Sign in

Showing all posts by "Gothique Angel"

Home  >  Forums  >  Showing all posts by "Gothique Angel"

Posted in Intranasal Oxytoxcin on 26 Nov, 2014 - 1:25 pm

I'm in contact with some in the medical profession who brought this to my attention...

Read closely folks, that's not the opioid medication Oxycontin, but the "Love hormone" Oxytocin.
Intranasal Oxytocin.[/L

Unfortunately, at this point the supporting literature and studies are behind pay-walls for Practitioners eyes only.

Posted in Magnesium on 16 Oct, 2014 - 5:55 pm

Vasodilation as a "cause" for CH is part of the now defunct theory of "Vascular Headache".
If we had a "cause" for CH, then we would all be closer to that "cure" we seek.
There is no known cause in CH.

The Vascular theory of headache, taught to most current practicing GPs is outdated and no longer applicable, they need to brush up on this:

The Vasoconstrictive effect of Imigran is a side-effect of the drug.
Mean arterial constriction seen in cross-sections of blood vessels, conducted during studies of Imigran is less than 10%. The mechanism of action behind Imigran in CH is still not known, although 5HT Serotonin receptors are implicated.

See: The vascular theory of migraine—a great story wrecked by the facts, by Peter Goadsby.

And, Cluster Headache: What has changed since 1999? Here on this site.

Magnesium, may help unlock stores of Vitamin D.
Batch's Vitamin D regimen is still gleaning positive results on the US forum.
The Vitamin D regimen is somewhere on this site, under "Medications and treatments".
Perhaps only when sufficient Vitamin D is supplemented, can Magnesium assist as a co-factor in CH relief.

Posted in Subconscious Mind on 01 Jul, 2014 - 4:35 pm

shrek_2226 said: "I made up my first cluster headache to get out of what I had to do, the rest were just automatic recalls of that excuse. With that, I am cured."

You and your video (yes I saw it) should be removed, kicked off the site. You are a blight on the CHers condition with nothing genuine to offer anyone else, no support for others, just me me me. You've hijacked other's symptoms for your own convenience.
How immoral and insulting to those who have helped you for years here and degrading to those with genuine CH, in some people here have CH going on for longer than you have been alive.

Yours is not the kind of awareness anyone with true CH seeks to raise. Ive watched your story for 4 years Alex and read all your posts. Ive seen probably more cluster attacks than you've ever had and that video was attention seeking , self-harm bullshit, posted under a fake name too, Pinnock. That was not a cluster attack, that was bullshit.
People having cluster attacks don't usually operate cameras, watch themselves in a monitor, carefully check their knife for traces of blood, add a soundtrack and then host it on youtube. A REAL CH OBVIOUSLY HURTS TOO MUCH FOR THAT CRAP!
What a joke!
It has been reported to youtube but for some reason they wont take it down even though it is self harm and a breech of their terms.

When the person I support starts to go into attack, he quietly shuffles off to his room, where he bangs his head against a pillow for 3 hours, not a wall, in case someone might hear him. He is very private about having his attacks.
He does not want to inflict the vision of a CH attack onto any person and suffers alone.
He does not want to be heard, he does not want to be seen, he uses no knife or video camera to seek attention. He just wants the pain to stop asap.

You feel good now? There is Methadone in your madness.
For 4 years you've disrespected so many people with CH here and those who support them. How is anyone meant to raise awareness when fakes, self-harmers, attention-seeking, sympathy-milking and opiate addicted fools make representations on behalf of all people with CH, like in the tags on your video?

That was an appeal to the government to pay for multiple imigran injection every day?
No informed doctor would prescribe 80K worth of Imigran injection in a year, it is just ridiculous and bad medical advice. Do all CH sufferers a favour and take down that melodramatic LIE of a video, Pinnock.
I've shown it to quite a few people and even people without CH are enraged.
You have hindered rather than helped any CH sufferer and all rather selfishly I might add.

If you don't have CH, then what the hell are you doing on this site then?

Posted in New Supporter on 01 Jul, 2014 - 4:03 pm

You are doing a very noble thing helping someone with CH.
Its a shocking thing to see isnt it.
Cluster Headache supporters are the bestest people!
Be patient with Mark, clusters are difficult to understnand and sometimes so are the people that have them.

