Inderal and diazepam

Pyrazolam—the incomparably-safer, rapid-onset anxiolytic diazepine connivingly withheld for decades.

2018.02.20 01:02 newbieforever2016 Pyrazolam—the incomparably-safer, rapid-onset anxiolytic diazepine connivingly withheld for decades.

Pyrazolam is exceptional in its effect’s *unparalleled selectivity* for anxiolysis and minor muscular relaxation, relative to sedation, hypnosis, and peripheral (primarily anticonvulsant) diazepine effects. It’s estimated to have 12x the *anxiolytic* potency of diazepam, *but that’s just one measure of potency.* The *incomparably-safer,* rapid-onset anxiolytic diazepine *concealed from us for decades...*
[link]


2022.08.04 23:02 TwoForSue Medications for Anxiety

7 Popular Medication Classes For Anxiety, Explained By an RN

Selective Serotonin Reuptake Inhibitors SSRIs

citalopram, celexa, escitalopram, lexapro, fluoxetine, prozac, sarafem, symbyax, fluvoxamine, luvox, luvox CR, paroxetine, paxil, paxil CR, pexeva, sertraline, zoloft, vilazodone, viibryd
Drug class
This is a very common drug class; prescribed to treat anxiety, depression, bipolar disorders, migraines, panic attacks, eating disorders, PTSD, OCD, and even chronic pain.
Over 10% of the US takes an SSRI
What Do SSRIs Do?
What does every medication within this class have in common? They all increase the level of Serotonin in your brain. Serotonin is a neurotransmitter. When you take a Serotonin Reuptake Inhibitor, you’re blocking the neurons from reabsorbing Serotonin, meaning there is more Serotonin available.
Since this medication increases serotonin levels, you’ll have more of it to regulate your mood and symptoms of anxiety. Your brain also has to adapt to more Serotonin. It’s thought that by your brain having to restructure from an increase in serotonin, it becomes more able to “remodel” and better able to adapt to stressors like anxiety.
So what does Serotonin do? Well, A LOT. Serotonin influences our mood and emotional state, our digestion, appetite, and our sleep cycle. It is found in your brain, in your intestines and even in your blood. One could argue that it impacts everything.
Did You Know?
Serotonin is even in animals, plants and fungus. We can measure the levels in our blood, but we can’t measure the levels within our brain. Meaning we’re all in the dark as to how much we have in our brain.

Azapirones

Buspar Buspirone
Drug Class
Buspirone is in the drug class of Azapirones. There is no addiction risk, overall there are less side effects than many other anxiolytic medicines. It can take up to a month for the medication to work fully. Typically prescribed for generalized anxiety.
What Does It Do?
This drug class impacts serotonin and dopamine receptors. The full mechanism of the drug aren’t known actually. But, because it seems to take 2-4 weeks to make a difference, that would mean it likely has to do with the receptors for serotonin and dopamine.
It is thought that by the receptors adjusting, it can make them more adaptive and therefore better able to handle stress. Another possibility is that by blocking serotonin receptors, an increase of serotonin is available, which improves symptoms for some types of anxiety disorders.
Did You Know?
The drug Buspar was originally developed for schizophrenia, but wasn’t useful. It did however seem to help people with anxiety. Dizziness seems to be one of the most common complaints as far as side effects.

Antihistamines

brompheniramine, dimetane, benadryl, diphenhydramine, carbinoxamine, clistin, clemastine, tavist, doxylamine, unisom, hydroxyzine, atarax, vistaril, promethazine, phenergan, triprolidine, triafed
Drug Class
Commonly used for allergies but also used for anxiety. Antihistamines are divided into different ‘generations’ & target different histamine receptors in our body.
What Do Antihistamines Do?
We’re actually still learning a lot about histamines but what we do know is that anti-histamines are usually anticholinergic; blocking receptors for choline.
Vistaril, hydroxyzine and Atarax are commonly prescribed for anxiety.
While your risks with this drug class are much less severe than when taking benzodiazepines, these are first generation antihistamines. Therefore, they do have a sedating effect (precisely why they can relieve tension) but this also means they can impair our ability to remember, think and learn. Especially the first generation antihistamines that easily penetrate our brain.
An example of second generation antihistamines are Claritin & Zyrtec. Unlike first generation antihistamines, these do not cross the blood-brain barrier as easily. Therefore, they relieve many effects of allergies, but do not have as many sedating properties or memory impairments associated with them. When it comes to anxiety though, Claritin & Zyrtec won’t do you much good.
Did you know?
The only drug within this class that can be given intravenously is Benadryl. Since Benadryl is a first generation, it impacts our body in many ways in addition to the reason why it’s administered. Since first generation antihistamines are much less specific in their effects, they have more side effects.
Though, being the only IV antihistamine available, it is still widely used in hospital settings (for anxiety included).

