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| Men's Health Forum: This is a discussion on Adderall Question--marianco, HeadDoc, Others? within the Anabolic Steroids forums, part of the extensive steroid information at MESO-Rx; I have Adult ADD and have been considering trying the drug Adderall XR. It is my understanding that several side ... |
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I have Adult ADD and have been considering trying the drug Adderall XR. It is my understanding that several side effects can be expected such as: 1. Weight Loss. 2. Increased Cortisol Levels. 3. Brain receptor burn out. 4. Addictive. First, is the weight loss that happens a result of loss of appetite, speed up in metabolic rate, or muscle wasting due to increased cortisol levels? Just how much do cortisol levels increase on such a drug (at say 20mg per day XR)? and what are the negatives of increased cortisol? Is it something to be concerned about, and can muscle wasting be controlled with lots of protein, glutamine, and phosphytelSerine? My ND told me receptor burn out can be fixed by supplementing with SAMe at 200mg X 3 times per day. Thoughts? Just how addictive is this stuff, and have you seen people that this became a serious problem with? Thanks for any info you can offer, I already have made a great deal of improvement with natural methods, but this stuff makes me feel incredible. BTW I feel that my ADD/LD problems are due to my mother smoking throughout her pregnancy with me. I had low birth weight, no breast feeding, and was in a home for about 2 months before being adopted. The good news is I have been recently reunited with my mother and it has been awesome! I read a study that smoking prohibits the dendrites in the brain from growing long enough, so they are not as long as they should be do to nicotine toxicity, and I suppose (guessing) oxygen deprivation. Last edited by Vforcer2; 12-21-2005 at 09:50 PM. |
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I take Adderall because I also have ADD. I've been taking it for a year and before that, I used to take Ritalin. Adderall curbs my appetite a lot more than Ritalin did, but if I don't eat, it makes me jittery and feeling weird. So I eat and there's no problem. I haven't really lost weight because I enjoy eating too much. But I've talked to other people who've lost weight and it was due simply because the Adderall curbed their appetite. The drug itself didn't eat away at the muscles or anything. As far as addictive, I don't take it for recreational purposes. I take it everyday just to be able to focus. But I don't overdo it either. I take 30 mg a day. |
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I'm on 30 mg right now cause I'm on a budget with no insurance, but I actually think I need to increase my dosage slightly. I get better results when I take 15 mg (half tab) in the morning, then take another 15 mg (other half) two hours later. That keeps me focused throughout the day until early afternoon where I just take another 15. So I think my ideal dosage is actually 45 mg, but I only take that much when I really need to get things done because I tend to ration the tablets considering it's a controlled substance and I have to go through a lot of BS to get a refill. And keep in mind that I'm also taking generic so that may weaken the pills I take. The doc says most people take at least 60 mg a day. |
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[quote=Vforcer2] Have you experienced any side effects? I did some reading and there was some controversy over brain receptor burn out that lead to anti depressent type drugs later on due to the brain being unable to produce dopamine and/or seratonin after extended use. QUOTE] I really don't know about brain receptor burnout and now you're scaring me. I do know that without the medication, it's extremely hard to focus. I was on ritalin for ten years before that. And before that, I was the typical ADD case. When I was a kid, I was always in trouble for something or another. I couldn't sit still. The teachers always told me I would be a success -- if only I learned to channel my abundant energy. |
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Perhaps some of the more knowledgble gentlemen here can expound a bit on the receptor burnout issue and the aftermath of being dependent on anti depressents later on. This specific issue is what kept (scared) me from using Adderall on a permenant basis a few months ago, however since then my ND recommends supplementing with SAMe while using Adderall, saying it refreshes the receptors. I have tried Adderall at doses of 5mg, and even as small as 2.5 mg, and all I can say is I can feel my brain "light up" and I go from being unorganized and easily distracted to an efficient focused work machine. I have a hard time imagining using more than 20 mg per day. I think that would make me extremely wired, but I am somewhat hypersensitive to stimulants. I can't even consume coffee past 6 p.m. or I might not be able to get to sleep. This is still a new area to me, so it will require a bit more research on my part. |