Posted in CH and Chronic Sinusitis on 01 Jul, 2014 - 3:57 pm

Fig 2 The trigeminovascular reflex. Nerve endings containing pain receptors innervate structures of the face and cranial vault, particularly the pain producing dura mater and cerebral blood vessels (the durovascular complex). This nociceptive information is carried to the brainstem in the trigeminal nerve, via the trigeminal ganglion. Within the brainstem, trigeminal fibres synapse in an area known as the trigeminocervical complex (TCC). From here, information ascends to the hypothalamus, thalamus, and cortex via pain processing pathways. In addition, the afferent trigeminal signals arriving at the TCC also stimulate the cranial parasympathetic system via the superior salivatory nucleus. This results in increased firing of parasympathetic fibres carried from the brainstem in the facial nerve and then greater superficial petrosal nerve, which synapse at the sphenopalatine ganglion. These fibres innervate facial structures (including the lacrimal gland and nasal mucosa, thus causing the lacrimation and rhinorrhoea seen with attacks) and the durovascular complex. Neurotransmitter release at these parasympathetic terminals (vasoactive intestinal polypeptide) causes further irritation of trigeminal sensory nerve endings and release of calcitonin gene related peptide, which potentiates the trigeminovascular reflex arc. It is this reflex that is responsible for the pain and facial parasympathetic signs of cluster headache attacks. The ptosis and miosis seen with attacks arise from interruption of the oculosympathetic fibres that run with the internal carotid artery and through the cavernous sinus, where they are thought to be affected by local vascular distension.

Posted in Batch's anti-inflammatory regimen for CH on 31 May, 2014 - 9:33 pm

I can't get this site to post the damn study!!!

Print this off for your Neuro
Link here:

Thanks to Batch for this.

Posted in Batch's anti-inflammatory regimen for CH on 31 May, 2014 - 9:28 pm

Hi Megan,

Last month the D3 regimen in Cluster Headache was published in the most widely read and highly-cited, peer-reviewed Neurology Journal.
The Official Journal of the American Academy of Neurology, thanks to Pete Batcheler's ongoing work and the input of all the survey participants worldwide.

The Journal of Neurology article:

A Survey of Cluster Headache (CH) Sufferers Using Vitamin D3 as a CH Preventative (P1.256)

Peter Batcheller

Neurology April 8, 2014 vol. 82 no. 10 Supplement P1.256


OBJECTIVE: To present survey results of 110 CH sufferers (CH'ers) using a daily anti-inflammatory regimen of vitamin and mineral supplements including 10,000 IU/d vitamin D3, (cholecalciferol) and Omega-3 fish oil as a CH preventative.

BACKGROUND: Cluster headache is one of the most painful and disabling headache disorders known to man. Results from an informal survey CH’ers using the anti-inflammatory regimen as a CH preventative indicated a surprisingly high efficacy. A survey was needed to qualify and quantify the efficacy of this regimen.

DESIGN/METHODS: A questionnaire was developed to capture efficacy, 25(OH)D lab results along with essential demographic and epidemiological information. Participants were advised to consult with their PCP or neurologist before starting this regimen and to ask for the 25(OH)D lab tests before and after 30 days of use or a favourable response.

RESULTS: 80% of CH'ers reported significant reductions in frequency, severity and duration of their CH. 60% reported remaining substantially PF. Average starting 25(OH)D was 23.4 ng/mL. Average 25(OH)D response after 30 days or favourable response was 76 ng/mL. Regimen appears equally effective for both ECH and CCH, although ECH'ers enjoy a slightly higher efficacy of 85% vs. 70% for CCH. A stress test of 25(OH)D reserves after 13 mo. PF, resulted in a return of CH after 8 days without vitamin D3. 33% reported comorbidities. There were no major adverse events reported.

CONCLUSIONS: Empirical data suggest a possible causal relationship between a vitamin D3 insufficiency/deficiency and cluster headache. At

Posted in Once a month vaccination against CH - Antibody targets CGRP release on 28 Apr, 2014 - 2:45 pm

Press release:

CGRP-targeted migraine prevention drugs succeed in phase II

By: MICHELE G. SULLIVAN, Ob.Gyn. News Digital Network

Two investigational migraine prevention drugs that target a vasodilating peptide significantly decreased the number of migraine days per month, compared with placebo, during a pair of phase II studies.

Both drugs reduced mean migraine headache days per month by more than 4 days overall, and one even eliminated migraine in up to 30% of patients.

Dr. Peter Goadsby

Each is a monoclonal antibody that inhibits calcitonin gene–related peptide (CGRP). Activated trigeminal sensory nerves release the peptide, which dilates intra- and extracranial blood vessels and modulates vascular nociception.

The antibodies could be game changers for migraine patients, Dr. Peter Goadsby said in an interview.

"Here are the first mechanism-based preventive treatments for migraine," said Dr. Goadsby of the University of California, San Francisco. "They are easy to use, biweekly or even monthly injections, which are effective and well tolerated. For neurologists it means the first major addition to the preventive armamentarium for a generation or more, and for patients, a tangible advance that they can look forward to enjoying soon."

During the annual meeting of the American Academy of Neurology, Dr. Goadsby will present the findings on ALD403, developed by Alder Biopharmaceuticals. His colleague Dr. David W. Dodick of the Mayo Clinic, Rochester, Minn., will present findings on LY2951742, which is being developed by Arteaus Therapeutics in conjunction with Eli Lily. Both presentations are scheduled for May 1.

