![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 28. This is the beginning of the thread.
Posted by linkadge on April 1, 2003, at 15:47:22
Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
Thanks in advance.
Linkadge
Posted by Larry Hoover on April 1, 2003, at 15:58:06
In reply to Any cheap effective anticortisols out there, posted by linkadge on April 1, 2003, at 15:47:22
> Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
>
> Thanks in advance.
>
> LinkadgeVitamin A, zinc, gingko biloba, and acetyl l-carnitine.
Posted by JLx on April 1, 2003, at 20:17:07
In reply to Any cheap effective anticortisols out there, posted by linkadge on April 1, 2003, at 15:47:22
> Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
8 hours of sleep per night -- very cheap. :)
I also suggest the book "The Cortisol Connection" by Shawn Talbott for many other ideas.
Posted by Ritch on April 1, 2003, at 23:06:44
In reply to Re: Any cheap effective anticortisols out there, posted by Larry Hoover on April 1, 2003, at 15:58:06
> > Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
> >
> > Thanks in advance.
> >
> > Linkadge
>
> Vitamin A, zinc, gingko biloba, and acetyl l-carnitine.
>Larry, given that Vitamin A has anti-cortisol activity would Cod Liver Oil be a better source of EPA than regular fish oil?
Posted by Larry Hoover on April 2, 2003, at 8:32:17
In reply to Re: Any cheap effective anticortisols out there » Larry Hoover, posted by Ritch on April 1, 2003, at 23:06:44
> > > Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
> > >
> > > Thanks in advance.
> > >
> > > Linkadge
> >
> > Vitamin A, zinc, gingko biloba, and acetyl l-carnitine.
> >
>
> Larry, given that Vitamin A has anti-cortisol activity would Cod Liver Oil be a better source of EPA than regular fish oil?I wouldn't make cod liver oil my only source of omega-3s, but it would be a good additional source. Recent reports of bone density problems associated with vitamin A supplements make me wonder about just how safe pre-formed vitamin A really is. Beta-carotene is converted to vitamin A as needed, so it's probably safer. A moderate dose of cod liver oil would probably be safe.
Posted by Ritch on April 2, 2003, at 9:59:18
In reply to Re: Any cheap effective anticortisols out there, posted by Larry Hoover on April 2, 2003, at 8:32:17
> > > > Is anyone aware of a nutrient or vitamin or something relativly cheep that reduces cortisol?
> > > >
> > > > Thanks in advance.
> > > >
> > > > Linkadge
> > >
> > > Vitamin A, zinc, gingko biloba, and acetyl l-carnitine.
> > >
> >
> > Larry, given that Vitamin A has anti-cortisol activity would Cod Liver Oil be a better source of EPA than regular fish oil?
>
> I wouldn't make cod liver oil my only source of omega-3s, but it would be a good additional source. Recent reports of bone density problems associated with vitamin A supplements make me wonder about just how safe pre-formed vitamin A really is. Beta-carotene is converted to vitamin A as needed, so it's probably safer. A moderate dose of cod liver oil would probably be safe.
>
>
Thanks Larry, hate to bug you one more time, but you mentioned Gingko Biloba as an anti-cortisol agent. Could you elaborate some about that? I know Gingko is used for alertness, which I could use more of. thanks for any info.
Posted by falconman on April 2, 2003, at 11:07:03
In reply to Any cheap effective anticortisols out there, posted by linkadge on April 1, 2003, at 15:47:22
Hi,
I've heard siberian ginseng can be quite effective. Don't know what anyone else thinks about this?
Peace
Mark
Posted by jemma on April 2, 2003, at 11:50:49
In reply to Re: Any cheap effective anticortisols out there, posted by falconman on April 2, 2003, at 11:07:03
Rhodiola rosea has also been shown to lower cortisol levels.
- jemma
Posted by Ron Hill on April 2, 2003, at 12:33:29
In reply to Re: Any cheap effective anticortisols out there, posted by jemma on April 2, 2003, at 11:50:49
Hi Jemma,
> Rhodiola rosea has also been shown to lower cortisol levels.
