I haven't used the blog as a venting platform in a while so please indulge me now.
In sum, Sasha was doing pretty well through the end of the holiday season and seemed to be quite happy in the beginning of January- he has been developing his friendship with his buddy, A, and his health has been good (except for a regular cold and the weird crisis with his blurry vision a few weeks ago). His BMI had reached the lowest ever after his continuous weight loss over the previous four months. He did start to gain weight at the end of the December which happened to coincide with the start of testosterone. I wasn't concerned about the weight gain since his BMI has been kept steady by the increase in his height (currently he is 5'9.25" and 158 pounds or 175.9 cm and 72 kg).
However, by mid February, I started to also notice the return of some of his food intensity. I wondered if he needed to change his dose of oxytocin so I raised it from 6 iu to 9 iu starting on Feb 17. During this time, his food seeking seemed to worsen. We saw some signs of empty snack food wrappers in his room (that were somehow snuck out of our locked kitchen cabinet... not sure how?) and I also noticed that he was more preoccupied with food and had more emotional meltdowns than he had had in prior months. It was stressful and painful to watch the regression and to be reminded of how he used to be but the telltale signs were there. After about 10 days on the 9 iu oxytocin, we returned him to 6 iu on Feb. 27. To make matters worse, I just received news from his case manager teacher at school that kids have been complaining about "missing cards" at lunch time. No evidence has appeared to apprehend Sasha but the suspicion rests on Sasha for his history of taking cards. Although there is no proof that he took the cards recently, I'm sure he has taken them in the past and perhaps he took them recently or perhaps it is merely the bad reputation he has established for himself, alas.
Things got even worse when he took a walk yesterday with our friend, M, and her three dogs. While walking down the street by the supermarket, he reported to her that he had a sudden urge to pee. She had no choice but to let him go into the store and because she had three dogs with her, she also had no choice but to let him into the store unsupervised. Well, of course it was the perfect opportunity for Sasha to steal food. When he came home, his dad searched his pockets and found a large handful of candy bars in his pocket. Sure enough, he admitted that the temptations were too strong when he saw the candy and he succumbed to taking the candy. You can't imagine the disappointment we felt. He was immediately sent to his room and took to his bed, falling into a convenient slumber to temporarily block out his shame and self-loathing. As his parents, we were left feeling very much raw with emotion- angry, powerless, frustrated, demoralized, and yes, very discouraged.
It appears that he has regressed from his prior state of improved satiety and decreased food intensity and food seeking. The behaviors we have seen lately resemble what we used to experience before oxytocin took effect: preoccupation with food, evidence of food sneaking, and emotional meltdowns over food. WHY? I wish we knew. After picking myself off the floor and licking my wounds after this disappointing week, I had no choice but to put on my detective hat again in search of answers in order to get us back on track.
As far as we know, the only changes to his lifestyle since we've observed these worsening behaviors have to do with his medication regimen where one hormone was added, one hormone went missing, and another hormone was (temporarily) increased and then returned to its original dose. The few clues I have about the changes in Sasha have led me to explore the involvement of:
1. skipping melatonin for about 4 weeks in mid- Jan to Feb. 19 (this was entirely by default- we ran out and kept forgetting to order more).
2. adding testosterone starting Dec 21 (after continuous weight loss from Sept 1 to Dec 21, he began to gain weight almost exactly one week after starting T).
3. increasing oxytocin from 6 iu to 9 iu for 10 days starting on Feb. 17 (this period of time seemed to be associated worsening food intensity and moodiness but it is hard to tell if this is causative, correlative, or just my imagination?)
Through some networking with oxytocin researchers (special shout out to Dr. Sue Carter of the Kinsey Institute), it was brought to my attention that melatonin is another hormone that is instrumental not only in regards to regulating circadian rhythm for sleep, but also for other important homeostatic functions.
Some papers on the deficiency of melatonin among survivors of craniopharyngioma:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715212/
2. http://www.eje-online.org/content/170/6/873.full.pdf
A reduction of melatonin production has been shown to induce insulin resistance, glucose intolerance, sleep disturbance, metabolic circadian disorganization, all of which leads to obesity. Once again, its mechanism is complex and beyond my understanding but endogenous melatonin secretion is something that appears to be lacking due perhaps to the damage to the suprachiasmatic nuclei of the hypothalamus (the area that regulates melatonin secretion by the pineal gland).
