10 replies to this topic

[username]

I started taking several supplements for my mental health problems (depression, hallucinations, isolation) and made a topic here on it as well. I now found out that not only vitamin B9 and B12 can lower my homocysteine level (which, unfortunately, I don't know), but also NAC and omega-3, which I also take.
I now upped my dosage of l-methylfolate from 2mg to 5mg and feel more alert. I'll now stick with the higher dosage. I take 5mg of B12 on a weekly basis.

I was really surprised to see how many diseases actually correlate with high homocysteine levels. It almost seems like every disease out there correlates with high homocysteine?

http://www.lef.org/p...eduction_01.htm
vascular damage, congestive heart failure, migraines, macular degeneration, hearing loss, alzheimer's

http://evolutionaryp...s-elevated.html
schizophrenia, bipolar disorder, depression

Could this be "a big thing"? Something that everyone seems to overlook and could be of great benefit to a huge part of the population?

http://www.lef.org/p...duction_les.htm
l-methylfolate, methylcobalamin, NAC, SAMe, taurine and many more can lower homocysteine.

What do you guys think? What if every person going to the doctor's would get their level checked and would then receive the substances mentioned above? Couldn't that possibly save society billions of dollars and additionally decrease suffering?

[dunbar]

I was once told by an angiologist that high homocysteine can be lowered through folic acid BUT the risk for diseases
still remains which means that high homocysteine is not a cause but a marker. I never heard this before and thought maybe
it's wrong but then I read the same thing again. If this is true then taking folic acid wouldn't change much.

[YoungSchizo]

Eating meat daily shouldn't that be enough to get the needed B12/B's?

I still have 5000mcg methyl-B12 stored, bought it a long time ago because of it's relationship to schizophrenia, however, only took it once, it gave me some sort of uncomfortable caffeine buzz

[blood]

Seems to be a link between homocysteine levels and dementia/ shrunken brain volumes in the elderly.

Brain atrophy associated with elevated homocysteine:

Int Psychogeriatr. 2010 Aug;22(5):804-11. doi: 10.1017/S1041610210000499. Epub 2010 Apr 7.

Homocysteine is associated with hippocampal and white matter atrophy in older subjects with mild hypertension.

Firbank MJ, Narayan SK, Saxby BK, Ford GA, O'Brien JT.



Abstract



BACKGROUND:

Plasma homocysteine has been associated with reduced brain volumes in cross-sectional studies. We aimed to investigate if homocysteine is associated with ongoing atrophy, and if so, if this is localized to gray or white matter.

METHODS:

In a group of 80 hypertensive subjects aged 70-90 years (from the SCOPE study) MRI images were obtained at two time points two years apart. Rates of gray and white matter and hippocampal atrophy were determined by calculating the difference in segmentation probability maps using SPM5. Plasma homocysteine, folate, B12 and creatinine were measured at study end.

RESULTS:

Homocysteine levels correlated with white matter atrophy rate (p = 0.006) hippocampal baseline volume (p = 0.011) and hippocampal atrophy rate (p = 0.004) but not global gray matter atrophy or baseline gray or white matter volumes. The correlations remained significant (p < 0.05) after controlling for subject age, blood pressure, folate levels and white matter lesion volume.

CONCLUSION:

In older hypertensives, plasma homocysteine levels are associated with increased rates of progressive white matter and hippocampal atrophy.

PMID: 20374668 [PubMed - indexed for MEDLINE]

B vitamins appear to prevent brain shrinkage in older subjects already suffering from mild cognitive impairment:

http://www.ncbi.nlm....les/PMC3677457/

Proc Natl Acad Sci U S A. 2013 Jun 4;110(23):9523-8. doi: 10.1073/pnas.1301816110. Epub 2013 May 20.
Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.

Douaud G, Refsum H, de Jager CA, Jacoby R, Nichols TE, Smith SM, Smith AD.




Abstract



Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.

KEYWORDS:

causal modeling, clinical trial, degeneration, hippocampus, structural neuroimaging

[username]

I was once told by an angiologist that high homocysteine can be lowered through folic acid BUT the risk for diseases
still remains which means that high homocysteine is not a cause but a marker. I never heard this before and thought maybe
it's wrong but then I read the same thing again. If this is true then taking folic acid wouldn't change much.

