http://ajpregu.physiology.org/content/287/1/R87.short
3. Leptin targets a specific subpopulation of oxytocin neurons and that this action may be important for leptin’s ability to reduce body weight in both control and obese rats:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059625
4. Oxytocin and its analogs have multi-level effects in improving weight control, insulin sensitivity and insulin secretion, and that oxytocin has a potential role in treating obesity and diabetes:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658979/
5. Therapeutic levels of oxytocin may raise blood glucose levels: http://www.karger.com/Article/Abstract/181018
These are but a few research papers reporting on oxytocin's potential role in decreasing appetite, weight, and the phenomena of hyperinsulinemia and leptin resistance. Have hope!
P.S. Sasha used to be a hyperinsulin secreter (OGTT with insulin tested two years ago indicated that he had this common problem associated with HO). His last OGTT with insulin test at the end of December showed that he is no longer hypersecreting insulin- due in part to his weight loss from oxytocin?
For the normal (non-HO) person:
1. Low blood sugar (hypoglycemia) triggers the hypothalamus to signal the sense of hunger.
2. When food (let’s say, a slice of pizza) is available, the hungry person eats it and this raises blood sugar, satisfying the person and making energy available for the person.
3. The pancreas produces and sends out insulin to facilitate blood glucose uptake into the cells to be immediately used for energy. Excess glucose is stored in fat cells as free fatty acids for later use.
4. In the absence of food, hunger triggers the person to secrete corticosteroids to convert stored glucose (glycogen), proteins, fats and carbs to raise blood glucose.
5. Corticosteroids also act like a traffic cop for glucose, slowing the flow of glucose into the cell, and preventing blood glucose from dropping too quickly.
6. In sum, the normal person's hypothalamus behaves in a way to respond to the low blood sugars using the feedback loop between his/her corticosteroids and insulin, creating a balanced system: insulin makes it possible for glucose to be used for energy as needed and any extra glucose to be stored as free fatty acids to be saved for another time when energy is needed in the absence of food. This process makes if possible for a person’s weight to remain stable.
For the HO person with hyperinsulinemia (who also has AI, Adrenal Insufficiency):
1. Low blood sugar (hypoglycemia) triggers the hypothalamus to signal a sense of hunger.
2. When food is available (pizza), the HO/AI hungry person eats it and this raises blood sugar (same as above).
3. Insulin does its job by sending glucose into the working cells and fat storage cells. However, in the case of the HO person, there is an oversecretion of insulin in response to the amount of glucose in the blood. See* below #5 for the explanation why HO person may hypersecrete insulin.
3. Glucose leaves the blood quickly as soon as insulin arrives but insulin takes longer to clear from the blood. As long as insulin is still in the blood, free fatty acids (stored in fat cells) cannot be accessed or released in the blood for later use.
4. The HO/AI person feels hungry (again), eats in response to the hunger, and the cycle continues with the insulin never being cleared from the body and more fatty acids being stored/trapped in the fat cells (making the person fatter).
5. In the absence of food, corticosteroids are not available to convert stored glucose, proteins, fats, and carbs to raise blood glucose. Unlike the normal person who can utilize corticosteroids to raise the blood glucose levels under the stressful conditions of hunger, the HO/AI person’s blood glucose drops further. *This state of low blood glucose is physically stressful and it causes insulin to increase because demand for energy in cells is greater.
6. In this low blood sugar state, the HO/AI person feels hungrier and is driven to eat. If s/he eats (esp carbs), glucose spikes, insulin rises in response and stays elevated, glucose drops again, fatty acids cannot be accessed for energy and the person becomes fatter. This becomes the vicious cycle familiar to HO sufferers.
Role of Leptin:
Known as the “satiety hormone”, leptin, a hormone released from the fat cells located in adipose (fat) tissues, sends signals to the hypothalamus in the brain. This particular hormone helps regulate and alter long-term food intake and energy expenditure, not just from one meal to the next like insulin. The primary design of leptin is to help the body maintain its weight.
