I'm returning to the DHEA topic. Patient has taken a two week break from DHEA after taking for a couple months. One problem Patient has battled with lately is not having a regular sleep schedule, despite continuing Melatonin. Patient has typically been very tired around 7-8PM and gone to bed only to wake up at 1-2am.
While looking at possibilities to get the schedule under control I have decided to give DHEA a shot at it. Will request Patient take DHEA 2.5mg in late afternoon. Idea being that Patient will get a small burst of energy/activity boost to carry into evening hours for a target 10-11pm sleep time. Six to seven PM has also been typically when Patient has delusional thoughts so I want to see how DHEA affects this time of day.
I suggest you read the following links for a better understanding of the role of these hormones within the body.
"...It is this rebound response that is the large area of stimulated nerves
that cause the seizures. Once the brain has stimulated sufficient DHEA, then the seizure stops." (1)
(1) http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/hypermail/neuroscience/1998-January/030264.html
I've updated the protocol on right side of page with info about max levels of DHEA. I should add that it is estimated that males levels naturally are 10-15 mg daily, female levels are up to 20% less than male levels. Upregulation does not occur when DHEA is taken orally, so do not exceed the natural levels. Why on earth would anyone take 25, 50, 100mg ???
--gjh
Saturday, February 24, 2007
Thursday, February 15, 2007
Phosphatidylserine (PS)
I found an excellent brief on Phosphatidylserine located at the link below. I did not find anything to suggest it would increase seizure activity, so I may introduce it for its list of benefits.
"PS is a fat-soluble nutrient and would be expected to require at least several days' dosing to build up in the nerve cell membranes." "PS appears in the blood at about 30 minutes. After a few more minutes uptake begins into the liver and, later, the brain." "Given orally, PS is rapidly absorbed and readily crosses the blood-brain barrier to reach the brain. There, its sites of action appear to be exclusively in cell membrane." "Structurally, PS protected the hippocampus (a major memory center) from the loss of dendrite connections that normally occurs with aging (see Nunzi et al, 1987)." "Nunzi and co-workers (1992) found that in the rat hippocampus, a fall-off in nerve growth factor receptor density occurs with aging. PS reversed this receptor density decline and seemed to enhance NGF production." "PS given to these athletes prior to starting exercise produced an impressive degree of down-regulation of the stress hormones"(1)
Regarding dosing: "A reasonable supplementation strategy with PS is to begin at 300 mg per day with meals for a month, then go into a maintenance mode at a lower level of intake (100 to 200 mg daily). There is no indication of potential problems from long-term supplementation with PS."(1)
"As a general rule, because PS is so safe the more severe the subject's problems the more aggressive can be the supplementation strategy. Patients with severe memory problems can be kept on all their other supplements and medications, and be given PS with their meals at 300 to 500 mg per day on an ongoing basis. Subjects afflicted with motor problems may respond better at 500 mg per day. Mood problems may require a starting dose of 400 mg per day. For age-related cognitive decline (ARCD), a daily intake of 300 mg may be appropriate. "(1)
(1) "Phosphatidylserine, A Remarkable Brain Cell Nutrient"
http://www.springboard4health.com/books_online/ps/phosphatidylserine.html
--gjh
"PS is a fat-soluble nutrient and would be expected to require at least several days' dosing to build up in the nerve cell membranes." "PS appears in the blood at about 30 minutes. After a few more minutes uptake begins into the liver and, later, the brain." "Given orally, PS is rapidly absorbed and readily crosses the blood-brain barrier to reach the brain. There, its sites of action appear to be exclusively in cell membrane." "Structurally, PS protected the hippocampus (a major memory center) from the loss of dendrite connections that normally occurs with aging (see Nunzi et al, 1987)." "Nunzi and co-workers (1992) found that in the rat hippocampus, a fall-off in nerve growth factor receptor density occurs with aging. PS reversed this receptor density decline and seemed to enhance NGF production." "PS given to these athletes prior to starting exercise produced an impressive degree of down-regulation of the stress hormones"(1)
Regarding dosing: "A reasonable supplementation strategy with PS is to begin at 300 mg per day with meals for a month, then go into a maintenance mode at a lower level of intake (100 to 200 mg daily). There is no indication of potential problems from long-term supplementation with PS."(1)
"As a general rule, because PS is so safe the more severe the subject's problems the more aggressive can be the supplementation strategy. Patients with severe memory problems can be kept on all their other supplements and medications, and be given PS with their meals at 300 to 500 mg per day on an ongoing basis. Subjects afflicted with motor problems may respond better at 500 mg per day. Mood problems may require a starting dose of 400 mg per day. For age-related cognitive decline (ARCD), a daily intake of 300 mg may be appropriate. "(1)
(1) "Phosphatidylserine, A Remarkable Brain Cell Nutrient"
http://www.springboard4health.com/books_online/ps/phosphatidylserine.html
--gjh
Friday, February 9, 2007
Patient Update February 9, 2007
Patient has not followed supplement protocol over the period of past week and reports from family about paranoia and psychosis have been relayed. Work schedule and vacation interferes with daily updates. I decided daily updates will not be necessary for blog at this time.
