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Supplements for Vitiligo

Vitiligo is an autoimmune condition and as such certain dietary protocols as well as supplements can be used to support the immune system for those that experience the characteristic skin depigmentation. The scope of this article however is to discuss the supplements that have been shown in clinical trials to help the repigmentation of the skin.

In most cases supplementation was accompanied by the use of light therapy.

Khellin.

For thousand of years the treatment of “leukoderma” (vitiligo) involved the topical application or ingestion of seeds or plant extracts and the subsequent exposure to sunlight. Khellin is an extract from the seeds of the plant khella found in the eastern Meditteranean area. Supplementation of Khellin has been repeatedly shown (Abdel-Fattah, A. et al., 1982, Orecchia, G. et al., 1998, de LEEUW, J. et al., 2003) to improve the repigmentation of the skin.

 

There have been cases though (Ortel, B. et al., 1988) that after 4-6 weeks of khellin supplementation the elevation of transaminases was observed and for these individuals had to discontinue the treatment.

 

L-phenylalanine.

In search for re-pigmentation solutions for vitiligo, a group of scientists in Amsterdam – NL (Cormane R et al., 1985), noted that patients with phenylketonuria (who among other symptoms have lighter than normal skin) when administrated tyrosine and were incubated with UV-light had normal melanin production. Cormane’s team initially tried the tyrosine & UV-A protocol in a pilot study of 5 without any success. Sequentially they tried phenylalanine (a precursor of tyrosine) seeing improvement in 95% of the subjects after 6 to 8 months. The theory put forward on why phenylalanine benefits vitiligo patches was that it stops antibodies and allows sun radiation to stimulate melanocytes from other areas to migrate to the damaged ones (Camacho, F. and Mazuecos, J., 1999).

 

50 mg/kg of body weight per day of phenylalanine was administered 1 hour prior to UV A irradiation (twice per week). Of the 19 participants:

i. 5 noted dense re-pigmentation in 6 to 8 months

ii. 13 saw sparse re-pigmentation in the same period

iii. and 1 had no re-pigmentation even after 8 months.

Since the 1980’s there has been no more research examining the benefits of phenylalanine for vitiligo. All 3 studies combining the administration of the amino acid & UVA exposure as well as the 1 that used just the amino acid reported positive outcomes (Szczurko, O. and Boon, H.S., 2008).

 

Additional supplements.

PABA is an ingredient often used in sunscreen lotions. One study showed PABA to support repigmentation (Sieve B F, 1942) but currently there is limited research to confirm these findings. An 8 years old girl developed hemolytic anemia and hepatotoxicity after administration of PABA for 4 months. Symptoms were reversed 2 months after discontinuing the supplement (Tootoonchi, P., 2018). PABA has also been reported to cause depigmentation (Hughes, C. G., 1983)

 

Vitamin E (Szczurko, O. and Boon, H.S., 2008) and vitamin C have also been shown to support re-pigmentation potentially due to their antioxidant properties.

 

Conclusion.

The results in the above studies are very promising. However, as I mentioned already, in certain cases there have been adverse effects such as the development of cirrhosis which highlights the importance of complimentary testing and supervision.

 

 

References.

Abdel-Fattah, A., Aboul-Enein, M. N., Wasset, G. M., & El-Menshawi, B. S. (1982). An approach to the treatment of vitiligo by khellin. Dermatology165(2), 136-140.

 

Camacho, F. and Mazuecos, J., 1999. Treatment of vitiligo with oral and topical phenylalanine: 6 years of experience. Archives of dermatology, 135(2), pp.216-217.

 

Cormane, R.H., Siddiqui, A.H., Westerhof, W. and Schutgens, R.B.H., 1985. Phenylalanine and UVA light for the treatment of vitiligo. Archives of Dermatological Research, 277(2), pp.126-130.

 

de LEEUW, J., MAIERHOFER, G., & NEUGEBAUER, W. D. (2003). A case study to evaluate the treatment of vitiligo with khellin encapsulated in L‐phenylalanin stabilized phosphatidylcholine liposomes in combination with ultraviolet light therapy. European Journal of Dermatology13(5), 474-477.

 

Hughes, C. G. (1983). Oral PABA and vitiligo. Journal of the American Academy of Dermatology9(5), 770.