Have you tried it? If so, do you still take it?
-- Ron
Posted by Larry Hoover on April 2, 2003, at 13:35:51
In reply to Re: Any cheap effective anticortisols-Gingko? » Larry Hoover, posted by Ritch on April 2, 2003, at 9:59:18
> Thanks Larry, hate to bug you one more time, but you mentioned Gingko Biloba as an anti-cortisol agent. Could you elaborate some about that? I know Gingko is used for alertness, which I could use more of. thanks for any info.
>Somebody else posted a link a few weeks or so ago, with excellent graphs showing cortisol reduction after gingko treatment. Anybody save the link?
Lar
Posted by Larry Hoover on April 2, 2003, at 14:33:22
In reply to Re: Any cheap effective anticortisols-Gingko? » Larry Hoover, posted by Ritch on April 2, 2003, at 9:59:18
> Thanks Larry, hate to bug you one more time, but you mentioned Gingko Biloba as an anti-cortisol agent. Could you elaborate some about that? I know Gingko is used for alertness, which I could use more of. thanks for any info.
>Damn. I can't find it. There was a recent posting that had an excellent graphical representation of the decrease in cortisol.....
Well, here's some supportive evidence:
Life Sci 1998;62(25):2329-40
Effect of chronic administration of Ginkgo biloba extract or Ginkgolide on the hypothalamic-pituitary-adrenal axis in the rat.Marcilhac A, Dakine N, Bourhim N, Guillaume V, Grino M, Drieu K, Oliver C.
Laboratoire de Neuroendocrinologie Experimentale, INSERM U 297, Institut Jean Roche, Faculte de Medecine Secteur Nord, Marseille, France.
The hypersecretion of glucocorticoids during exposure to various stressors may induce or worsen pathological states in predisposed subjects. Therefore it is of interest to evaluate drugs able to reduce glucocorticoid secretion. It has recently been shown that chronic administration of a Ginkgo biloba extract (EGb 761) inhibits stress-induced corticosterone hypersecretion through a reduction in the number of adrenal peripheral benzodiazepine receptors. The present study was designed to analyze the effect of EGb 761 and one of its components, Ginkgolide B on the biosynthesis and secretion of CRH and AVP, the hypothalamic neurohormones that regulate the pituitary-adrenal axis. Chronic administration of EGb 761 (50 or 100 mg/kg p.o. daily for 14 days) reduced basal corticosterone secretion and the subsequent increase in CRH and AVP gene expression. Under the same conditions, surgically-induced increase in CRH secretion was attenuated while the activation of CRH gene expression, ACTH and corticosterone secretion following insulin-induced hypoglycemia remained unchanged. Chronic i.p. injection of Ginkgolide B reduced basal corticosterone secretion without alteration in the subsequent CRH and AVP increase. However, the stimulation of CRH gene expression by insulin-induced hypoglycemia was attenuated by Ginkgolide B. These data confirm that the administration of EGb 761 and Ginkgolide B reduces corticosterone secretion. In addition, these substances act also at the hypothalamic level and are able to reduce CRH expression and secretion. However the latter effect appears to be complex and may depend upon both the nature of stress and substance (Ginkgolide B or other compounds of EGb 761).
Cell Mol Biol (Noisy-le-grand) 2002 Sep;48(6):633-9Use of ginkgolide B and A ginkgolide-activated response element to control gene transcription: example of the adrenocortical peripheral-type benzodiazepine receptor.
Amri H, Drieu K, Papadopoulos V.
Department of Cell Biology, Georgetown University Medical Center, Washington, DC, USA.
