Cyproheptadine + Aspirin Safety?

[tomisonbottom]

You can get internal bleeding if you have bad ulcers. You can also get bleeding in the brain, even though the studies using aspirin only found it reduced that type of bleeding. Not sure if adding cyproheptadine makes it worse, but I would not risk it. I think adding 5mg K2 is a wise idea if using both aspirin and cypro.

I take aspirin and cypro and didn't know they were contraindicated. Is bruising considered internal bleeding? Is that the best way to know if there's a problem if there's no obvious pain?

 

[DaveFoster]

I've taken 16 mg cyproheptadine for months with around 1 - 2 grams aspirin daily: no bleeding issues, but I've taken occasional famotidine (40 mg ~once per week).

 

[Deleted member 5487]

Never seen anything to imply it is not safe. However, since both of them sedate people I'd use at night. You don't want to get groggy on the road or at work.

I have been experiencing stimulation with cypro and not being able to go bed till 3am(as im writing this) with .5mg 2x a day. I am tired during the day but energized at night now. Dosing in the morning and night.

Any thoughts on why?

 

[InChristAlone]

I have been experiencing stimulation with cypro and not being able to go bed till 3am(as im writing this) with .5mg 2x a day. I am tired during the day but energized at night now. Dosing in the morning and night.

Any thoughts on why?

Try just a few hrs before bed.

 

[Logan-]

@tara, could you write an update on your pizotifen experience? Are you still using it for the migraine prophylaxis? I have been suffering from chronic migraines for years and found this medication (theoretically) to be not as bad as the other prophylactic agents. I'd appreciate it if you could write your experiences and thoughts on it.

 

[Logan-]

@haidut, what's your take on the long term use of pizotifen for the prophylaxis of migraine? Would it cause permanent changes/harm in the brain? Which one is safer to use long term, cyproheptadine or pizotifen?

 

[haidut]

@haidut, what's your take on the long term use of pizotifen for the prophylaxis of migraine? Would it cause permanent changes/harm in the brain? Which one is safer to use long term, cyproheptadine or pizotifen?

They basically the same molecule. I think no drug should be used as the sole method for controlling a condition, including migraines. I posted a few studies showing that migraines are due to high serotonin and low brain ATP. So, if metabolism recovers there should be no need to use pizotifen indefinitely. Pizotifen, cyproheptadine and ketotifen are basically the same molecule and ketotifen seems to have the fewest reports of side effects but it is weaker as a serotonin antagonist than pizotifen and cypro. So, in terms of safety I would probably rank them as ketotifen, pizotifen, cypro and in terms of helping with migraine the ranking would be exactly the opposite.

 

[Logan-]

They basically the same molecule. I think no drug should be used as the sole method for controlling a condition, including migraines. I posted a few studies showing that migraines are due to high serotonin and low brain ATP. So, if metabolism recovers there should be no need to use pizotifen indefinitely. Pizotifen, cyproheptadine and ketotifen are basically the same molecule and ketotifen seems to have the fewest reports of side effects but it is weaker as a serotonin antagonist than pizotifen and cypro. So, in terms of safety I would probably rank them as ketotifen, pizotifen, cypro and in terms of helping with migraine the ranking would be exactly the opposite.

Thank you. I've been consuming about 20-25 grams of ginger powder every day for my chronic migraines. What do you think about this dosage? Toxicity studies suggest that ginger is one of the least toxic substances out there, but this dose is still high. The only problem I can think of is brain hemorrhage due to its anti-thrombotic action, but I supplement with Thorne K2 every day. Could you share your views on the long term use of ginger powder with this dosage?

Here is the study that opened my eyes to this:

Maghbooli, M., Golipour, F., Moghimi Esfandabadi, A. and Yousefi, M. (2014), Comparison Between the Efficacy of Ginger and Sumatriptan in the Ablative Treatment of the Common Migraine. Phytother. Res., 28: 412–415. doi:10.1002/ptr.4996

 

[haidut]

Thank you. I've been consuming about 20-25 grams of ginger powder every day for my chronic migraines. What do you think about this dosage? Toxicity studies suggest that ginger is one of the least toxic substances out there, but this dose is still high. The only problem I can think of is brain hemorrhage due to its anti-thrombotic action, but I supplement with Thorne K2 every day. Could you share your views on the long term use of ginger powder with this dosage?

Here is the study that opened my eyes to this:

Maghbooli, M., Golipour, F., Moghimi Esfandabadi, A. and Yousefi, M. (2014), Comparison Between the Efficacy of Ginger and Sumatriptan in the Ablative Treatment of the Common Migraine. Phytother. Res., 28: 412–415. doi:10.1002/ptr.4996

I think 25g ginger daily is fine. Many cultures around the world consume even more on a daily basis. Its main benefit is probably due to ginger being serotonin (5-HT3) antagonist. VItamin B2 is also used clinically for migraine as it increases serotonin degradation. Methylene blue may also help in low doses (1mg daily).

