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Ice baths

Cold exposure : 3 benefits

The popularity of cold exposure has increased since 2017 in continental Europe, US & Australia through the work of Wim Hof. Whether it is through cryotherapy or cold water immersion more and more people practice and hashtag: #coldexposure. Cold therapy has its roots back in South East Asian yogic traditions and Eastern European-Scandinavian cultures. In this article I will cover 3 benefits training with cold has for those of us living a modern lifestyle.

 

How old is cold therapy?

The moment you ask this question you realise that cold has been accompanying humans from the very start of our existence. As temperatures in nature constantly fluctuate, humans have been exposed to cold : voluntarily or not for a long time.

 

As from a therapy stand point, cold exposure is listed in “The Edwin Smith Papyrus” dated 3,500 BC (Wang H et al., 2006). In certain parts of the globe (ie. Russia, Bulgaria, Scandinavian countries) cold training has been part of the culture, practiced in banya or plunge pools, as well as a standard procedure in hospitals to prevent further damage in patients with cardiovascular (Ref) and neurological conditions (Ref).

 

In recent years Wim Hof (a dutchman Guinness record holder) popularised cold training through his workshops across the globe. It was my training with Wim in 2016 that initiated my journey in cold exposure.

 

1. Cold exposure improves Circulation & Cardiovascular Function

Think of cold exposure as a workout for the circulatory system.

Most people think of cardio when it comes to improving their cardiovascular function. Cold exposure though offers a unique way to strengthen one’s cardiovascular system (cvs).

Our cardiovascular system is surrounded by epithelial muscles which facilitate the circulation of the blood. At low temperatures the epithelial muscles surrounding the veins and arteries of our extremities constrict – preserving the blood and the nutrients carried in it for the more vital organs in the trunk and the head. When the body returns to higher temperatures the epithelial muscles in our extremities dilate again allowing for the blood to flow freely there. In a similar way that our biceps get stronger as they contract during bicep curls (or chaturangas) our cardiovascular system can get stronger through cold exposure.

 

 

Good circulation means no athletes foot, no cold extremities, better cognitive function, ability to heal/recover faster and perform better in sports.

 

2. Cold exposure as a meditation technique

Those that practice cold water immersions for some time report a sensation of stillness in mind (usually 30 seconds to a minute after the initial exposure). A friend of mine Luke Wills (founder of the Optimal Health Method) said he reached a similar state of mind in his 2nd ice bath, with that on the 7th day of a vipassana meditation retreat. Anecdotal evidence like this were confirmed to be valid in a study published in May 2018 titled “Brain over Body“.  In this study participants with no previous experience in cold exposure and Wim Hof, were interchangeably exposed to cold and neutral temperatures. One of the most striking differences between the inexperienced subjects and Wim was the Dutchman’s ability to reduce activity in the insular cortex part of the brain during cold exposure. Insular cortex is an area involved in emotional attachment to external stimuli and self-reflection. Activity in this part of the brain has been shown to be linked with meditation and control in emotional eating.

 

Meditation is the 5th of the 8 limbs of yoga. Cold exposure is one of the many ways to enter into a state of meditation.

 

3. Cold exposure helps overcome fears

Cold exposure is demanding on many levels:

• the adrenal glands

• musculoskeletal system

• circulation and

• the brown fat tissue are activated at low temperatures.

Aside though the multiple biochemical adaptations in the rest of the body:

our brain also changes when we are exposed to cold.

The initial response is that of: “fight or flight”. A small area of the brain called amygdala (Greek word for almond) – activates the HPA (Hypothalamic Pituitary Adrenal) axis – signalling a stress response to the rest of the body. While this initial stage is universal the way one deals with cold thereafter depends on his/her experience and ability to use her breath.

By training the body to deal with a stressful situation (ie. a cold immersion) in a controlled environment (such as a shower or a bath) we can reprogram our mind to deal with stressful situations which are out of our control. Our main tool is our breath. Dealing with fear was the focus of a workshop I gave in 2017 to a group of actors.

