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Monday, August 2, 2010

Effect of Bupron (Bupropion SR) - 150 mg

I discontinued fluoxetine and then I took bupropion 150 mg extended release once daily in the morning along with neurogistics multivitamin capsules for 3-4 weeks.

Positive effects:
  • Improved mood - No negative thoughts, No depressed mood
  • Improved energy
  • No procrastination - I could meet the deadline in my job first time in the last 3 years.
  • More focus - can remain in a task for more period of time enabling me to complete the work.
  • More concentration - can think faster and do faster processing
  • No sexual side effects - but no increased libido or strong erections
  • Maximum resolution of anxiety - After 2-3 weeks, I experienced a maximum resolution of anxiety which was haunting me for more than 10 years. No worrying thoughts before driving the car. No worrying thoughts before the class. Sometimes, I used to feel tachycardia. This tachycardia went off after taking few deep breaths.
  • My eye vision improved. I was not taking omega-3 supplements. Even then my vision did not deteriorate. I could see more brightness in the night while driving. Earlier, this lack of brightness was causing me more anxiety while driving in the night.
  • Improved olfactory functions - Taste and smell sensation improved.
Negative effects:
  • More aggressiveness - led to more fights with my wife.
  • No difference in the affection. I was not able to like and love my family (This condition was there before taking medicines. So no improvement in this part.)
  • Music was not enjoyable as like before.
  • Dizziness and syncope
Suggestion:
  • I may need a less dosage of bupropion to reduce the side effects
  • OR I have to include 5-HTP once daily (either morning or in evening) to counteract the probable decrease in serotonin and GABA due to elevated dopamine levels.

    Effect of Fludac (Fluoxetine)

    I took the fludac (Fluoxetine) 20 mg once daily along with neurogistics multivitamin capsules. I could not continue (discontinued after 4 days) the drug because of its sexual side effect (observed within 1 day).

    Positive effects:
    • No negative thoughts
    • No depressed mood
    Negative effects:
    • Mild anxiety
    • Anorgasmia
    • Weak erections
    • Loss of sensation in the penis - so after penetrating, the striking movements are not pleasurable leading to weakened erection inside vagina.
    Neutral Effects:
    • Not a significant effect on stuttering
    • No effect on motor activity - No increased pain, no lethargy, no increase of inertia and immobility

    Sunday, June 6, 2010

    My Headache

    My headache comes in two types.
    1. Left sided head pain - lasts for maximum 1 day and disappears with 5-HTP intake and sometimes with rice eating. (serotonin deficiency)
    2. Right sided head pain - Lasts for two days and disappears with DL-Phenylalanine intake and vitamin C intake. (either dopamine or NE deficiency)

    Wednesday, May 12, 2010

    My exact condition - Is it atypical depression with psychomotor retardation or ADD/ADHD?

    Today I was reading research articles. I found references for my exact condition. Based on the following refefences, I can say that I have a atypical depression with impaired dopamine transmission which accounts for the psychomotor retardation.

    The following information is from wikipedia on atypical depression.

    The DSM-IV-TR defines Atypical Depression as a subtype of Major Depressive Disorder with Atypical Features, characterized by:


    a) Mood reactivity (i.e., mood brightens in response to actual or potential positive events)

    b) At least two of the following:

    • Significant weight gain or increase in appetite;
    • Hypersomnia (sleeping too much, as opposed to the insomnia present in melancholic depression;
    • Leaden paralysis (i.e., heavy, leaden feelings in arms or legs);
    • Long-standing pattern of interpersonal rejection sensitivity (not limited to episodes of mood disturbance) that results in significant social or occupational impairment.

    c) Criteria are not met for Melancholic Depression or Catatonic Depression during the same episode.