Had conversation with Patient about options: supplements or drugs. Since I am not seeing a significant reverse of paranoia or psychosis or memory deficit baseline behavior without heavy supplementation, I am ready to test a drug.
Based on the findings of the PRODH deficiency study, I have faxed a 24 page document to the Neurologist requesting a review and comment on the study as well as recommendation for a test period of Lamotrigine (drug.) I provided the study and info from wikipedia about the drug which I had been searching for over the past few weeks since finding the study details.
Here's my Letter to the Doctor:
I am providing information for your review and comment regarding prescribing Lamotrigine for Patient (blank). I have been keeping a blog (web journal http://orthosz.blogspot.com) of research and daily progress for Patient. Based on the findings of a study and what I have learned by controlling diet and supplements and monitoring daily, I would like to have you review the attached information for comment and possible prescription to target the regulation of glutamate. The findings of the study essentially report the following:
1. glutamate toxicity factor - loss of PRODH gene function directly causes hyperactivity of nerves that use glutamate to signal other nerves.
2. dopamine toxicity factor - loss of PRODH gene function causes upregulation of COMT gene responsible for encoding the enzyme that breaks down dopamine.
3. upregulation of COMT gene is not possible in patients with 22q11 microdeletion which causes toxic buildup of dopamine {and psychosis/paranoa in Patient.}
4. PRODH deficiency increases release of glutamate at synapses in hippocampus and inhibits LTP, important step in forming memories.
5. Lack of glutamate regulation due to loss of PRODH contributes to learning difficulties.
Over the period of time since our last visit I have learned that the supplement L-Theanine (apparently) has a direct boost effect on Dopamine and for this Patient, caused paranoia and psychosis. We have known for a long time that excess sugar in the diet has also triggered the psychosis and paranoia, just not as quickly as Theanine (a green tea extract.)
Lamotrigine would target the glutamate regulation, help to control the seizures, and control the drop attacks. I am hopeful that it may prevent the chain reaction of Dopamine toxicity as well. If the glutamate release at hippocampal neurons is presently toxic, this drug may help improve the memory which at is a steady, slow deficit currently.
Patient's mother suffered from seizures that eventually robbed her of memory. Patient has been experiencing daily morning dizziness. I am aware that for many people seizures occur in the twilight sleep just as they begin to wake up. We have used a GABA enhancing supplement called Kavinace (Phenibut, Taurine) which eliminated seizures and dizziness during the day. However, this is smoke and mirrors if what is broken has to do with regulating glutamate. Even with morning and evening doses of Kavinace we did not prevent the morning dizziness that occurred when first getting out of bed-possibly a partial seizure.
end of Letter
Had conversation with Patient about options: supplements or drugs. Since I am not seeing a significant reverse of paranoia or psychosis or memory deficit baseline behavior without heavy supplementation, I am ready to test a drug.
Based on the findings of the PRODH deficiency study, I have faxed a 24 page document to the Neurologist requesting a review and comment on the study as well as recommendation for a test period of Lamotrigine (drug.) I provided the study and info from wikipedia about the drug which I had been searching for over the past few weeks since finding the study details.
Here's my Letter to the Doctor:
I am providing information for your review and comment regarding prescribing Lamotrigine for Patient (blank). I have been keeping a blog (web journal http://orthosz.blogspot.com) of research and daily progress for Patient. Based on the findings of a study and what I have learned by controlling diet and supplements and monitoring daily, I would like to have you review the attached information for comment and possible prescription to target the regulation of glutamate. The findings of the study essentially report the following:
1. glutamate toxicity factor - loss of PRODH gene function directly causes hyperactivity of nerves that use glutamate to signal other nerves.
2. dopamine toxicity factor - loss of PRODH gene function causes upregulation of COMT gene responsible for encoding the enzyme that breaks down dopamine.
3. upregulation of COMT gene is not possible in patients with 22q11 microdeletion which causes toxic buildup of dopamine {and psychosis/paranoa in Patient.}
4. PRODH deficiency increases release of glutamate at synapses in hippocampus and inhibits LTP, important step in forming memories.
5. Lack of glutamate regulation due to loss of PRODH contributes to learning difficulties.
Over the period of time since our last visit I have learned that the supplement L-Theanine (apparently) has a direct boost effect on Dopamine and for this Patient, caused paranoia and psychosis. We have known for a long time that excess sugar in the diet has also triggered the psychosis and paranoia, just not as quickly as Theanine (a green tea extract.)
Lamotrigine would target the glutamate regulation, help to control the seizures, and control the drop attacks. I am hopeful that it may prevent the chain reaction of Dopamine toxicity as well. If the glutamate release at hippocampal neurons is presently toxic, this drug may help improve the memory which at is a steady, slow deficit currently.
Patient's mother suffered from seizures that eventually robbed her of memory. Patient has been experiencing daily morning dizziness. I am aware that for many people seizures occur in the twilight sleep just as they begin to wake up. We have used a GABA enhancing supplement called Kavinace (Phenibut, Taurine) which eliminated seizures and dizziness during the day. However, this is smoke and mirrors if what is broken has to do with regulating glutamate. Even with morning and evening doses of Kavinace we did not prevent the morning dizziness that occurred when first getting out of bed-possibly a partial seizure.
end of Letter
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