Feeling sleepy from B vitamins

[Gondwanaland]

I thought I was ready to retry with the basics and soon be able to feel the benetifts from mB12 again...

Since Saturaday I have been trialing with 1/2 dose of the following B complex:

B1 15mg
B2 5mg
Niacin 20mg
B5 30mg
P5P 10mg
B7 300mcg
magnesium 10mg

Then took 100mcg of mB12 + fifteen micrograms of mfolate which made me even more sleepy but with fast gears turning close to the xiphoid process.

On Sunday I added 10mg of benfothiamine but felt no effects from it.

Yesterday and today I took no Bs and feel sleepy as well.

I had been playing with hyB12, mB12 and folinic sublingual drops for a month (+ Bcomplex above) with the same results (feeling sleepy).

The things that have made me more alert lately have been:

-silymarin (can't take very often or a really effective dose due to strong detox and end up brain fogged again, but it stabilized my body temperature)
-multimineral (waiting for a new delivery)
-digestive enzymes (waiting for a new delivery without protease as alerted by @picante )

It seems like anything I take works for a short while and then I start detoxing and feel no more benefits at all.

I would be thankful for any suggestions ( @ahmo coffee enemas, I know ).

 

[ahmo]

Ha ha.

It seems like anything I take works for a short while and then I start detoxing and feel no more benefits at all.

I wonder if this means that your body is overloaded w/ toxins, and therefore attempts to get rid of them whenever there's a stimulus??

 

[Gondwanaland]

OK, just got my bloodwork and I have low T3.

Coffee enemas would definetly help.

 

[Critterina]

OK, just got my bloodwork and I have low T3.

That would totally explain your sleepiness! I would lay off any coffee enemas while your thyroid has a chance to respond to the medication. After a few weeks, maybe, see if you still want to. I'm guessing not. And see if your body temperature will be more stable (and likely higher), too, with or without the silymarin. (My average morning temp went up about 1.5 degrees F with 50 mg T4.) Good going, getting the lab work done!

 

[Gondwanaland]

with or without the silymarin

Silymarin definetly helped with the adrenal type of temperature variation! I have been feeling very comfortable re temperature, but then it is late spring here and already very hot. Will have my temps measured, thanks, Crit!

 

[aaron_c]

Hi Yall,

@Gondwanaland thought it would be a good idea to move this conversation from "private" to a thread. The conversation arose from this thread on vitamin K, but these bits were not about vitamin k.

Hi Aaron

Re the B vits:
B1 - Always took it in a Bcomplex and can't evaluate its effect. Once I took 10mg of Benfothiamine on its own, but in that day I ate asparagus and I think both pooled to lower my T3. High dose B1 can be very beneficial for HYPERthyroid AFAIK.

B2 - I played a lot with the doses of B2 in my Bcomplex (locally compounded). I started with 5mg and it seemed well balanced with the others. Then I upped to 8mg and felt awful - low serotonin/high ammonia symptoms

B3 - niacin seemed more helpful than niacinamide. My liver felt stuck with niacinamide which slows phase I.

B5 - can't say anything about its effects. I tried extra 25mg Panthetine apart from the complex and felt nothing.

B6 - B6 with low magnesium is a recipe for disaster

B7 - At some point I took 700mcg with my Bcomplex and at first felt increased appetite, later I think It increased my acidity. SO I am keeping with 300mcg now.

B9 - disater

CyB12 - toxic - I think I have serious problems with it

mB12 - love at 1st dose, then got intermittent fatigue

Right now both the Bcomplex and the mB12+mB9 (I take them separately) make me sleepy

I started taking ((only a fraction of a capsule) an all activated B complex (Swanson's) and felt OK for like 3 days, then low serotonin / high ammonia crept up.

Does this help?

forgot to add that when I lowered it to 2mg I had the same symptoms as with 8mg

At the time I introced it I was getting hyperthytoid and definetly had symptoms of low B1. Run into low potassium, high ammonia and high uric acid (acidosis) as per this chart:
http://forums.phoenixrising.me/inde...bolism-simplified-chart-and-b-vitamins.34375/

 

[aaron_c]

First, I want to say that it sounds like you might still in the process of getting some sort of toxin out of your body...and if this is the case, it makes it even more likely that I am missing something here.

Then took 100mcg of mB12 + fifteen micrograms of mfolate which made me even more sleepy but with fast gears turning close to the xiphoid process.

Could you describe that bit about fast gears in a different way?

I had been playing with hyB12, mB12 and folinic sublingual drops for a month (+ Bcomplex above) with the same results (feeling sleepy).