 

Szczurko, O. and Boon, H.S., 2008. A systematic review of natural health product treatment for vitiligo. BMC dermatology, 8(1), p.2.

 

Sieve, B. F. (1942). The clinical effects of a new B-complex factor, para-aminobenzoic acid, on pigmentation and fertility. South Med Surg104(135), 9.

 

Orecchia, G., Sangalli, M. E., Gazzaniga, A., & Giordano, F. (1998). Topical photochemotherapy of vitiligo with a new khellin formulation: preliminary clinical results. Journal of dermatological treatment9(2), 65-69.

 

Ortel, B., Tanew, A., & Hönigsmann, H. (1988). Treatment of vitiligo with khellin and ultraviolet A. Journal of the American Academy of Dermatology18(4), 693-701.

 

Tootoonchi, P. (2018). Hemolytic Anemia and Other Side Effects of Para-amino Benzoic Acid in an 8-Year-Old Girl. Iranian Journal of Pediatric Hematology & Oncology8(3).

Reversing Vitiligo

(Updated: 17th Oct 2018)

Vitiligo (also called “leukoma”) is an autoimmune condition where loss of pigment from areas of the skin result in irregular white patches, the texture of which remain normal. Similar with all autoimmune disorders:

i. the body is attacking its own tissue. In the case of vitiligo the body is attacking the melanocytes (the cells responsible for skin colouring).

ii. the triggering cause may vary. I have seen 1 case where it started after a car accident at an early stage of life & another where it developed after a stressful period at late 40s.

iii. the development of the disease is the result of genetic predisposition as well as environmental factors.

iv. there is a higher than normal risk for the simultaneous presence of other autoimmune conditions.

 

Cease the Fire.

As an autoimmune condition vitiligo has to be treated as an immunological problem and not solely as a skin one. While the symptoms manifest in the skin it is the immune system that is over-reacting. This is the reason why in many cases immunosuppressive drugs are prescribed (Boone B., et al., 2007). Stopping the over-activity of the immune system may not be as straight forward as we wish. Foods, heavy metals, infections have been shown or speculated to be the root cause of this unfavourable behaviour of the immune system (IS).

In order to address each of the above one can:

i. follow an anti-inflammatory diet.

ii. remove any obvious toxic deposits in the body (i.e. mercury fillings, tattoos)

iii. get tested for carrying any of the common viruses associated with autoimmunity (i.e. Epstein Barr virus)

 

Test for other AI conditions.

While there are 100s of autoimmune conditions, Hashimoto’s & Celiac Disease have been shown to have a higher prevalence among patients of vitiligo. Hashimoto’s can be easily diagnosed through an inexpensive blood test for TPO (Thyroid peroxidase) & TgAB (Thyroglobulin) antibodies. The diagnosis of Celiac Disease requires a biopsy which is why a lot of patients with vitiligo decide to eliminate gluten from their diet without going through the hustle of testing.

 

If the body is attacking more than one of its own tissue it is best for all autoimmune cases to be supported at the same time.

 

Light Therapy.

For the depigmentation is of the “milky” patches the 2 versions of light therapy have been used successfully are: Narrowband UVB & Targeted light therapy (Grimers PE 2005).

 

Narrowband UV-B involves the use of UV lamps with a peak emission around 311 nm. It induces local immunosuppression while stimulating the production of melanocyte-stimulating hormone, and the increase of melanocyte proliferation and melanogenesis. In a study (Njoo M D et al., 2000) where 51 children with generalised vitiligo were treated with narrowband UV-B:

a) 53% achieved >75% of repigmentation

b) 29% had 26-50% of repigmentation

c) 18% had <25% of repigmentation

 

The main advantages of narrowband UV-B include:

a) safety for both adults & children

b) lack of systemic adverse effects

Source: Njoo M D et al., 1998

 

A number of supplements have been shown to help reverse vitiligo. Accompanying light therapy with supplementation is likely to amply its benefits.

 

Which Genes?

NLRP1 gene

NLRP1 is a gene involved in the production of proteins called inflammasomes. Inflammasomes participate in the regulation of the immune system & mutations in NLRP1 have been associated with the presence of autoimmune disorders. The rs6502867 variant of the NLRP1 gene (risky allele: T) was associated with vitiligo in an Indian study (Dwivedi M et al., 2013).

