Posted by ed_uk2010 on February 15, 2015, at 16:28:37
In reply to Re: Depression vs. 'negative' psychotic symptoms » ed_uk2010, posted by Tomatheus on February 15, 2015, at 14:50:28
Hi Tom,
>Thank you for responding to what I've written again and for offering your thoughts on my responses to your questions.
You're very welcome, I enjoy writing to you.
>It also seems that vitamin D may boost tyrosine hydroxylase activity, leading to increased dopamine synthesis, which offers a possible explanation as to why vitamin D might have influenced my psychotic symptoms in the way that it seemed to.
That's very interesting. I didn't know that so I just looked into it a little. Thanks for the information.
Now for some speculation!! :)
I was thinking, unless vitamin D deficiency is actually beneficial for psychosis by reducing tyrosine hydroxylase activity, which seems a little unlikely, it also seems improbable that therapeutic dose supplementation in the treatment of biochemically proven deficiency would be psychologically harmful - supplementation should help to normalise rather than disrupt your metabolic functions. Even in the unlikely event that vitamin D deficiency actually is antipsychotic, low dose oral supplementation would presumably lead to a very gradual change in symptoms, following the gradual increase in serum levels.
I can think of some reasons why your worsened psychotic symptoms might perhaps have been due to some other cause:
1. At the doses of D3 you were taking ie. not mega-doses, it would take weeks or months to fully treat the deficiency. I would therefore not expect any rapid change in symptoms. During the early stage of treatment, your vitamin D level was probably still sub-normal and increasing very gradually. A 300 000 unit single dose can often normalise D3 levels within a week, but you didn't do that.
2. D3 (cholecalciferol) is a pro-hormone. Except in huge overdose, toxicity is uncommon because it requires a two-step metabolic process to produce the active substance, 1,25-dihydroxy D3. As a rule, the body only produces as much active vitamin D as it needs.
First, vitamin D3 (cholecalciferol) is converted to 25-hydroxy D3 (calcidiol) in the liver.. and then 25-hydroxy D3 is converted to 1,25-dihydroxy D3 (calcitriol) in the kidney. The body does not produce more active calcitriol than it needs unless it is subject to a massive vitamin D overdose, or because of some physiological abnormality of vitamin D metabolism, as occurs in the disease sarcoidosis.
Patients with chronic kidney failure need to take active vitamin D because their diseased kidneys cannot product enough, calcitriol itself can be used, or more commonly a related synthetic such as alfacalcidol or paricalcitol. These active vitamin Ds require much more careful dosing than standard supplemental D3 because there is no safety net; they are already active and too much will cause toxicity. None of these active Ds are suitable for the treatment of simple deficiency; there are only used in chronic renal failure. The latest, paricalcitol is especially useful for the bone disease which occurs in kidney failure.
3. Massive vitamin D overdose causes symptoms, in some cases, which appear to be due to hypercalcaemia. Toxicity may require several hundreds of thousands, or millions of units. Reducing calcium levels appears to relieve the symptoms. I doubt that overdose would increase tyrosine hydroxylase levels to above normal levels.... It's often possible to inhibit enzyme activity with drugs, but stimulating it to supra-normal levels is difficult, so many factors are involved.
4. Those with primary hyperparathyroidism and sarcoidosis are often sensitive to vitamin D supplements. PH is most common in post-menopausal women. If you had sarcoid you'd probably have symptoms. Even so, a blood calcium level may be advisable during long term vitamin D supplementation if any unexpected symptoms develop. Your doctor can easily measure your calcium at the same time as your vitamin D level (in general, 25-hydroxy D3 is measured). Serum calcium is a very cheap and routine test. Much more so than vitamin D levels.
Symptoms of hypercalcaemia (elevated calcium) include depressive symptoms, fatigue, abdominal discomfort 'stomach acid', constipation and bone/join aches and pains. I seriously doubt you're hypercalcaemic, but there's little reason not to check the next time you have a blood test, particularly considering your symptoms.
>21.9 ng/mL.
>I will see if I can do that.Exeellent. See if you can get a D3 level and a calcium level (often done as part of a 'bone panel' including phosphate, albumin and alk phos).
Also, consider asking about a CBC *with* differential, an ESR and a thyroid panel (TSH and fT4, or just TSH for screening)... plus anything your doctor wants to check. Everyone on antipsychotics should have occasional fasting glucose tests and plasma lipids. All of the above tests are fairly routine, nothing obscure.
>my white blood cells always come back as being elevated....
I noticed the private lab did a CBC without differential. All CBCs include a differential WBC count here. I think that's what your PCP would do too. A mildly elevated WCC on its own is not particular revealing. If it persists, follow up includes a repeat WCC with differential. If abnormal, a blood smear should be performed by the lab for microscopic analysis. In toxoplasmosis, the usual finding, I believe, is an elevated WCC due to lymphocytosis, with atypical lymphocytes visible on the smear. A similar picture is seen in infectious mononucleosis. These finding are typical during the acute infection, I don't know about chronically. Still, the same process can still be followed for initial investigation of an abnormal WCC on CBC.
>but can't T. gondii also be caught by eating undercooked meat?
I think so, yes.
>I tend to have a low tolerance for agitation and irritability.
I can imagine. Any type of aggressive irritation leads to trouble.
Take care.
poster:ed_uk2010
thread:1076218
URL: http://www.dr-bob.org/babble/20150129/msgs/1076679.html