Folinic acid uses ATP to enter the rest of the folic acid cycle via conversion to 5,10 methenylTHF, so it is not surprising that this would make you sleepy.

I have read two guesses about why mB12 might make people sleepy. The first is that SAMe donates a methyl group in the rate limiting step that turns serotonin into melatonin. This might produce enough melatonin to make you sleepy. Have you taken melatonin, and if so, what happened?

EDIT: I said that THF is used to make serotonin. I misread a diagram! It was BH4, converted to q-BH2.

For what it is worth, I tried taking melatonin last year and taking maybe half a mg--the lowest dose pills I could find were 1mg--made me exhausted for...perhaps 12 hours or so? I continued on the dose, however, and developed a tolerance. I assume what happened is that I was so starved of melatonin that my body had produced a high number of melatonin receptors. Melatonin inhibits cortisol release: See this study: Melatonin exerts direct inhibitory actions on ACTH responses in the human adrenal gland.

The second guess as to why mB12 would make one sleepy is that mB12 could help inactivate histamine in the central nervous system through converting 5MTHF to THF, which is then converted to DHF by a methyltransferase which turns histamine into glutamate. If you have enough manganese and B6, the glutamate could then be turned into GABA. I am not suggesting that heightened GABA would knock you out, but if you had high histamine, lowering it might? This second mechanism seems much less likely to me.

-silymarin (can't take very often or a really effective dose due to strong detox and end up brain fogged again, but it stabilized my body temperature)
-multimineral (waiting for a new delivery)
-digestive enzymes (waiting for a new delivery without protease as alerted by @picante )

Very cool observation on silymarin. I skipped my silymarin after lunch today and had cold feet...perhaps this is why?

You digestive enzymes didn't include betaine, right?

OK, just got my bloodwork and I have low T3.

Was this "free" T3? Was your free T4 low as well?

Finally: For whatever it is worth, I completely support your reservations about vitamin K. I also continue to hope that it will prove to be an important piece of the puzzle for myself and others.

 

[Gondwanaland]

Thanks, @aaron_c I will come back soon for a detailed reply!

 

[Gondwanaland]

First, I want to say that it sounds like you might still in the process of getting some sort of toxin out of your body...and if this is the case, it makes it even more likely that I am missing something here.

I have found several names to it upon researching: detox, die-off, candida, SIBO, HIT, etc

Could you describe that bit about fast gears in a different way?

It is something happening between the liver lobes

Folinic acid uses ATP to enter the rest of the folic acid cycle via conversion to 5,10 methenylTHF, so it is not surprising that this would make you sleepy.

Interestin, it ould be that, could be ammonia building up...

I have read two guesses about why mB12 might make people sleepy. The first is that SAMe donates a methyl group in the rate limiting step that turns serotonin into melatonin. This might produce enough melatonin to make you sleepy. Have you taken melatonin, and if so, what happened?

Sorry, I did not meant THAT kind of sleepy. When I took continued high doses of mB12 I felt really sleepy. But now that I have been retrying with low doses, it's more like a "brain-fog sleepy". I never took melatonin.

The second guess as to why mB12 would make one sleepy is that mB12 could help inactivate histamine in the central nervous system through converting 5MTHF to THF, which is then converted to DHF by a methyltransferase which turns histamine into glutamate. If you have enough manganese and B6, the glutamate could then be turned into GABA. I am not suggesting that heightened GABA would knock you out, but if you had high histamine, lowering it might? This second mechanism seems much less likely to me.

This is an excellent explanation for the real sleepiness

Very cool observation on silymarin. I skipped my silymarin after lunch today and had cold feet...perhaps this is why?

I love silymarin and am really happy to be able to tolerate it now.

You digestive enzymes didn't include betaine, right?

No betaine, just pepsin, bromelain and protease. I found that I tolerate the protease very well with dinner ( @picante ). Will retry it with lunch as well

Was this "free" T3? Was your free T4 low as well?

Unaltered FT4 and T3 (not tested FT3 at that time) was below range, but later I found out it was due to eating asparagus... But I found great benefit from changing the T4 only to T4+T3.

Finally: For whatever it is worth, I completely support your reservations about vitamin K. I also continue to hope that it will prove to be an important piece of the puzzle for myself and others.

I am more than willing to take it at least once a week, but I will have to establish a powerful anti-inflammatory supplementation. Suggestions?
I currently take fishoil, Gamma E and astaxanthin (haven't noticed nothing from it).

 

[Gondwanaland]

Could you describe that bit about fast gears in a different way?