 

Phytonutrient (EGCG) in green tea has been shown to inhibit the action of the NLRP1 gene (Ellis L et al., 2010).

 

Methylation

Methylation is a process responsible for many functions in the body including cell replication and DNA repair. A study published among 80 individuals (40 with vitiligo & 40 controls) (Yasar, A et al., 2012) showed no correlation between mutations in MTHFR or the levels of serum folate & vitamin B12 among the patients. Had the study measured red blood cell folate and vitamin B12 their findings would have been more significant.

Both folate & vitamin B12 (which directly support the methylation pathway) have been used by vitiligo patients with positive outcomes.

 

Case Study.

The photos in the image above are from a female client in her 50’s. She was following the Wahls dietary protocol for 6 months as an anti-inflammatory / auto-immune friendly approach. The main adjustments in her diet where the increase of fats through nuts & seeds as well as progressing from 2 meals and 1 snack a day to a 16-8 hours fast and then to 1 meal a day (twice per week). Breathing exercises as well as progressive exposure to cold (through showers) were also part of her protocol.

 

References.

Boone, B., Ongenae, K., Van Geel, N., Vernijns, S., De Keyser, S. and Naeyaert, J.M., 2007. Topical pimecrolimus in the treatment of vitiligo. European Journal of Dermatology, 17(1), pp.55-61.

Dwivedi, M., Laddha, N.C., Mansuri, M.S., Marfatia, Y.S. and Begum, R., 2013. Association of NLRP1 genetic variants and mRNA overexpression with generalized vitiligo and disease activity in a Gujarat population. British Journal of Dermatology, 169(5), pp.1114-1125.

Ellis, L.Z., Liu, W., Luo, Y., Okamoto, M., Qu, D., Dunn, J.H. and Fujita, M., 2011. Green tea polyphenol epigallocatechin-3-gallate suppresses melanoma growth by inhibiting inflammasome and IL-1β secretion. Biochemical and biophysical research communications, 414(3), pp.551-556.

Grimes, P. E. (2005). New insights and new therapies in vitiligo. Jama293(6), 730-735.

Njoo, M. D., Bos, J. D., & Westerhof, W. (2000). Treatment of generalized vitiligo in children with narrow-band (TL-01) UVB radiation therapy. Journal of the American Academy of Dermatology42(2), 245-253.

Njoo, M. D., Spuls, P., Bos, J. T. A., Westerhof, W., & Bossuyt, P. M. M. (1998). Nonsurgical repigmentation therapies in vitiligo: meta-analysis of the literature. Archives of dermatology134(12), 1532-1540.

Yasar, A., Gunduz, K., Onur, E. and Calkan, M., 2012. Serum homocysteine, vitamin B12, folic acid levels and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism in vitiligo. Disease markers, 33(2), pp.85-89.

 

 

How to detect vitamin B12 deficiency

Vitamin B12 is common and unfortunately one cannot rely on serum vitamin B12 to detect a deficiency. Vitamin B12 is carried in the blood by either of 2 proteins: haptocorrin and holotranscobalamin. While the majority of vitamin B12 is carried by haptocorrin, this vitamin B12 is considered inactive* [1]. A serum vitamin B12 test cannot differentiate between the active and inactive form and as a result while the level may appear healthy, the active form of vitamin B12 may be significantly low.

 

Which test is best to identify vitamin B12 deficiency?

The most direct why to detect vitamin B12 deficiency is to measure your active form of B12: holotranscobalamin. Biolab in UK offers that test.

If that test is not available to you, your 2nd best option is to measure your homocysteine levels. Homocysteine is a protein humans synthesise in their body and it’s considered one of the most significant biomarkers of cardiovascular health. Its production relies on the availability of vitamin B12, folate & protein.

source: PMID 16702348 [4]

As multiple other factors though affect the levels of Homocysteine, one cannot drive conclusive results for her vitamin B12 just knowing her homocysteine level.

 

 

Which symptoms indicate vitamin B12 deficiency?