Because it comes from fat cells, leptin amounts are directly connected to an individual’s amount of body fat. When the body is functioning properly, excess fat cells will produce leptin, which will trigger the hypothalamus to lower the appetite, allowing the body to dip into the fat stores to feed itself which keeps the person at a normal, stable weight. Unfortunately, when someone is obese, that individual will have too much leptin in the blood. This can cause a lack of sensitivity to the hormone, a condition known as leptin resistance and the person’s appetite does not get lowered. Because the individual keeps eating, the fat cells produce more leptin to signal the feeling of satiety, leading to increased leptin levels, more leptin resistance, more weight gain, etc. Similarly, if a person decreases fat/calories (by dieting, for example), leptin will also decrease and appetite will increase. Leptin may be the reason why it is impossible to keep weight off in the long run after initially losing weight from a diet. Dieting may in fact, drive down leptin and drive UP appetite.
Between the vicious cycle of glucose, hyperinsulin secretion, overeating and weight gain, the weight maintaining function of leptin, and weight gaining effects of leptin resistance, it is not looking good for the sufferer of HO.
WHAT TO DO?
When it comes to an eating regimen, the low carbohydrate diet is known as one of the best choices for people with HO. By keeping the sugar levels from precipitously rising (and falling and this prevents the triggering of the glucose/insulin roller coaster), rapid weight gain can be stopped or slowed. Maintaining a more stable weight also prevents the overproduction of leptin and the development of leptin resistance.
Bariatric surgery and many drugs have been tried to find a cure and stop the scourge of HO but still, to my knowledge, this is still a work in progress.
So, where does oxytocin fit in as a possible therapeutic agent for HO, and in particular, hyperinsulinemia and leptin resistance?
1. Oxytocin may be an effective treatment against impaired leptin signaling or leptin resistance.
http://journal.frontiersin.org/article/10.3389/fendo.2015.00119/full
2. Oxytocin may cause increased sensitivity to satiety signals:
http://ajpregu.physiology.org/content/287/1/R87.short
3. Leptin targets a specific subpopulation of oxytocin neurons and that this action may be important for leptin’s ability to reduce body weight in both control and obese rats:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059625
4. Oxytocin and its analogs have multi-level effects in improving weight control, insulin sensitivity and insulin secretion, and that oxytocin has a potential role in treating obesity and diabetes:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658979/
5. Therapeutic levels of oxytocin may raise blood glucose levels: http://www.karger.com/Article/Abstract/181018
These are but a few research papers reporting on oxytocin's potential role in decreasing appetite, weight, and the phenomena of hyperinsulinemia and leptin resistance. Have hope!
P.S. Sasha used to be a hyperinsulin secreter (OGTT with insulin tested two years ago indicated that he had this common problem associated with HO). His last OGTT with insulin test at the end of December showed that he is no longer hypersecreting insulin- due in part to his weight loss from oxytocin?
Wednesday, February 15, 2017
72) A mystery explained: endocrinological bases of compulsive behaviors
In addition to my son's history of food obsession and food seeking (hyperphagia), Sasha has engaged in a peculiar habit of needing to acquire and sort things for a collection. Since the early days after tumor surgery, I noticed that we had an awfully large number of pens, pencils, erasers, and other various office supplies in our house that I know we didn't purchase. When I paid attention, I noticed that he had a way of organizing his collections in little plastic baggies which he kept hidden away in his desk. Sometimes he would be seen sorting and organizing them (sometimes even in the middle of the night). He was compelled to collect these office supplies (a lot of them!) and his compulsion was so strong that he even stole things from other people including classmates, teachers, and merchants.
Although we didn't need to have hundreds of pencils and pens in our house, we didn't mind that he wanted to collect office supplies. We DID mind that he resorted to stealing these items. It became clear to us after we admonished, lectured and disciplined him, that he was unable to control this behavior. It was then that I decided to conduct a survey to find out if this was a common behavior pattern among his craniopharyngioma cohorts. After conducting a survey, I received responses from 146 subjects and was astounded to learn that there was a high prevalence, 33-42%, of cranios who compulsively acquired non-food items. The rates increased to 41-51% when I filtered for cranios who had HO (hypothalamic obesity) and decreased to only 9-12% among cranios who did NOT have HO! Although I was investigating the specific compulsion of collecting and hoarding non-food items, I also received comments from some respondents that other compulsive behaviors including skin picking, ordering, needs for symmetry, etc. were also present.
