Foods and supplements in the management of migraine headaches

The New York Headache Center, New York, NY 10021, USA.
The Clinical journal of pain (Impact Factor: 2.7). 07/2009; 25(5):446-52. DOI: 10.1097/AJP.0b013e31819a6f65
Source: PubMed

ABSTRACT Although a wide range of acute and preventative medications are now available for the treatment of migraine headaches, many patients will not have a significant improvement in the frequency and severity of their headaches unless lifestyle modifications are made. Also, given the myriad side effects of traditional prescription medications, there is an increasing demand for "natural" treatment like vitamins and supplements for common ailments such as headaches. Here, we discuss the role of food triggers in the management of migraines, and review the evidence for supplements in migraine treatment.
A review of the English language literature on preclinical and clinical studies of any type on food triggers, vitamins, supplements, and migraine headaches was conducted.
A detailed nutritional history is helpful in identifying food triggers. Although the data surrounding the role of certain foods and substances in triggering headaches is controversial, certain subsets of patients may be sensitive to phenylethylamine, tyramine, aspartame, monosodium glutamate, nitrates, nitrites, alcohol, and caffeine. The available evidence for the efficacy of certain vitamins and supplements in preventing migraines supports the use of these agents in the migraine treatment.
The identification of food triggers, with the help of food diaries, is an inexpensive way to reduce migraine headaches. We also recommend the use of the following supplements in the preventative treatment of migraines, in decreasing order of preference: magnesium, Petasites hybridus, feverfew, coenzyme Q10, riboflavin, and alpha lipoic acid.

Download full-text


Available from: Alexander Mauskop, Jun 11, 2015
1 Follower
  • Source
    • "Some patients with migraine, be it VM or other variants, appear to have dietary or environmental triggers, and avoiding such triggers can result in relief of symptoms. Both the use of caffeine and caffeine withdrawal have been suggested to be triggers of migraine for some patients, yet caffeine is a component of over-the-counter migraine medications and has also been used in clinical trials as a therapy against migraines [4] [5] [6] [7] [8] [9]. In an effort to resolve the ambiguity currently in the literature regarding the role of caffeine in migraine and to identify an effective method to treat patients with VM and CDUE, the authors retrospectively reviewed the records of patients presenting to the clinic with the primary complaint of dizziness to evaluate the efficacy of a therapeutic pathway to VM and CDUE with long-term caffeine cessation as a first step and pharmacotherapy with nortriptyline or topiramate as the second step. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to evaluate the efficacy of a therapeutic pathway for vestibular migraine (VM) and complex dizziness of undetermined etiology (CDUE) with caffeine cessation and pharmacotherapy. This study is a retrospective chart review. Patients were recommended to stop intake of caffeine and other putative migraine-triggering agents. Pharmacotherapy was initiated with nortriptyline or topiramate if symptoms persisted despite diet modification. Self-reported dizziness is the main outcome measure. Vestibular migraine and CDUE were considered contributing factors to dizziness in 34 and 10, respectively, of 156 patients. Fourteen percent of patients reported improvement in symptoms upon caffeine cessation, whereas 46% of patients reported a reduction in dizziness after nortriptyline therapy (P = .007). Topiramate reduced symptoms in 25% of patients. In total, 75% of VM patients and 56% of patients with CDUE received sufficient benefit from this therapeutic pathway to not progress to other treatments. Vestibular migraine and CDUE can be treated effectively with a therapeutic pathway consisting of caffeine cessation followed by pharmacotherapy.
    American journal of otolaryngology 06/2011; 33(1):121-7. DOI:10.1016/j.amjoto.2011.04.010 · 1.08 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We show here how the discrete Petri nets, languages and automata, and max-algebra approaches to DEDS yield complementary results. Using a simple discrete event dynamic system, we show how this complementarity may be used for the optimal control of a DEDS: the conditions ensuring liveness of the Petri net model yield admissible control strategies; the automaton of the system then exhibits nondeterministic situations, and suggest unambiguous control policies. Each of these policies can then be analysed. In each case, we get general timed PNs, which are not TEGs, and spectral theory in the min-max algebra yield the periodicity of the system. An optimal control strategy may then be selected
    Petri Nets and Performance Models, 1999. Proceedings. The 8th International Workshop on; 02/1999
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Practitioners of oral medicine frequently encounter patients with complaints of taste disturbance. While some such complaints represent pathological processes specific to the gustatory system, per se, this is rarely the case. Unless taste-bud mediated qualities such as sweet, sour, bitter, salty, umami, chalky, or metallic are involved, 'taste' dysfunction inevitably reflects damage to the sense of smell. Such 'taste' sensations as chicken, chocolate, coffee, raspberry, steak sauce, pizza, and hamburger are dependent upon stimulation of the olfactory receptors via the nasopharynx during deglutition. In this paper, we briefly review the anatomy, physiology, and pathophysiology of the olfactory system, along with means for clinically assessing its function. The prevalence, etiology, and nature of olfactory disorders commonly encountered in the dental clinic are addressed, along with approaches to therapy and patient management.
    Oral Diseases 09/2009; 16(3):221-32. DOI:10.1111/j.1601-0825.2009.01616.x · 2.40 Impact Factor
Show more