    I have (a) mood reactivity - My mood usually improves when I travel long distance; when I meet people and talk with whom I can make jokes and laugh. If I am alone, my depressive thoughts start occupying my mind.

    in (b) I have significant weight gain - very difficult to lose weight. If I starve very much, then only I can lose my weight. Then I have hypersomnia - I sleep for almost 9-11 hours per day. If I don't sleep this much time, I don't feel energized or refreshed. Leaden paralysis is not there. I don't feel heavy feelings in my arm or legs. My arms and legs are very weak and I am unable to get out of sofa or car seat as like normal people of my age. I think I had strong interpersonal rejection sensitivity and body dysmorphic disorder (because of my pimples) when I was 13-18 years old. Later on, it subsided to some extent. However, it did not go fully.

    (c) I don't have a supressed mood always. The problem with me is the mood is unable to reach its maximum pleasure levels. I don't sink into depression also. I am unable to enjoy the pleasures in my everyday life. My anxiety is very high, incapacitating enough to make me avoid normal operations in life.

    So, collectively these things imply that I have atypical depression and probably with psychomotor retardation. Actually my depression was not a problem for me in my adolescent age. Those days, I didn't have neurological issues. From 2003, my erections were not as strong as before. In 2004-2005, I started to have involuntary head twitches and sudden fainting-like feeling for few seconds.

    There could be a
    • dopamine and noradrenaline deficiency - accounting for psychomotor, lack of motivation, lack of reward sensing and sexual issues
    • GABA deficiency - accounting for high anxiety
    • Acetyl choline deficiency - accounting for impaired memory and stomach bloating.

    My serotonin levels seems to be normal. I have done the brain neurotransmitter survey on this site (http://www.antiagingnow.com/secure/test_forms/edge_effect_intro.html) and the results indicated that I have severe deficiency of dopamine, GABA, acetylcholine and not serotonin.

    The treatment strategies for atypical depression could be as follows:

     600 microgram/day

    I may need a dopamine reuptake inhibitor to really alleviate my psychomotor retardation. And I may not have parkinson's disease also.

    References:

    Motor and cognitive aspects of motor retardation in depression. Journal of Affective Disorders 57 (2000) 83–93.

    Abstract

    Background: Motor retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychomotor retardation, must exhibit motor slowing of sufficient severity to be observed by others. However, overt presentations of motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuromotor disturbances.
    Methods: We examined cognitive and neuromotor aspects of motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit motor programming disturbances in addition to psychomotor impairment. A novel instrumental technique was used to assess motor programming in terms of the subject’s ability to program movement velocity as a function of movement distance. A traditional psychomotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of motor retardation.
    Results: The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychomotor function as measured by the traditional battery; whereas over 60% exhibited some form of motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like motor programming deficits. A five-factor model consisting of motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. Limitations: The ability of motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients.
    Conclusions: These findings suggest that a subgroup of depressed patients exhibit motor retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.

    Clinical and psychometric correlates of dopamine D2 binding in depression. Psychological Medicine (1997), 27:1247-1256 Cambridge University Press.

    Update on 15 October 2012:

    I used to feel heavily sleepy after drinking coffee especially if the coffee is taken after a good meal either in the breakfast or in the lunch. I first observed this effect in 1997 when I was taking a training in an industry. I used to feel like that most of the times after taking coffee. Today I googled on it and found a yahoo answer saying that getting sleepiness after taking coffee is one of the physiological indications of attention deficit disorder (ADD) / attention deficit hyperactivity disorder (ADHD). I got interest and searched on the symptoms of ADD/ADHD. I found a very good website detailing all information on ADD/ADHD (http://www.helpguide.org/mental/adhd_add_adult_symptoms.htm).

    The major symptoms which I may have under the heading of disorganization and forgetfulness include the following:

    Disorganization and forgetfulness

    • poor organizational skills (home, office, desk, or car is extremely messy and cluttered)
    • tendency to procrastinate
    • trouble starting and finishing projects
    • chronic lateness
    • frequently forgetting appointments, commitments, and deadlines
    • constantly losing or misplacing things (keys, wallet, phone, documents, bills)
    • underestimating the time it will take you to complete tasks

    The suggested treatment plan

    Wednesday, April 21, 2010

    My best condition of mood and stuttering - The ideal one

    I have experienced ideal conditions also. I mean to say, I had experienced good mood, no depression, no anxiety and no stuttering. I had such incidents under the following conditions. If I could understand the possible underlying mechanisms and if I could reproduce these effects daily by using nutraceutical or pharmacological means, I could be a happy person.

