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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 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



Not affected by IgA deficiency

Not prone to interpretation


Appropriate for children <2 years old






Anti-Actin IgA



classic Anti-gliadin (AGA) antibody IgA


1. relatively cheap


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)




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)


1. relatively insensitive (Fasano A, 2013)


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


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


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)


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

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


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)


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)



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






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).

Carbon Dioxide: The missing piece in a metabolic jigsaw puzzle

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?



The two breath parameters: Frequency & volume

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?



The role of carbon dioxide in oxygen transport

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.

A good reference book on this topic is: “Oxygen Advantage” by Patrick Mckeown. On the Youtube Oxygen Advantage channel you can find several exercises to improve your tolerance to CO2.



Fun fact

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.



  1. Bland, J., Costarella, L., Levin, B., Liska, D., Lukaczer, D., Schiltz, B. and Schmidt, M.A., 1999. Clinical nutrition: A functional approach. The Institute for Functional Medicine, Gig Harbor, Wash, USA.
  2. Bohr, C., Hasselbalch, K. and Krogh, A., 1904. Über einen in biologischer Beziehung wichtigen Einfluss, den die Kohlensäurespannung des Blutes auf dessen Sauerstoffbindung übt. Acta Physiologica16(2), pp.402-412.
  3. Satish, U., Mendell, M.J., Shekhar, K., Hotchi, T., Sullivan, D., Streufert, S. and Fisk, W.J., 2012. Is CO2 an indoor pollutant? Direct effects of low-to-moderate CO2 concentrations on human decision-making performance. Environmental health perspectives120(12), p.1671.
  4. Huckstepp, R.T. and Dale, N., 2011. Redefining the components of central CO2 chemosensitivity–towards a better understanding of mechanism. The Journal of physiology589(23), pp.5561-5579.
  5. Cheung, S., 2010. Advanced environmental exercise physiology. Human Kinetics.
  6. Oe, K., Ueha, T., Sakai, Y., Niikura, T., Lee, S.Y., Koh, A., Hasegawa, T., Tanaka, M., Miwa, M. and Kurosaka, M., 2011. The effect of transcutaneous application of carbon dioxide (CO 2) on skeletal muscle. Biochemical and biophysical research communications407(1), pp.148-152.
  7. Sechzer, P.H., Egbert, L.D., Linde, H.W., Cooper, D.Y., Dripps, R.D. and Price, H.L., 1960. Effect of CO 2 inhalation on arterial pressure, ECG and plasma catecholamines and 17-OH corticosteroids in normal man. Journal of Applied Physiology15(3), pp.454-458.


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.

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.

🔑  Things to consider

👉🏻 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.

👉🏻 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.

👉🏻 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.

👉🏻 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 towards 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 all together. I have been consuming them freely. Two things that can help a lot in extending your fasting periods are:
👉🏻 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.

👉🏻 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.




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.

Leaky gut: the trojan horse to food allergies?

Leaky Gut is a digestive track with a compromised permeability (like a hose with holes).


While the SYMPTOMS OF A LEAKY GUT ARE NOT ONLY ASSOCIATED WITH DIGESTION many people suffering from it experience food sensitivities. That’s why in my opinion:

  1. Elimination diets (i.e. FODMAP, low oxalate, low histamine diets) do not work long term: foods that cause reactions are removed but the reason why the reaction was there are 1st place stays.
  2. Most chronically ill patients have restricted diets: the body is not able to renew the epithelial tissue in the gut  leading to poor gut integrity ➛ increased gut permeability  ➛ food sensitivities.
  3. Diversity in gut flora is positively associated with health: A diverse gut flora supports gut integrity.


The reason why the above hold true can be traced to the double role of the gut:

  1. digest and absorb nutrients
  2. host part of the immune system

The immune system in the gut has the delicate role of balancing between: Tolerating or Reacting to the foods it comes in contact with. The evolutionary benefit of this role is the following:

Foods we consume can be degraded or containing toxins and thus be poisonous to the body. In these cases the activation of the immune system can kill the pathogenic substances and protect us.  This process is mediated through a series of steps leading to the increase of intestinal permeability.