Vitamin B12 plays a critical role in the methylation cycle [3] (which consists of the folate & methionine cycle). As a result any problems associated with methylation may be driven due to:

  1. low vitamin B12 intake (important for vegans and vegetarians)
  2. poor absorption (relevant for those with poor gastrointestinal function) [2] or
  3. compromised metabolism (possibly due to MTR & MTRR polymorphisms)

 

 

 

* due to the fact that haptocorrin receptors are found mainly in the liver.

 

  1. Morkbak, A.L., Poulsen, S.S. and Nexo, E., 2007. Haptocorrin in humans. Clinical Chemical Laboratory Medicine, 45(12), pp.1751-1759.
  2. Schjønsby, H., 1989. Vitamin B12 absorption and malabsorption. Gut, 30(12), p.1686.
  3. Miller, A., Korem, M., Almog, R. and Galboiz, Y., 2005. Vitamin B12, demyelination, remyelination and repair in multiple sclerosis. Journal of the neurological sciences, 233(1), pp.93-97.
  4. Refsum, H., Nurk, E., Smith, A.D., Ueland, P.M., Gjesdal, C.G., Bjelland, I., Tverdal, A., Tell, G.S., Nygård, O. and Vollset, S.E., 2006. The Hordaland Homocysteine Study: a community-based study of homocysteine, its determinants, and associations with disease. The Journal of nutrition, 136(6), pp.1731S-1740S.

What helps Histamine Intolerance?

Histamine is a hormone involved in digestion, immune & nervous system function. While anti-histamine drugs are often prescribed for asthma, they are also given to those with food allergies.

 

Anti-histamine drugs can be life saving in times of crisis. At the same time if one doesn’t deal with what causes the reaction at 1st place she/he is trying to put off a fire by removing the battery from the fire alarm.
Which raises the question “What helps histamine intolerance?”

 

What is Histamine Intolerance?

Histamine is a hormone with varying functions in different tissues.

 

Histamine intolerance symptoms are due to histamine’s relation with the immune system. Histamine activates immune cells (basophils & mast cells) while causing blood vessels to dilate so that immune cells can be quickly transferred to kill pathogens. In that sense you can think of histamine as a fire alarm.

“Histamine intolerance is a fire alarm going on when there is no fire.”

 

To be more precise histamine intolerance results from imbalance between accumulated histamine and the capacity to break it down. In most cases it is due to limited histamine breakdown capacity. Like all hormones histamine needs to be eliminated from the body when it has done its job. While it is broken down by a few different enzymes (HNMT, NAT1,2 & DAO), it is the DAO (Maintz, L. and Novak, N., 2007) responsible for the breakdown of ingested histamine.

 

Histamine’s link with Digestion.

Gastrointestinal problems are very common among those with histamine intolerance.

While histamine is necessary for proper gut function excess levels can cause digestive complications. Bellow are a few facts highlighting the link between histamine intolerance and gut health:

a. all 4 histamine receptors H1R-H4R are found in the digestive track and they have excitatory actions there (Breunig E. et al., 2007).

b. In a study conducted in Italy, 13 out of 14 subjects (with food intolerances) reported benefits in at least 1 food after DAO supplementation (Manzotti G. et al., 2015).

c. The capacity of both histamine breakdown pathways: HNMT and DAO have been reported to be reduced in those with food intolerances (Kuefner MA et al., 2004).

d. Elevated levels of histamine in the brain have been shown to suppress appetite. (Malmlöf, K. et al., 2005)

 

“Diet can help histamine intolerance in 2 ways: i. reduce the histamine load ii. support histamine breakdown”

 

Histamine Intolerance foods to avoid

 

There are 2 categories of foods those with histamine intolerance need to avoid: a. Those that contain histamine & b. those that can cause the release of histamine in the body although they don’t contain histamine (Maintz, L. and Novak, N., 2007)

#Foods to be avoided with Histamine IntoleranceContain HistamineLow in Histamine (but may trigger its release)DAO blockingVegetarianVeganFruits
Vinegar containing foods (ie pickles, mayonnaise, olives)XXX
Fermented foods (ie saurkraut, soy sauce, kombucha, kefir, yogurt)XXXX
Fermented foods (ie saurkraut, soy sauce, kombucha, kefir, yogurt)XX
Cured Meats (ie bacon, salami, hot dogs)X
Soured foods (ie sour cream, sour milk, buttermilk)XX
Dried fruitXXXX
Aged cheese (ie gouda, camembert, cheddar, goat cheese)XX
Nuts (walnuts, cashews, peanuts)XXX
Smoked fish & shellfishX
Chickpeas, soybeansXXX
Banana, Papaya, Pineapple, StrawberriesXXXX
ChocolateXXX
Cow's milkXX
TomatoesXXX
Black, green, mate teaXXX

