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Acetium - clinical trial

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Tony Only mentions Acetium in another thread, which I didn't want to potentially hijack with this message.  A clinical trial of Acetium for CH is apparently underway, as Tony said there.


Biohit Oyj Stock Exchange Release April 29, 2014 at 4:30 pm local time (EEST)

Biohit Oyj initiates two clinical trials for prevention of migraine-type headache attacks, testing the efficacy of Acetium® capsule in novel clinical indications. The purpose of the trial is to assess the effect of Acetium® capsule in prevention of headache attacks   among patients suffering from migraine or cluster/Horton headache. Both studies will be conducted as multi-center clinical trials in collaboration with Terveystalo Oy and Aava Medical Center altogether in six cities in Finland.

The study hypothesis is based on the fact that acetaldehyde liberates histamine from the mast cells which are ubiquitous in all human tissues.  Histamine in turn is a well-known trigger of the acute attacks of vascular-type headaches (migraine, cluster).  By preventing the local effects of acetaldehyde with Acetium® capsules, it might be possible to prevent the headache attacks in these two categories of patients.

Both studies will be conducted as placebo-controlled, double-blind clinical trials, where half of the subjects will receive the active compound and the other half will receive a placebo.

    Acetium® capsule in prevention of headache attacks among patients with cluster headache:

    altogether, 100 subjects with clinically diagnosed cluster headache will be enrolled in the study.<<

There's also a "discussion" of Acetium over at CH.com, characterized in part by the fierce skepticism that seems to greet any new idea there. http://www.clusterheadaches.com/cgi-bin/yabb2/YaBB.pl?num=1381768499/23

It seems that Acetium can be purchased throughout Europe, but not in the US.  Maybe I'm reading that wrong. 

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Acetium has helped me quite a lot, but it's too expensive for me and and almost same results could be achieved getting rid of or staying away from acetaldehyde. It's interesting to follow this one though since it has already seemed to help so many (in Finland).

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No, they didn't want me, I am doing "too well". I think they need people in a cycle who don't have means to control their CH. It has been available here for quite a while already, one can buy it without prescription from a pharmacy.

I only use it when I am stupid enough to smoke cigarettes which equals trouble for my CH. E-cigarettes don't form acetaldehyde so mainly use those nowadays.

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  • 3 weeks later...

Acetaldehyde belongs to the larger chemical family of aldehydes, which are pervasive environmental toxins. The human body possesses enzymes that convert it to a less-harmful substance and therefore is protected from small exposures. However, acetaldehyde at toxic levels can make its way into the brain from sources such as alcohol consumption, Candida sp. (yeast) overgrowth, breathing air contaminated with acetaldehyde from cigarette and other smoke, smog, vehicle and factory exhaust, synthetic fragrances and many commercially manufactured materials. Acetaldehyde and its close relative formaldehyde are used in the synthesis of chemicals such as plastics, dyes, fabrics, adhesives, fuels, plywood, particleboard, insulating foam, fragrances, preservatives and more. Besides being an occupational hazard, these materials are found throughout the home especially in new carpets, furniture and floors and can out-gas aldehydes into the air for years, creating continuous exposure. Aldehydes are among the top chemicals released into the environment daily.

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I did notice my son taking TUMS yesterday .. i have noticed that in the past with the CH comes the acid reflux ,, related or coincidence i don't know .. but an observance non the less.

Acetaldehyde Exposure


One of the main significant acetaldehyde exposure routes is through alcohol (ethanol) consumption. Ethanol metabolism starts with the conversion of alcohol to acetaldehyde, which is at least 30 times more toxic than alcohol. Ideally, acetaldehyde is then oxidized to acetic acid and ultimately into Acetyl-CoA, which will be used for cellular energy. Unfortunately, in many if not most people, this conversion is slow and not always efficient due to genetic variations of the enzymes that perform this step, insufficient nutrient cofactors or exposure to related chemicals utilizing the same metabolic enzymes and nutrients. The result may be high acetaldehyde levels, which can cause significant damage to the liver where the bulk of alcohol metabolism occurs.1 Other alcohol metabolism sites that expose tissue to acetaldehyde’s damaging effects are the pancreas, gastrointestinal tract and in particular, the brain.2-3 Alcohol may result in “drunkenness”—the central nervous system effects of relaxation, loss of coordination and inhibition of judgment—but acetaldehyde is responsible for the “hangover,” the toxic side effects that can eventually damage the brain.