The trial of ALD403 comprised 163 patients who experienced 5-14 migraine headache days per month; 81 were randomized to receive a single infusion of 1,000 mg ALD403 and the rest received placebo. Patients were followed for 24 weeks. The primary outcome was the mean change in migraine days between weeks 5-8 and baseline.

Patients in the active treatment group fared significantly better than those in the placebo group, with a mean reduction in migraine headache days of –5.6, compared to –4.6 for the placebo group (66% vs. 52% decrease).

Most patients taking the study drug had at least a 50% reduction in migraine headache days at 12 weeks (60% vs. 30%); the proportions of those with at least a 75% reduction were 32% vs. 9%. A 100% reduction occurred in 16% of the active group and in none of the placebo group. These differences were all statistically significant.

Posted in Not sure of diagnosis on 01 Mar, 2014 - 4:27 pm

Cervicogenic headache?
Diagnosis by a headache specialist of correct type of headaches is essential.
Have a read of this one.

Posted in Cluster headache: what has changed since 1999? on 10 Jan, 2014 - 4:09 pm


Cluster headache: what has changed since 1999?

Massimo Leone • Alberto Proietti Cecchini • Vincenzo Tullo • Marcella Curone
• Paola Di Fiore • Gennaro Bussone
Springer-Verlag Italia 2013

The peripheral and central origin of pain in cluster headache (CH) and trigeminal autonomic cephalalgias (TACs) has been matter of debate. In the last decade, a number of information came from both animal and human studies. This paper briefly highlights main data from these studies. Taken together, there is now sufficient body of evidence indicating that CH and TACs can be regarded as a unique headache spectrum–syndrome, due to involvement of specific brain areas.

Until 1988, cluster headache (CH) was classified together with migraine under the section of ‘‘vascular headaches’’ [1]. For the first time in 1988 the International headache society (IHS) classification separated CH from migraine [2]. In the second IHS classification [2] CH was grouped together with other two primary headache forms: paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) [3]. This group was named the trigeminal autonomic cephalalgias (TACs) and is characterised by attacks of unilateral head pain associated with ipsilateral craniofacial autonomic manifestations. Attack duration is the main feature that distinguishes the three TAC forms.

The term TAC was first introduced by Goadsby and Lipton [4] in 1997 because of the simultaneous activation of trigeminal and parasympathetic craniofacial nerves both in these headache forms. The contemporary activation of these nerves could be due to pathological activation of the trigeminofacial brainstem reflex [4].

The peripheral and central origin of pain in TACs, mainly in CH has been matter of debate. Orbital phlebographies in CH and other headaches did not reveal differences and systemic signs of inflammation have never been reported in CH [5], thus excluding inflammation of the cavernous sinus as a source of the pain in CH.

Vasodilation seems not to be the cause of pain in CH:
Intracranial vasodilation is not specific to CH as it is observed in experimental forehead pain [6]. In addition, CH can occur even if vasodilation is blocked by trigeminal nerve section [7].

Sumatriptan efficacy is due to the antagonistic effect on peripheral 5-HT1D (at trigeminal nerve endings) and 5-HT1B receptors (on the walls of intracranial blood vessels) [8]
. Thanks to these effects on peripheral 5-HT1D and 5-HT1B receptors, sumatriptan could control CH pain by reducing the increased concentrations of calcitonin gene-related peptide in the ipsilateral jugular vein during CH attacks [9].

A peripheral origin of pain in CH and TACs also comes from secondary forms of these headaches: under such circumstances the clinical characteristics of CH and TACs are rather often difficult to differentiate the primary forms [10]. In many cases, the lesions are located in the sella turcica or the sinus cavernosus [10], and surgical removal leads to resolution of the pain.

Other observations indicate that activation of trigeminal nerve endings alone cannot explain the pain of CH (and other TACs). Other factors probably in the brain play a role in pain generation. Vasodilators such as alcohol, nitro-glycerine [11], and the 5-HT2B agonist m-chlorophenyl-piperazine [12], can precipitate CH attacks but only during the bouts. These observations point to a central permissive state allowing vasodilation being perceived as painful.

In a PET study, peripheral trigeminal activation occurs in CH [13] without provoking CH pain attacks; in addition, surgical lesioning of the trigeminal nerve does not always resolve the pain in CH as well as other TACs [14, 15].

It is of interest to note that sumatriptan retains its ability to stop CH attacks after complete trigeminal nerve section [7], indicating that its effect is not at peripheral level but in the brain.
Other data also suggest that the trigeminal nerve is not crucial in CH and TACs pain. In a large study on CH patients, 48 % reported the headache outside the trigeminal distribution [16]. In PH pain can occur in various non-trigeminal areas, occipital (42 %), neck (32 %), ear (13 %), ipsilateral shoulder (10 %), and arm (10 %) [17].

In SUNCT pain can occur in the back of the head and neck in 31 % and in the ear in 6 % [18]. The clockwork regularity of CH attacks and the seasonal recurrence of CH led to the hypothesis that a biological clock in the hypothalamus was involved in CH [11]. In the same direction go the observations that attacks can be provoked by napping [11], and the shift to their regular times after changing time zone [11].