 

Histamine Intolerance diet

The fresher the food the lower it is in histamine. Vitamin C supplementation has also been shown to reduce histamine levels (Hemilä, H., 2014).

#Diet for Histamine IntoleranceVegetarianVegan
Fresh cooked meat, poultry
Fresh caught fish
EggsX
Gluten free grains: rice, quinoaXX
Fresh fruits (ie mango, pear, watermelon, apples)XX
Fresh veggies (except: tomatoes, eggplant, spinach, avocado)XX
Dairy substitutes (ie coconut m rice, hemp, almond milk)XX
Cooking oils (olive & coconut)XX
Herbal teasXX

 

Blood sugar regulation and Histamine Intolerance

The link between histamine and diabetes goes back to the 1950 (Pini A et al., 2016).

Plasma histamine was shown to reduce after insulin administration in diabetic rats (Hollis T. et al., 1985). Two of the mechanisms through which insulin and histamine interact was that the activation of histamine 3 receptors (H3R) in pancreatic beta cells was shown to: a. inhibit insulin secretion (Nakamura T et al., 2014) b. reduce glucagon production in non-hyperglycemic state (Nakamura T et al., 2015). While the mechanisms of interaction between diabetes and histamine intolerance are currently not clear the correlation appears to be positive (Pini A et al., 2016).

To that extent a state of insulin resistance should be addressed in cases of histamine intolerance together with any other protocol.

 

How to test for Histamine Intolerance

Prior to treating any condition it is wise to diagnose it first. By measuring the levels of DAO enzyme in your blood you can assess your body’s capacity to breakdown histamine. The cut off level of serum DAO activity (for probable histamine intolerance) is <10 U/mL (Manzotti G. et al., 2015)

 

Labs that offer this service are:

Smart Nutrition in UK

ImmunoPro in Australia

Dunwoody Labs in US & UK (via Invivo clinical)  – In my opinion the best test for gut integrity currently available.

 

23andme results & Histamine Intolerance

23andme results can be useful in identifying potential blockages in the pathway of histamine. At the same time it is dangerous to drive conclusions solely from one’s genetic make up, let alone one gene. In many cases a person may have no SNPs in the gene that produces the DAO enzyme (AOC1 gene) and at the same time experience histamine-like reactions after the consumption of red wine for instance. The case bellow is such an example.

The woman is in her mid 40s, vegetarian with a more or less healthy lifestyle. She carries only 1 homozygous polymorphism in the AOC1 gene which has been shown to be beneficial.

 

Source: Opus23

 

While there seems to be no burden on the production of DAO if you look at the entire pathway you will see that she carries SNPs in the HNMT and MAOB genes. Both of which can tax DAO’s function.

 

Source: Opus23

 

How can this information be useful? 

For this woman supporting the function of HNMT and MAOB can help with histamine symptoms. For HNMT methylation support as well Salacia Oblonga (Oda, Y et al., 2015)  can be used while for MAOB vit B2.

 

Source: Opus23

 

This Nutrigenomics analysis would not be possible without access to Opus23 analytics.

 

 

References

Breunig, E., Michel, K., Zeller, F., Seidl, S., Weyhern, C.W.H.V. and Schemann, M., 2007. Histamine excites neurones in the human submucous plexus through activation of H1, H2, H3 and H4 receptors. The Journal of physiology583(2), pp.731-742.

 

Hemilä, H., 2014. The effect of vitamin C on bronchoconstriction and respiratory symptoms caused by exercise: a review and statistical analysis. Allergy, Asthma & Clinical Immunology10(1), p.58.

 

Hollis, T.M., Kern, J.A., Enea, N.A. and Cosgarea, A.J., 1985. Changes in plasma histamine concentration in the streptozotocin-diabetic rat. Experimental and molecular pathology, 43(1), pp.90-96.