The study this view is based on had huge methodological flaws
http://www.lef.org/m...r-Health_01.htm

-> those who took part in the study were very sick to begin with. Other factors were not considered.
-> dosage might have been too low. They used folic acid instead of methylfolate (more bioactive!)
-> If you died just days after the study began, you were considered a 'failure' (treatment failed). They didn't take into account that it takes a certain amount of time to actually lower homocysteine levels
-> They put subjects into 'categories' and the lowest category was <11 µmol/l while it would have been more reasonable to have used <8µmol/l (8-11 -> still increased risk), thus distorting the results

In one study, they looked at people with coronary heart disease. Those belonging to highest category (homocysteine) were almost 7x more likely to die in the next five years. It would be foolish not to assume that there is a causative relation. It seems tragic because, even if it isn't, lowering homocysteine won't do any harm. The substances used to do that are harmless and have no to very few side effects.

[username]

Eating meat daily shouldn't that be enough to get the needed B12/B's?

I still have 5000mcg methyl-B12 stored, bought it a long time ago because of it's relationship to schizophrenia, however, only took it once, it gave me some sort of uncomfortable caffeine buzz

When I took it for the first time, I felt "different", too. I tried it several years ago when I was 'only' depressed and saw some improvement. I had side effects, though, such as paresthesia (for up to a week!). I would definitely take active forms of B9, B12 and possibly B6 if I were you. Right now, I take B9 and B12 in their active form. B12 is extremely harmless. You won't be able to do any harm by taking it.
B12 alone won't be sufficient to treat high homocysteine. That's why I'd advise adding in methylfolate as well and NAC. Schizophrenics often have mthfr c667t mutations leading to high homocysteine. I think it would be a mistake not to give homocysteine-lowering substances a try.

in regard to eating meat:
Problems with absorbing B12 and genetic factors lead to B12 insufficiency or deficiency. Eating meat will NOT protect you from B12 deficiency. This is a frequent misconception. Vegans, vegetarians, and carnivores can all get a B12 deficiency. While carnivores are less likely to have a B12 deficiency than the other two groups, this difference is not 'huge'. Carnivores frequently have low levels of B12 as well.

Edited by longschi, 31 January 2014 - 10:21 AM.

[YoungSchizo]

Active form of B9 is L-Methylfolate right? I also had it laying around here from a long time ago, 1000mcg. I thought I might as well empty it see if it would make any difference, couple of days I took 7, other days 15mg, the recommended dose for schizophrenics. Didn't notice any improvements in these days (I know you have to take it for a long time at 15mg dosages to see if it will improve something, don't know if it is worth the money).

B6 I also still have, don't have the active form off it, I think I get enough B6 from my supplements which already contain B6.

B12 story is same as Sarcosine I guess. Sarcosine is found in chicken, eggs etc. which I already ate a lot but never improved any symptoms, Sarcosine alone does! I can pop the rest of the B12's, I have 5000mcg, what's the recommended dose?

[username]

It is worth the money

15mg methylfolate vs. placebo (6 months)


2mg folate, 25mg pyridoxine, 400mcg B12 vs. placebo (6 months)



There aren't any recommended doses, really. But 1000mcg per day of B12 should suffice.

[dunbar]

@ longschi

You mean this stuff about high homocysteine only being a marker is based on 1 study?

I also thought that what the doc said sounded a bit weird. I'd still take folate if my levels were high.

Is folic acid always a bad choice or does it work for some and not for others? I think I heard that women
cannot use folic acid and instead they need methylfolate.

[username]

http://chriskresser....e-vs-folic-acid
http://thehealthyele...late-vs-folate/

Folic acid supplementation does not reduce intracellular concentrations of homocysteine or any of its closely related substances. Rather, folic acid may disturb physiological regulation of intracellular one carbon metabolism [methylation] by interfering with SAM’s inhibitory effect on MTHFR activity. — Smith et al., Clinical Chemistry and Laboratory Medicine, Aug 2013

http://mthfr.net/folic-acid-awareness-week-2014-want-awareness-here-you-go/2014/01/08/

[albedo]

There is a strong link between oxidation stress, homocysteine levels and brain disorders. Please refer to the good video (in 3 parts) from Dr. Andrew Rostenberg, much in line with blood's post, explaining the balance you need to achieve in homocysteine levels (not too low, not too high, possibly 4-8) and providing also some clinical evidence from his practice:

 

http://beyondmthfr.c...teine-part-iii/