Neuroendocrinological abnormalities have been documented in CH substantiating hypothalamic involvement in CH [19]. CH and TACs should be regarded as a syndrome, with a central component predominating in primary forms and a peripheral component predominating in secondary forms.

Neuroimaging findings, clinical characteristics and neuroendocrinological abnormalities in CH and in the other TACs pointed to a hypothalamic involvement, prompting the idea that this brain area could act cluster generator [20].
In animals, a direct connection between the posterior hypothalamus and the trigeminal nucleus caudalis through the trigemino-hypothalamic tract has been demonstrated [21].

Sensory information from trigeminally innervated territories is conveyed to the hypothalamus via the trigemino-hypothalamic tract [21]. On the contrary, stimulation of the posterior hypothalamus modulates the activity of trigeminal nucleus caudalis neurons: this effect is mediated by a number of substances, such as orexins [22}.

In a PET study conducted in patients with chronic CH under hypothalamic stimulation [13], hypothalamic stimulation induced activation in both the ipsilateral hypothalamic grey and the ipsilateral trigeminal system documenting for the first time a connection between the hypothalamus and the trigeminal system in humans. In this study, activation of the trigeminal nerve and ganglion did not produce any headache nor head sensation suggesting that trigeminal activation is not sufficient to fully explain CH pain [13].

Taking together data from animals and humans, there is now sufficient body of evidence indicating that the posterior hypothalamus plays a role in head pain modulation.

High-frequency hypothalamic stimulation to treat chronic drug-resistant CH was introduced in 2000 to inhibit hyperactivity of this brain area previously detected by PET [23]. So far, experience from more than 60 patients with drug resistant chronic CH treated with hypothalamic stimulation shows a remarkable improvement in about 60 % of cases [24]. Hypothalamic stimulation is also effective in SUNCT [25–27] and in PH [28]. Acute stimulation does not improve ongoing CH attacks [29], and stimulation must continue for weeks or months before there is benefit [30].

Taken together, these observations suggest that the mechanism of action of hypothalamic stimulation is not the mere result of inhibition of hypothalamic neurons [30]. The increased threshold for cold pain in first trigeminal branch on the stimulated side in patients under chronic hypothalamic stimulation suggested modulation of the antinociceptive system [31].

Hypothalamic stimulation affects major pain-matrix areas: activation has been recorded in the thalamus, somatosensory cortex, precuneus, and anterior cingulate cortex, whereas deactivation occurs in the middle temporal gyrus, posterior cingulate cortex, and insula [13]. This suggests that it restores normal function of pain network in CH patients. The original hypothesis that the hypothalamus is the so-called CH generator was appealing, but recent neuroimaging findings and the accumulated experience with hypothalamic stimulation indicate other interpretations.

If the posterior hypothalamus was the CH generator, one would expect hypothalamic stimulation to trigger CH pain attacks, but this is not the case [30]. An alternative explanation about the role of the posterior hypothalamus in CH and TACs is that its activation leads to attack termination, thus regulating the duration of an attack [32]; this ability could explain the different attack durations in the various TAC forms.

Data accumulated in the last years, led to move beyond the search of a single trigger zone as previously thought in CH. Brain areas involved in a CH attack [20] are almost the same of those traditionally regarded as the pain matrix; moreover, these areas show a huge overlap with brain areas modified by hypothalamic stimulation [13].

These areas play a major role also in autonomic, cognitive and affective functions. A derangement in one or more of these areas, or alternatively a deficit in their interactions, could be the cause of a permissive state leading to disinhibition of the hypothalamo-trigeminal pathway that in turn may start a pain attack.

Conflict of interest
We certify that there is no actual or potential conflict of interest in relation to this article.

1. Ad Hoc Committee on Classification of Headache (1962) Clas-
sification of headache. JAMA 179(9):717–718

2. Headache Classification Committee of the International Head-
ache Society (1988) Classification and diagnostic criteria for
headache disorders, cranial neuralgias and facial pain. Cepha-
lalgia 8(Suppl 7)

3. Headache Classification Subcommittee of the International
Headache Society (2004) The international classification of
headache disorders: 2nd edn. Cephalalgia 24(Suppl 1):1–160

4. Goadsby PJ, Lipton RB (1997) A review of paroxysmal hemi-
cranias, SUNCT syndrome and other shortlasting headaches with
autonomic feature, including new cases. Brain 120:193–209

5. Nilsson Remahl I, Waldenlind E, Bratt J, Ekbom K (2000)
Cluster headache is not associated with signs of a systemic
inflammation. Headache 40:276–281

6. May A, Buchel C, Turner R, Goadsby PJ (2001) Magnetic res-
onance angiography in facial and other pain: neurovascular
mechanisms of trigeminal sensation. J Cereb Blood Flow Metab