Benzodiazepines

alprazolam, xanax, chlordiazepoxide, librium, clonazepam, klonopin, clorazepate, tranxene, diazepam, valium, lorazepam, ativan, oxazepam, serax, temazepam, restoril, triazolam, halcion
Drug Class
These are commonly used as anxiety medicines (though can be used for seizures, insomnia, and muscle spasms). They work by quickly slowing down important parts of our brain.
This drug class specifically targets the GABA-A receptor, enhancing its effect, which slows down our central nervous system; this makes us feel relaxed, because the drug has retarted a major gear in our system (sometimes this is EXACTLY what we need).
Anesthesiologists often give Versed (a benzodiazepine) so patients will not remember surgery?
The Drawbacks of Benzos
When Benzodiazepines were first discovered they offered an immediate solution to the overwhelming crippling anxiety that many people face, but the harsh reality is we’re now in a benzo addiction crisis. We’re learning over time as a society, and those changes don’t happen overnight.
This drug class changes our mental state & while the drug is advantageously quick acting, the effects linger. Short-term memory is not as affected, but long-term memory is specifically impaired. The memory loss may occur because events are not transferred from short-term memory to long-term memory.
The effects are similar to the long-term effects of alcoholism (alcohol is also a CNS depressant). Both of these substances, used long term actually damage our brain.
This is why a rehab center isn’t going to allow the use of this drug class while recovering. This is why therapists often (but not always) stray away from patients taking benzodiazepines while trying to work on trauma, recovery, etc. If the brain is not functioning at full capacity & you’re not able to retain information, progress becomes much more difficult.
The most effective aspects of benzodiazepines are precisely why individuals have a tendency to become dependent on them.
Obviously, there is a time and a place for benzodiazepines. They’re a life saver for the (hopefully) occasional panic attack. But how sadistic is that Benzodiazepines have addictive properties, which means that with consistent repeated use we will need increasingly higher doses.
Another point of concern is that this drug will inhibit your brain from initiating activity of GABA A (since the medication has so kindly been doing it). What this means is that after the drug is long gone from your system, your brain experiences a lag in restoring the normal GABA balance.
This is often what is referred to as rebound anxiety because your anxiety is likely to get worse, before it gets better after taking a benzodiazepine, especially if taken frequently and long term.
The mental health world is increasingly trying to move towards low dosing and only prescribing for a limited amount of time. I’ve even worked with prescribers who won’t prescribe them, period.
Now, Benzodiazepines are very dangerous to quit cold turkey, so please don’t go flush yours down the toilet after reading this!

Beta Blockers

acebutolol, atenolol, tenormin, bisoprolol, zebeta, metoprolol, lopressor, toprol XL, nadolol, corgard, nebivolol, bystolic, propranolol, inderal, innopran XL
Drug Class
A beta blocker is most often used for heart conditions since this drug class lowers blood pressure and heart rate. But, they do this by blocking epinephrine which we commonly refer to as adrenaline. By blocking adrenaline, you prevent the progression of the physical symptoms of anxiety, like increased heart rate and blood pressure.
These can be prescribed “as needed” and is also prescribed long term to be taken regularly. Sometimes doctors will prescribe them for public speaking, or other stressful events someone has to face.
What do Beta Blockers Do?
Well, they Block Beta-adrenergic receptors, preventing norepinephrine and epinephrine from activating those receptors. This relaxes heart muscles, slows the heart beat, and lowers blood pressure.
That might seem completely unrelated to anxiety to some people, but when anxiety starts it will create physical symptoms that tend to make us feel even more panicked. This is why it can be pretty helpful to stop the physical symptoms from escalating an already not-so-good state of mind.
Did you know?
Beta blockers can be used for tremors, migraines, abnormal heart rhythms, and chest pain too.
Summary
Beta blockers can be a useful anxiety medication. As a nurse some of the things I pay attention to when a patient is prescribed them are obviously heart rate and blood pressure. Energy level is always something that can be impacted too.
It’s not uncommon for someone to become tired, groggy, lightheaded, or get headaches from beta blockers. Even for people who take it for high blood pressure and heart rate, it can have a tendency to drop them too low.
Everyone is different, our diets change, our weight changes, our stress levels change, how hydrated we are fluctuates, our salt intake varies; and all of these impact our blood pressure. So, it’s always a good idea to be keeping an eye on your heart performance with a beta blocker and your doctor who is prescribing should be too.