 

 

Conclusion

The list above is not exhaustive of the benefits one can get from cold exposure :

• Controlling pain perception [Ref]

• Generation of Brown Fat [Ref]

• Strengthening of the immune system [Ref] • Improved tolerance to cold [Ref]

are also good reasons for modern “over-civilised” humans to train with cold.

 

 



supplements for vitiligo

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. supplements for vitiligoKhellin 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.

supplements for vitiligo

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 complementary 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).

How to test for Celiac Disease?

The only way you can get a definite YES or a NO for Celiac Disease (CD) is by doing an intestinal biopsy. As this is an invasive and expensive procedure, many prefer measuring serum antibodies as an initial screening process. When someone decides to test for antibodies against gluten it is necessary to keep in mind:

a) that the gluten protein is fairly complex and thus all antibodies need to be tested

b) that the blood test is not a substitute for the biopsy.

Whichever assessment method one decides to use it is important to know that:

For CD, early diagnosis means early intervention with treatment and prevention of long-term complications, including the development of severe and irreversible phenotypes and of other autoimmune disorders.” (Ventura A et al., 2010)

 

Intestinal biopsy is the golden standard for diagnosing Celiac Disease.

 

An individual is classified as celiac when a biopsy of the duodenal mucosa is taken which detects:

a) a reduction or disappearance of intestinal villi &

b) intraepithelial lymphocytes (IELs) higher than 25/100 enterocytes (Sapone A. et al., 2012).

Individuals presenting with significant villous atrophy are classified as CD March stage III, whereas normal villi but increased number of intraepithelial lymphocytes are classified as Marsh I or II (Hill ID et al., 2005). Marsh type II may also suffer from CD but positive serological tests is needed to strengthen the diagnosis (Hill ID et al., 2005). When only elevated IELs are observed but no damage of the intestinal lining, it is difficult to diagnose CD (Kakar eta l., 200). In literature this state is usually referred to as latent CD (Dewar et al., 2005) and further testing is required.

 

Can elevated IELs be due to a different cause other than Celiac Disease?

The presence of IELs can be due to gastrointestinal inflammation caused by H. pylori (Memeo et al., 2005) or tropical sprue (Ross et al., 1981). Unexplained neurological or psychiatric disorders such as autism, schizophrenia, and cerebellar ataxia (Cascella N et al., 2009, Burk K et al., 2009, Genuis S and Bouchard T, 2010) are also linked with elevated IELs and no mucosal damage.

 

Can a blood test confirm Celiac Disease?

No. However, a lot of the time serum antibody testing is used in the screening process. The ones necessary are: anti-DGP IgG & anti-tTG IgA

 

Antibodies for the diagnosis of Celiac Disease

Antibodies

Accurate

Not affected by IgA deficiency

Not prone to interpretation

Cheap

Appropriate for children <2 years old

AGA IgA

AGA IgG

EMA IgA

tTG IgA

DGP IgG

Anti-Actin IgA

 

 

classic Anti-gliadin (AGA) antibody IgA

Pros:

1. relatively cheap

Cons:

1. found in healthy individuals (Bizzaro N et al., 2012)

2. May fluctuate within the first 2 years of age (Simell et al., 2007)

3. relatively insensitive (Fasano A, 2013)

 

AGA-IgG

Pros:

1. useful for pediatric patients with CD who test negative for anti-tTG (Carlsson A et al. 2001, Lagerqvist C et al., 2008).

2. useful in patients with IgA deficiency (Villalta D et al., 2007).

3. reasonably cheap

3. Same results where obtained with the DGP IgG test (Liu E et al., 2007, Agardh D 2007, Basso D et al., 2009, Naiyer A et al., 2009).