Besides being relieved that my son wasn't the only one with a compulsive acquiring habit, I was fascinated that the prevalence was so high and that there was virtually no mention of it in the medical or psychiatric literature save for a couple of case study papers. I was also intrigued that the rates of compulsive acquiring increased among those who had HO and decreased significantly among those who did not have HO. What is the relationship between HO and compulsive acquiring? Why would collecting and hoarding non-food items be so much higher among cranios with HO compared to cranios without HO?
In the last 6 years since acting as a amateur endocrine researcher/mom, I have been totally fascinated by the endocrine underpinnings of my son's behavior. Who knew that our hormones control so much of who we are, how we feel, how we act, etc? After observing his peculiar collecting behaviors and learning about their existence in other cranios, I began to really wonder about the biological etiology of OCD and other compulsive behaviors. I proceeded to write a paper on it and hope to publish it in the medical/psychiatric literature to share this interesting finding.
Recently, I have felt extremely excited because I believe I have figured something out that solves a big mystery for me regarding the connection between compulsive behaviors and HO. I bet you can guess... in looking over the existing literature, I have found some clues that point to oxytocin as a significant player in explaining compulsive behaviors. Not only does it show up in research pertaining to autism and PWS (disorders known for obsessive compulsive behaviors and social impairment), it has been referenced in some papers on diabetes insipidus (DI). As you may know, DI is a disorder in which the brain no longer produces the anti-diuretic hormone, vasopressin. Like oxytocin, vasopressin is made in the hypothalamus and secreted by the posterior pituitary gland. Vasopressin must be replaced in people with DI or else they would be required to drink inordinate amounts of water to stay hydrated and to keep electrolytes in balance, or they would dessicate. Unlike vasopressin (as you know), oxytocin is typically NOT replaced.
Considering that both oxytocin and vasopressin are made and secreted from the same areas of the brain, it is interesting to read about the co-morbidity of DI and obsessive-compulsive behaviors. In these cases, might certain people with central DI also suffer from oxytocin imbalances/abnormalities to help explain their compulsivity? Here is a dated but fascinating report on nine cases examples of diabetes insipidus and "obsessional neuroses" (back in the day when psychoanalytic theory was alive and well!)
http://www.sciencedirect.com/science/article/pii/S0140673665910925
From a book chapter on childhood obsessional compulsive disorder:
https://books.google.com/books?hl=en&lr=&id=hEY0dmttheIC&oi=fnd&pg=PA208&dq=diabetes+insipidus+ocd&ots=ioSWj04uX2&sig=mls_uJV64JGoLWp7ODCHp8sjIEM#v=onepage&q=diabetes%20insipidus%20ocd&f=false
A paper on the role of central oxytocin in OCD and related normal behavior:http://www.sciencedirect.com/science/article/pii/0306453094900213
There may be other ways to show the connection between compulsive behaviors and HO hunger since oxytocin is likely to play an important role in mediating hunger and its associated stress. Using a psycho-endocrinological theory (which I just made up- finding evidence in the literature to support my theory is still a work in progress): Without oxytocin's ability to provide satiety, this drives up anxiety. In OCD, obsessions are the ruminative, anxious thoughts ("I will die if I touch germs") that plague the sufferer. Compulsions are the compensatory behaviors ("therefore I have to wash my hands 25 times") to relieve the sufferer of his/her anxiety. In the case of the HO sufferer who also compulsively acquires non-food, the obsession is hunger for food. Although the compulsion to collect non-food items may not be a direct compensation for their hunger, compulsions to acquire things (for example) may be a way for these oxytocin-impaired people to soothe themselves from their terrible pangs of hunger. Others may use other types of compulsive behaviors to find relief.