While Sasha has always taken 6 mg per night of melatonin, he neglected this important hormone for about 4 weeks after we ran out and kept forgetting to order more! We know that the hypothalamic damage to his brain affects his ability to regulate his circadian rhythm and that he suffers from chronic sleep disruption. Many cranios suffer from disrupted night time sleep AND day time somnolence. With melatonin replacement, he optimized his sleeping at night and maintaining wakefulness during the day. With some reflection and after restarting his nightly dose of melatonin, he did admit that his night time sleep quality/quantity was worse during the time he was not taking melatonin. Could it be that skipping the four weeks or so of melatonin contributed to the cause of his metabolic and subsequent behavioral regression? What other hormones might be affected by his 4-week-long neglect of taking melatonin?
Some papers on melatonin's role in metabolic health:
1. https://www.hindawi.com/journals/ije/2015/591729/
2. http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.2012.02410.x/full
3. https://link.springer.com/article/10.1007/s11154-009-9117-5
A paper describing melatonin deficiency and dysfunction:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354573/
As for the addition of testosterone- from what I gather and as I've mentioned before, I expect that it increases muscle mass, bone density, and promotes sexual development, etc. What I don't know is how much/if adding T affects the balance of his other hormones. Does adding T affect oxytocin and vice versa? Does T interact with melatonin or lack thereof? Does adding T affect other hormones, his mood, impulse control, appetite, etc.? Could it be that it makes him more temperamental, impulsive and hungry (aren't these stereotypes of teenage boys?) possibly causing increased food seeking? Who knows?!
As for what appeared to be his worsening symptoms for the 10 days when we raised his oxytocin to 9 iu (to confuse things more- for the first two days during his 10 day stint of 9 iu oxytocin dose, he wasn't taking melatonin and for the remaining 8 days, he started back at his usual 6 mg dose)- who knows? We did try increasing the oxytocin once before from 6 to 9 iu and it also seemed to worsen his behaviors. Perhaps this just confirms that 9 iu is NOT a helpful dose for Sasha. On the other hand, he wasn't on testosterone before when he was tried on 9 iu of oxytocin.
Today Sasha's weekly Na test showed us that (despite the increase of his food seeking), he LOST a significant amount of weight, 1.8 kg (5 pounds) in the past 7 days! Why? Was it the lowering of his oxytocin dose back to 6 iu? Was it the combination of being on the original lower oxytocin dose along with his resuming his nightly melatonin dose (first time both meds were taken together at their original dose since mid-January)?
Questions I ask:
1. Should I try to change the dose of oxytocin- higher or lower than his 6 iu dose?
2. Should his melatonin dose stay at 6 mg or go lower, perhaps as low as .5 mg (as I've read in some papers about the physiologic dose of melatonin)?
3. What other hormones might need adjusting now?
4. Did the subtraction of melatonin during the 4 weeks from mid-Jan to mid-Feb have anything to do with his weight gain and intensified food focus?
My weary head is spinning....managing replacement hormones IS like herding cats!
So while I fumble clumsily to try to grasp at the two most humbling tasks of my lifetime: 1) raising a child with cranionpharyngioma and 2) being a blind pioneer of this oxytocin experiment- I am humbled to my core. My utter desperation for a solution to the problem of HO and hyperphagia forced me to try this experiment and I cannot go back now after tasting a bit of normalcy and seeing that there IS hope for HO.
Our recent experience with this regression makes me think about a powerful book (Flowers for Algernon) I read in high school. In the book, the intellectually disabled protagonist (Charlie) undergoes an experimental surgery which greatly increases his intelligence to a genius level. With his newly acquired intelligence, Charlie's life expands and he ends up having many new experiences (not all good). At the peak of his intellectual power, Charlie ends up detecting a grave flaw made by the scientist who created the experiment. Sure enough, the lab mouse (Algernon) who was the test animal for this experiment eventually loses his intelligence and dies. It is a foreshadowing for what is to become of Charlie; he eventually regresses back to his lower-intelligent self. Of course, I shudder to think of Sasha ending up like Charlie in the story, permanently regressed back to his HO Monster self.
With some patience, luck, and help, I hope to regain our lost footing and to get back on track. I welcome any feedback, suggestions, info on illuminating studies, anecdotal information, and any ideas about what could be contributing to this (hopefully temporary) setback.
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