4. Remains constant the first 2 years of age (Simell et al., 2007)

Cons:

1. relatively insensitive (Fasano A, 2013)

 

EmA (Endomysial Antibodies – antigliadin) IgA (unless IgG requested)

Pros:

1. It is equally specific with the anti-tTG antibodies, meaning it recognizes the same antigens (Hill 2005)

Cons:

1. It is prone to subjective interpretation

2. It is less sensitive than the anti-tTG (Biagi F et al., 2001, Baudon J et al., 2004, Lock et al., 2004, Kaukinen K et al., 2007).

3. Not accurate in patients with selective IgA deficiency.

4. May fluctuate within the first 2 years of age (Simell et al., 2007)

5 *The IgG version has inferior sensitivity (Fasano A, 2013)

 

anti-tTG (antihuman tissue transglutaminase) IgA (unless IgG requested)

Pros:

1. As it is quantitative, automated and not prone to subjective interpretation

2. high diagnostic sensitivity (95%) specificity (97%) (Tozzoli et al., 2010)

Cons:

1. Anti-tTG IgA is not sensitive enough to be used alone and the addition of the anti-DGP IgG test would increase the accuracy for CD especially in children (Niveloni S et al., 2007, Villalta D et al., 2007, Volta U et al., 2010, Tonutti E et al., 2009, Villalta et al., 2010, Maglio M et al., 2010)

2. May fluctuate within the first 2 years of age (Simell et al., 2007)

3 *The IgG version has inferior sensitivity (Fasano A, 2013)

 

DGP antibodies IgG (deamidated gliadin peptide)

Pros:

1. antibodies comparable sensitivity and specificity to anti-tTG and EMA (Sugai E et al., 2006)

2. Remains constant the first 2 years of age (Simell et al., 2007)

3. DGP IgG test positive in 80% of cases of CD patients with IgA deficiency as compared to 40% for AGA IgG ( Villalta et al., 2010)

 

ANTI-ACTIN IgA

Pros: can evaluate the severity as it is related to the severity of intestinal damage (Granito A et al., 2004, Carroccio A et al., 2005)

Cons: limited usefulness for diagnosis

 

In monitoring of patients on a gluten-free diet, positivity with a low titer of anti-DGP antibodies suggests that the diet should be reassessed, even if the anti-tTG test is negative” (Tursi et al., 2006)

 

Interpretation of serological and biopsy test results

Biopsy

+

Serology

+

CD

Absence of CD and possible false-positive blood test. A negative genetic test can strengthen the negative diagnosis.

This result is treated as CD. However, inflammation in the lining can be due to other causes, including intolerances to other foods.

No CD. However, in the presence of other autoimmune conditions or genetic predisposition, future monitoring may be appropriate.

 

Which other blood biomarkers are available?

While the tests above are the ones most commonly done there is evidence that more thorough testing may be needed for those with negative results and positive symptoms. A complete antibody screening should include: Alpha gliadin, Omega gliadin, Gamma gliadin, Deamidated gliadin, TG2, TG3, TG6.

 

Deamidation is an acid or enzymatic treatment used by the food processing industry to make wheat, water-soluble so it mixes with other foods. It has been shown to cause severe immune responses to people (Leduc V et al., 2003).

Gliadin is broken down to alpha, omega and gamma fractions. If a lab tests only for alpha gliadin antibodies the results may be misleading (Quartesn H et al. 2001).

Elevated antibodies of TG2 indicated a reaction against the intestinal track (Thomas H et al., 2011). Transglutaminase 3 (TG3) is found in the skin. An autoimmune reaction to skin may lead to skin disorder known as dermatitis herpetidormis, which presents as itchy red blisters found usually in the knees, elbows, buttocks but can appear anywhere on the body (Stamnaes I et al., 2010). Elevated antibodies to transglutaminase 6 indicate an immune response against the nervous system (Alessio et al., 2012).

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 way 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 synthesize 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.

detect vitamin B12 deficiency

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.

detect vitamin B12 deficiency detect vitamin B12 deficiency detect vitamin B12 deficiency detect vitamin B12 deficiency

 

 

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.