Identification of the molecular switch controlling glucocorticoid synthesis might facilitate the development of pharmacological tools to control circulating cortisol levels. The transport of cholesterol from intracellular sources to the inner mitochondrial membrane represents the rate-determining step in the cascade of reactions leading to cortisol synthesis. A key element in this step is the peripheral-type benzodiazepine receptor (PBR). Several studies have indicated the beneficial effects of Ginkgo biloba on memory and stress control. Using pharmacological, biochemical and proteomic methods, we demonstrated that the standardized Ginkgo biloba extract EGb 761 and its isolated component ginkgolide B (GKB) inhibit PBR ligand binding and protein expression, resulting in decreased serum corticosterone levels. We further demonstrated that EGb 761- and GKB-induced inhibition of PBR protein is preceded by a decrease in mRNA-levels due to transcriptional suppression of PBR gene expression. Further studies indicated that the action of GKB is mediated by a transcription factor binding to the PBR gene promoter, thereby regulating PBR gene expression. These data indicate that EGb 761-induced inhibition of glucocorticoid production is due to specific transcriptional suppression of the adrenal PBR gene by GKB, and suggest that EGb 761 and GKB might serve as pharmacological tools to control excess glucocorticoid formation.
Curr Drug Targets 2000 Jul;1(1):25-58Ginkgo biloba extract (EGb 761) and CNS functions: basic studies and clinical applications.
DeFeudis FV, Drieu K.
Institute for BioScience, 153 West Main Street, Westboro, MA 01581, USA. defeudi@prime-x.net
The effects of EGb 761 on the CNS underlie one of its major therapeutic indications; i.e., individuals suffering from deteriorating cerebral mechanisms related to age-associated impairments of memory, attention and other cognitive functions. EGb 761 is currently used as symptomatic treatment for cerebral insufficiency that occurs during normal ageing or which may be due to degenerative dementia, vascular dementia or mixed forms of both, and for neurosensory disturbances. Depressive symptoms of patients with Alzheimer's disease (AD) and aged non-Alzheimer patients may also respond to treatment with EGb 761 since this extract has an "anti-stress" effect. Basic and clinical studies, conducted both in vitro and in vivo, support these beneficial neuroprotective effects of EGb 761. EGb 761 has several major actions; it enhances cognition, improves blood rheology and tissue metabolism, and opposes the detrimental effects of ischaemia. Several mechanisms of action are useful in explaining how EGb 761 benefits patients with AD and other age-related, neurodegenerative disorders. In animals, EGb 761 possesses antioxidant and free radical-scavenging activities, it reverses age-related losses in brain alpha 1-adrenergic, 5-HT1A and muscarinic receptors, protects against ischaemic neuronal death, preserves the function of the hippocampal mossy fiber system, increases hippocampal high-affinity choline uptake, inhibits the down-regulation of hippocampal glucocorticoid receptors, enhances neuronal plasticity, and counteracts the cognitive deficits that follow stress or traumatic brain injury. Identified chemical constituents of EGb 761 have been associated with certain actions. Both flavonoid and ginkgolide constituents are involved in the free radical-scavenging and antioxidant effects of EGb 761 which decrease tissue levels of reactive oxygen species (ROS) and inhibit membrane lipid peroxidation. Regarding EGb 761-induced regulation of cerebral glucose utilization, bilobalide increases the respiratory control ratio of mitochondria by protecting against uncoupling of oxidative phosphorylation, thereby increasing ATP levels, a result that is supported by the finding that bilobalide increases the expression of the mitochondrial DNA-encoded COX III subunit of cytochrome oxidase. With regard to its "anti-stress" effect, EGb 761 acts via its ginkgolide constituents to decrease the expression of the peripheral benzodiazepine receptor (PBR) of the adrenal cortex.
Posted by jemma on April 2, 2003, at 15:19:19
In reply to Re: Rhodiola rosea » jemma, posted by Ron Hill on April 2, 2003, at 12:33:29
To be honest, I'm not entirely sure how effective it is. I'm feeling better since replacing ritalin with low-dose selegiline, and I started taking rhodiola and alphalipoic acid at the same time. So I'm not sure what's doing what, but I'm happy with the overall result. I was attracted to rhodiola precisely because of its cortisol-lowering potential, and because, like ginseng, it has a touted ability to bring the endocrine system into balance. But I'm sure that, as with most herbs, its effect is gradual and incremental.