Tricyclic Antidepressant TCAs

anafranil, clomipramine, asendin, amoxapine, elavil, amitriptyline, norpramin, desipramine, pamelor, nortriptyline, sinequan, doxepin, surmontil, trimipramine, tofranil, imipramine, vivactil, protiptyline
Drug Class
The word “tricyclic” refers to the three molecular ring shapes associated with this drug class. These existed before SSRIs, but they seem to cause more side effects. This has led to SSRIs being more commonly prescribed nowadays.
TCAs are still often prescribed for things like anxiety, depression, migraines, panic disorder, eating disorders, mood disorders, insomnia, hormone disorders, bedwetting, and even nerve pain.
What do Tricyclic Antidepressants Do?
What do all TCAs have in common? Similar to an SSRI, tricyclic antidepressants impact neurotransmitters. But, in addition to serotonin, they also block the reabsorption of norepinephrine. They ALSO block acetylcholine receptors.
These key differences from SSRIs create a cascade of effects in the body that make them a bit more likely to cause side effects; like dry mouth, blurred vision, and urinary retention.
Did You Know?
In 1945, the Sulphur bridge of the phenothiazine ring of promethazine was altered to synthesize G22355 (a weak antihistamine and mild anticholinergic with sedative properties). The new ‘invention’ was tested as an antipsychotic. It was ineffective for schizophrenia, but did have antidepressant properties. Thus, the first clinically useful tricyclic antidepressant (TCA) was discovered.
Summary
These drugs interfere with our bodies baseline of norepinephrine and acetylcholine. As with any drug; sometimes they create an optimal effect on a person, as for others, not so much. If a person is too excitable and anxious, a TCA can improve their quality of life, while for another it can leave a bad impression.
*Note each drug within the class impacts the degree of these effects a little differently.

Antipsychotics

sometimes referred to as major tranquilizers or neuroleptics
risperidone, risperdal, quetiapine, seroquel, olanzapine, zyprexa, ziprasidone, zeldox, paliperidone, invega, aripiprazole, abilify, clozapine, clozaril, fluphenazine
Drug Class
Commonly used as the first line treatment for schizophrenia & sometimes used for mood disorders, depression, personality disorders, Tourette’s syndrome, Huntington’s disease, and anxiety.
What Do They Do?
Most drugs in this class work to block Dopamine, though some do impact other chemicals in the brain.
Schizophrenia is the major psychotic disorder we use antipsychotics for. Some of the main symptoms are delusions, lack of motivation, unusual behaviors, and hallucinations. Dopamine has been thought to regulate our brains understanding of our surroundings and what it all means to us. So, it’s to be expected that drugs within this class target Dopamine.
This class is broken up into two categories;
First Generation (old, typical): Block Dopamine-2 Receptors, which means they also block acetylcholine, histamine and norepinephrine. which can impact our cognition and the complex way in which we store memories.
*More movement disorders come with the first generation antipsychotics.
Second Generation: (new, atypical): Block Serotonin and Dopamine Receptors. Less risk of extra movements, increased risk of diabetes, high cholesterol, and weight gain.
Hopefully this helps clarify some information on these common 7 classes of medications. If not feel free to submit a question in the comments, or by using my contact form below and I’ll do my best to answer.
Original Post https://twoforsue.com/medications-for-anxiety/
submitted by TwoForSue to mentalhealth [link] [comments]