    Conditions:
    1. I was taking Zincovit multivitamin tablets (Pls find the composition below). After taking it for few days, I felt some what uneasy feelings of tiredness and low mood. Then I stopped the tablet for one day. On the day of stopping, my energy level was up and almost no stuttering. My voice was louder. During this time, I was with my family. So, social support also play a role in this.
    2. I was taking neurogistics multivitamin caps, 5-HTP, magnesium, glycine, taurine, vitamin C and bioflavonoids. I went to to my relative's house where I didn't take these supplements. I applied coconut oil on my head hair. After 1 hour, my voice was louder, no stuttering. If no coconut oil is applied, the effect was not there. This time also, I was with my close relatives.
    3. Yesterday night (20 may 2010), I slept with a new cotton pillow which is quite fluffy. So it is big. No pillow cover. Today morning I could get up easily without laziness and my mind was full of energy. I felt energetic physically also. My stuttering is also very much reduced today (It is not completely absent). I suspect some anamoly in my neck area which would prevent proper drainage of blood, CSF and other fluids from head to main body. When I sleep with raised head, the drainage seems to occur properly. Other than this, I could not think of any other reason for this.  

    Unusual and non stutterable pause in stuttering

    I experienced an unusual and unstutterable pause during my speech when I was taking certain supplements.


    In 2008, I took Renerve capsules http://www.grandix.in/products_neuro.html

    The composition is given below. After taking this caps, I experienced this kind of stuttering for the first time. I speak faster and after 5-15 minutes, the unusual pause of 3- 7 seconds comes in. It is like an epilepsy attack (may be an absence seizure). During that pause, I was not able to make any sound from my throat. But, no loss of consciousness, no loss of memory and no impairment of other functions. And, no other symptoms also. I used to feel like paralysis of my vocal cord. I assume that this could be due to dopamine (either increased or decreased levels) or some minerals.


    Products
      Packing
            Composition
    ReNerveSoft
    Gel
    Caps
    10x10'sMethyl Cobalamin
    Alpha Lipoic Acid
    Vitamin E Acetate
    Vitamin B1 HCl
    Vitamin B6
    Vitamin A Concentrate
    Calcium Pantothenate
    Selenium Dioxide
    Folic Acid
    Chromium polynicotinate
    Inositol
    500 mcg
    100 mg
    25 mg
    10 mg
    1.5 mg
    2500 IU
    10 mg
    163.6mcg
    5 mg
    200 mcg
    100 mg    


    The same effect was observed when I was taking neurogistics multivitamin capsules also. The composition is given below. Here, Vitamin B12 is present as methylcobalamin. So, it could be due to methylcobalamin. when I switched over to other vitamin tablets with Vitamin B12 as cyanocobalamin, this effect was not there. However, this effect could be due to some other component/mechanism also.


    This effect was more observed during the time when I was taking DL-phenylalanine 1000 mg (500 mg X 2) daily in mornings. When I was taking this neurogistics multivitamin caps together with 5-HTP along with magnesium, taurine and glycine, this effect was not there. So, I assume the culprits as dopamine and methyl cobalamin. The clear mechanism is unknown. It could be a form of vocal cord dystonia induced by excess dopamine also.

    I was taking zincovit multivitamin tablets in 2008. That also caused this effect. But it was less severe. The worst was with neurogistics multivitamin + vitamin C + DL-phenylalanine.