7. Matharu MS, Goadsby PJ (2002) Persistence of attacks of cluster
headache after trigeminal nerve root section. Brain 125:976–984

8. Moskowitz MA (1990) Basic mechanisms in vascular headache.
Neurol Clin 8:801–815

9. Goadsby PJ, Edvinsson L (1994) Human in vivo evidence for
trigeminovascular activation in cluster headache. Neuropeptide
changes and effects of acute attacks therapies. Brain 117:427–434

10. Favier I, van Vliet JA, Roon KI et al (2007) Trigeminal auto-
nomic cephalgias due to structural lesions: a review of 31 cases.
Arch Neurol 64:25–31

11. Kudrow L (1980) Cluster headache, mechanism and manage-
ment, 1st edn. Oxford University Press, New York

12. Leone M, Attanasio A, Croci D et al (1997) The
m-chlorophe- nylpiperazine test in cluster headache: a study on central serotoninergic activity. Cephalalgia 17:666–672

13. May A, Leone M, Boecker H et al (2006) Hypothalamic deep
brain stimulation in positron emission tomography. J Neurosci

14. Jarrar RG, Black DF, Dodick DW, Davis DH (2003) Outcome of
trigeminal nerve section in the treatment of chronic cluster
headache. Neurology 60:1360–1362

15. Black DF, Dodick DW (2002) Two cases of medically and sur-
gically intractable SUNCT: a reason for caution and an argument
for a central mechanism. Cephalalgia 22:201–204

16. Torelli P, Cologno D, Cademartiri C, Manzoni GC (2001)
Application of the International Headache Society classification
criteria in 652 cluster headache patients. Cephalalgia 21:145–150

17. Cittadini E, Matharu MS, Goadsby PJ (2008) Paroxysmal hemi-
crania: a prospective clinical study of 31 cases. Brain

18. Cohen AS, Matharu MS, Goadsby PJ (2006) Short-lasting uni-
lateral neuralgiform headache attacks with conjunctival injection
and tearing (SUNCT) or cranial autonomic features (SUNA)—a
prospective clinical study of SUNCT and SUNA. Brain

19. Leone M, Bussone G (1993) A review of hormonal findings in
cluster headache. Evidence for hypothalamic involvement.
Cephalalgia 13:309–317

20. May A, Bahra A, Buchel C, Frackowiak RS, Goadsby PJ (1998)
Hypothalamic activation in cluster headache attacks. Lancet

21. Malick A, Strassman AM, Burstein R (2000) Trigeminohypo-
thalamic and reticulohypothalamic tract neurons in the upper
cervical spinal cord and caudal medulla of the rat. J Neurophysiol

22. Bartsch T, Levy MJ, Knight YE, Goadsby PJ (2004) Differential
modulation of nociceptive dural input to [hypocretin] orexin A
and B receptor activation in the posterior hypothalamic area. Pain

23. Leone M, Franzini A, Bussone G (2001) Stereotactic stimulation
of posterior hypothalamic gray matter for intractable cluster
headache. N Engl J Med 345:1428–1429

24. Magis D, Schoenen J (2012) Advances and challenges in neur-
ostimulation for headaches. Lancet Neurol 11(8):708–719

25. Leone M, Franzini A, D’Andrea G, Broggi G, Casucci G, Bus-
sone G (2005) Deep brain stimulation to relieve severe drug-
resistant SUNCT. Ann Neurol 57:924–927

26. Lyons MK, Dodick DW, Evidente VG (2008) Responsiveness of
short-lasting unilateral neuralgiform headache with conjunctival
injection and tearing to hypothalamic deep brain stimulation.
J Neurosurg 26:1–3

27. Bartsch T, Falk D, Knudsen K, Reese R, Raethjen J, Mehdorn
HM et al (2011) Deep brain stimulation of the posterior hypo-
thalamic area in intractable short-lasting unilateral neuralgiform
headache with conjunctival injection and tearing (SUNCT).
Cephalalgia 31(13):1405–1408

28. Walcott BP, Bamber NI, Anderson DE (2009) Successful treat-
ment of chronic paroxysmal hemicrania with posterior hypotha-
lamic stimulation: technical case report. Neurosurgery 65:E997
(discussion E997)

29. Leone M, Franzini A, Broggi G, Mea E, Proietti Cecchini A,
Bussone G (2006) Acute hypothalamic stimulation and ongoing
cluster headache attacks. Neurology 67:1844–1845

30. Leone M, Franzini A, Proietti Cecchini A, Bussone G (2013)
Success, failure and putative mechanisms in hypothalamic stim-
ulation for drug-resistant chronic cluster headache. Pain

31. Jurgens T, Leone M, Proietti-Cecchini A, Busch V, Mea E,
Bussone G, May G (2009) Hypothalamic deep-brain stimulation
modulates thermal sensitivity and pain thresholds in cluster
headache. Pain 146(1–2):84–90

32. May A (2005) Cluster headache: pathogenesis, diagnosis, and
management. Lancet 366:843–855
Neurol Sci (2013) 34 (Suppl 1):S71–S73

Posted in Batch's anti-inflammatory regimen for CH on 15 Oct, 2013 - 1:28 pm

This post is from Batch on, as an update on news and safety for D3 users.