2021.11.10 22:24 JP1021 WebMD Kava Article Discussion

Hello kava lovers!
I took quite a bit of time today to dig into this. It's been a long running issue that when you type in "Kava" in google you get some dubious results on the first page. I'm taking it upon myself to list those here, and refute them where they have issues.
Search Results for "Kava" on google in incognito window.
Result 1: Webmd
  1. Overview
  1. No issues with point one.
  1. And my issues start here. “Cases of liver damage and even some deaths have been traced to kava use” is a hotly contested conclusion, and rather inflammatory when such paltry evidence exists to support it. The paragraph then goes on to state “However, most countries have allowed kava to return to the market since that time.” My issue here is; why are we not seeing these cases of liver failures and injury in countries where it’s freely available today, if it’s as liver toxic as it was said to be?
  1. “But there is no good scientific evidence to support these uses.” Hilariously they give quite good scientific evidence to support these uses directly in their references. Kava and kava extracts have been proven in double blind placebo controlled studies to reduce anxiety scores, and increase sleep duration/quality.
  2. How does it work?
  1. No issues with this. This has been demonstrated repeatedly in research.
  2. Possibly Effective for
  1. Strangely, they just got finished saying there is no good scientific information on which to support these theories. Extra note: WS-1490 is an extract that has been embroiled in controversy. The extract is contested on the grounds that it was changed several times throughout the research periods from an ethanolic extract to an acetonic extract with no indication. You can see this by noting how the kavalactone percentage changes arbitrarily from 30% to 70%.
  2. Possibly Ineffective for
  1. They conveniently don’t mark their sources in the article, but this one comes from Dr. Sarris in Australia in 2020. This research concluded that kava was more suitable for the reduction in stress and tension related to ‘situational’ anxiety, than it was for direct treatment of G.A.D.
  2. Insufficient Evidence for
  1. It can reduce anxiety, but the actual physical withdrawal is not treated by any action of the kavalactones themselves. It’s likely that the steady tapering of the BZP drug was what allowed these participants to cease their use with less acute withdrawal. Kava definitely helps, but it has different actions at the GABA-A receptor that are not similar to that of benzodiazepine drugs. Benzos target the BZP allosteric site on the GABA-A receptor where they exert their effect. Kava and flumazenil (a very potent anti-benzo or BZP antagonist) were administered at the same time in studies, and the effect of kava was not blocked.
  1. I would say this “insufficient evidence” is actually an order of magnitude more studied and documented than the “liver damage” at the very beginning of this article. I’ve added additional citations below this papers citations, and I stopped citing at 12 research studies that show anti-cancer effects.
  1. The World Health organization monograph (2002) describes insomnia as a state supported by clinical data. This is generally accepted, however there were participants in studies on kava that dropped out due to insomnia complaints. While kava is overall a good fit for sleep issues, it likely won’t present that way to 100% of the people who drink it. We actually do see people complain about not being able to get to sleep after a strong kava. I say this to agree with the above paragraph where it states the research is inconsistent. It helps me with sleep, but that doesn’t mean it will be the same for everyone.
  1. While maybe insufficient, there is good evidence to support this. Two individual studies found improvement in mood, reduction in depression, and reduction in anxiety in perimenopausal individuals.
  1. This is an odd one to say has insufficient evidence. A number of researchers including Münte, Sarris, Cropley, and Aporosa have found kava reduces symptoms associated with mentally stressful tasks.
  1. This is in line with reality. We only see glimpses into kava’s ability to modulate glutamate. Kavain was shown to inhibit veratridine-activated sodium channels. It’s possible that kava may help reduce seizures, but as said, there is insufficient evidence to say it precisely.
  1. This I don’t agree with, and it’s a strange one to be saying there’s insufficient evidence for. Kava has marked antinociceptive (pain relieving) and muscle-relaxing properties. A good number of independent research studies have confirmed this.
  1. I’m not really sure what to say here. I suppose it’s quite accurate to say that there is insufficient evidence for kava causing superhero-like powers to emerge.
  2. Side Effects
  1. This is good, and goes pretty far based on the double blind placebo controlled studies. The one issue I have is the 6 month limit. There really isn’t any indication that taking kava beyond this time frame causes issues, it’s just when they cut the time limit of the study. Empirical evidence suggests kava, when consumed as a beverage, is safe indefinitely as shown by the South Pacific people who drink kava on a daily basis and have for generations. In regards to driving, I fully agree. If you’re consuming anything that makes you question your abilities with driving, call an ubelyft.The risk is simply not worth it.
  1. That’s pretty honest, however the phrase “The use of kava for as little as 1-3 months has resulted in the need for liver transplants and even death in some people” really understates “some people”. The number of individuals allegedly harmed by kava is limited to less than 10. There has been no intrinsic (unable to be separated) toxicity seen in kava or any kava extracts, however idiosyncratic reactions of the immunologic type have occurred. This is extremely rare. I can’t say that enough. We’re talking on the scale of winning the lottery, being hit by lightning, and finding Jimmy Hoffa all at the same instant. If we turn our attention to things such as green tea extracts or acetaminophen we see intrinsic, predictable toxicity to the liver. This does not exist with kava.
  2. Special Precautions and Warnings
  1. They’re speaking about kavalactones, and they’re not “dangerous chemicals” however we don't fully understand the function of GABAergic substances on the developing brain. Kavalactones are known as lipophilic, meaning they tend to combine or dissolve in fats. This means they could likely also pass on through breastfeeding. There is no data confirming this suspicion, however with no experience available, kava is not recommended for use by pregnant or breast-feeding women. It’s much better to err on the side of caution. In regards to kava affecting the uterus, I’m afraid there is absolutely nothing confirming this. It’s an old myth from Fiji that kava stimulates the uterus, this doesn’t happen, and shouldn’t be listed as a precaution. Histopathology was performed on rats at 2.0g/kg of kavalactones and found no-effect level on the uterus. (2012. “Toxicology and Carcinogenesis Studies of Kava Kava Extract (CAS No. 9000-38-8) in F344/N Rats and B6C3F1 Mice (gavage Studies).” National Toxicology Program 571 (1): 1–186. https://ntp.niehs.nih.gov/publications/reports/t500s/tr571/index.html)
