...maybe



yup, it's fixed.

First, thanks for the fixing work. Superbe.

Hello, Annsie

I'll try try to give you a global answer while I comment on specific points on your message. It's clear that CH is complex, so here we are crumbling as we can. I don't know what kind of "answer" ar you looking for, I settled myself today with a better quality of life, and now I'm going there.

Nor do I understand on the basis of which states that maintain or increase levels of serotonin did not give the reply. I think, at your words, that already tried to do this, otherwise left to know if it has been really achieved. And no, I think, there's not an "answer", but a long way to go. I share the words of monty: "If a serotonin deficiency is a main cause of clusters (as was asserted above), there is much that can be done in response to that.".

Nor do I share other statements, such as the level of serotonin is strictly controlled, and by the hypothalamus. If you want to comment on where you read this, it would be a good contribution to the discussion, because nothing that I've studied so far supports that idea at all.

Moreover, in the first post I explain the circadian and circanual rhythms based on the hypothesis. It's the first thing I did, it might not please everyone and of course it's subject to discussion, but I did. Please review it.

And if we withdraw the alleged control of the hypothalamus, and we agree that lower levels at night (up to 80% lower than on the day), and if I say that 2% of serotonin is in the brain, 8% in platelets and 90% in the intestine and that we are interested in 2% and 8% and not only at brain's 2%, we can continue to seek ways to increase these levels.

But again as we move through the discussion we'll arrive to practical conclusions, but surely not "the answer" yes, but, as I said, to a better quality of life. I hope.

Salut.

Thank you, This is the best post i seen since i have been part of this site. My only question right now is, if sertonin is the main thought process here, how does mushroom stop so many people with clusters, do the mushrooms raise their sertonin levels? i Will be following this post. 


                   Challening, more assertive.. Coach Bill

coach_bill wrote on Feb 19^th, 2009 at 9:20pm:


WE'll arrive here soon. For the moment i think I've read LSD and Mushrooms have a strong affectation to the serotonin recepeteurs. No much idea at this moment, but I think in this thread we need to pass over nearly all the CH affections, including this one.

Regards

Gonzalo wrote on Feb 19^th, 2009 at 9:00pm:



Hi Gonzalo,

I read about serotonin control in this article:

Solms, Mark (2000) DREAMING AND REM SLEEP ARE CONTROLLED BY DIFFERENT BRAIN MECHANISMS,  Behavioral and Brain Sciences 23 (63)

and from the other articles as quoted in that article.

You may need a subscription or online purchase to be able to access it though.

I have been reading up on pineal gland and REM and nonREM sleep, the bioneurological mechanism of different stages of sleep, not in a CHer but in normal and mentally ill patients. What I read I was surprised to find how much it could be related to CH and the mechanism of CH. However, it is so complicated that it is almost impossible to summarise into an easily understandable presentation.

The level of serotonin and melatonin changes throughout the day and night, according to the circadian rhythm, which in turns is affected both by internal factors such as the hypothalamus and the pineal gland etc , and external factors like the weather, the different seasons etc.

Since personally I am finding it difficult to discern the most important pathway or element, I am hoping that by discussing it with others will make things clearer.

My main interest in to come up with some strong enough evidence that I can present to the specialists at medical conferences to raise their interest, with view to pushing for research. So far, I have not been able to develop a concise enough hypothesis that I can present and defend.

Thanks for helping.

Quote:


SSRIs don't raise the actual amount of serotonin in the body; they only increase the effective level of serotonin in certain areas of certain nerves (and as you noted, that may not even be how they work - it may be indirect effects on other things).  So the fact that SSRIs don't usually improve clusters is good to know, but it is limited in scope.

SSRIs have a very different type of action than a MAO inhibitor or a serotonin precursor or and indoleamine deoxygenase inhibitor, all of which can actually raise the level of serotonin.  And the work on lactose/fructose intolerance shows that some individuals with anxiety/depression do respond quite well to increasing the levels of serotonin in the blood - tryptophan is converted to serotonin, but nor/epinephrine and dopamine require the amino acid tyrosine.


Quote:


Again, SSRIs do not make more serotonin available everywhere. They make each pulse of serotonin in some nerves more likely to last longer or be more intense - and they do this by blocking the reuptake in certain nerves.  

When low serotonin levels reduce melatonin production, SSRIs do not necessarily change that. (Some SSRIs do, but they do it indirectly by inhibiting other enzymes, and some SSRIs do not affect melatonin at all.)  On the other hand, taking tryptophan or 5-htp has been shown to raise melatonin fairly consistently, especially when serotonin levels were low to start.