- jemma
Posted by Ron Hill on April 2, 2003, at 16:49:43
In reply to Re: Rhodiola rosea » Ron Hill, posted by jemma on April 2, 2003, at 15:19:19
Posted by zero on April 2, 2003, at 17:12:25
In reply to Any cheap effective anticortisols out there, posted by linkadge on April 1, 2003, at 15:47:22
Posted by Larry Hoover on April 2, 2003, at 21:23:11
In reply to cheap effective anticortisols- phosphatidylserine? (nm), posted by zero on April 2, 2003, at 17:12:25
Yes, phosphatidylserine, but I don't consider it to be cheap.
Posted by Ritch on April 2, 2003, at 22:36:34
In reply to Re: Any cheap effective anticortisols-Gingko?, posted by Larry Hoover on April 2, 2003, at 14:33:22
Wow, thanks a lot Larry! Adrenal peripheral benzodiazepine receptors-that's interesting.
Got one more question. Months before I had all of my thyroid troubles I was on lithium and got hypercalcemia (idiopathic). This was found out after I started getting hives on the bottom of my feet and I had to go to ER for prednisone treatment. I was referred back to my GP and got some electrolyte workup, etc. that found the hypercalcemia. Anyhow I was prescribed several different antihistamines to treat the hives and they weren't very effective. I was waiting on seeing an immunologist to find out what was causing it in the meantime. Anyhow, I found that NSAID's (especially ketaprofen) were VERY effective in alleviating the itching and stopping the hives, whereas several antihistamines were relatively useless (Claritin, Allegra, Benadryl, etc.) I was under a lot of stress (cortisol connection?) during all of this time. Question is: IF I responded to NSAID's instead of antihistamines-does that "tell" anything about my HPA axis/cortisol "picture" that is noteworthy or remarkable in any way? I know that NSAID's act on prostaglandins. Are prostaglandins and cortisol linked? Thanks again for any info-your posts are very informative!
Posted by bluedog on April 2, 2003, at 22:53:46
In reply to Re: Any cheap effective anticortisols-Gingko?, posted by Larry Hoover on April 2, 2003, at 13:35:51
> > Thanks Larry, hate to bug you one more time, but you mentioned Gingko Biloba as an anti-cortisol agent. Could you elaborate some about that? I know Gingko is used for alertness, which I could use more of. thanks for any info.
> >
>
> Somebody else posted a link a few weeks or so ago, with excellent graphs showing cortisol reduction after gingko treatment. Anybody save the link?
>
> Lar
>
LarryI saved this link months ago but I hope it helps you some.
http://www.bentham.org/cdt1-1/defeudis/defeudis.htm
regards
bluedog
Posted by Larry Hoover on April 3, 2003, at 12:33:14
In reply to Re: thanks! ...one more question..... » Larry Hoover, posted by Ritch on April 2, 2003, at 22:36:34
> Wow, thanks a lot Larry! Adrenal peripheral benzodiazepine receptors-that's interesting.
>
> Got one more question. Months before I had all of my thyroid troubles I was on lithium and got hypercalcemia (idiopathic). This was found out after I started getting hives on the bottom of my feet and I had to go to ER for prednisone treatment. I was referred back to my GP and got some electrolyte workup, etc. that found the hypercalcemia. Anyhow I was prescribed several different antihistamines to treat the hives and they weren't very effective. I was waiting on seeing an immunologist to find out what was causing it in the meantime. Anyhow, I found that NSAID's (especially ketaprofen) were VERY effective in alleviating the itching and stopping the hives, whereas several antihistamines were relatively useless (Claritin, Allegra, Benadryl, etc.) I was under a lot of stress (cortisol connection?) during all of this time. Question is: IF I responded to NSAID's instead of antihistamines-does that "tell" anything about my HPA axis/cortisol "picture" that is noteworthy or remarkable in any way? I know that NSAID's act on prostaglandins. Are prostaglandins and cortisol linked? Thanks again for any info-your posts are very informative!I don't feel qualified to give you a definitive answer, as the interactions between the various products of cyclooxygenase enzymes are exceedingly complex. In general, COX inhibitors suppress ACTH (adreno-corticotropin hormone) and cortisol release. So, a non-specific COX inhibitor like ketoprofen will suppress stress responses. This will suppress, in turn, inflammatory cytokines like TNF-alpha. TNF-alpha can induce release of the inflammatory and urticaritic (hive-producing) prostaglandin D2. So, COX inhibitors can have direct and indirect effects suppressing inflammation, including hives.