By the way, now that Sasha is taking oxytocin, he has stopped his compulsive acquiring of office supplies. He still tries to sneak food and money every once in a while, but it has greatly reduced in frequency since oxytocin.
I am excited to finish writing this paper in order to expose the prevalence of these co-morbid phenomena in the medical literature. Please feel free to comment and to share your observations especially if you believe you/your loved one also suffer from oxytocin deficiency (HO, DI without a thirst mechanism, PWS, autism) and compulsive behaviors.
Although we didn't need to have hundreds of pencils and pens in our house, we didn't mind that he wanted to collect office supplies. We DID mind that he resorted to stealing these items. It became clear to us after we admonished, lectured and disciplined him, that he was unable to control this behavior. It was then that I decided to conduct a survey to find out if this was a common behavior pattern among his craniopharyngioma cohorts. After conducting a survey, I received responses from 146 subjects and was astounded to learn that there was a high prevalence, 33-42%, of cranios who compulsively acquired non-food items. The rates increased to 41-51% when I filtered for cranios who had HO (hypothalamic obesity) and decreased to only 9-12% among cranios who did NOT have HO! Although I was investigating the specific compulsion of collecting and hoarding non-food items, I also received comments from some respondents that other compulsive behaviors including skin picking, ordering, needs for symmetry, etc. were also present.
Besides being relieved that my son wasn't the only one with a compulsive acquiring habit, I was fascinated that the prevalence was so high and that there was virtually no mention of it in the medical or psychiatric literature save for a couple of case study papers. I was also intrigued that the rates of compulsive acquiring increased among those who had HO and decreased significantly among those who did not have HO. What is the relationship between HO and compulsive acquiring? Why would collecting and hoarding non-food items be so much higher among cranios with HO compared to cranios without HO?
In the last 6 years since acting as a amateur endocrine researcher/mom, I have been totally fascinated by the endocrine underpinnings of my son's behavior. Who knew that our hormones control so much of who we are, how we feel, how we act, etc? After observing his peculiar collecting behaviors and learning about their existence in other cranios, I began to really wonder about the biological etiology of OCD and other compulsive behaviors. I proceeded to write a paper on it and hope to publish it in the medical/psychiatric literature to share this interesting finding.
Recently, I have felt extremely excited because I believe I have figured something out that solves a big mystery for me regarding the connection between compulsive behaviors and HO. I bet you can guess... in looking over the existing literature, I have found some clues that point to oxytocin as a significant player in explaining compulsive behaviors. Not only does it show up in research pertaining to autism and PWS (disorders known for obsessive compulsive behaviors and social impairment), it has been referenced in some papers on diabetes insipidus (DI). As you may know, DI is a disorder in which the brain no longer produces the anti-diuretic hormone, vasopressin. Like oxytocin, vasopressin is made in the hypothalamus and secreted by the posterior pituitary gland. Vasopressin must be replaced in people with DI or else they would be required to drink inordinate amounts of water to stay hydrated and to keep electrolytes in balance, or they would dessicate. Unlike vasopressin (as you know), oxytocin is typically NOT replaced.
Considering that both oxytocin and vasopressin are made and secreted from the same areas of the brain, it is interesting to read about the co-morbidity of DI and obsessive-compulsive behaviors. In these cases, might certain people with central DI also suffer from oxytocin imbalances/abnormalities to help explain their compulsivity? Here is a dated but fascinating report on nine cases examples of diabetes insipidus and "obsessional neuroses" (back in the day when psychoanalytic theory was alive and well!)