Another important exposure route to toxic acetaldehyde levels is through its production by the opportunistic yeast, Candida albicans. In small numbers, this yeast may be kept in check in the gut by the immune system and friendly bacteria such as Lactobacillus sp. and Bifidobacterium sp. But in many people, increasing carbohydrates, especially sweets, will cause chronic Candidiasis. Candida produces acetaldehyde in the GI tract by sugar fermentation. The typical American diet along with drug and antibiotic therapies, hypochlorhydria (low stomach acid), chronic stress, environmental toxins, etc. have altered gut integrity and immunity and predisposed millions of people to yeast overgrowth or the “Candida Syndrome.”4 A person with this condition who also drinks beer, wine or liqueurs not only produces acetaldehyde from the alcohol but also delivers more sugar for yeast production of acetaldehyde, creating a double-barreled dose. Acetaldehyde produced in the gut can eventually reach more parts of the body, flooding the system and increasing the risk for damage.5


Through the burning of tobacco, petroleum fuels, natural gas, wood and trash, aldehydes, including acetaldehyde, are present in the air we breathe. Vehicle and factory exhaust can create a chronic but significant exposure source to those who live near heavily trafficked areas or who spend hours commuting on freeways. Acetaldehyde contributes to photochemical “smog” formation when it reacts with other volatile substances in the air. Open car windows increase exposure, as does breathing in acetaldehyde-containing fumes near gas pumps. Cigarette smokers and others around them are exposed through inhaling smoke. According to the Environmental Protection Agency (EPA), wood smoke from campfires, wood-burning stoves and residential fireplaces is more toxic than cigarette smoke. But the acetaldehyde level released from burning items such as plastics, styrofoam and batteries is even higher.6 While acetaldehyde exposure from auto exhaust and cigarettes may be less than that from alcohol, research shows that low dose chronic exposure may still be sufficient to gradually damage proteins, enzymes and other cellular structures in the brain and other organs.7

Furthermore, most fragrances today are made from synthetic chemicals, many of which are toxic. Air fresheners, scented candles, cleaning products, cologne or perfume and more can create a source of chronic exposure to many toxic chemicals including acetaldehyde. Children and babies are particularly susceptible. Additionally, the Environmental Working Group (EWG) lists acetaldehyde as one of the contaminants released from polyethylene plastic bottles.8

Detrimental Effects

Acetaldehyde is classified as a probable human carcinogen linked to nose and throat irritation and cancer as well as a toxicant to the neurological (neurotoxin), respiratory, endocrine and immune systems. Animal research also shows that this chemical crosses the placental barrier causing skeletal deformities, reduced birth weights and infant death.9

Acetaldehyde significantly compromises brain function. It is considered to be the substance that directly contributes to the toxic effects and the chemical dependency to alcohol and cigarettes. Addictive, opiate-like biochemicals are formed in the brain when acetaldehyde combines with the key neurotransmitters, dopamine and serotonin. In acetaldehydeÂ’s presence, dopamine is converted into salsolinol and serotonin into beta-carboline, both of which are very addictive tetrahydroisoquinolines (TIQs).10-11 Moreover, metabolites of salsolinol are neurotoxic to dopaminergic neurons inducing cell death and eliciting symptoms nearly identical to idiopathic ParkinsonÂ’s disease.12-13

Acetaldehyde damages the membranes of red blood cells (RBC) making them less flexible in passing through tiny capillaries, and it can alter hemoglobin, the oxygen transporter in the RBC.14 These two effects reduce available oxygen to the cells, especially in the brain.

Acetaldehyde disables the protein tubulin from assembling into microtubules in the brain.15 Microtubules structurally and nutritionally support the dendrites, the feathery-looking extensions from the nerve cellsÂ’ main body, which connect many nerve cells to each other. Without the microtubules, the dendrites atrophy and die. This can be seen in chronic alcoholism and AlzheimerÂ’s disease.

Acetaldehyde and Nutrient Deficiencies

In addition to its toxic effects, acetaldehyde induces deficiencies of nutrients used for its detoxification. As an example, vitamin B1 (thiamine) is depleted through alcohol and acetaldehyde detoxification.16 B1 is essential in carbohydrate metabolism for energy production, of which  the brain uses 20 percent. Acetaldehyde-induced B1 depletions exacerbate the already low B1 levels common in the population due to diuretics and other drugs, over-consumption of simple carbohydrates (dysglycemia) and adrenal stress. In addition to its many functions, thiamine, the “nerve vitamin,” is critical to nerves and neurotransmitters. Even mild, chronic B1 deficiency can produce brain-related symptoms such as emotional instability, confusion, depression, fatigue, irritability, headaches, sensitivity to noise, insomnia, decreased short-term memory, brain-fog and a feeling of impending doom.17-18

Relevant to this time of year, B1­deficiency-related lactic acidosis can make people more vulnerable to bug bites, since many insects, particularly mosquitoes, are attracted to mild acids.19

Furthermore, people with chemical sensitivities to aldehydes may also be sensitive to seemingly unrelated substances like sulfites (preservatives) from wines and foods, and the smell of chlorine from pools and bleach.