Quote:


Agree fully. I think the hypothalamus/pineal factors and the serotonin/melatonin factors are close to the center of the mechanism, and as such deserve special attention. But other things can destabilize or disturb the system.

Quote:


One curious thing I came across recently was the idea that the pineal gland can get calcified and less responsive. This can happen naturally, but high fluoride levels are also one way this can happen. Three of us here are from the same small town, which was one of the first to fluoridate water.  Coincidence?  Maybe. I'm sure there are other factors - traumatic injury to the head (I also have that), genetic predisposition, poor sleep hygiene, etc. etc.


Quote:


Agree with you on this for the most part.  Lifestyle can be very important, but it is not always a direct or consistent pattern. We know that what works for some won't work for others.  In a sense this is similar to migraines - 'therapeutics' include the triptans and other quick acting medicines, a few preventives, but lifestyle is even more nebulous and harder to predict, so many throw up their hands with respect to lifestyle modifications.  

Here are some links on sugar malabsorption and serotonin and related conditions, along with some other reports that simply consuming more beta-lactalbumin (a milk protein) can increase serotonin levels and improve mood.

Malabsorption of carbohydrates and depression in children and adolescents. PMID: 15861016

Fructose malabsorption is associated with decreased plasma tryptophan.
PMID: 11336160

Fructose- and sorbitol-reduced diet improves mood and gastrointestinal disturbances in fructose malabsorbers.
PMID: 11099057

Dietary carbohydrates: effects on self-selection, plasma glucose and insulin, and brain indoleaminergic systems in rat.
PMID: 7537031

Lactose malabsorption is associated with early signs of mental depression in females: a preliminary report.
PMID: 9824144

Kallikrein and serotonin in the blood of patients with lactose intolerance
PMID: 4407879

Fructose malabsorption is associated with early signs of mental depression.
PMID: 9620891

Dietary influences on neurotransmission.
PMID: 3026151

Alpha-lactalbumin-enriched diets enhance serotonin release and induce anxiolytic and rewarding effects in the rat.
PMID: 14684242

Effect of different tryptophan sources on amino acids availability to the brain and mood in healthy volunteers. PMID: 18648776

Effects of alpha-lactalbumin on emotional processing in healthy women.
PMID: 17446205

Diet rich in alpha-lactalbumin improves memory in unmedicated recovered depressed patients and matched controls.
PMID: 16174675

Hi Monty,

Thank you very much for the articles on lactose/fructose intolerance, I will read up on them. 

Regarding the second article, it discussed the role of serotonin in general in application to vertebrates and invertebrates' behaviours, more specifically leech. I am talking about the finding of the effects of SSRIs in human.

Anyway, I think we are getting a bit side tracked. The original posts discuss the hypothesis that by modifying serotonin, via diet changes, that we might see an improvement in CH. My point is from what I have learnt about the mechanisms possibly involved in the genesis of CH, it is not the central point. I believe that the key point is the control pathways via feedback system by which the hypothamalamus and the pineal gland maintaining homeostasis for the body. CH seems to be the byproduct of the break down of such. I feel that the key to unravel how and where and why the break down occurs is the functions of the autonomic nervous system, and therefore the "cure" most possibly lies here.

So far, the only chemicals that seem to have the power to completely halt CH in its track are those that have a profound effects on the autonomic nervous system, namely ergotamine and its derivatives.

Well, let's get organized and we are in order. I proposed three points relating to the possible increase of serotonin, as I said in the conclusions (2) of my first post of the approach hypothesis. The three points are:

a) Increase the availability of tryptophan
b) Avoid the path of conversion of tryptophan quinurenina
c) To facilitate the conversion of tryptophan to serotonin

With your permission, I would like to initiate discussion on item (a).

Years ago, this was my starting point in my studies and I do not remember in detail all aspects related to this issue, so I write what I remember, I would incur in a multitude of mistakes and I would appreciate your corrections.

Necessarily ingested tryptophan in the diet, that's a fact. Most of the tryptophan consumed remains in the intestine, but a small fraction is able to pass to the blood flow (tryptophan-free call) and a part of it can enter the brain.