 

Kuefner, M.A., Schwelberger, H.G., Weidenhiller, M., Hahn, E.G. and Raithel, M., 2004. Both catabolic pathways of histamine via histamine-N-methyltransferase and diamine oxidase are diminished in the colonic mucosa of patients with food allergy. Inflammation Research, 53, pp.S31-S32.

 

Malmlöf, K., Zaragoza, F., Golozoubova, V., Refsgaard, H.H.F., Cremers, T., Raun, K., Wulff, B.S., Johansen, P.B., Westerink, B. and Rimvall, K., 2005. Influence of a selective histamine H3 receptor antagonist on hypothalamic neural activity, food intake and body weight. International journal of obesity, 29(12), pp.1402-1412.

 

Manzotti, G., Breda, D., Di Gioacchino, M. and Burastero, S.E., 2015. Serum diamine oxidase activity in patients with histamine intolerance. International journal of immunopathology and pharmacology, p.0394632015617170.
Maintz, L. and Novak, N., 2007. Histamine and histamine intolerance. The American journal of clinical nutrition, 85(5), pp.1185-1196.

 

Pini, A., Obara, I., Battell, E., Chazot, P.L. and Rosa, A.C., 2016. Histamine in diabetes: is it time to reconsider?. Pharmacological research111, pp.316-324.

 

Nakamura, T., Yoshikawa, T., Noguchi, N., Sugawara, A., Kasajima, A., Sasano, H. and Yanai, K., 2014. The expression and function of histamine H3 receptors in pancreatic beta cells. British journal of pharmacology, 171(1), pp.171-185.

 

Nakamura, T., Yoshikawa, T., Naganuma, F., Mohsen, A., Iida, T., Miura, Y., Sugawara, A. and Yanai, K., 2015. Role of histamine H 3 receptor in glucagon-secreting αTC1. 6 cells. FEBS open bio, 5, pp.36-41.

 

Oda, Y., Ueda, F., Utsuyama, M., Kamei, A., Kakinuma, C., Abe, K. and Hirokawa, K., 2015. Improvement in Human Immune Function with Changes in Intestinal Microbiota by Salacia reticulata Extract Ingestion: A Randomized Placebo-Controlled Trial. PloS one, 10(12), p.e0142909.

 

 

 

5 steps towards optimal health

5 Steps towards optimal health

 

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There are 5, logical in my opinion, steps towards optimising our health. Depending on where someone is with his/her health there may not be a need to go through all them. However the earlier steps have to be in place before one proceeds to the later ones.

1. Gut health and pathogen elimination

2. Cell/mitochondria membrane health & weight management

3. Methylation

4. Detoxification

5. Hormone and Neurotransmitter balancing

In the video attached I explain a bit about each step. Here are a 2 examples why it can be a waste of time or dangerous when this order is not followed.

 

Detoxification prior to weight losing weight

This is a classic. My guess is that “detoxification” is among the top 3 health related searches on google, together with “yoga leggings” and “one minute 6 pack routines”. No surprise some yoga teachers at the forefront of fashion call their classes detoxifying. Toxins can be both water and fat soluble. The fat soluble ones are stored in fat tissue (adipose tissue as well as bone marrow). When forcing someone’s detoxification process while overweight we are POTENTIALLY encouraging the release of many toxins in the bloodstream. In this scenario are the toxins going to cross the blood brain barrier making the person feel horrible and call it “healing crisis”?

 

Hormone balancing prior to methylation optimisation

Methylation is responsible for hormone production. Won’t you want to make sure there is water supply prior to fixing the bath tap?

 

 

Is folic acid dangerous for the brain?

” Is folic acid dangerous for the brain? ” would probably get no response from some of you and a negative one from the rest. After all you, like myself, were brought up thinking that B vitamins are good for you. Folic acid is a SYNTHETIC form of vitamin B9. I highlight the word synthetic because that’s something most people are missing. Now let’s try to answer our question on folic acid’s impact on the brain.