 

References

  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.

Fasting Diet: progressions

 

Updated: 26 Sep 2018

 

This article is written with deep respect in the process of fasting and consciousness that its epigenetic effects are far reaching. Fasting in my opinion is something we all need to be comfortable with. There are many disputes on what the healthiest diet is, with advocates of the different diets often trying to support their view using ethnological and ancestral data. It is clear though to everyone that our ancestors had to survive periods of fasting independent of their diet (whether the famine was caused due to lack of game or a disaster in the crops).

My Journey with the Fasting Diet

I have been following a Fasting Diet on and off since September 2009. In my first attempt to fast (after reading my first book on nutrition called: Food Governs your Destiny) I set x3 2hour slots in the day during which I allowed myself to eat. Outside these windows I would consume only liquids. I stayed on the diet for 6 months, during which I:

?? reduced my waist circumference from 34 to 29 inches.

?? lost 7.5 kilos.

?? achieved mental clarity I have never experienced before.

During a big part of these 6 months I was vegetarian.

In 2016 I decided that as a way of monitoring my metabolism I would like to measure the production of ketones in my body. Between October 2016 and February 2017 I monitored my Blood Glucose (BG) and Ketone Bodies (KB) – beta-hydroxybutyric acid on a daily basis. Monitoring can be useful:

?? as feedback for one’s response to food / exercise.

?? for compliance when BG & KB targets are set.

During this period there were weeks of following a vegetarian diet but most days I consumed meat.

Fast Diet: Progressions

Bellow I share what I consider to be a natural progression of fasting. Of course everyone’s starting point is different: not everyone starts with a: 3 meals and 2 snacks diet and neither do we all have the same tolerance to the changes each step requires. I imagine you have not been eating the same way all your life, after all. If you are not sure how quickly you should progress from one stage to the next I suggest you err on the safe side. Most people will find progressions comfortable if they spend 1-2 months on each stage. Those with a healthy relationship to food will evolve our fasting practice over our lifespan.

⏱ Time restrict your eating

I consider the 16-8h type-diet to be an easy one for most people to adopt. During this diet you restrict your caloric intake over an 8 hour window. The remaining 16 hours one is allowed to have non-caloric drinks such as water, coffee and tea. The easiest way to get into it, is to prolong the overnight fast. Assuming one sleeps for 8 hours and stops eating 4 hours prior to going to bed, she / he can achieve the 16/8h fast by eating 4 hours after waking up. If the idea still feels daunting here are a few tips to ease your way into it:

?? Start with a 12-12h diet and gradually increase the fasting window. The danger here is not to be consistent. Decide which window schedule suits you and stick to it for at least 1 week before increasing the fasting phase.

?? Take days off if you find the idea of doing it daily suffocating. However have the days scheduled before hand and do not change them. You know you are ready to proceed when you have completed 4 consecutive weeks with 5 days per week on your “Time Restricted Eating” schedule.

🌞 Eat while the sun is up

While I acknowledge that many people working in offices have more physically active evenings than mornings; the body’s biological clock will not flip upside down because you signed up at the 20:30 CrossFit class. Neither your sleeping time can accommodate all the digestion you wish just because your gym class finishes at 22:00. As a next step to a “Time Restricted Eating” I consider to be the swift of the eating window earlier in the day. How early is early? – you decide. My suggestion is to finish eating prior to the sunset and ideally by midday. As you can see in the infographic from a 2018 paper [1], time restricting food to the earlier part of the day causes an number of beneficial effects:

Actions that helped me with this transition:

?? Exercise earlier in the day.

?? Make sure the quality of my sleep is not compromised. Supplements as well as breathing practices can support a good night sleep. Initially prolonged fasts can lead to elevated cortisol levels which will mess up with sleep. Poor sleep leads to tiredness and erratic appetite the next day.