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I'm like you, very sensitive to caffeine and stimulants. But it also takes me a while for my mind to focus in the morning. Even if I drink coffee and I'm very hyper, my mind is still foggy in the morning. It's still hard for me to accomplish mental tasks. The other thing about adderall, is that even though it is a stimulant, it doesn't make me wiry (unless I don't eat). I'm wiry without it. Wiry yet unfocused. Moving a lot yet doing nothing. Lately, I'm beginning to think there is a connection between hypogonadism and ADD because some of the symptoms of ADD are also the symptoms of low T and/or high E. |
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the following is a post I've been following over at Avant. The author raises some points realted to the questions. Hope you find this useful. Something has always bothered me about the generalizations people draw with regards to dopaminergic drugs. The generalizations I speak of state that any drug that is dopaminergic, whether it be so through reuptake inhibition (methylphenidate), release of dopamine (amphetamine) or agonization of the DR (bromocriptine), should basically have similar effects on body comp. However, I have simply not found that to be true. In brief, I have not benefited from desireable changes in body composition using either DRI's (methylphenidate) or dopa releasers (Dexedrine). As well, these medications have given unreliable and unreplicable cognitive effects. When using direct dopamine agonists, however, I usually can get repeated positive effects on body comp. This always has interested me and I have wondered if there really is something to all this or it is just all in my head. I mean, after all it is certainly understandable why the generalizations are made, increased dopaminergic tone, is increased dopaminergic tone right? Well, this is what can be so exciting about the biomedical sciences, the reality is often different than what we opine based on human reasoning. Anyway, usually, if you have a sense that something is not right, it usually is not. Call it what you will, spider sense, dumb luck, or thinking outside the box, but to that end, medical puzzles that don't fit require cavernous deliberation. I know that amphetamine and amphetamine-type drugs often cause acute increases in cortisol levels, especially at higher doses. This has always bothered me because for stress hyper-responders, undesireable effects both cognitively and superficially can precipitate. Interestingly enough however, some studies are begginning to show that dopamine agonists may be of value in reducing stress levels (measured via ACTH). This is fascinating to me because there is no way you would ever consider an amphetamine type medication for diseases such as Cushing's or Nelson's. Below are two abstracts that lend some evidence to this scenario. Is this where the dichotomy between DA agonists and other dopaminergics lies with regards to their effects on body comp: cortisol? I mean both will stimulate the DA receptors, but there is something else going on. If this pans out to be true, it shows how complex and beguiling mother nature can be. 1) Horm Res. 2004;62(6):300-5. Epub 2004 Nov 19. Related Articles, Links Nelson's syndrome: complete remission with cabergoline but not with bromocriptine or cyproheptadine treatment. Casulari LA, Naves LA, Mello PA, Pereira Neto A, Papadia C. Neurosurgery Unit, Hospital de Base do Distrito Federal, Escola Superior em Ciencias da Saude, FEPECS, Brasilia, Brazil. lacasulari@unb.br A woman affected by Cushing's disease underwent bilateral adrenalectomy followed by radiotherapy of the hypothalamic-pituitary area when she was 18 years old. Thereafter, she used hydrocortisone acetate replacement therapy (35.5 mg divided into two daily doses). At the age of 26 years, the patient exhibited the clinical signs of the Nelson's syndrome, i.e. skin and gingival hyperpigmentation accompanied by amenorrhea, and elevated ACTH plasma levels (2,850 pg/ml, normal range 15-80 pg/ml). The magnetic resonance imaging (MRI) analysis of the sellar region evidenced a pituitary macroadenoma, measuring 14 x 13 mm. The patient was initially treated with cyproheptadine hydrochloride (12 mg/day) for 18 months. There was a partial improvement of the symptoms, with a reduction of the ACTH plasma levels to 112 pg/ml, but without any modification of the tumor mass. Due to sleepiness and weight gain, the cyproheptadine treatment was interrupted and substituted by a cabergoline (0.5 mg twice a week) therapy. Soon after cabergoline was applied an improvement of the clinical symptoms and signs was observed such as a regression of the tumor mass and the normalization of the ACTH plasma titers (38 pg/ml). Later, cabergoline was substituted by bromocriptine (7.5 mg/day) and the plasma levels of ACTH increased again (247 pg/ml), and headache and cutaneous hyperpigmentation were recorded. When cabergoline was reintroduced there was a clinical improvement and normalization of ACTH plasma levels (64 pg/ml). The MRI analysis of the sella region demonstrated a complete remission of the pituitary adenoma. The results obtained show for the first time that a long-term treatment with cabergoline also brings about a complete remission of Nelson's syndrome in the presence of a pituitary macroadenoma. 2) J Clin Endocrinol Metab. 