I think I got it:

@Kimsie, I believe many of the issues you are finding could be related to gut dysbiosis. Prebiotics, such as resistant starch, can increase uric acid. See this quote for example:

by Vegas:

So let's say we increased your purine metabolism, or at least the activity of xanthine oxidases which generates uric acid. One absolute consequence would be the increased production of superoxide and peroxynitrite. An increase in this part of the metabolism likely signifies that there is an increase in the ability to suppress superoxide radicals and peroxynitrite simply because ONOO levels will inhibit this reaction. Put another way, as peroxynitrite levels rise this down-regulates xanthine oxidase activity and all the byproducts of this reaction, including uric acid, are suppressed. This serves to reduce the demands on the entire antioxidant network and the dehydrogenase enzymes, in particular. The increased activity of XO would seemingly suggest that the prebiotics have reduced ONOO levels.

The mechanism by which glyconutrients or resistant carbohydrates could result in an increase in uric acid likely involves the provision of SCFA's, particularly butyrate, where it is needed. Increases in butyrate would seemingly have the ability to influence every single consequences of enhanced purine metabolism that comes to mind. In fact, I think it perfectly fits this equation. I think it is also notable that while butyrate is taken up by the colonocytes, it is also principally utilized in the liver. It is certainly not coincidental that in humans, xanthine oxidase, which creates uric acid, is chiefly and almost exclusively expressed in the liver and intestinal tract.

 

[adreno]

@Gondwanaland, I think you should attribute that quote above to it's rightful origin (vegas). I didn't write that quote.

 

[Gondwanaland]

@Gondwanaland, I think you should attribute that quote above to it's rightful origin (vegas). I didn't write that quote.

If you click the quote you'll be redirected to Vegas post, but I added his name now, thanks!

 

[aaron_c]

@Vegas, might we snag you into our discussion? I found your post very interesting, but I do not think I understood most of it.

So let's say we increased your purine metabolism, or at least the activity of xanthine oxidases which generates uric acid. One absolute consequence would be the increased production of superoxide and peroxynitrite.

If I read you right, you are saying that uric acid increases superoxide and peroxynitrite production. I don't know a great deal about uric acid, but wikipedia (citing a study I cannot immediately get access to) says that it accounts for "over half the antioxidant capacity of blood plasma" in humans. Are you saying that we produce more free radicals, in effect, because we have the increased antioxidant capacity to accommodate that? Or am I missing something important about what heightened uric acid does?

Talking about the results of decreased xanthine oxidase activity and this decreased uric acid levels, you said:

This serves to reduce the demands on the entire antioxidant network and the dehydrogenase enzymes, in particular.

Again, I am confused, because wikipedia has me thinking that uric acid is an antioxidant, so I do not understand how lowered uric acid levels would "reduce the demands on the entire antioxidant network." In particular, I would be curious to know what dehydrogenase enzyme(s) you had in mind.

Increases in butyrate would seemingly have the ability to influence every single consequences of enhanced purine metabolism that comes to mind. In fact, I think it perfectly fits this equation. I think it is also notable that while butyrate is taken up by the colonocytes, it is also principally utilized in the liver. It is certainly not coincidental that in humans, xanthine oxidase, which creates uric acid, is chiefly and almost exclusively expressed in the liver and intestinal tract.

Would you mind explaining this more thoroughly, or perhaps linking to a page where you have already explained it? It seems important, but the link between butyrate and pretty much any part of purine metabolism is a mystery to me. I am only aware of butyrate as something that can aid in the excretion of ammonia, and also as a source of energy for the colon.

I've also noticed that my tolerance to caffeine (a methyl xanthine) has steadily risen over the last six months. This is very possibly an indication of improvement in this particular metabolic process as caffeine can reduce the activity of xanthine oxidase, thus its effects have become less noticeable.

[...]I have days when my hands get very cold, and days when a little bit of caffeine has a very pronounced diuretic effect. With uric acid primarily excreted in urine, I think this is a compensatory measure.

Finally, I hope you can help me wrap my head around this detail. It seems like if increased diuresis from caffeine was compensating for caffeine's effect on xanthine oxidase, caffeine would need to increase production of uric acid, not decrease it. Put another way: It seems like you are saying that the increased urine volume from caffeine is "compensating" for an extra high uric acid level, when in fact you said that " caffeine can reduce the activity of xanthine oxidase." What am I missing?