Recall that the brain serotonin must to be produced in the brain itself, since it does not cross the blood-brain barrier, so it is vital that tryptophan reaches the brain. To do this, it need a transport, but to gain such transport it must compete with other amino acids "neutral" who have greater capacity to transport than him (tyrosine, phenylalanine, leucine, isoleucine and valine)

Although the pineal gland is outside the blood-brain berrera, it captures only tryptophan combined with albumin against the blood circulation, so the transport remains essential. At least two chemicals help tryptophan to join transport over the other amino acids: insulin and carbohydrate.

Nor should we forget that an excess of tryptophan automatically produces an elevation of T-pirrolasa leading tryptophan to the quinurenina, and since this is a self-regulatory body, does not seem much less desirable exceeding consumption. A normal diet (Western) provides more than enough tryptophan to meet the needs of the organism.

With all that, I theorize some mechanisms to increase the general availability of free tryptophan and brain

1) Do not ingest external tryptophan, at least not in high doses, the effect would be contrary to that sought. When the ingestion of Tryptophan is prescribed, it start at high doses, which decreases over time and stages of abstinence in order to avoid this possible effect.
2) Improve the diet for the tryptophan ingested substances is accompanied by to help you reach the brain, eat something sweet and / or carbohydrate (potatoes, bread, ..)
3) Check that the tryptophan is not eated with a large number of amino acid competitors. In this sense, red meat (cow, pig, etc.). have a lot of tryptophan, but also large amounts of other amino acids. Foods that have tryptophan with less competitors and even transport facilitators are: bananas, turkey meat, whole grains, milk and eggs.
4) Make the ingestion of these foods preferably separated from other ingestions.

Recalling that the excess is counterproductive, and that the availability of brain tryptophan occurs in one or two hours after ingestion, I propose as a first good idea to eat some turkey meat and potatoes, or a turkey sandwich with whole grain cereals, or a banana for dessert. Any of these things looking to do a couple of hours before the scheduled time for the crisis.

Probably, this is not the way to get a significant improvement, much less, but could be a condition “sine qua non" for the points b) and c) can be met.

I do not forget the possible ingestion of 5-HTTP or other issues, but I prefer to concentrate on this first point the mere availability of tryptophan.

I look forward to corrections, comments or ideas.

      I dont beleive diet can improve CH, Wouldnt this thought have something in line with how we draw "triggers" from certain foods Some people eat candy bar and get CH, Same as smells draw CH.

       Im not understanding the differance of sertonin, and free sertonin, I believe it is in the transmission, and the sertonin and the mushroom chem break down are almost exatlly the same. I know im not that smart and i dont really understand all this but here it is.

     I never got a cycle that started any other time but in the fall, Always after the time change. So something in the brain is sending out cells that lack sertonin and on path back up if they dont have the proper sertonin.. CH.  This is where the mushroom chem breakdown comes into play and fools returning cell into beleive that it is corrected, Because the cem make-up is almost identical.

    So if you can trick the brain with the LSD on returning cells, So dont that mean the problem starts in the cemical make-up of the cells themselfs. I hope this dont sound stupid.


                                Challening, More assertive.. Coach Bill 

Mechanism of action of drugs.

To not reject a hypothesis, it should at least explain the common observed facts. So little by little I’ll try to present a minimal explanation of how the various drugs that are prescribed for the CH operate.

Ergotamine.

Ergotamin does not deserve much discussion. Its action is predominantly vasoconstrictive, and very powerful. So much so, that combined with other vasoconstricting as triptans, may be fatal.

Ergotamin causes significant vasoconstriction throughout the body, so it would be classified in my first group of hypotheses, the idea of preventing inflammation of the nerve.

I must say that I have consulted some doctors that asked surprised if it’s still prescribed today. The first option seems to be the triptans, the ergot is full of contra-indications, warnings, etc. ..

As a general warning, in addition to substances that are contraindicated with ergot, a leaflet that lacks information: cocaine. Powerful vasoconstrictor, has already resulted in limb amputations in patients due to lack of blood flow. Remember: if you take ergotamine, do not to consume cocaine.

