LONGECITY

Hi all,

 

I have received my results of the amino acid analysis through 24 hours urine.

1-methylhistidine has been elevated alot, it's extremely high.

 

1-methylhistidine: 973 umol/24u (normal range: 128 - 392).

 

3-methylhistidine: 216 (this is good).

 

A google search gave me a probably leaky gut syndrome (http://www.aminoacid....com/blog/?p=11).

 

Can anyone tell me more what this means? Can it be lowered with food/supplements?

You might want to check with your doctor.

 

 

One-methylhistidine (1-MHis) is derived mainly from the anserine of dietary flesh sources, especially poultry. The enzyme, carnosinase, splits anserine into b-alanine and 1-MHis. High levels of 1-MHis tend to inhibit the enzyme carnosinase and increase anserine levels. Conversely, genetic variants with deficient carnosinase activity in plasma show increased 1-MHis excretions when they consume a high meat diet. Reduced serum carnosinase activity is also found in patients with Parkinson's disease and multiple sclerosis and patients following a cerebrovascular accident. Vitamin E deficiency can lead to 1-methylhistidinuria from increased oxidative effects in skeletal muscle.

 

 

 http://www.hmdb.ca/m...lites/HMDB00001

http://books.google....stidine&f=false

Edited by Metagene, 26 October 2014 - 08:44 PM.

Thanks Metagene.

 

I just found the following information: 1. 1-methylhistidine. If the individual has an elevation in this marker, s/he probably has leaky gut syndrome. (http://www.aminoacid....com/blog/?p=11)

 

On an other site i found:

 

 1-Methylhistidine is found to be elevated; it is a component of the dietary peptide anserine. Anserine is
beta-alanyl-1-methyl-L-histidine, and it is known to come from chicken, turkey, duck, rabbit, tuna and salmon. Other
food sources (especially trout and fowl) also are likely but are not documented. The peptidase enzyme that
hydrolyzes anserine is present in the small intestine and also present in liver, spleen, and kidney tissues and in blood
serum. Some direct uptake of dietary anserine is normal, and moderate levels of urinary 1-methylhistidine are
normal. However, high levels suggest increased uptake of short-chain peptides, possibly increased gut permeability,
and increased hydrolysis of short-chain dietary peptides by peptidases in blood, liver and spleen. Elevated
1-methylhistidine suggests one or more of: dietary overload of anserine-source foods, increased gut permeability, and
decreased activity of digestive peptidases in the small intestine. There may or may not be associated
symptomatology. 1-Methylhistidine itself is not known to be detrimental.

Source: http://www.homeopath...n/r_AAurine.pdf

 

I will discuss the results next week with the doctor, my guess is that he doesnt know much about it. Are there any particular doctors which know more about this?

 

Oh btw, hereby a summary of other amino's which are not normal:
GABA: 3 umol/24u ( 7 - 35)
Methionine: 7 umol/24u (16-62)
Phenylalanine: 30 umol/24u (31 - 95)
Tyrosine: 36 umol/24u (40 - 168)
Phosphoethanolamine: 16 umol/24u (19 - 55)
1-methylhistidine: 973 umol/24u (128 - 392)

Leaky gut syndrome is not a recognized medical diagnosis, but a proposed condition that is claimed to be the root cause of many ailments, including chronic fatigue syndrome and multiple sclerosis.

http://en.m.wikipedi...ky_gut_syndrome

Is your doctor a GP?
Edited by Metagene, 29 October 2014 - 08:26 PM.

These are the reference values from Medline Plus.

1-methylhistidine

Children: 41 to 300

Adults: 68 to 855

3-methylhistidine

Children: 42 to 135

Adults: 64 to 320

http://www.nlm.nih.g...icle/003366.htm

Hey Jason30 I saw your post on Phoniex Rising. Have you ruled out Temporomandibular disorder?

Features of Temporomandibular Disorders in Fibromyalgia Syndrome

http://www.ncbi.nlm....5027730/related

Evidence of oxidative stress in temporomandibular disorders: a pilot study.

http://www.ncbi.nlm....?report=classic

Pain Intensity, Illness Duration, and Protein Catabolism in Temporomandibular Disorder Patients with
Chronic Muscle Pain

In support of the depletion of body reserves of amino acids and the gradual development of pain and whole body symptom expression,
patients with the longest illness duration had lower levels of urinary metabolites and increases in 3- methylhistidine. Increases in 3-methylhistidine strongly suggest that there is an increase in degra- dation of muscle fibers and cytoskeletal actin indicating the possible depletion of the nonfibrillar protein source. Also supportive of a protein turnover problem is the increase in urinary 1- methylhistidine for both pain intensity and illness duration.1-Methylhistidine and 3-methylhistidine are components that originate from cytoskeletal actin, but may also be found in urine of subjects eating meat products. In this case, the levels corre- late with symptom expression and appear to indi- cate the degradation of cytoskeletal proteins that usually occurs in the late stage of cancer or under severe protein degradation situations.

https://docs.google....sp=docslist_api
Edited by Metagene, 30 October 2014 - 01:14 AM.