What was found to be the cause of the hypercalcemia? It can directly cause release of TNF-alpha.
Posted by Ritch on April 3, 2003, at 13:52:57
In reply to Re: thanks! ...one more question....., posted by Larry Hoover on April 3, 2003, at 12:33:14
> > Wow, thanks a lot Larry! Adrenal peripheral benzodiazepine receptors-that's interesting.
> >
> > Got one more question. Months before I had all of my thyroid troubles I was on lithium and got hypercalcemia (idiopathic). This was found out after I started getting hives on the bottom of my feet and I had to go to ER for prednisone treatment. I was referred back to my GP and got some electrolyte workup, etc. that found the hypercalcemia. Anyhow I was prescribed several different antihistamines to treat the hives and they weren't very effective. I was waiting on seeing an immunologist to find out what was causing it in the meantime. Anyhow, I found that NSAID's (especially ketaprofen) were VERY effective in alleviating the itching and stopping the hives, whereas several antihistamines were relatively useless (Claritin, Allegra, Benadryl, etc.) I was under a lot of stress (cortisol connection?) during all of this time. Question is: IF I responded to NSAID's instead of antihistamines-does that "tell" anything about my HPA axis/cortisol "picture" that is noteworthy or remarkable in any way? I know that NSAID's act on prostaglandins. Are prostaglandins and cortisol linked? Thanks again for any info-your posts are very informative!
>
> I don't feel qualified to give you a definitive answer, as the interactions between the various products of cyclooxygenase enzymes are exceedingly complex. In general, COX inhibitors suppress ACTH (adreno-corticotropin hormone) and cortisol release. So, a non-specific COX inhibitor like ketoprofen will suppress stress responses. This will suppress, in turn, inflammatory cytokines like TNF-alpha. TNF-alpha can induce release of the inflammatory and urticaritic (hive-producing) prostaglandin D2. So, COX inhibitors can have direct and indirect effects suppressing inflammation, including hives.
>
> What was found to be the cause of the hypercalcemia? It can directly cause release of TNF-alpha.
>
>
Thanks for the response! I was primarily curious why on earth antihistamines were doing practically nothing, but one tab of ketaprofen nearly eliminated the systemic reaction (for a few hours anyways). The reaction was so bad at times that most of my skin all over my body was uncomfortably hot, with hives on my feet, and extremely itchy. Hydrocortisone creams helped somewhat, but only ketaprofen and prednisone worked quite effectively. The cause of the hives was found to be a severe dust-mold allergy that presented itself only systemically (1-3 days after exposure). Did immunotherapy for that (allergy shots) and it cleared up. The hypercalcemia "cause" was never found. I would get one test and it would be well above the normal range, get another test and it would be normal, then get another one and it would be only moderately high. Then it just went away. But just a few months after that was when I got my thyroid tumor. Hidden tumors are also a cause of hypercalcemia, so it may have been related to thyroid, but I didn't have any symptoms to suspect that, until my GP found the enlargement in my thyroid.
Posted by Larry Hoover on April 3, 2003, at 14:26:16
In reply to Re: hypercalcemia » Larry Hoover, posted by Ritch on April 3, 2003, at 13:52:57
>Hidden tumors are also a cause of hypercalcemia, so it may have been related to thyroid, but I didn't have any symptoms to suspect that, until my GP found the enlargement in my thyroid.
The only problem I have with this scenario is that calcium regulation is a function of the parathyroid gland. Following treatment for the thyroid tumour, was you blood calcium monitored?
Posted by jemma on April 3, 2003, at 15:07:10
In reply to Re: hypercalcemia, posted by Larry Hoover on April 3, 2003, at 14:26:16
This is interesting to me. I have ndi - nephrogenic diabetes insipidus - which has caused hypercalcuria and high blood phosphate, low sodium, etc. I control it with 25 mg. of hydrochlorthiozide. Because of ndi, I can't take lithium, which causes ndi in many people. So Mitch, your hypercalcemia may have been a result of lithium.