The under appreciated essential trace mineral molybdenum is also involved with acetaldehyde metabolism. A molybdenum deficiency not only affects this process but also other enzymes in the body that require molybdenum as a cofactor—for example, sulfite oxidase, responsible for converting irritating sulfites into harmless sulfates for use in liver detoxification and cartilage. Sulfur-containing amino acids, as important free radical scavengers, also use this molybdenum-dependent pathway. Molybdenum has been shown to reduce sulfite sensitivity by increasing sulfite oxidase activity.20 Sulfites also destroy vitamin B1’s biological activity, contributing to a deficiency. Nutrient depletion leads to sensitivity to other chemicals that use these same pathways. This has been demonstrated in patients with Candidiasis as the excess stress put on the enzyme systems to detoxify acetaldehyde often leave them with sensitivities to multiple chemicals especially fragrances. Supplementing with the appropriate cofactors may improve an individual’s ability to handle Candida-generated acetaldehyde.21

Acetaldehyde Relief

Acetaldehyde toxicity can be acute or chronic. In order to stop this toxicity, levels of key nutrients that metabolize and clear acetaldehyde must be adequate. Some of these nutrients are cofactors to the enzymes that metabolize acetaldehyde and others, such as sulfur-containing compounds, are necessary to scavenge or “mop up” any stray un-metabolized acetaldehyde. Supplementation with specific nutrients offers an important level of prevention and protection from toxicity. In one animal study, pretreatment of the animals with B1, vitamin C and the sulfur-containing amino acid cysteine completely blocked the LD-90 dose of acetaldehyde (the dose that would normally kill 90 percent of the animals).22 In another study, cysteine lowered in the digestive tract the amount of acetaldehyde produced by smoking and alcohol consumption. Both of these risk factors are considered the main causes of upper digestive tract cancer in 75 percent of developed countries with acetaldehyde as the probable cause.23

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ok one more comment on this

last year he had the same problem ... right after 4th of July hit with clusters for 4 - 6 days ...

this year right after 4th of July hit with clusters for 1 day

and why would the 4th be significant you ask

because FIREWORKS are legal in my city ,, and they shoot them off in the street .. our streets are covered in smoke from these fireworks ...

why were his headaches worse last year and not this year  ??

because last year they shot off 120$ worth of them

this year only 25$ ,,

im thinking there may be something to this Acetaldehyde ???

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ok i just cant stop reading about this ... so i found a link where Molybednum can reduce this acetaldehyde so i kept going and found where molybdenum is found in food ,, and i rememberd my son having a long period of no CH's (like the last 6 months) and he's been eating tons of Sunflower seeds (some of you might remember my mentioning that)

Human dietary intake and deficiency[edit]

Molybdenum is an essential trace element and crucial for the survival of animals.[66] Four mammalian Mo-dependent enzymes are known, all of them harboring a pterin-based molybdenum cofactor [Moco) in their active site: sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase, and mitochondrial amidoxime reductase.[67] People severely deficient in molybdenum have poorly functioning sulfite oxidase and are prone to toxic reactions to sulfites in foods.[68][69] The human body contains about 0.07 mg of molybdenum per kilogram of weight.[70] It occurs in higher concentrations in the liver and kidneys and in lower concentrations in the vertebrae.[33] Molybdenum is also present within human tooth enamel and may help prevent its decay.[71]

The average daily intake of molybdenum varies between 0.12 and 0.24 mg, depending on the molybdenum content of the food.[72] Pork, lamb, and beef liver each have approximately 1.5 parts per million of molybdenum. Other significant dietary sources include green beans, eggs, sunflower seeds, wheat flour, lentils, cucumbers and cereal grain.[5] Acute toxicity has not been seen in humans, and the toxicity depends strongly on the chemical state. Studies on rats show a median lethal dose (LD50) as low as 180 mg/kg for some Mo compounds.[73] Although human toxicity data is unavailable, animal studies have shown that chronic ingestion of more than 10 mg/day of molybdenum can cause diarrhea, growth retardation, infertility, low birth weight and gout; it can also affect the lungs, kidneys and liver.[72][74] Sodium tungstate is a competitive inhibitor of molybdenum. Dietary tungsten reduces the concentration of molybdenum in tissues.[33]