 

[Logan-]

I think 25g ginger daily is fine. Many cultures around the world consume even more on a daily basis. Its main benefit is probably due to ginger being serotonin (5-HT3) antagonist. VItamin B2 is also used clinically for migraine as it increases serotonin degradation. Methylene blue may also help in low doses (1mg daily).

I have tried eating that much, even more fresh ginger for migraines, but that didn't work. Only the powder form works with this efficiency. I think the powder form has a significantly higher and faster absorption rate, thus making it quite different from eating the fresh ginger (which has poor absorption). You said "Many cultures around the world consume even more on a daily basis.", I think people generally consume ginger in its fresh form, or am I wrong? Don't you think consuming it in its powder form makes a difference in regards to its dosing?

Serotonin antagonism, inhibition of nitric oxide synthesis, reduction of lipid peroxidation in the brain, inhibition of prostaglandin synhesis, reduction in the cerebral inflammation etc. all could be playing roles in the abortive effect of ginger, I guess. Ginger is considered as a "dual acting anti-inflammatory", which makes it safer for the gut.

"Several mechanisms have been proposed to justify the analgesic action of ginger, including the inhibition of arachidonic acid metabolism via the cyclooxygenase (COX) pathways, similar to the non-steroidal anti-inflammatory drugs (5). Ginger also acts to block lipoxygenase (LOX), another enzyme associated with the arachidonic acid pathway (11). The concomitant inhibition of COX and LOX may increase anti-inflammatory action and reduce its side effects (12).
...
During migraine attacks, trigeminal nerve fibers are activated releasing neuropeptides that trigger the production of inflammatory mediators such as cytokines, bradykinin and prostaglandins, which activate nociceptive pathways (29,30). Drugs used in the treatment of pain usually act by altering the transduction and/or modulation of nociception (31). Previous studies have shown that ginger components, mainly gingerols and shogaols, are able to decrease prostaglandin production through COX-2 inhibition, inducing pain relief (6,31,32). Leukotriene production is also decreased by ginger components through 5-lipoxygenase (5-LOX) inhibition (11). Concomitant blocking of COX-2 and 5-LOX potentiates anti-inflammatory effects and reduces the side effects observed when only COX-2 is inhibited (12). Furthermore, 6-shogaol modulates neuroinflammation by inhibition of proinflammatory cytokines expression in microglial cells (13). Together, the proposed mechanisms and the available evidence suggest a potential role of ginger in acute migraine."
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Dual acting anti-inflammatory drugs.

Leone S1, Ottani A, Bertolini A.

Author information

Abstract

Drugs able to inhibit both cyclooxygenases (COX-1 and COX-2) and 5-lipoxygenase (5-LOX) (dual acting anti-inflammatory drugs) have been designed in order to obtain compounds that retain the activity of classical nonsteroidal anti-inflammatory drugs (NSAIDs) while avoiding their main drawbacks. The classical NSAIDs display their anti-inflammatory action mainly through inhibition of COX and one of their main drawbacks is the curtailed production of gastroprotective prostaglandins (PGs) being associated with the concurrent increased production of the gastro-damaging and bronchoconstrictive leukotrienes (LTs). Leukotrienes and cysteinyl-leukotrienes are moreover pro-inflammatory and increase microvascular permeability. One of the leukotrienes (LTB(4)) is the most potent chemotactic agent and it induces chemotaxis of eosinophils, neutrophils and monocytes in the inflamed tissue, increases superoxide generation and proinflammatory cytokines production. It is further advantageous for a drug to have both COX and 5-LOX inhibiting activities because prostaglandins enhance leukotriene-mediated inflammation. Various structural families of dual inhibitors have been designed and several compounds are currently undergoing clinical development. In the post-COX-2 selective inhibitors era, these dual acting inhibitors may turn out to be promising new drugs to treat inflammatory diseases and possibly other diseases. Indeed, both COX-2 and 5-LOX are also involved in the development and progression of several types of cancer; in these conditions, selective inhibition of COX-2 alone may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway, and therefore the blockade of both COX-2 and 5-LOX may produce a better anticancer response. In addition, the dual inhibition of both COX and 5-LOX is neuroprotective by suppressing toxic actions of reactive microglia and macrophages, that are increased in aging brain and in age-related degenerative conditions, particularly Alzheimer's and Parkinson's diseases. Finally, the blockade of 5-LOX does not impair the synthesis of lipoxins (LXs), which are mainly produced by further lipoxygenation of 15-HPETE, and which have potent anti-inflammatory properties and can be considered as stop-signal mediators. Leukocyte 15-LOX and platelet 12-LOX by intercellular mechanism via leukocyte/platelet cell-cell interaction convert 15-HPETE into lipoxins.

Dual acting anti-inflammatory drugs. - PubMed - NCBI


I have been taking 400 mg riboflavin every day for migraine prophylaxis. I guess it's helping, especially for the ocular problems.

Magnesium glycinate is also helpful.

I had read methylene blue increases the brain serotonin level at 1 mg, so I didn't investigate it further for migraine. It could be wrong though. Why do you think MB would help? Because of its effects on energy metabolism? Do you suggest its use as an every day prophylactic, or as an abortive?