  1. Well this sounds familiar. This will be the 3rd time this website has decided it was pertinent to warn us of liver damage. What they’ll throw at you sometimes is the instance of GGT elevation in metabolism tests seen in kava users in the late 80s and early 90s in Australia's Northern Territory. This is NOT indicative of liver damage. It indicates liver adaptation and is seen in kava drinkers that consume about a pound of dried kava per week. AST and ALT increases are not seen. I would even go as far to say here that kava is not even detrimental to those with liver problems. Kava is not intrinsically toxic to the liver in any way.
  1. This one is interesting. You have research on one side saying kava has no or very little activity at dopamine, then you have other research indicating that some kavalactones drop dopamine levels considerably. The one kavalactone in question here is Yangonin. Yangonin has shown in research to lower dopamine to below detectable levels. I personally believe that this is happening evidenced by the extrapyramidal movements seen in kava drinkers that went way overboard. They end up looking like they have parkinsons. If you are on medication such as levodopa that is specifically meant to increase free dopamine levels in the brain, kava can counteract this effect and cause the resurgence of parkinson's symptoms. So yes, I agree with this statement. If you have parkinsons it’s best to skip the kava.
  1. This is not talked about very much but should be taken into close consideration when approaching a surgery. Kava has many properties that haven’t been studied all that intensively. Kava has shown to have some mild antithrombotic actions. This means it may be able to prevent, to a degree, blood clotting. Give yourself at least a week if not two before any surgery to let your system flush out. Kava has also been shown to increase the sedation of anesthetic drugs. You’ll want to observe this just to be on the safe side.
  2. Major Interactions
  1. Agreed
  1. Agreed as well. Sedation seems to be the pharmacodynamic interaction here.
  2. Moderate Interactions
  1. I believe this to be correct. Levodopa is a medication meant to increase the levels of dopamine in the brain. Yangonin can decrease dopamine levels in the brain and counteract this medication.
  1. This is also correct. CYP1A2 is the pathway of metabolization for caffeine. Kava causes inhibitory actions at this pathway and as such causes caffeine to appear in serum levels for much longer than without kava in the system. The individual effect of this combination may differ from person to person. CYP1A2 activity has a range of 40% between individuals. As such it’s quite difficult to make predictions of which drugs will do what when this pathway is inhibited.
  1. Correct as well; however, issues at this cytochrome with drugs that use this pathway are not heavily researched in regards to kava. They generally encompass the sedative effects and their increase when in combination with the drugs above. Caution should still be taken when combining these drugs with kava as it will likely make them stay in your system for considerably longer periods of time. DMY seems to be the most potent inhibitory kavalactone in this regard.
  1. This inhibition was seen strongest with methysticin, the number 6 on chemotypes. The effect seen with methysticin was low, with only 1% of the strength of their positive control (Sulfaphenazole). I truly believe this would not have a strong impact on drugs that also use this pathway being kava/kavalactones have such a low affinity for it.
  1. This is incorrect. Kava has no inhibition property at this cytochrome even at absurdly high concentrations, and as such this is wrong.
  1. Again methysticin is the only kavalactone shown to interact with this cytochrome and it does it quite weakly. I wouldn’t suspect any immediate issues with drugs that use this pathway combined with kava.
  1. This effect, if present, will be very light. Kava has shown very slight inhibitory properties at CYP3A4 with methysticin being the most potent inhibitor. Methysticin has shown to be about 1% the inhibitory properties of their positive control, Ketoconazole. I would not expect major interactions with pharmaceuticals along this pathway with kava.
  1. A single dose of 800mg kavain gave a serum concentration level of 40ng/ml or .1um. This plasma level is unlikely to cause any significant inhibition of P-gp in vivo. Also, 800mg of kavain is quite unlikely to be consumed at once in a typical kava consuming session. The likelihood of inhibition here is very low. Results obtained in vitro vs in vivo were contradictory.
  1. It should be obvious to limit the intake of liver toxic compounds, however some of them are rather ubiquitous. Acetaminophen, also known as APAP, Panadol, Paracetamol, and Tylenol is a potent hepatotoxic drug due to its metabolites. Kava likely does not interact with these drugs other than APAP. There is research leaning to indicate that the combination of APAP and kava should be avoided on the issue of glutathione degradation. IF kava does indeed reduce glutathione levels, mixing it with APAP would increase its toxicity.
  2. Dosing
  3. Paragraph 1 “By Mouth: For anxiety: 50-100 mg of a specific kava extract (WS 1490, Dr. Willmar Schwabe Pharmaceuticals), taken three times daily for up to 25 weeks, has been used. Also, 400 mg of another specific kava extract (LI 150, Lichtwer Pharma) taken daily for 8 weeks has been used. Five kava tablets each containing 50 mg of kavalactones have been taken in three divided doses daily for one week. One to two kava extract tablets has been taken twice daily for 6 weeks. Calcium supplements plus 100-200 mg of kava taken daily for 3 months have also been used.”
  4. This really doesn’t tell us anything to go by for our own personal dosing. In truth, there is no recommended dosage for powdered kava. These dosage recommendations come from several studies as well as the German Commission E. I take it that these numbers indicate the minimum amount of kavalactones it requires to see any effect without seeing intoxication. Seeing that many of us aim for intoxication these numbers are simply meaningless.
Citations Removed for length. See kavaforums post for full citations.
Kavaforums Discussion Thread: https://kavaforums.com/forum/threads/webmds-article-on-kava.19070/
submitted by JP1021 to Kava [link] [comments]