* * * * * * *

The founder of VitaminDWiki has been kind enough to post a web page on the use of vitamin D3 as a cluster headache preventative at the following link:

I'm not a physician or nutritionist... but I did stay at a Howard Johnson a few years back...

Seriously... all I can do is provide you information based on my experience with, and what I've learned over the last three years about vitamin D3, Omega-3 Fish Oil and the rest of the vitamin D3 cofactors: calcium, magnesium, zinc, boron, vitamin A (retinol) and vitamin K2 (MK-4 & MK-7). Armed with this information, you can make your own decisions.

For starters, you've likely already discovered that most PCPs and too many neurologists have no real first-hand clinical experience treating patients with cluster headaches... That should be understandable... We suffer from an orphan disorder... When patients present with a condition they've not treated previously... like cluster headache, most physicians use a cookbook approach with treatment recommendations from Standards of Care Guidlines... Many of these guidelines are excellent... That said, it all depends on when the cookbook (Guideline) was published...

Unfortunately, the same can be said for the benefits of nutrition and the use of supplements on the many health issues we face...

This shouldn't be surprising either... Most medical school curricula provide an average of 1 hour on primary headaches and about the same amount of time on the use of nutrition as a mode of preventative and interventional treatments.

Furthermore, most of the exciting medical breakthrough discoveries in the last ten years have come as a result of molecular biochemistry at the cellular and nuclear level... in short, rise of the genetic-based pharmaceutical companies...

To put this in perspective, the Human Genome Project wasn't declared substantially complete until April 2003 with sequencing of the last remaining chromasome not completed until May of 2006.

Getting back to the pharmacokinetics of vitamin D3, the real exciting stuff has come as a result of gold standard RCTs completed in the last five years and the use of vitamin D3 as a preventative for cluster headache didn't start until three years ago when I developed the basic anti-inflammatory regimen.

Moreover, until now, the only first hand information on the efficacy of vitamin D3 as a preventative for cluster headache has only been available here at Other sites like ClusterBusters and a couple cluster headache organizations in Europe have been watching.

Sooo... unless physicians have been taking CME specific to vitamin D3 and nutrition... they've likely never been exposed to the health benefits of vitamin D3 and the vitamin D3 cofactors.

With that as a preface... here's what I suggest. VitaminDWiki provides the most complete and up to date compendium of all things vitamin D3 including excerpts, and links to the latest RCTs...

For example, here's the link to the benefits of taking vitamin D3 to control cholesterol:

The really cool thing about vitamin D3, 25(OH)D and 1,25(OH)2D3, (calcitriol), the active hormonal form of vitamin D3 is its capacity to stimulate genetic expression...

In simple terms calcitriol triggers certain genes to produce products our bodies need to heal themselves and turn off genes to prevent them from making products that make us sick.

It's this capacity of vitamin D3 we think is responsible for the down-regulation/suppression of Calcitonin Gene-Related Peptide (CGRP) that studies have found elevated during cluster and migraine headaches. Dr. Peter Goadsby, M.D., one of the world's top cluster headache neurologists, conducted one of these studies.

In order to help make genetic expression happen, we need to supplement with adequate amounts of vitamin D3, calcium, magnesium, zinc, boron, vitamin A (retinol) and vitamin K2 (MK-4 & MK-7). The following graphic provides a high level illustration of how this happens...

You can find more about the synergy between vitamin D3, vitamin A and vitamin K2 at the following link:

Finally, no discussion of vitamin D3 therapy is complete without discussing safety. The following graphic tells the tale on safety of the doses we take. Note that it's not just the dose but also the duration of dose that adds up...

This graphic doesn't tell the whole story... It's not so much the dose and duration but rather how much 25(OH)D the body produces in response to these doses over time.

Even that can be misleading as it's not the serum concentration of 25(OH)D that indicates toxicity... It's the serum concentration of calcium...

If you read through the papers on vitamin D3 toxicity you'll find there are no studies (RCT's) that intentionally set out to define the vitamin D3 dose and serum level of 25(OH)D that triggers a toxic reaction... That would be unethical...

Instead, they gathered data from cases of unintentional and accidental overdoses due to mislabeled or improperly prepared vitamin D3 that resulted in calcium serum concentrations above the normal reference range. These cases were then used to approximate vitamin D3 dosing and 25(OH)D thresholds where a toxic reaction occurred as indicated by too much serum calcium and or too much calcium in the urine.

In nearly every case, authors reporting toxic levels build in a large safety margin... For example, if the lowest threshold for vitamin D3 toxicity from any study (with or without peer review), was found to be 200 ng/mL, the "Safe" upper limit of the normal reference range is set at 100 ng/mL.

