Our body’s capacity to produce energy is dependent on oxygen. Our cells are capable of producing much more energy in the presence of oxygen compared to a non-aerobic state *. Approximately 90% of the oxygen in our cells is used for energy production (1). So how can we ensure the delivery of adequate oxygen to our cells?
When most people are out of breath, they tend to breathe faster and take bigger breaths. Both of these actions will offer a temporary release for the air-hunger sensation but will not improve cell oxygenation – at least not in the long run.
In order to grasp how erroneous the idea of air hunger equating lack of oxygen is, think of the following: During an asthma attack patients are advised to breathe through a brown bag. If they need more oxygen, why should they restrict their oxygen intake?
Most people take between 10 and 16 breaths per minute. The volume of air that we inhale is approximately 500 millilitres per breath . This translates to approximately 6 litres per minute. When increasing the frequency of breaths, the volume of air per breath is reduced and vice versa, keeping the total volume of air inhaled the same.
Strange as it may sound, the increase of air in the lungs is not what is required for better oxygenation of our cells. Inhalations allow the body to take oxygen in. Most of the time though, the body retains high oxygen saturation levels. By using an oxygen meter we can prove that our blood contains 95-99% of its total oxygen capacity most of the time. If our blood constantly contains good levels of oxygen, why do we “run out of breath” at the end of a strenuous workout or when walking quickly up stairs?
Carbon Dioxide** is a by-product of fat and carbohydrate metabolism (aerobic and anaerobic). It exists in the fresh air at concentrations of 0.036-0.041% (36-41ppm). At 1% (10,000 ppm) concentration it can cause sleepiness and between 7 – 10%*** suffocation.
In 1904 **** physiologist Christian Bohr discovered the Bohr effect. Based on the Bohr effect, haemoglobin in the blood requires Carbon Dioxide (CO2) in order to release Oxygen (2). Low levels of CO2 in the blood, increase the affinity of oxygen to haemoglobin, preventing it from moving to the cells.
So, while at high levels CO2 can be toxic (3), at low levels it can deprive our cells of oxygen (based of the Bohr effect). Which raises the question, “what is the optimal level of CO2”? Before answering this question we need to review one more function of CO2: its role to signal our need to inhale!
Our brain is responsible for the control of our breathing cycle. Receptors in the brain continuously monitor a number of blood markers to signal the need for the next inhalation (4). Among these, the most critical, marker, is the levels of CO2 in the blood (5). When the levels of CO2 reach our tolerance point we get the urge for the next inhalation. Those familiar with the sport of underwater diving are aware of this concept.
So in order to deliver oxygen to our cells efficiently we need to prolong our urge for the next inhalation (i.e. increase our tolerance to CO2) and not increase our body’s levels of CO2. The beneficial metabolic effects of temporary exposure to an elevated CO2 state has been demonstrated in scientific studies. In one study the application of CO2 to transcutaneous tissue led to the proliferation of mitochondria, similar to the one observed during aerobic exercise (6).
It is worth pointing out that in most medical centres the saturation of oxygen (SpO2) in the blood is monitored regularly. Nonetheless, good levels of SpO2 in the blood do not equate good levels of SpO2 in the organs. Our ability to deliver oxygen to our cells is dependent on our tolerance to CO2.
The concept of better delivery of oxygen to cells is also the reason for which some athletes train at high altitude. High-altitude training became popular after the 1968 Mexico Olympics. Mexico is located at 2,300 metres above sea level. During this Olympiad, many athletes surpassed their previous performances, which prompted coaches to question if the location, was conducive to athletic performance. At high altitude the oxygen is reduced. At a hypoxic (low in oxygen) environment, the body is forced to produce more red blood cells. More blood cells means more available vehicles to carry oxygen to the cells. However, soon after an athlete, returns to sea level, the number of red blood cells returns to normal levels.
* One molecule of glucose will produce two molecules of Adenosine Triphosphate (ATP – our body’s energy currency) in an anaerobic state, as opposed to thirty six molecules of ATP in an aerobic state.
** Carbon Dioxide, a natural-occurring product of metabolism, that should not to be confused with Carbon Monoxide, a flammable gas that does not occur naturally in the atmosphere.
*** In one study subjects were exposed to air containing 7-14% of CO2 for 10-20 mins. All subjects had a complete recovery of their physiology 10 mins after the end of the experiment (7).
**** That was 33 years before Han’s Krebs’ discovered the eponymous Krebs cycle.
(Updated: 18th Dec 2017)
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.
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 elimination diet for foods.
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)
This is the 1st step of the ROSE system I base most cases on (i.e. Removal of ongoing pathogens).
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).
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.
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 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.
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.
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.
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.
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.
Szczurko, O. and Boon, H.S., 2008. A systematic review of natural health product treatment for vitiligo. BMC dermatology, 8(1), p.2.
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.