http://www.sciencedirect.com/science/article/pii/S0140673665910925
From a book chapter on childhood obsessional compulsive disorder:
https://books.google.com/books?hl=en&lr=&id=hEY0dmttheIC&oi=fnd&pg=PA208&dq=diabetes+insipidus+ocd&ots=ioSWj04uX2&sig=mls_uJV64JGoLWp7ODCHp8sjIEM#v=onepage&q=diabetes%20insipidus%20ocd&f=false
A paper on the role of central oxytocin in OCD and related normal behavior:http://www.sciencedirect.com/science/article/pii/0306453094900213
There may be other ways to show the connection between compulsive behaviors and HO hunger since oxytocin is likely to play an important role in mediating hunger and its associated stress. Using a psycho-endocrinological theory (which I just made up- finding evidence in the literature to support my theory is still a work in progress): Without oxytocin's ability to provide satiety, this drives up anxiety. In OCD, obsessions are the ruminative, anxious thoughts ("I will die if I touch germs") that plague the sufferer. Compulsions are the compensatory behaviors ("therefore I have to wash my hands 25 times") to relieve the sufferer of his/her anxiety. In the case of the HO sufferer who also compulsively acquires non-food, the obsession is hunger for food. Although the compulsion to collect non-food items may not be a direct compensation for their hunger, compulsions to acquire things (for example) may be a way for these oxytocin-impaired people to soothe themselves from their terrible pangs of hunger. Others may use other types of compulsive behaviors to find relief.
By the way, now that Sasha is taking oxytocin, he has stopped his compulsive acquiring of office supplies. He still tries to sneak food and money every once in a while, but it has greatly reduced in frequency since oxytocin.
I am excited to finish writing this paper in order to expose the prevalence of these co-morbid phenomena in the medical literature. Please feel free to comment and to share your observations especially if you believe you/your loved one also suffer from oxytocin deficiency (HO, DI without a thirst mechanism, PWS, autism) and compulsive behaviors.
Saturday, February 11, 2017
71) Medical scare... so grateful to our medical care- how do insurance coverages compare?
It's been quite a week. On Wednesday afternoon, Sasha had a sudden loss of his vision in which his vision became very blurred for about ten minutes then cleared a bit but stayed blurry. Sasha already has visual impairment from the optic nerve atrophy caused by his tumor and surgery back in 2011. He is able to correct his right eye to 20/100 (with glasses) but his left eye is uncorrectable at 20/360. Without his glasses, he is considered legally blind (right eye is 20/200 uncorrected) and with his glasses, he is considered "low vision." In any case, the sudden change in his vision was alarming and led us to bring him to the emergency department at the hospital. There, he had a CT scan to check for any large mass (his tumor has a tendency to regrow) or large brain bleed. Fortunately, the CT scan was reassuring and ruled out these problems but he still needed an MRI and an ophthalmological exam for more a more detailed view of what might be causing his vision changes. The very next day (yesterday), Sasha was offered a MRI followed by an appointment with the ophthalmologist. To our relief, the MRI and eye exam were also negative (NO news is GOOD news in the medical world). Although his vision has remained blurry and we still have no explanation for his vision changes, we are relieved to know that they are not caused by the scary problems my overly active imagination were conjuring up. Due to his atrophied optic nerve, we were told that sometimes there are changes to vision and that all we can do is "wait and see" if the vision changes back to its former state. We will also have his eyes checked by an optometrist in case his vision problems are refractory in nature and might be helped by corrective lenses.
In the last 6 years since Sasha's tumor diagnosis and surgery, I have felt so fortunate for the amazing medical care we have with our medical insurance and provider, Kaiser Permanente. In this recent situation, Sasha was treated in the emergency department, had a CT scan, MRI scan, ophthalmology exam, and was informed of the reassuring results- all in less than 24 hours!
Kaiser (the largest HMO in the US) is a major medical provider in California where we live and provides "one stop shopping" by offering comprehensive medical care all under one roof. In Northern California alone, there are 20 hospitals and 54 outpatient clinics totaling 8000 physicians in the region. All medical providers in all departments are connected under one system and use the same electronic medical records (for ease of referrals, communications, etc). As a Kaiser provider myself (psychologist), I find it very patient-friendly since my job is to focus solely on treating my patients. Unlike other medical providers who work in other types of clinics, I have absolutely no responsibilities to bill or collect fees or hassle with insurance matters.