I’ll gradually try to address all drugs and substances as well known by us. Of course, some help would be welcome  

Ok, a longer list of tryptophan as a percent of LNAA:

Sesame seed flour,  9.17
Wheat flour, whole grain, 7.94
Potato, baked, flesh and skin, 7.48
Cocoa powder, unsweetened, 7.05
Quinoa, uncooked, 7.04
Wheat flour, white, 13% protein, 6.99
Oyster mushroom, raw, 6.96
Tofu, made with nigari, 6.92
Amaranth grain, uncooked, 6.82
Sunflower seeds, 6.79
Whey milk protein, sweet, dried, 6.46
Pumpkin seed (pepitas), 6.37
Shrimp, mixed species, cooked moist heat, 6.25
Soybeans, mature seeds, boiled, 6.25
Pistachio nuts, roasted, salted,  6.23
Peanut butter, smooth, no salt, 5.78
Banana, 5.57
Rice, brown, long grained, cooked, 5.49
Chicken, broilers or fryers, breast, stewed, 5.25
Lamb, trimmed retail cuts, cooked, 5.18
Coconut water, 5.12
Dates, Medjool, 5.12  
Egg, whole, omlet,  5.08
Cod, broiled, 5.01
Salmon, broiled, 5.01
Beans, baked, canned, plain, 4.81
Turkey Breast, 4.81
Milk, skim, 4.73
Bologna, Pork, 4.66
Corn flour, whole grain yellow, 2.75
Ground Beef, 80% lean, 2.26
Yogurt, plain, skim milk,      1.9

Thoughts:  

1) Don't eat crunchy beef tacos!  Corn and beef are very low in tryptophan compared to other LNAAs, and a diet heavy in either of these could reduce the amount of serotonin that can formed in the brain. Lamb is a better red meat with respect to tryptophan (and in many other ways, IMO).

2) Turkey is over-rated when it comes to tryptophan. It is equal to baked beans, less than chicken and many other foods. Actually calculating which foods have the best ratio gives a rather different list than is spread in the urban legends and oral traditions.  I have long said that the Thanksgiving drowsiness is due to eating way too much, not to the amount of tryptophan in turkey. I have taken a large dose of pure tryptophan on an empty stomach, and it has never made me feel like I feel after stuffing myself on Thanksgiving day.

3) A desert dessert concoction of dates, sesame paste, pistachios, sunflower seeds, and maybe a little chocolate and honey could be good - Halva is pretty popular across the Mediterranean ... it is based on ground sesame seeds, and sometimes contains some of the other things I mentioned.  Dates have a good ratio of tryptophan, but the total amount is low ... but they are sweet and tasty, so could be a good mix.

4) Wheat is better than rice, whole wheat is better than white refined wheat. All of these are better than most meats if the goal is to raise brain tryptophan/serotonin.

5) Milk is not that great of a source of tryptophan, but one particular protein in milk (alpha-lactalbumin) is much better. Some of the research on the effects of diet and neurotransmitters uses a purified form of this protein. So far, I haven't found a supplement that is pure alpha-lactalbumin, except when buying in huge volume (1000 kg dried). Whey protein (which is used by many in bodybuilding) is better than normal milk. Yogurt may be good for many reasons, but tryptophan is not one of them.

Foods that are high in protein can overwhelm those that are are medium or low protein. For example, combining four ounces of beef with 4 ounces of wheat bread would not be the average of the two... not ((7.94+2.26)/2) or 5.1.  Since the meat has about 3 -4 times more protein than bread per ounce, the true weighted average for a hamburger would be down around 3.4 to 3.7, which is still quite low. A quarter pounder lambburger would weigh in around 5.8, which is considerably better.  

A stir-fry dish with shrimp, tofu, wheat noodles and a good dash of ground sesame would be above 7 -- twice as much brain-available tryptophan as a hamburger.  

More reasonable over the long term - if someone's diet had a weighted average of 4-5, and they raised it to a 6, that could translate to a 20% to 50% increase in the tryptophan available to the brain. I've run some sample diets, and think that a 20-25% increase is possible without banning or prohibiting any foods, simply eating less of the foods on the low end, more on the high end.

This could actually be done consuming the same amount of tryptophan, so I don't think the enzymes to degrade tryptophan would go up, unless they are controlled by the balance of LNAA instead of the amount of tryptophan.

Because the mechanism for transporting LNAA to the brain is relatively slow and gets saturated, the timing of the food may be important as Gonazalo previously said. Eating foods with a high score first (morning meal, pre-meal (soup/salad) and snacks/empty stomach) could make a difference.

No doubt, vitamin A can be toxic at certain doses. I am wondering what the original article meant by 'excessive' - it could be that anything over 100% of the daily allowance might be considered excessive. Doubling or tripling or quadrupling that for a short time would have little toxicity, not sure if that would be enough to reduce the tryptophanase activity for a cycle.

I think a diet limited to polar bear liver has 100,000x the daily allowance - that gets toxic quick.