In short, the vitamin D3 experts, endocrinologists specializing in treating vitamin D3 deficient patients will say... vitamin D3 toxicity is very rare...

Finally, I've tried to put this on an apples to apples comparison of relative risk... I was unaware of any deaths reported to the FDA over the last 9 years due to vitamin D3... so I checked a web site that tracks reports like this... I think you'll find the following list an eye-opener...

From Q1 2004 to Q3 2012, (9 years), the FDA received adverse reaction reports on the following prescription medications and over the counter supplements: Check out the following link to see for yourself. Plug in prescribed and over-the-counter medications and supplements you’ve been taking… one at a time, to see what’s been reported to the FDA about these medications over the last 9 years. Click on the “Show More” button to see the entire list of adverse reaction reports for each choice.

Prescription Medications Used To Treat Cluster Headache and Related Symptoms
Deaths due to VERAPAMIL 229
Deaths due to DEPAKOTE 168
Deaths due to TOPAMAX 66
Deaths due to LITHIUM CARBONATE 56
Deaths due to LYRICA 703
Deaths due to GABAPENTIN (Neurontin) 202
Deaths due to VALPROIC ACID 194
Deaths due to BACLOFEN 102
Deaths due to PREDNISONE 513
Deaths due to PREDNISOLONE 163
Deaths due to COUMADIN 458
Deaths due to IMITREX 32
Deaths due to INDOMETHACIN 18
Deaths due to OCTREOTIDE 1317
Deaths due to CALAN 208
Deaths due to CLOMIPHENE CITRATE 8 Intra-uterine Deaths
Deaths due to PROPRANOLOL HCL 67
Deaths due to ATENOLO 62
Deaths due to AMITRIPTYLINE 184
Deaths due to PAXIL 357
Deaths due to LIPITOR 865
Deaths due to CRESTOR 238
Deaths due to NEXIUM 357
Deaths due to AMBIEN 243
Deaths due to PRILOSEC 0
Deaths due to OXYGEN 0

Over The Counter NSAIDs
Deaths due to NAPROXEN (Aleve) 142
Deaths due to ASPIRIN 645
Deaths due to TYLENOL 964
Deaths due to EXCEDRIN 500
Deaths due to IBUPROFEN 661

Over The Counter Supplements/Nutrients
Deaths due to MELATONIN 0
Deaths due to MAGNESIUM OXIDE 0
Deaths due to CALCIUM CITRATE Not Listed
Deaths due to BORON Not Listed
Deaths due to VITAMIN A (Retinol) 6
Deaths due to VITAMIN B (Complex) 2
Deaths due to VITAMIN B 12 0
Deaths due to VITAMIN C 0
Deaths due to Vitamin E 2
Deaths due to VITAMIN D3 0
Deaths due to VITAMIN K 2
Deaths due to VITAMIN K2 Not Listed
Deaths due to ZINC OXIDE Not Listed

So there you have it... The next time a nervous Nellie cries "Wolf" in a post about taking vitamin D3... at the doses we take in the anti-inflammatory regimen... take a deep breath and remember the sage sayings... Too much of anything isn't good... and... All things in moderation...

Good people of Clusterville... Our healthcare system is going down the dumper at a frightening pace... The smart thing to do now is stay healthy. The anti-inflammatory regimen is a very safe regimen with health benefits that go well beyond preventing cluster headaches.

And if you do get sick and need to see a doctor... be informed... Ask for an explanation of any prescribed medication including side effects.

Take care,

V/R, Batch

Posted in Opioids don't work in CH. on 12 Sep, 2013 - 10:19 pm

On the TV news tonight

Posted in When to start Complex B supps on 12 Sep, 2013 - 10:10 pm

Posted in Miscarriage; a little word with huge consequences on 07 Apr, 2013 - 2:43 pm

Let me start by saying I’ve never had a cluster headache in my life, nor do I want to. I only know about CH because I support someone who does suffer from them and as such I occasionally read the posts on this site.

While I admit to having very little understanding about CH one thing I do understand only too well is miscarriage. Why am I posting this on a CH site you may wonder? The answer is simple; I don’t want to have anyone go through the pain of miscarriage if they can avoid it and some of the posts on this site pertaining to the use of castor oil in CH – mostly without a disclaimer that such treatments can lead to miscarriage in pregnant women – are potentially dangerous.

Statistically one in five pregnancies end in miscarriage and that’s without well-meaning advice that can induce a woman to miscarry. It’s naturally hard enough to carry a baby to term as it is without half-truths and hearsay making it harder; or even impossible. What happened to me was no one’s fault, but that doesn’t make dealing with it any easier.

Like the name CH, the word miscarriage does nothing to explain the depth of pain the condition can cause. Miscarriage is a life sentence. I’m sure you’ll say the same about CH, but while CH sufferers have remission, miscarriage is something that never goes away.