As a very high maintenance patient, Sasha has truly reaped the many benefits from Kaiser- all of his physicians work in the same system and he has seen A LOT of them! Besides his regular pediatrician, he has had treatment by providers from the following specialities: emergency medicine, radiology, endocrinology, neurosurgery, neurology, physical therapy, speech therapy, occupational therapy, dermatology, nutrition, genetics, ophthalmology, psychiatry, pharmacy, otolaryngology, and sleep medicine/pulmonology. We have never had any problems whatsoever fighting for his care because whatever has been needed (referrals, medicines, treatments, equipment, etc.) for him has been granted swiftly and easily. When Kaiser has not been able to offer the care with its own providers, Kaiser has paid outside contractors (such as with his speech therapy, psychotherapy, overnight sleep studies). The only exception to this (ironically) has been oxytocin but that is because it is considered too experimental a drug to prescribe and is not in the Kaiser drug formulary. Besides the excellent care, I am an employee of Kaiser and I have the option for bargain-priced coverage: $70 comes out of my paycheck each month which covers myself and family for medical coverage. This includes NO cost for hospitalization, surgery, MRI, etc. (big ticket items) and other routine items like laboratory tests; $25 for emergency room visits; $10 for prescription drugs; $10 for all other outpatient appointments. There is never any deductible. After talking to a friend this morning who has had to fight tooth and nail for her medical care from the insurance company while still dealing with a high deductible AND high co-pays, there is just no comparison between her experience and ours. She even shared an absurd story with me about bringing her son into the emergency department because he cut himself on his thumb by accident- he didn't need stitches as they feared he would- he needed only a butterfly bandage. Cost of visit= $2,000! She will probably end up having to pay for 40% of that visit, $800 for a bandage, ugh!!
I am VERY grateful to Kaiser (both as my employer and my health insurance provider) for the excellent care Sasha has received. I know that others are not as fortunate with health coverage and I think this is WRONG. In our current political climate, there is much talk now about repealing/replacing the Affordable Care Act (Obamacare). Irrespective of one's political opinion about what is best to do in regards to our country's health care, most would agree that having excellent and affordable health care is a MUST especially if one has serious and chronic medical conditions such as Sasha.
If you care to share about your satisfaction with your medical care, medical insurance coverage, and costs, I would be very interested in learning about it. Please write your comments below, thank you!
In the last 6 years since Sasha's tumor diagnosis and surgery, I have felt so fortunate for the amazing medical care we have with our medical insurance and provider, Kaiser Permanente. In this recent situation, Sasha was treated in the emergency department, had a CT scan, MRI scan, ophthalmology exam, and was informed of the reassuring results- all in less than 24 hours!
Kaiser (the largest HMO in the US) is a major medical provider in California where we live and provides "one stop shopping" by offering comprehensive medical care all under one roof. In Northern California alone, there are 20 hospitals and 54 outpatient clinics totaling 8000 physicians in the region. All medical providers in all departments are connected under one system and use the same electronic medical records (for ease of referrals, communications, etc). As a Kaiser provider myself (psychologist), I find it very patient-friendly since my job is to focus solely on treating my patients. Unlike other medical providers who work in other types of clinics, I have absolutely no responsibilities to bill or collect fees or hassle with insurance matters.