The concentration of MeTH folate, a reduced form of vitamin B9, in the cerebrospinal fluid (CSF) is 4 times higher than in plasma, in healthy individuals (Sepctor and Johanson, 2006). This indicates the importance of vitamin B9 for the nervous system. In order for vitamin B9 to enter the brain* though it has to be in its reduced form (Levitt, 2009, Sepctor and Johanson, 2006 ). The fact that the brain, cannot use folic acid unless it metabolises it to a reduced form, is NOT a small issue as folic acid may still be binding to vitamin B9 receptors** and potentially obstructing the reduced form’s function.

 

 

Knowing all the above what can you do?

1. I encourage everyone to do for $100 a DNA test and find out if they have any polymorphisms in the MTHFR gene: 23andme. MTHFR is a high polymorphic gene, responsible for the conversion of folic acid to its reduced forms (See graph bellow).

 

2. Avoid any foods fermented with folic acid (most processed food will be) and when supplementing opt for the (reduced) natural forms. Always work with a healthcare professional.

 

 

methylation-map

Further reading:

In a paper published in April 2014 Richard Frye’s et al. discusses the implications of low cerebral folate levels in Autism Spectrum Disorder (ASD) kids and the correlation of folate receptor antibodies in hypothyroidism.

 

* For those interested in the logistics folate enters the brain not through the blood brain barrier (BBB) by via the Choroid Plexus (CP), the place in the brain where CSF is produced (Spencer, 2009).

** Folate receptors are tightly regulated by the body. Upregulation of folate receptors are linked with certain cancers including ovarian (Cambel et al., 1991).

 

References

Cambel et al. (1991) Folate-binding protein is a marker for ovarian cancer. Cancer Research. 51: 5329.

Levitt M., Nixon P. F., Pincus J. H. and Bertino J. R. (1971) Transport characteristics of folates in cerebrospinal fluid; a study utilizing doubly labeled 5-methytetrahydro- folate and 5-formyltetrahydrofolate. J. Clin. Invest. 50, 13011308.

Spector R. (2009) Nutrient transport systems in brain: 40 years of progress. Journal of Neurochemistry. 111: 315-320.

Spector R. and Johanson C. E. (2006) Micronutrient and urate transport in choroid plexus and kidney: implications for drug therapy. Pharm. Res. 23, 25152524.

Frye R. eta l., (2014) Folate Receptor Alpha Autoantibodies Modulate Thyroid Function in Autism Spectrum Disorder. North American Journal of Medicine and Science. Accessed: http://najms.net/wp-content/uploads/v07i02p053.pdf 21 Nov 2014.

Creatine and pregnancy

Many women prior to getting pregnant advise fertility experts. That I think is a wise idea. Unfortunately though the advise many times comes down to the very dangerous one liner: “Take 1 gr of folic acid per day.”. Why this is a dangerous statement I will discuss in a future post but today I would like to touch on creatine. Creatine is a very essential organic acid with many functions in the body. As the image above tells creatine is very popular among athletes. So why should future mothers care?

“Growing evidence supports the potential for creatine as an antioxidant, neuromodulator and key regulator of energy metabolism, to improve depressive symptoms in humans and animals, especially in females.” (Patricia A, 2013) Knowing that it should come as no surprise that Seattle’s Children’s hospital screens women planning to get pregnant for GAMT gene SNPs and and healthy creatine levels (Braissant O and Henry H, 2008). You still wander what’s the big deal?

Low creatine levels in the mother have been linked with:

speech delay

autism

developmental delay

movement disorders

retardation

 

So what can you do now that you know that?

Evaluate your creatinine levels via a lab test. Keep in mind that low creatinine levels may be due to a series of issues such as low SAMe, blocked methylation, B12 deficiency, oxidative stress.

 

ps: Feel free to forward the post to your healthcare practitioner. Hopefully he/she will already be aware of creatine’s importance and will be keen to share his/her knowledge with me.

 

 

 

References:

Patricia A (2013) Influence of Chronic Creatine Supplementation on Neurogenesis, Synaptic Plasticity and Affective Behavior: Implications for Sex-Specific Differences, TUFTS UNIVERSITY, 210 pages; 3564114.

O. Braissant O, Henry H. (2008) AGAT, GAMT and SLC6A8 distribution in the central nervous system, in relation to creatine deficiency syndromes: A review, Journal of Inherited Metabolic Disease. Volume 31, Issue 2, pp 230-239.