I lost my first child to miscarriage and the pain of which, I wouldn’t wish on my worst enemy. They say time heals all wounds; well I’m here to tell you it doesn’t. Yes the physical pain of miscarriage fades and over time you do forget it, but there is no escaping the emotional and psychological toll miscarriage takes on a woman.

My miscarriage happened back in October 1997 and I’m still dealing with it. I lost not just my precious baby but also I ended up losing my husband, my job, my home, my financial security, all my hopes and dreams for the future and for a while my sanity as well.

The first ultrasound I had showed a healthy embryo with a strong and steady heartbeat. Everything looked good. Then a week later I began to spot bleed but even then, I was sure I would go on to deliver a happy healthy baby. A subsequent ultrasound performed by an obstetrician showed a different picture. There is nothing that can prepare you for when you’re told that your embryo is no longer viable because it wasn’t just an embryo to me; it was my baby.

I’d spent my whole life waiting for the day when I would hold my newborn in my arms. As soon as I heard I was pregnant it was a baby to me. I already loved this tiny being growing inside me. I allowed myself to have hopes and dreams for a future together and six simple words could shatter all that. Your embryo is no longer viable.

Suddenly you are thrust into this secret world of darkness and despair. You become a member of an exclusive club that no one wants to join. And for the most part you’re left to deal with it alone because even these days miscarriage is seen as the last great taboo.

People, even friends and family with the best of intentions are ill-equipped to help grieving parents cope with their loss. Trust me when I say that unless you’ve been there you have NO idea what it’s like… you can imagine what you think it’s like, but the imagination doesn’t come close to the horror of reality; the same as you Cher’s report.

To this day it is still thought best to avoid the topic with bereaved parents, as if not talking about it will make it go away. The truth is, we need to talk and remember the children we’ll never meet if we ever hope to heal. Our entire world has just crumbled around us and people think the best thing is not to acknowledge it. All that really does is spare them the embarrassment of talking about something they don’t really understand and isolate the bereaved even more.

When my baby died I lost not only my child, but all the hopes and dreams that I’d had for that child. I lost all the special moments I’d have had with them. I’d never see them walk, or talk. Drive a car, start dating. Marry. I lost the grandchildren that they’d never get to give me.

And yet the rest of the world went on as if nothing had happened.

Never had I felt so alone in my life. Society gives grieving parents about a six week window in which to grieve, by which time they assume we should be over it. Nobody speaks about it, except in hushed tones. This is why I speak out about it. I did nothing wrong, I have nothing to be ashamed of and I refuse to sweep my feelings under the carpet so that others can remain in ignorant bliss.

Losing a baby hurts and not just physically. I think I’ve found acceptance in what happened to me, but it took years to get there. Even now, there are triggers that can set me off and send me right back to when it all happened. Nowadays it tends to be around the anniversary of my miscarriage, but for many years it could be anything; from seeing a newborn baby through to seeing kids walking to school and knowing my child will never get the chance to do that.

I suffer severe clinical depression, whereas before my miscarriage I was a happy well-adjusted person. Yes I’ve thought of ending it all, but I’ve never actually tried and to this day I still can’t work out whether that’s because I was too strong or too cowardly to go there.

I’m not writing this looking for sympathy. I’m writing this because when you read a disclaimer - that often the castor oil posts on this site don’t have – stating that miscarriage is a possible side effect, it looks harmless enough. Miscarriage an insidious little word with such far reaching consequences that people aren’t aware of until it’s too late.

Please be careful when looking for so called cures to your CH. Do your research before you try these remedies. I’m sure the people who post them like Les do so with the best intentions but you can’t undo a miscarriage. It’s permanent, irreversible and will be with you forever.

Even a subsequent baby won’t undo the damage of miscarriage. Yes, you have a precious little bundle of joy to share your love with, but you still always grieve the child you lost. Milestones in your subsequent child’s life are always tinged with sadness because inevitably you remember your other baby that never got to make them. I know this from speaking to a lot of women who have suffered one or multiple miscarriages.

I never got a second chance at motherhood; I have no children. I’ll never know the joy of holding my baby in my arms but not a day goes by that I haven’t stopped to think about the baby I lost and what could have been. I don’t think I’ll ever stop thinking of him or her. My heart is full of love, yet my arms remain empty. As full as my life may be, I will always consider it only half lived because I believe I was born to be a mother; never did I want to be anything but.

If you or your partner have suffered the death of a baby, I’m sorry if this post brings your feelings of grief to the surface. If you’re one of the lucky ones that haven’t been there, perhaps this will give you a better insight into what pregnancy loss is like, but if this post can potentially save just one baby I will consider it worthwhile.

If you are, or suspect you might be, pregnant please be very careful when seeking relief for CH. I’d advise running any alleged treatments past a medical practitioner first, just to be sure of possible side effects such as miscarriage.

You’ve already lost enough to CH, I’d hate to see you lose a baby to it as well.