As a very high maintenance patient, Sasha has truly reaped the many benefits from Kaiser- all of his physicians work in the same system and he has seen A LOT of them! Besides his regular pediatrician, he has had treatment by providers from the following specialities: emergency medicine, radiology, endocrinology, neurosurgery, neurology, physical therapy, speech therapy, occupational therapy, dermatology, nutrition, genetics, ophthalmology, psychiatry, pharmacy, otolaryngology, and sleep medicine/pulmonology. We have never had any problems whatsoever fighting for his care because whatever has been needed (referrals, medicines, treatments, equipment, etc.) for him has been granted swiftly and easily. When Kaiser has not been able to offer the care with its own providers, Kaiser has paid outside contractors (such as with his speech therapy, psychotherapy, overnight sleep studies). The only exception to this (ironically) has been oxytocin but that is because it is considered too experimental a drug to prescribe and is not in the Kaiser drug formulary. Besides the excellent care, I am an employee of Kaiser and I have the option for bargain-priced coverage: $70 comes out of my paycheck each month which covers myself and family for medical coverage. This includes NO cost for hospitalization, surgery, MRI, etc. (big ticket items) and other routine items like laboratory tests; $25 for emergency room visits; $10 for prescription drugs; $10 for all other outpatient appointments. There is never any deductible. After talking to a friend this morning who has had to fight tooth and nail for her medical care from the insurance company while still dealing with a high deductible AND high co-pays, there is just no comparison between her experience and ours. She even shared an absurd story with me about bringing her son into the emergency department because he cut himself on his thumb by accident- he didn't need stitches as they feared he would- he needed only a butterfly bandage. Cost of visit= $2,000! She will probably end up having to pay for 40% of that visit, $800 for a bandage, ugh!!
I am VERY grateful to Kaiser (both as my employer and my health insurance provider) for the excellent care Sasha has received. I know that others are not as fortunate with health coverage and I think this is WRONG. In our current political climate, there is much talk now about repealing/replacing the Affordable Care Act (Obamacare). Irrespective of one's political opinion about what is best to do in regards to our country's health care, most would agree that having excellent and affordable health care is a MUST especially if one has serious and chronic medical conditions such as Sasha.
If you care to share about your satisfaction with your medical care, medical insurance coverage, and costs, I would be very interested in learning about it. Please write your comments below, thank you!
Monday, February 6, 2017
70) Over-expression of oxytocin= William's Syndrome
Poor Sasha is home sick with a stomach bug today. While he naps, I peruse the internet for interesting articles. I am preparing to finish up a paper on the phenomenon of compulsive acquiring of non-food items and HO (particularly in association with the hyperphagic component of HO) in craniopharyngioma. As I read up on the various connections between oxytocin, social impairment, PWS, autism, compulsive behaviors, hyperphagia, etc. etc., I stumble upon an absolutely fascinating syndrome (William's Syndrome). This is a rare genetic disorder in which oxytocin is over-expressed. I learn from my reading that it is characterized by medical problems, including cardiovascular disease, developmental delays, and learning disabilities. Most people with WS have an average IQ of 69 (70 is considered two standard deviations below the normal 100 IQ). However, people with WS have an extraordinary command of language (with respect to their IQ) AND impressive social motivation (friendliness). Here are some articles I found on William's Syndrome:
A (non-academic) story about WS printed in the New York Times Magazine:
http://www.nytimes.com/2007/07/08/magazine/08sociability-t.html
An article about WS from the Salk Institute newsletter:
http://www.salk.edu/news-release/trust-hormone-oxytocin-found-at-heart-of-rare-genetic-disorder/
And for you diehard scientists, here are some academic papers on WS:
1. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0038513
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330921/
Finally, a very interesting paper on two mirror-image genetic disorders: PWS and WS
5. PWS and Williams Syndrome: http://www.aaiddjournals.org/doi/pdf/10.1352/0895-8017%281999%29104%3C0158%3ARBPPIW%3E2.0.CO%3B2
As I read these papers, I am intrigued by what we can learn from studying various disorders and from multiple angles... We can see how oxytocin deficiency may be expressed by the overlapping phenotypic behaviors among syndromes/disorders including PWS and autism. Both disorders may exhibit symptoms including repetitive and restrictive behaviors, self-injurious behaviors, language impairment, and communication difficulties (among others). Those with PWS and craniopharyngioma (called "acquired PWS" in the PWS community) share some common phenotypic traits including obesity/hyperphagia, hypogonadism, growth hormone deficiency, and compulsive behaviors. The social impairment or lack of social motivation observed in craniopharyngioma survivors is another behavior that is shared by those with PWS and autism and is likely a result (or at least correlated with) oxytocin deficiency.
What can we learn from William's Syndrome then? Personally, I find it very interesting that the over-expression of oxytocin is implicated for the high level of friendliness/sociability and language abilities among these folks. Maybe William's Syndrome and its over-expression of oxytocin can provide more evidence about the important role of oxytocin in social motivation and teach us more about those disorders which under-express oxytocin.