    Composition of zincovit tablets:

    Vitamins
    Ascorbic acid as coated75 mg
    Niacinamide50 mg
    Alphatocopheryl Acetate concentrate (Powder form)15 mg
    Thiamine mononitrate10 mg
    Riboflavine10 mg
    Calcium Pantothenate2 mg
    Pyridoxine Hydrochloride2 mg
    Folic aicd1 mg
    Vitamin A con. Powder form (as acetate)5000 I.U.
    VitaminD3 (Cholecalciferol)400 I.U.
    Minerals
    Zinc sulphate monohydrate63 mg
    Magnesium oxide30 mg
    Manganese sulpahte monohydrate2.8 mg
    Copper sulphate2 mg
    Colloidal Sillicon Dioxide (equ. To Sillica)1 mg
    Pottassium Idodie (Eq. to Iodine)150 mcg
    Sodium Borate (Equ. Boron)150 mcg
    Selenium di oxide monohydrate70 mcg
    Chromium picolinate (equ to Chromium)25 mcg
    Sodium molybdate Dihydrate (equ to molybdenum)25 mcg
     (Source: http://www.apexlab.com/html/zincovit.html)

    Today, I had this effect when I was talking to my landlord (luckily she was counting the rental money I gave to her, So I had some time to observe my pause). Oh my God! What a horrible disturbances in this life? I took Vitamin C (500 mg NOT slow release) + bioflavonoids and DL-phenylalanine 500 mg in the lunch time. Around 7 pm I had this effect.

    Possible mechanism:
    1. Vitamin C increases noradrenaline synthesis and DL-phenylalanine increases noradrenaline, dopamine and adrenaline.
    2. I feel this increase may be an excess or there may not be a matching increase in serotonin and GABA. So I should try increasing serotonin (5-HTP) and GABA (Mentat)
    Reduced effect of unstutterable stuttering - Update on 12 may 2010:

    For the past few days, I am taking the supplements as follows:

    Morning: 1 capsule of 5-HTP - 50 mg; 1 capsule of DL-phenylalanine - 500 mg, 2 capsules of neurogistics multivitamin; 1 tablet of l-lysine - 600 mg

    Lunch/evening: 1 capsule of DL-phenylalanine 500 mg

    Evening/night: 1 capsule of neurogistics multivitamin; 1 capsule of omega -3 (EPA + DHA = 780 mg)

    Diet:

    Morning - oats or noodles (not much of protein)

    Lunch - rice, vegetables and 1 piece of fish

    Dinner - rice or dosa with chicken drum stick 1 piece

    This condition has reduced my unstutterable stuttering to greater level. Not much of longer pauses like before. I am not taking vitamin C and magnesium. They are said to have antidepressant properties but they may interact with noradrenergic and dopaminergic systems. I suspect the magneisum very much for this effect. Need to explore more on this area.

    Ascorbic acid administration produces an antidepressant-like effect: Evidence for the involvement of monoaminergic neurotransmission
    Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 33, Issue 3, 30 April 2009, Pages 530-540.

    Abstract


    Ascorbic acid is highly concentrated in the brain, being considered as a neuromodulator. This study investigated the effect of ascorbic acid in the tail suspension test (TST) and in the forced swimming test (FST) in mice and the contribution of the monoaminergic system to its antidepressant-like effect. Moreover, the effects of fluoxetine, imipramine and bupropion in combination with ascorbic acid in the TST were investigated. Ascorbic acid (0.1-10 mg/kg, i.p., 1-10 mg/kg p.o. or 0.1 nmol/mice i.c.v.) produced an antidepressant-like effect in the TST, but not in the FST, without altering the locomotor activity. The effect of ascorbic acid (0.1 mg/kg, i.p.) in the TST was prevented by i.p. pre-treatment with NAN-190 (0.5 mg/kg), ketanserin (5 mg/kg), MDL72222 (0.1 mg/kg), prazosin (62.5 microg/kg), yohimbine (1 mg/kg), propranolol (2 mg/kg), haloperidol (0.2 mg/kg), sulpiride (50 mg/kg), but not with SCH23390 (0.05 mg/kg, s.c.). Additionally, ascorbic acid (1 mg/kg, p.o.) potentiated the effect of subeffective doses (p.o. route) of fluoxetine (1 mg/kg), imipramine (0.1 mg/kg), or bupropion (1 mg/kg) in the TST. The combined treatment of ascorbic acid with antidepressants produced no alteration in the locomotion in the open-field test. In conclusion, our results show that administration of ascorbic acid produces an antidepressant-like effect in TST, which is dependent on its interaction with the monoaminergic system. Moreover, ascorbic acid caused a synergistic antidepressant-like effect with conventional antidepressants. Therefore, the present findings warrant further studies to evaluate the therapeutical relevance of ascorbic acid for the treatment of depression and as a co-adjuvant treatment with antidepressants.
     