⏰ Set your eating times

That stage could also be called: Stop snaking. Most of us (living a western lifestyle) have constant access to food and numerous stressors during our day. The combination of the two in many cases lead to binging / snaking. Whether you call it comfort food or not, every extra meal (and by meal let’s call anything containing more than 20 calories) requires the activation of the pancreas and the subsequent release of insulin. Insulin is a hormone with multiple roles in our biochemistry other than food metabolism. With that in mind I don’t find strange that hormonal imbalances are common in those with erratic eating patterns.

If one attempts to “Set her Eating Times” while she is eating during daytime only, I expect this transition not to be a big challenge. On the other hand shifting from a 16-8h fast to a “Set Eating Times” schedule can be a bigger step.

Setting the times when someone eats is a personal issue and can be scheduled around her lifestyle. My suggestion is to schedule no more than 3 meals a day and if for whatever reason a meal is lost not to be replaced.

☝ Eat once a day

If you have been following the progression described above I would be surprised if you are eating more than twice a day by now. Eating once can be something you want to try occasionally based on your energy expenditure & mood.

😶 Eat only when hungry & as much as you need

Even when I eat once a day I sometimes find hard not to overeat. I consider our relationship with food complex and the addictive aspect of it multidimensional. We can be addicted to:

?? certain foods.

?? the sensation of fullness.

Whatever the addiction is it will always manifest to emotions which make it hard to break loose off. To that extent I would like to clarify that:

“I consider eating one of the big joys of life & fasting can only enhance this sensation.”

Fasting works as a challenge for the body. This doesn’t mean it makes it makes the body weaker. In the same way that you would not assume a runner to be doing harm to her body just because her legs are weak at the end of a training session, don’t be afraid of fasting.

Fast Diet: Considerations

Most people when they consider fasting, they are worried about their energy levels and muscle mass maintenance. The energy levels may fluctuate initially: that is due not to lack of energy but to poor hormone regulation. Even if you have 9% of body fat, there is enough energy stored in your body to keep you alive for days. Fluctuations in energy levels can be caused because your metabolism has no access to your fat. If you are concerned with maintaining muscle mass I suggest you keep your protein intake high when you eat (~x1.6 gr of protein per body weight in kg)

Those that depend on constant energy supply (ie. 3 meals a day + 2 snacks) are the ones that would benefit the most from fasting.

4 Things to consider

1 Always keep your (AME) Appetite, Mood and Energy levels in check. If one of them is not under control adjustments may be necessary. In most cases soon after one gets out of control the other 2 follow.

2 Our life changes constantly and so will our mood, circadian cycle, appetite, needs for nutrients etc. I hope this article works as a road map not an itinerary.

3 Food composition can affect your Blood Glucose and consequently your fasting phases. Fibre, fat, protein can slow down your meals’ metabolism which is necessary initially.

4 Metabolism is complex and its efficiency depends on many factors including oxygen availability & insulin sensitivity. Practicing yoga, breathing exercise and cold exposure can be very useful for improving metabolic efficiency and supporting a fasting practice.

Things to consume while fasting

In order to maintain the calories low during fasting my suggestion is to limit your liquid intake to coffee & teas. If stimulants play havoc in your metabolism & appetite you should avoid caffeinated drinks altogether. I have been consuming them freely. Two things that can help a lot in extending your fasting periods are:
1 Water – in particular carbonated. I think it is easier if one takes sips during the day aiming for 1-3 litters as opposed to drinking 3 glasses when filling peckish.

2 Magnesium Citrate powder (I like the one from Designers for Health). Its sweet taste can help deal with a sweet tooth while the Magnesium supports the adrenals & promotes gut mobility.

?? Brushing teeth after eating. Making sure mouth hygiene is in check can help in 2 ways: 1. some associate a clean mouth with the end of eating 2. food leftovers will stop triggering taste buds receptors.

 

References:

1. Sutton, E. F., Beyl, R., Early, K. S., Cefalu, W. T., Ravussin, E., & Peterson, C. M. (2018). Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes. Cell Metabolism.