2020.12.06 13:27 Hustle-IE My recent experience

long post sorry
Hi folks.
I feel comfort in reading these posts. To know your not alone is very powerful. I just want to explain what’s going on with me currently.
So I guess I started have a general feeling on being unwell two weeks ago now. I was visiting my folks, sitting on the sofa 🛋 and all of a sudden out of the blue I thought I was going to die. I got this sensation up my body into my head. Then felt like there was a very tight belt around my head squeezing my brain. I had to get up and walk away. I went to the bathroom, my pupils were completely dilated. I just felt TERRIFIED. I was hot and bothered and at this stage my heart started to race. I didn’t hyperventilate and was able to breath but I felt HORRENDOUS. Jelly legged and super heightened. My eyes were sensitive. Hot. Focusing was harder. I can’t explain the feeling other than I literally thought I was a gonner. This continued for 30 minutes and then I stated to calm down. Pulse was returning to near normal. But I was left with this band like feeling around my head, pressure on the top of my head and it was radiating up from my neck into my head. It wasn’t a headache as such. You know not the “bang bang” but there was pressure there. My eyes were also just bothered. Hot, sore, strained etc. (Granted I do a lot of work with screens but this is different) anyways I was super annoyed that this happened to me as I hadn’t experienced something similar to this in about 5 years.
5 years ago I was prescribed 10mg of lexapro (for two years) and diazepam a couple times a day for a month to probably combat the side effects of lexapro I’m assuming. So for a few years I’ve been great. I started weaning off lexapro 3 years ago. I had gained a stone and wanted to get that under control.
Anyways since my episode two weeks ago, i just haven’t been well. I’m not eating, I’m worried all the time. I’ve lost 10lbs. I can’t think of anything else other than how I’m feeling. I’m catastrophizing everything. I also have “avoidance health anxiety” meaning I absolutely fear what the doctor is going to tell me. Like to the point I didn’t go to the GP from age 13 to 25. At 25 (5 years ago) I reached a point of complete despair.
Anyways this past two weeks I tried battling alone. I just felt terrible a lot of the time. I had 6 months of 5mg lexapro in my cupboard and decided to take it. It makes me nauseous and super awake, tension headaches are not going away, not sleeping etc. So of course I was driving myself DEMENTED with all the possible scenarios. I was crying daily through sheer helplessness and sick of feeling the way I felt so on Friday evening I got an emergency appointment with my doctor. I had spent 3 hours that day crying. Gagging on food. Horrible feeling in my head. Eyes burning. Etc etc etc. I had reached the end of my tether.
Anyways I went in TERRIFIED so so so scared. The minute he sat in front of me I burst into tears. He was so supportive, I’m very lucky. Anyways, he convinced me that he needed to check my blood pressure, my heart and my lungs. All were fine. Obviously my heart was running faster due to the sheer stress of being in the practice but he said it was all very normal. Then he checked my eyes with two different Ophthalmoscope. One to see how my pupils reacted to light and the other to look at the entire back of my eye. This was scary. Because he took a bit of time to do this properly and I had expressed my eyes being very annoying currently. Anyways he told me they were perfect so I sat there looking at him like “why am I such a psycho” and he just explained that the symptoms I feel are very real but it’s my body doing it to me. I have to pluck up the courage soon to get a full blood panel ran but waiting for the meds to be in my system for a while.
Anyways he has upped the 5mg of Lexapro that I started myself to 10mg immediately. He put me on 5mg of Diazepam 3 times per day for 3 weeks. Also prescribed Inderal (a beta blocker used for anxiety) 4 times a day at 10mg a dose. I didn’t really want to be put on Inderal, I have a resting heart rate of 58-60. I’m normally very active with sport (not the in past two weeks due to feeling awful) and I have low-normal blood pressure all the time. I started taking the diazepam and instantly felt a lot better. Tension not fully gone but it was definitely take the edge off it. I was also able to sleep.
BUT..... on day 2 on inderal I had a very scary experience, I was out in the cold for a half hour. Granted probably not wearing enough clothes and my face, hands and feet were FROZEN. My mouth, tongue, face got so cold I could barely speak. I came in and looked at my gums and they were SNOWWWWW white. I really frightened myself. Of course I went to “omg I’m bleeding internally” ... “omg I have very dangerous anemia” but I believe it was most definitely the inderal having an effect on my thermoregulation. After a hot cup of green tea and a blanket around me my gums returned to their pink colour. But I was honestly none the better of the fright I got. I felt AWFUL. So I’ve stopped taking the beta blocker until I speak with the doctor tomorrow. It may just not be for me. I’m 5”6 and 154lbs. With good cardiac health.
I just can’t keep thinking that there’s really something wrong. I’m sick to my stomach when I wake up in the morning. My appetite is gone. I have a general feeling of unease. Mornings and nights seem to be the worst. The Valium definitely gets me to sleep and keeps me asleep which is something was has been really needed. I know it’s only been two days.
My question is, is this normal????? Is it me? Is it the lexapro? I honestly feel like the Lexapro made me worse. I’m probably 8 days in at 5mg of lex and 2 days in at 10mg.
Am I going to feel normal soon? I just feel so helpless.
submitted by Hustle-IE to HealthAnxiety [link] [comments]


2019.07.15 00:44 decrepit_plant I believe I am the definition of treatment resistant bipolar depression. I have tried 33 different medications (list below). I have completed over 30 rounds of ECT (Electroconvulsive therapy). I’m halfway through TMS (Transcranial magnetic stimulation). What other treatments are our there?