Larry, how does any of this affect my meds? Currently I take 250 mg modafinil and 10 mg selegiline, along with the hydrochlorthiozide and HRT. I've often wondered if my brain fox came from a lack of vasopressin receptors in my hypothalamus, as well as my kidney. My ndi appears to be genetic, but it's labelled idiopathic for 'who knows?' I've had a lot of weird things go wrong, including postcapsular cataracts. I'm 47, and not diabetic.
Feel free to ignore this. But I've come to admire the scope of your knowledge of the brain's and body's chemistry.
- jemma
Posted by Larry Hoover on April 3, 2003, at 18:26:38
In reply to Re: hypercalcemia, posted by jemma on April 3, 2003, at 15:07:10
> This is interesting to me. I have ndi - nephrogenic diabetes insipidus - which has caused hypercalcuria and high blood phosphate, low sodium, etc. I control it with 25 mg. of hydrochlorthiozide. Because of ndi, I can't take lithium, which causes ndi in many people. So Mitch, your hypercalcemia may have been a result of lithium.
Fascinating that a diuretic controls a disorder of diuresis. Have you ever been advised to use an NSAID? The combination is more effective than the thiazide alone.
> Larry, how does any of this affect my meds? Currently I take 250 mg modafinil and 10 mg selegiline, along with the hydrochlorthiozide and HRT.
None of these should be affected by your kidney disorder. Surely you were dose-titrated with foreknowledge of the NDI, yes?
>I've often wondered if my brain fox came from a lack of vasopressin receptors in my hypothalamus, as well as my kidney.
Were your psychotropic meds prescribed to deal with brain fog, in particular? They seem to be appropriate for that.
As I understand it, the hypothalamus senses solute concentrations directly, and thus mediates vasopressin release, rather than responding to it. Or have I got that mixed up?
> My ndi appears to be genetic, but it's labelled idiopathic for 'who knows?'
Ya. I hear ya. If experts don't know, who does?
>I've had a lot of weird things go wrong, including postcapsular cataracts. I'm 47, and not diabetic.
Well, I hate to say it, but you're of an age where things, idiopathic things, tend to become prominent.
> Feel free to ignore this. But I've come to admire the scope of your knowledge of the brain's and body's chemistry.
>
> - jemmaI will always be a student. I have an infinite curiosity. Glad to find that suits others, too.
;-)Lar
Posted by Ritch on April 3, 2003, at 23:01:42
In reply to Re: hypercalcemia, posted by Larry Hoover on April 3, 2003, at 14:26:16
> >Hidden tumors are also a cause of hypercalcemia, so it may have been related to thyroid, but I didn't have any symptoms to suspect that, until my GP found the enlargement in my thyroid.
>
> The only problem I have with this scenario is that calcium regulation is a function of the parathyroid gland. Following treatment for the thyroid tumour, was you blood calcium monitored?
>
>Yes, that is true. When, my first high calcium blood tests came back, my GP was thinking about the parathyroid glands first off and specifically mentioned them. Some tests were done to check those from what I remember and nothing was found that was unusual. The next theory was kidney dysfunction-after a CAT scan they were OK. After discovering the severe dust/mold allergy and getting a few allergy shots, the hives disappeared, a serum calcium level showed OK and that seemed to be the end of things for a few months. Anyhow, a few months later my pdoc and I were tinkering with Adderall (for the first time), with Neurontin and Risperdal. I got a dystonic reaction and gait disturbances from the Risperdal and I flipped to Seroquel. The dystonia resolved somewhat, but after a few weeks I started to get more and more anxious. It may have been the Adderall, but I wasn't sure, so I stopped the Adderall. Anyhow, I started to get panicky after a few days following stopping the stimulant and had trouble swallowing. Went back to GP, and he thought it was just anxiety, but did yet another thyroid exam and felt a slight enlargement. They did that radioactive iodine test thingie and found the tumor. All I know is the thing grew real fast and it was called a folicular hyrtle cell adenoma. They surgically removed that half and the middle (isthmus) of my thyroid. They did a "cold section" after surgery and said it was benign. No follow up on serum calcium was done after all of that except for one test done about a year following which showed normal calcium levels.