       
    Evidence for the involvement of the monoaminergic system in the antidepressant-like effect of magnesium. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Mar 17;33(2):235-42. Epub 2008 Nov 27.


    Abstract


    Literature data has shown that acute administration of magnesium reduces immobility time in the mouse forced swimming test (FST), which suggests potential antidepressant activity in humans. However, its mechanism of action is not completely understood. Thus, this study is aimed at investigating the antidepressant-like action of magnesium and the possible involvement of the monoaminergic system in its effect in the FST. The immobility time in the FST was significantly reduced by magnesium chloride administration (30-100 mg/kg, i.p.) without accompanying changes in ambulation when assessed in an open-field test. The pre-treatment of mice with NAN-190 (0.5 mg/kg, i.p. a 5-HT(1A) receptor antagonist), WAY100635 (0.1 mg/kg, s.c., a selective 5-HT(1A) receptor antagonist), ritanserin (4 mg/kg, i.p., a 5-HT(2A/2C) receptor antagonist), ketanserin (5 mg/kg, a preferential 5-HT(2A) receptor antagonist), prazosin (1 mg/kg, i.p., an alpha(1)-adrenoceptor antagonist), yohimbine (1 mg/kg, i.p., an alpha(2)-adrenoceptor antagonist), haloperidol (0.2 mg/kg, i.p., a non selective dopaminergic receptor antagonist), SCH23390 (0.05 mg/kg, s.c., a dopamine D(1) receptor antagonist) or sulpiride (50 mg/kg, i.p., a dopamine D(2) receptor antagonist) 30 min before the administration of magnesium chloride (30 mg/kg, i.p.) significantly prevented its anti-immobility effect in the FST. Moreover, the administration of sub-effective doses of fluoxetine (10 mg/kg, i.p., serotonin reuptake inhibitor), imipramine (5 mg/kg, i.p., a mixed serotonergic noradrenergic reuptake inhibitor), bupropion (1 mg/kg, i.p., dopamine reuptake inhibitor) was able to potentiate the action of sub-effective doses of magnesium chloride. In conclusion, the present study provides evidence indicating that the antidepressant-like effect of magnesium in the FST is dependent on its interaction with the serotonergic (5-HT(1A) and 5-HT(2A/2C) receptors), noradrenergic (alpha(1)- and alpha(2)- receptors) and dopaminergic (dopamine D(1) and D(2) receptors) systems.


    Update on 8 may 2015:

    For the past 3 months, I was taking zinc in order to improve my testosterone and dopamine levels. I took zinc 15 mg + vitamin C 250 mg daily in mornings after food. During February 2015, I took proviton capsules + zinc 15 mg + vitamin C 250 mg combination. This produced good energy and mood. However, it produced mild non-stutterable pause also. Also, it increased blood pressure to 156/100 mmHg during the lunch time. The blood pressure dropped to normal levels during the evening hours. So, I had to change the multivitamin from proviton to Supradyn recharge. I continued the zinc but without vitamin C since supradyn recharge has enough vitamin C. This combination also produced non-stutterable pause and caused big embarrassment when I was speaking with my boss. What a pity life I live! Also, it caused poor concentration, unable to focus and less motivation to start doing things. Then, I reduced the dose of zinc to 7.5 mg by taking half tablet. Still the effects persisted with reduced intensity. I stopped zinc one day. On that day of no zinc, I felt great energy, mood and no non-stutterable pause. After that, I stopped taking zinc. That non-stutterable pause is not coming again. However, this non-stutterable pause may be caused by other minerals/vitamins also. I need to explore further and confirm.

    In my research with my stuttering and interventions, I suspect the following for the non-stutterable pause. The mechanism could be lack of dopamine in the speech circuit.

    1. Zinc
    2. Folic acid
    3. Methyl cobalamin
    4. Methylfolate
    5. Selenium