Medications have only provided me with negative side effects and very little remission.
List of the medications I have tried -
Antidepressants: Desvenlafaxine (Pristiq), Bupropion (Wellbutrin), Duloxetine (Cymbalta), Fluoxetine (Prozac), Venlafaxine (Effexor), Paroxetine (Paxil), Citalopram (Celexa), Sertraline (Zoloft)
Anxiolytics and Hyrnotics: Zolpidem (Ambien), Alprazolam (Xanax), Buspirone (BuSpar), Clorazepam (Klonopin), Lorazepam (Ativan), Propranolol (Inderal), Diazepam (Valium)
Antipsychotics: Asenapine (Saphris), Ziprasidone (Geodon), Aripiprazole (Abilify), Brexpiprazole (Rexulti), Cariprazine (Vraylar), Quetiapine (Seroquel), Risperidone (Risperdal), Lurasidone (Latuda), Chlorpromazine (Thorazine), Olanzapine (Zyprexa)
Mood Stabilizers: Lamotrigine (Lamictal), Valproic acid/divalproex (Depakote), Gabapentin (Neurontin), Lithium (Eskalith)
ADD/ADHD: Amphetamine salts (Adderall), Atomoxetine (Strattera), Lisdexamfetamine (Vyvanse), Methylphenidate (Ritalin, Concetta)
ECT brought my suicidal depression down from a 12/10 to a 5/10. It is much more manageable but still didn’t give me the full remission. Also my depression got worse 6 months after treatment stopped.
TMS seemed promising but I’m halfway through already and I haven’t experienced much relief from my depression.
I feel like I’m at my wits end. I just want to feel better.
submitted by decrepit_plant to bipolar [link] [comments]


2018.05.28 01:54 ExpensiveDonut Experience with treatments for CFS, depression and anxiety

Hello fellow redditors! I decided to make this post about treatments to share my trials and errors so far and to see if there are people on here who's had some sort of succesfull response to a supplement or medication for their CFS.
Long story short i have been battling with chronic fatigue for several years now (7-8 years) with loads of other symptoms that has fluctated in severiy througout the years. Recently it got so bad that i had to drop out of school and postpone everything indefinately. I have been suspicious of having CFS for years now but because i also struggle with anxiety and depression my doctors have always pointed to those being the sole reason for my fatigue (which i always knew it wasnt). The fatigue always persisted regardless if i was depressed or not.
Although i havent officially been diagnosed with ME/CFS yet, i have been thouroughly examined by my doctor and have gone through loads of testing to rule out any other possibilities for my symptoms (hypothyroidism, celiac, addisons etc). My doctor is confident that what i have is CFS and has sent a refferal to a CFS specialist for further examination and diagnosis. The only other test i havent had yet to completely rule out other possible causes for my symptoms are a sleep test to check for sleep apnea and narcolepsy. This i will get done eventually.
Symptoms:
Besides the chronic fatigue, the symptoms that bother me the most are the constant brain fog and lack of mental clarity that makes focusing on everything from reading to thinking hard. Also the constant anhedonia makes everyday life miserable. Pain is also a small problem but not as big as the others.
I know that some of the symptoms might be caused or exacerbated by the depression and anxiety, but i also believe that these are very intertwined with the CFS and can be symptoms of the desease itself. So therefore im going to list up the generally most debilitating symptoms that i am looking to get treatments for.
Treatments:
Since i've got these symptoms i am eager as all of you to find things (supps, meds) that will actually help me feel better and function better in everyday life. I have been reading alot lately about potential treatments for CFS and have tried some of them already to minimal success. NAC, vitamin D, vitamin B complex, omega 3 and magnesium. I have also tried loads of medications for anxiety and depression over the years that has indirectly had a positive (or negative) effect on my CFS. What i have responded best to in this regard is Lyrica (Pregabalin).
The most effective medications i have tried thus far is:
Meds that slightly worked:
Meds that didnt work or make me feel worse:
After extensive reading i have found the following supps and meds might be worth a shot:
Questions:
Im sorry for the lengthy post, i just decided i might as well get it all out there while im at it. Also sorry if you feel i went too off topic, but as i said, i feel like depression and anxiety are so intertwined with CFS that i feel they are relevant.TLDR: See questions at the bottom.
UPDATE 10/06/18:
I have now ordered several supplements to try and treat my various symptoms. These are supplements (antioxidants, herbs) i have read alot about and they seem to be effective for various symptoms of CFS. I will write the list of supplements i have ordered and will report back once i know their effects.
Supplements i have ordered:
All of the info i got on these various supplements are taken from various anecdotal sources around the web, mainly the Pheonix Rising forums and here on Reddit. I will report back in a few weeks on how these supplements affects me.
Some of the posts where i read about the various supplements:
https://forums.phoenixrising.me/index.php?threads/five-ways-to-reduce-your-me-cfs-wired-but-tired-hyperaroused-brain-state.44269/
https://forums.phoenixrising.me/index.php?threads/what-fixed-aided-your-brain-fog.43340/
https://forums.phoenixrising.me/index.php?threads/completely-eliminated-my-severe-anxiety-symptoms-with-three-supplements.18369/
Update 19/6:
I have now gotten ahold of most of the supplements i ordered, as well as tramadol for pain. Im also back on LDN.
Tramadol was not as effective as i expected. It doesnt do much for my backpain and i cant really notice much effect at the 50-100mg doserange. I would actually say that lyrica is just as effective for pain management.
While waiting for sarcosine and a few additional supplements i ordered (5-htp, jarro-dophilus (probiotic) im also trying out a FODMAP diet to fix my stomach issues and hopefully brain fog.
Current regimen:
Morning:
Supps:
Meds:
Evening:
Supps:
Meds:
PRN: PQQ, Bacopa, L-theanine, baclofen, valium.
submitted by ExpensiveDonut to cfs [link] [comments]