2004 May;89(5):2452-62. Related Articles, Links Dopamine receptor expression and function in corticotroph pituitary tumors. Pivonello R, Ferone D, de Herder WW, Kros JM, De Caro ML, Arvigo M, Annunziato L, Lombardi G, Colao A, Hofland LJ, Lamberts SW. Department of Internal Medicine, Erasmus Medical Center, 3015 GE Rotterdam, The Netherlands. rpivone@tin.it The role of dopamine agonist treatment in corticotroph pituitary tumors is controversial. The aim of this study was to evaluate D(2) receptor expression in 20 corticotroph pituitary tumors and to correlate it to the in vitro effect of dopamine agonists on ACTH secretion and the in vivo effect of short-term cabergoline treatment on cortisol secretion. D(2) expression was evaluated by receptor-ligand binding, immunohistochemistry, and RT-PCR. A 50% or more decrease in daily urinary cortisol levels was considered a significant clinical response. At receptor-ligand binding, specific binding of [(125)I]epidepride was found in 80% of cases. At immunohistochemistry, specific D(2) immunostaining was found in 75% of cases. D(2) expression was found in 83.3% of cases (D(2long) in 40%, D(2short) in 20%, and both in 40%) by RT-PCR. Significant in vitro inhibition of ACTH secretion was found in 100% of D(2)-positive cases, but not in 100% of D(2)-negative cases by either bromocriptine or cabergoline. A significant in vivo inhibition of cortisol secretion after 3-month cabergoline treatment was found in 60%, although a normalization of cortisol secretion was found in 40% of cases. All cabergoline-responsive cases were associated with D(2) expression, whereas all noncabergoline-responsive cases but one were not associated with D(2) expression. In conclusion, functional D(2) receptors were expressed in approximately 80% of corticotroph pituitary tumors. The effectiveness of cabergoline in normalizing cortisol secretion in 40% of cases supports its therapeutic use in the management of Cushing's disease.
__________________ And we'll collect the moments one by one. I guess that's how the future's done. Feist, "Mushaboom", 2005. |
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I am not ADD but suffer from bad fatigue and brain fog. My Dr. put me on Concerta when it came out a slow release Ritalin. Man did this help with the fatigue and brain fog I was not doing SWALE's protocol at the time and could do with out it but don't want to. Have any of you tried this no sides.
__________________ Don't believe anything you hear and only half of what you see. Phil |
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Also if you suffer from brain fog a lot, I would take a look at your carb consumption, and try to balance every meal with at least 40-50% protein. Dr. Amen recommends a relatively low carb, low glycemic index diet for most patients. Imbalances in blood sugar can cause fog. I always used to get severe brain fog and fatigue after eating pasta, white potatoes, or pastries. I have eliminated them from my diet except for special occasions, and I am all the better for it.......and so is my waistline |
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I have been on it since it came out now doing 36 mgs. of Concerta I tried Adderall it made my BP go up and my heart race. I don't do a lot of carb's I follow the Weight Watchers weight loss program for a long time over 15 yrs. or I would have gotten up to 500 lbs when I was house bound for 3 yrs. My first problem with low T was fatigue so bad I could not go to work. Was told it was depression, CFS, and low iron. After 5 yrs being treated for Depression and not feeling any better I found out it was low T not depression. Had to go into re-hab to get off all the drugs for depression they had me on. I feel still to this day I lost 5 yrs of my life to AD drugs. Starting on SWALE's protocol the first of this yr. I dropped a lot of weight went down from 325 to 260. I am doing the best I every did on TRT in the last 21 yrs. My E2 is a problem but it is a small price to pay to feel this good. I feel that I will get down to 200 lbs next yr. and this will help with my E2 been working out for the last 6 months. Not bad seeing how this time last yr. I had such bad joint and muscle pain I could hardly walk.
__________________ Don't believe anything you hear and only half of what you see. Phil |
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I think my hypogonadism was either caused by the menengitis I had as a kid and/or a serious injury I had around the same time where I was struck hard between my nose and forehead with a huge object. I still have a scar. That may have caused the ADD as well because I believe both the pituarity gland and the dopamine glands (or whatever they're called) are located in the frontal lobe of the brain. A few years ago when I had an MRI done to determine that I did not have a tumor, the doctor said there is some "mass" in that area. Not sure what it meant, but it was not a tumor. I do tend to focus better and be in better spirits when my testosterone is working fine, but you know how hard it can be to get it to the right levels so I think the ADD medication is very helpful. Even though I've always considered the two conditions separate, lately I'm becoming to see a stronger connection between the two. |
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Phil that is some impressive weight loss. I can see why getting a handle on the aromitizaton was so important. My hat's off to you man!
__________________ And we'll collect the moments one by one. I guess that's how the future's done. Feist, "Mushaboom", 2005. |
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