Posted by Ritch on April 3, 2003, at 23:18:52
In reply to Re: hypercalcemia, posted by jemma on April 3, 2003, at 15:07:10
> This is interesting to me. I have ndi - nephrogenic diabetes insipidus - which has caused hypercalcuria and high blood phosphate, low sodium, etc. I control it with 25 mg. of hydrochlorthiozide. Because of ndi, I can't take lithium, which causes ndi in many people. So Mitch, your hypercalcemia may have been a result of lithium.
>
> - jemmaThat's interesting, because I was still on lithium when the first serum calcium showed up abnormal. Thanks for mentioning that. What I find also very interesting is that you also experience low blood sodium (hyponatremia). Perhaps that is why I found Trileptal difficult to tolerate?
Posted by jemma on April 4, 2003, at 11:54:09
In reply to Re: hypercalcemia, posted by Larry Hoover on April 3, 2003, at 18:26:38
> > This is interesting to me. I have ndi - nephrogenic diabetes insipidus - which has caused hypercalcuria and high blood phosphate, low sodium, etc. I control it with 25 mg. of hydrochlorthiozide. Because of ndi, I can't take lithium, which causes ndi in many people. So Mitch, your hypercalcemia may have been a result of lithium.
>
> Fascinating that a diuretic controls a disorder of diuresis. Have you ever been advised to use an NSAID? The combination is more effective than the thiazide alone.
I'll ask my endo about this - thanks.
>
> > Larry, how does any of this affect my meds? Currently I take 250 mg modafinil and 10 mg selegiline, along with the hydrochlorthiozide and HRT.
>
> None of these should be affected by your kidney disorder. Surely you were dose-titrated with foreknowledge of the NDI, yes?
>
Actually, I pretty much titrate the doses myself. After so many meds over the years, I've developed a pretty finely honed sense of what I need to feel well. And modafinil and low-dose selegiline aren't meds that my psychopharmacologist has much experience with.> >I've often wondered if my brain fox came from a lack of vasopressin receptors in my hypothalamus, as well as my kidney.
>
> Were your psychotropic meds prescribed to deal with brain fog, in particular? They seem to be appropriate for that.I found these meds and sold my pdoc on them. But yes, my depression is of the anhedonic, anergic, brain fog variety. Ssri's made things worse - after nine years on zoloft I discovered it had been downloading catecholamine receptors. Serzone turned me into a blithering idiot, and lamictal wasn't much better. Even wellbutrin made me fall asleep. Finally we tried modafinil, and voila - energy and motivation for the first time in a decade. Then he tried ritalin and it felt like valium, but with a wicked rebound effect. So I talked him into the selegiline, and its working a treat.
>
> As I understand it, the hypothalamus senses solute concentrations directly, and thus mediates vasopressin release, rather than responding to it. Or have I got that mixed up?Like most things neurochemical, the V2 receptors seems to be pretty much a mystery. I do know that vasopressin not only prevents diuresis but also sharpens the mind and memory brilliantly.
>
> > My ndi appears to be genetic, but it's labelled idiopathic for 'who knows?'
>
> Ya. I hear ya. If experts don't know, who does?
>
> >I've had a lot of weird things go wrong, including postcapsular cataracts. I'm 47, and not diabetic.
>
> Well, I hate to say it, but you're of an age where things, idiopathic things, tend to become prominent.Don't I know it. Like a car, wearing out its parts one by one. Damn, I wish I'd spent more time on early maintenance :^). Still, I have a lot of pretty weird things going on.
>
> > Feel free to ignore this. But I've come to admire the scope of your knowledge of the brain's and body's chemistry.
> >
> > - jemma
>
> I will always be a student. I have an infinite curiosity. Glad to find that suits others, too.
> ;-)
>
> LarLucky for us. Thanks, Larry.
- jemma
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