Dietary molybdenum deficiency from low soil concentration of molybdenum has been associated with increased rates of esophageal cancer in a geographical band from northern China to Iran.[75][76] Compared to the United States, which has a greater supply of molybdenum in the soil, people living in these areas have about 16 times greater risk for esophageal squamous cell carcinoma.[77][citation needed]

Molybdenum deficiency has also been reported as a consequence of non-molybdenum supplemented total parenteral nutrition (complete intravenous feeding) for long periods of time. It results in high blood levels of sulfite and urate, in much the same way as molybdenum cofactor deficiency. However, presumably since pure molybdenum deficiency from this mechanism is seen primarily in adults, the neurological consequences have not been as marked as for the congenital cofactor deficiency.[78]

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I tried the L-Cystine 600mg from the heath food store. I took one pill a day for two weeks, no results. So I had my pharmacist make a 100 mg pill from what she said was a better grade of  L-Cystine. I have been on this for a week and no results. I finally found a place to buy Acetium on the internet, it came in today. I will let you know what happens. peace

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yeah the MJ seemed like it held such promise too .. well I guess if people get some relief from it then its worth trying ?  please let me know about the Acetium ,, that really interests me.  My son was eating an entire bag (almost) of sunflower seeds there for a while .. im wondering.. hmmm

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i going to post early results, cats out of the bag on another post, and i want to be respectful of her post. Acetium, i'm running my own trail, i'm chronic 7 years, get small hit during the day and bigger hits evening and night, i use o2, D3 and lsa, i ordered from this link, http://acetiumusa.com/Contact/index.html, i have been on Acetium for 3 1/2 days, got results first evening i took 100 mg pill, i take two pills a day, pain and CH that is always around my right eye is gone, i'm very skeptical, but hey my TCM doctor wanted to cure my CH through my stomach, liver & gall balder, only time will tell, i will report back in early next week, a thunder storm is brewing tonight and tomorrow, that will be a good test. peace

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my daughter, who is episodic and in cycle....

Ugh, that's disturbing to hear she's back in cycle - seriously, with all of CHf's tremendous and constant help for CH'ers, shouldn't she be a CH'er who is allowed to "pass cycle and collect 200 dollars"??!!  :(  I guess I kinda already knew there is no justice in beast-ville, but this is rank.  >:(

All digits now crossed that the acetium experiment will bring some positive results ASAP for CHf'sDaughter and anyone else trying it.

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Acetium seems to be working for me, here is a 5 1/2 day report. I am taking Acetium at 7 am and 6 pm. The Acetium  last about 10 hours before I start to feel shadows. I am trying to stay on this schedule for testing. I get my biggest hit of the day around 7 pm. The storm triggered a 4:30 pm hit. I took Acetium then and by 7 pm it was gone. I did not take another Acetium that night (should have) and woke up with a bad CH, in the eye and down the neck, normally it's just in the eye. I used coffee, O2 and Acetium, about 30 minutes later CH was gone. The storms were still here, so I took a noon, and 9 pm pill, no CH the next am. The storms left, back to am and pm schedule. So far Acetium seems to be a good preventive, just need to know when to dose, only time will tell. I going to stay on D3 and use o2 if needed, skipping my lsa preventive dose, just to see what happens. peace

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This is the product I have been using for quite some time, maybe this will help all of you further:


You can get the site in english (clicking english flag on top right corner) .

Ingredients of my Acetium capsules:


Eudragit RS-PO



titanium dioxide

And the brief description:

"Microbes in the mouth and pharynx, which result from anacidic stomach or the use of anti-acid medication, will survive and increase in the stomach. The microbes always produce acetaldehyde when you consume sugary foods and beverages or when you consume alcohol. Acetium binds carsonigenic acetaldehyde in your stomach."

Smoking can be added to this list as well. For these reasons I have believed for years acetaldehyde being the Mother Trigger for us. It may even have a larger role.

And whatever the discussion about Acetium involves at the moment, in no way it was developed for clusters or the manufacturer was not even aware such thing as cluster headaches. Through several reports where people had just noticed by accident it's efficiency in their clusters, the manufacturer took interest to research this. And possibly make a zillion dollars.

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I am also going to add that my sons clusters seem to come in October during the Santa Ana winds when the pryomaniacs are out and the southland is on fire ?? smoke in the air, so far this seems consistant.  CHf ,, is there anything going on in your area that would kick this off with your daughter ? any pollutants in the air she has recently been exposed to ??  a beach fire perhaps,, family bbq with bonfire ?

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