Hi Metagene,

I am sorry, what do you mean with a GP doctor?

The references of medline plus are in micromoles per deciliter (micromol/dL). My lab uses micromol/24u. I am not sure if they use per deciliter or liter. I will ask this.

I have look into the Temporomandibular disorder. I do have chronic muscle pain, but i have no pain in the mouth or muscles that move the jaw. My main symptoms are pain in the legs (mostly in the night) and fatigue, but those are not symptoms of Temporomandibular disorder.  So i guess that could be ruled out?

The quote:
Also supportive of a protein turnover problem is the increase in urinary 1- methylhistidine for both pain intensity and illness duration.

What do they mean with a protein turnover problem? Is this in other words; a protein conversion problem?

What can i do to improve this?

I do not eat alot of meat or proteins.

I'll guess i'll have to start with a good amino acid supplement.
Do you think that this will lower the 1-methylhistidine?

Thanks for the info and thinking with me, much appreciated!

GP is short for general practitioner. I should have asked about your symptoms earlier but everything makes sense within the context of CFS/fibromyalgia. 

 

 

Temporomandibular disorder can definitely be ruled out although fibromyalgia may actually cause TMD.

 

 

http://www.ncbi.nlm....pubmed/10901602

http://www.ncbi.nlm....pubmed/20466595

 

 

 

Increased oxidative stress is still a factor.

 

Oxidative stress and antioxidative parameters and metal ion content in patients with fibromyalgia syndrome: implications in the pathogenesis of the disease.

 

 

http://www.ncbi.nlm....pubmed/24373371

 

 

 

"Protein turnover is the balance between protein synthesis and protein degradation. More synthesis than breakdown indicates an anabolic state that builds lean tissues, more breakdown than synthesis indicates a catabolic state that burns lean tissues."

 

http://en.wikipedia....rotein_turnover

 

 

 

 

After you see a specialist hydrogen water might be worth looking into. Wish you all the best.

 

Edited by Metagene, 30 October 2014 - 05:23 PM.

Hi Metagene,

 

Yes indeed, he is a general practitioner.

 

About the oxidative stress, this has longer my attention. But i don't know if that applies to me.

I do know that my Malondialdehyde was good in my last blood results (this month): 0.90 umol/l  (Malondialdehyde could be a marker for oxidative stress, http://en.wikipedia....Malondialdehyde ).

 

I am sorry, i don't understand what you mean with:

"Protein turnover is the balance between protein synthesis and protein degradation. More synthesis than breakdown indicates an anabolic state that builds lean tissues, more breakdown than synthesis indicates a catabolic state that burns lean tissues."

 

How is this relevant for me?

 

Molecular hydrogen, that looks interesting. I can't figure it out if that's H2o2 or something else? (i check if i can order this)

 

Again, thanks alot for your time.

 

 

Malondialdehyde is only one marker for oxidative stress. 3-methylhistidine is a useful marker for muscle protein break down (catabolism) which is normal in your case.

   

 

Overview of Metabolism - Anabolism and Catabolism

 

 

 

"High levels of 1-MHis tend to inhibit the enzyme carnosinase and increase anserine levels."

 

Carnosine (beta-alanyl-L-histidine) is a dipeptide of the amino acids beta-alanine and histidine. It is highly concentrated in muscle and brain tissues.

Carnosine and carnitine were discovered by Russian chemist V.Gulevich.^[2] Researchers in Britain,^[3] South Korea,^[4] Russia^[5][6] and other countries^[7][8][9] have shown that carnosine has a number of antioxidant properties that may be beneficial. Carnosine has been proven to scavenge reactive oxygen species (ROS) as well as alpha-beta unsaturated aldehydes formed from peroxidation of cell membrane fatty acids during oxidative stress.

 

http://en.wikipedia.org/wiki/Carnosine

 

The roles of carnosine in aging of skeletal muscle and in neuromuscular diseases.

 

Skeletal muscles undergo specific alterations that are related to the aging process. The incidence of several neuromuscular diseases (e.g., amyotrophic lateral sclerosis (ALS), myasthenia gravis, polymyositis, drug-induced myopathies, late-onset mitochondrial myopathy) is age-related. The increased sensitivity to disease of aging muscle represents an additional age-related negative influence in the presence of existing risk factors (such as a genetic predisposition). The potential significance of carnosine lies on one hand in its possible influence on specific physiological changes in muscle associated with the aging process, and on the other in its effect on oxidative stress and the antioxidative system in specific neuromuscular diseases such as ALS or polymyositis.

 

 

http://www.ncbi.nlm....pubmed/10951106

 

 

You should definitely speak to a rheumatologist.

 

 

See post #2130 for hydrogen water products

 

http://www.longecity...-71#entry693298

 

 

Edited by Metagene, 31 October 2014 - 06:53 PM.