 

[aaron_c]

Said another way, when we loose the microbes that create enzymes that participate in the breakdown of macronutrients and indigestible or resistant polysaccharides, there is a similar inhibition of our own human digestive enzymatic capacity. We commonly see this when someone is afflicted with severe ME/CFS and starts to develop severe food intolerance, weight loss, fat malabsorption, and obvious pancreatic insufficiency. Think about what this achieves functionally, it suppresses the immune response, which is mediated by many of the compounds and micronutrients contained in our foods. Availability of zinc, fat soluble vitamins A, E, D, & K. This is of course comes with adverse immune consequences, including the creation of antibodies, but I would argue that the higher priority, in the setting of a compromised intestinal epithelium barrier involves suppressing the immune/inflammatory response. As I have studied ME/CFS, I see level after level of ways this has done and the provision of butyrate has a special ability to start to reverse many of these processes unlike anything else I have found.

@Gondwanaland: You have probably already read this post by Vegas, but as they mention "severe food intolerance" and "weight loss"--which to my understanding is atypical in ME/CFS, I think we usually gain weight--I thought it might be of interest. Not that it suggests anything you haven't already tried, of course.

 

[WillowJ]

@Gondwanaland: You have probably already read this post by Vegas, but as they mention "severe food intolerance" and "weight loss"--which to my understanding is atypical in ME/CFS, I think we usually gain weight--I thought it might be of interest. Not that it suggests anything you haven't already tried, of course.

Thanks for the interesting repost there. There is indeed a significant subset of PWME having weight loss, including severe weight loss (enough to scare a doctor, if we can manage to get in), which may be associated with severe food intolerance, malabsorption/maldigestion, etc.

 

[Sidereal]

@Gondwanaland: You have probably already read this post by Vegas, but as they mention "severe food intolerance" and "weight loss"--which to my understanding is atypical in ME/CFS, I think we usually gain weight--I thought it might be of interest. Not that it suggests anything you haven't already tried, of course.

There are plenty of people with ME/CFS who can't keep weight on. Often such patients are suspected of having anorexia nervosa by mainstream docs. But you are right, it is less typical than the abnormal weight gain most of us experience. The latter group gets accused of being depressed and overeating and told to exercise and lose weight and all problems will go away. Both groups are unable to extract usable energy from food, it would appear, but one group seems to develop malabsorption issues so they keep wasting away while the weight gain type seems to just store everything they eat as fat.

Personally, since my crash, I can eat as little as 1400 calories a day and not lose any weight at all. If I restrict food intake in any way I just become even more weak and dizzy, muscles feel more acidic and I urinate continuously leading to even worse problems with low blood volume and electrolyte wasting.

 

[Vegas]

@Vegas, might we snag you into our discussion? I found your post very interesting, but I do not think I understood most of it.



If I read you right, you are saying that uric acid increases superoxide and peroxynitrite production. I don't know a great deal about uric acid, but wikipedia (citing a study I cannot immediately get access to) says that it accounts for "over half the antioxidant capacity of blood plasma" in humans. Are you saying that we produce more free radicals, in effect, because we have the increased antioxidant capacity to accommodate that? Or am I missing something important about what heightened uric acid does?

Talking about the results of decreased xanthine oxidase activity and this decreased uric acid levels, you said:


Again, I am confused, because wikipedia has me thinking that uric acid is an antioxidant, so I do not understand how lowered uric acid levels would "reduce the demands on the entire antioxidant network." In particular, I would be curious to know what dehydrogenase enzyme(s) you had in mind.



Would you mind explaining this more thoroughly, or perhaps linking to a page where you have already explained it? It seems important, but the link between butyrate and pretty much any part of purine metabolism is a mystery to me. I am only aware of butyrate as something that can aid in the excretion of ammonia, and also as a source of energy for the colon.



Finally, I hope you can help me wrap my head around this detail. It seems like if increased diuresis from caffeine was compensating for caffeine's effect on xanthine oxidase, caffeine would need to increase production of uric acid, not decrease it. Put another way: It seems like you are saying that the increased urine volume from caffeine is "compensating" for an extra high uric acid level, when in fact you said that " caffeine can reduce the activity of xanthine oxidase." What am I missing?

Sorry, lots of questions and none too simple to answer succinctly, at least today. Uric acid is both an anti and pro-oxidant. In some instances I am talking about negative expression of a gene not the chemical coordinate.
The link between the purine metabolism relates to the PDHC. Butyrate increases the capacity of the nitrogen /purine metabolism in a number of different ways, both direct and indirect. At a sub-cellular level, this has been shown to occur via enhanced expression of the entire pyruvate dehydrogenase complex.

Perhaps you can start by reading this:

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0006759