Unfortunately in certain people the same reaction is triggered not only by toxins but also by regular foods. In these cases after the consumption of the “trigger food” the individual experiences a reaction such as: foggy brain, bloatness, diarrhea, stomach cramps, increased heart rate, running nose, anxiety, irritability. Reducing gut permeability (i.e. healing leaky gut) can make previous “trigger foods” tolerable again.


Testing for leaky gut.

Our gut wall consists of just one cell thick epithelial tissue (Sturgeon, C. and Fasano, A., 2016) . The space between each epithelial cell is called tight junction.


Lactulose/Mannitol test

The test that has been used the longest for detecting leaky gut is the lactulose/mannitol urine test. The test is simple: after an overnight (12 hour) fast you collect the urine then have a solution of lactulose & mannitol and 6 hours later you collect the urine again.

Mannitol enters the body through the epithelial cell membrane, while lactulose goes through the tight junctions (FlemIng, S.C. et al., 1990)

The loss of absorptive areas ➛ ↓ the absorption of mannitol.

The loss of mucosal integrity ➛ ↑ lactulose absorption.


An elevated lactulose : mannitol ratio indicates the presence of leaky gut. The test is available from many labs including Genova Diagnostics. The results can be affected by the use of  NSAIDS, alcohol and according to Dr. Alesio Fasano the results are very sensitive to the collection process and thus may not be reliable when done outside a lab.


3 stool markers of leaky gut (α1-Antitrypsin – sIgA – calprotectin)



is a protein of the liver. When detected in stool (sourced from the intestines) it indicates a severe case of intestinal permeability and thus is not a sensitive enough marker of leaky gut (Biancone, L. et al., 2003)


is part of the immune system and functions as a tag for substances that need to be excreted.


is a protein linked with intestinal inflammation. It is used to distinguish between IBD & IBS (Leblhuber, F., et al., 2015).

3 blood markers of leaky gut (Zonulin – LPS – DAO)



Zolulin is a protein responsible for the modulation of tight junctions (Sturgeon, C. and Fasano, A., 2016).

↑ levels of Zonulin ➛ Opening of tight junctions ➛ influx of dietary & microbial antigens in the blood


The 2 main triggers of Zonulin release have been found to be:

  1. Bacteria: including Eschericha coli, lab E. coli, virulent E. coli, and Salmonella typhi (El Asmar et al. 2002)
  2. Gliadin: a protein found in gluten (Clemente, M et al., 2003)

Elevated levels of Zonulin have been linked in literature (Sturgeon, C. and Fasano, A., 2016) to:

  1. autoimmune conditions such as: Type 1 Diabetes, Celiac Disease, Multiple Sclerosis, Intestinal Bowel Diseases
  2. metabolic disorders such as: Obesity & PCOS
  3. Asthma
  4. Coronary Heart Disease
  5. Systemic infections
  6. Gluten Sensitivity
  7. Necrotizing Enterocolitis
  8. Brain cancer (Skardelly, M et al., 2009) by altering the integrity of the Blood Brain Barrier.


Lipopolysaccharide Bacterial Endotoxin

Lipopolysaccharide (LPS) is a component of the wall of gram-negative bacteria (Trent, M.S et al., 2006) responsible for the activation of the innate immune system. LPS have 3 regions. Lab tests measure the lipid A region which is also known as endotoxin. Germ-negative bacteria live in the lumen of the gut but should not be found in the blood. Detection of LPS endotoxins in the blood is sign of leaky gut.



Dunwoody Labs measures the levels of DAO enzyme in their intestinal permeability test. DAO is responsible for the break down of histamine. Histamine while necessary for good gut health when elevated can cause problems. Low levels of DAO thus is also a sign of leaky gut. Genetic polymorphisms in the AOC1 gene (which encodes the DAO enzyme) can impair the body’s ability to produce the DAO. Those with low levels can check their genetic burden using the table bellow.

source: InstagramOpus23


The future of leaky gut testing

While not currently available for the general public I-FABP is a marker of gut permeability used in laboratories. Intestinal fatty acid binding protein (I-FABP), is a marker of early enterocyte cell death (Derikx, J.P. et al., 2010)



How to support leaky gut.