A (non-academic) story about WS printed in the New York Times Magazine:
http://www.nytimes.com/2007/07/08/magazine/08sociability-t.html
An article about WS from the Salk Institute newsletter:
http://www.salk.edu/news-release/trust-hormone-oxytocin-found-at-heart-of-rare-genetic-disorder/
And for you diehard scientists, here are some academic papers on WS:
1. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0038513
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330921/
Finally, a very interesting paper on two mirror-image genetic disorders: PWS and WS
5. PWS and Williams Syndrome: http://www.aaiddjournals.org/doi/pdf/10.1352/0895-8017%281999%29104%3C0158%3ARBPPIW%3E2.0.CO%3B2
As I read these papers, I am intrigued by what we can learn from studying various disorders and from multiple angles... We can see how oxytocin deficiency may be expressed by the overlapping phenotypic behaviors among syndromes/disorders including PWS and autism. Both disorders may exhibit symptoms including repetitive and restrictive behaviors, self-injurious behaviors, language impairment, and communication difficulties (among others). Those with PWS and craniopharyngioma (called "acquired PWS" in the PWS community) share some common phenotypic traits including obesity/hyperphagia, hypogonadism, growth hormone deficiency, and compulsive behaviors. The social impairment or lack of social motivation observed in craniopharyngioma survivors is another behavior that is shared by those with PWS and autism and is likely a result (or at least correlated with) oxytocin deficiency.
What can we learn from William's Syndrome then? Personally, I find it very interesting that the over-expression of oxytocin is implicated for the high level of friendliness/sociability and language abilities among these folks. Maybe William's Syndrome and its over-expression of oxytocin can provide more evidence about the important role of oxytocin in social motivation and teach us more about those disorders which under-express oxytocin.
Sunday, February 5, 2017
69) Gaining "density"- Does oxytocin help muscle development too?
Sasha has been having relatively good (disaster-free) weeks. He had the incident of taking the extra graham crackers a couple of weeks ago and overindulged in some Girl Scout cookies that were offered to him yesterday, but all in all, he's been pretty good about not sneaking extra food. He's been enjoying his friendships with two boys with whom he plays MTG cards every Saturday and at lunchtime during the school week. As a matter of fact, Sasha is over at his friend's house right now as I am writing this! Weirdly, I am having some free time to myself. Did I mention it is weird? My daughter is 11 and has always had a very busy social life with her friends and activities but we have always had to find ways to entertain Sasha especially on the weekends. I am getting a little taste of what it must feel like for parents of typical kids as they come into their tweens/teens. I must admit, it is very nice! I am enjoying the increased free time to myself but most of all, I am happy for Sasha that he has a friend with whom to hang out on the weekends. I also met his mom over lunch a few days ago and learned about how much they have in common in their personalities. We plan to have A and mom over for dinner next weekend and look forward to our growing friendship with the family.
Meanwhile, we are noticing that Sasha continues to put on weight (but is also growing taller so his BMI is persisting the same 89-90% range). I was curious about whether or not oxytocin interacts with testosterone. After losing weight steadily since September 1, Sasha started to gain weight one week after he began his very first testosterone dose at the end of December. In fact, there is some evidence of oxytocin's role in muscle regeneration as I found in PubMed:
I don't know about the interaction (if any) between testosterone and oxytocin but I can't help but wonder if the addition of the testosterone (in combination with the oxytocin he has already been taking) is responsible for this weight gain. I have noticed that his upper arms are looking and feeling more lean, solid and muscular. While testosterone is commonly known to increase muscle mass, I wanted to see the research data for myself and found several articles which describe the change from fat to muscle in replacing testosterone in hypogonadal men:
If it is true that testosterone contributes to increased muscle mass and decreased fat mass and that oxytocin contributes to increase bone density and muscle regeneration, might it be that Sasha's weight gain is well explained by his body's overall increasing density?
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