2014.06.13 15:50 gheyddit Drugs that may cause impotence

The following is a list of medications and nonprescription drugs that may cause impotence in men:
Antidepressants and other psychiatric medications:
Amitriptyline (Elavil) Amoxapine (Asendin) Buspirone (Buspar) Chlordiazepoxide (Librium) Chlorpromazine (Thorazine) Clomipramine (Anafranil) Clorazepate (Tranxene) Desipramine (Norpramin) Diazepam (Valium) Doxepin (Sinequan) Fluoxetine (Prozac) Fluphenazine (Prolixin) Imipramine (Tofranil) Isocarboxazid (Marplan) Lorazepam (Ativan) Meprobamate (Equanil) Mesoridazine (Serentil) Nortriptyline (Pamelor) Oxazepam (Serax) Phenelzine (Nardil) Phenytoin (Dilantin) Sertraline (Zoloft) Thioridazine (Mellaril) Thiothixene (Navane) Tranylcypromine (Parnate) Trifluoperazine (Stelazine) 
Antihistamine medications (certain classes of antihistamines are also used to treat heartburn):
Cimetidine (Tagamet) Dimenhydrinate (Dramamine) Diphenhydramine (Benadryl) Hydroxyzine (Vistaril) Meclizine (Antivert) Nizatidine (Axid) Promethazine (Phenergan) Ranitidine (Zantac) 
High blood pressure medicines and diuretics ("water pills"):
Atenolol (Tenormin) Bethanidine Bumetanide (Bumex) Captopril (Capoten) Chlorothiazide (Diuril) Chlorthalidone (Hygroton) Clonidine (Catapres) Enalapril (Vasotec) Furosemide (Lasix) Guanabenz (Wytensin) Guanethidine (Ismelin) Guanfacine (Tenex) Haloperidol (Haldol) Hydralazine (Apresoline) Hydrochlorothiazide (Esidrix) Labetalol (Normodyne) Methyldopa (Aldomet) Metoprolol (Lopressor) Nifedipine (Adalat, Procardia) Phenoxybenzamine (Dibenzyline) Phentolamine (Regitine) Prazosin (Minipress) Propranolol (Inderal) Reserpine (Serpasil) Spironolactone (Aldactone) Triamterene (Maxzide) Verapamil (Calan) 
Among the antihypertensive medications, thiazides are the most common cause of ED, followed by beta-blockers. Alpha-blockers are, in general, less likely to cause this problem.
Parkinson's disease medications:
Benztropine (Cogentin) Biperiden (Akineton) Bromocriptine (Parlodel) Levodopa (Sinemet) Procyclidine (Kemadrin) Trihexyphenidyl (Artane) 
Chemotherapy and hormonal medications:
Antiandrogens (Casodex, Flutamide, Nilutamide) Busulfan (Myleran) Cyclophosphamide (Cytoxan) Ketoconazole LHRH agonists (Lupron, Zoladex) 
Other medications:
Aminocaproic acid (Amicar) Atropine Clofibrate (Atromid-S) Cyclobenzaprine (Flexeril) Cyproterone Digoxin (Lanoxin) Disopyramide (Norpace) Estrogen Finasteride (Propecia, Proscar, Avodart) Furazolidone (Furoxone) H2 blockers (Tagamet, Zantac, Pepcid) Indomethacin (Indocin) Lipid-lowering agents Licorice Metoclopramide (Reglan) NSAIDs (Ibuprofen, etc.) Orphenadrine (Norflex) Prochlorperazine (Compazine) Pseudoephedrine (Sudafed) 
Opiate analgesics (painkillers)
Codeine Fentanyl (Innovar) Hydromorphone (Dilaudid) Meperidine (Demerol) Methadone Morphine Oxycodone (Oxycontin, Percodan) 
Recreational drugs: Alcohol Amphetamines Barbiturates Cocaine Marijuana Heroin Nicotine
Source: http://www.nlm.nih.gov/medlineplus/ency/article/004024.htm : http://www.webmd.com/erectile-dysfunction/guide/drugs-linked-erectile-dysfunction
submitted by gheyddit to ScumbagMedicine [link] [comments]


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