When it comes to supporting leaky gut I like to split the nutrients in 2 categories:

  1. the ones affecting the mechanisms that cause the problem (these are the ones that ultimately will heal the intestines)
  2. the ones that suppress the symptoms – commonly referred to as anti-inflammatory (these are the ones that should help ameliorate the symptoms)


Avoid trigger foods

While I consider elimination diets not a good idea long-term in the short run it is important to remove any trigger foods to control inflammation. IgG food intolerance tests can be very useful for that matter.



I consider the use of probiotics the most potent yet the most tricky in implementation among all interventions. Certain probiotic strains have been found to induce cell proliferation in gut cells:

Bifidobacterium breve R0070 & Lactococcus lactis R1058 when taken taken together seem to have synergistic effects and both can be found in the Jarrow-Dophilus EPS. (Grimoud, J. et al., 2010 *)

Some others that were shown to suppress inflammation induced by LPS levels are:

  1. Bifidobacterium longum subsp. Infantis, Bifidobacterium longum, Bifidobacterium bifidum, Lactobacillus rhamnosus – in the order mentioned (Laetitia, R. et al., 2013)
  2. Lactobacillus reuteri strain, ATCC PTA 6475 – available from Biogaia. (Thomas, C.M. and Versalovic, J., 2010)
  3. Bifidobacterium infantis 35624 (Groeger, D. et al., 2013)


* The French study by Julien Grimoud is a goldmine of information.



Edible & medicinal mushrooms have been shown to activate & modulate the  immune system in the gut acting this way as anti-inflammatory in LPS toxicity.  A. bisporus, C. cibarius and L. deliciosus (Saffron Milkcap mushroom) are mushroom extracts available in supplemental form (Moro, C. et al., 2012).


Berberine is an alkaloid found in some plants shown to inhibit the inflammatory effects of LPS (Mo, C. et al., 2014Wu, Y.H., et al., 2012). Berberine has been shown to interact with 57 genes, so cross-checking polymorphisms related to other symptoms is worth doing.











source: Opus23


Other agents

Quercetin & CoQ10 were also shown to have anti-inflammatory effects in  LPS toxicity (Abd el-gawad, H.M. and Khalifa, A.E., 2001). Fish Oils were shown to restore intestinal integrity by increasing DAO enzyme concentration in the gut (Liu, Y. et al., 2012).



L-glutamine acts as fuel for intestinal cells (Larson, S.D, et al., 2007) and to that extent supplementation can benefit leaky gut. Gradually building the dosage from as little as 2.5 gr per day to 20 gr should be a safe way to avoid adverse reactions. I have not seen any studies demonstrating the benefits of L-glutamine supplementation for leaky gut however it does support overall intestinal health.


Larazotide acetate

Larazotide acetate is a protein shown to inhibit Zonulin production without any adverse effects (Paterson, B.M et al., 2007). Alba Therapeutics an Indian pharmaceutical company is in the process of developing a drug with this protein.




Abd el-gawad, H.M. and Khalifa, A.E., 2001. Quercetin, coenzyme Q 10, and l-canavanine as protective agents against lipid peroxidation and nitric oxide generation in endotoxin-induced shock in rat brain. Pharmacological research, 43(3), pp.257-263.


Biancone, L., Fantini, M., Tosti, C., Bozzi, R., Vavassori, P. and Pallone, F., 2003. Fecal α1-antitrypsin clearance as a marker of clinical relapse in patients with Crohn’s disease of the distal ileum. European journal of gastroenterology & hepatology, 15(3), pp.261-266.


Clemente, M.G., De Virgiliis, S., Kang, J.S., Macatagney, R., Musu, M.P., Di Pierro, M.R., Drago, S., Congia, M. and Fasano, A., 2003. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut, 52(2), pp.218-223.


Derikx, J.P., Luyer, M.D., Heineman, E. and Buurman, W.A., 2010. Non-invasive markers of gut wall integrity in health and. World J Gastroenterol, 16(42), pp.5272-5279.


El Asmar, R., Panigrahi, P., Bamford, P., Berti, I., Not, T., Coppa, G.V., Catassi, C. and Fasano, A., 2002. Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure. Gastroenterology, 123(5), pp.1607-1615.


FlemIng, S.C., Kapembwa, M.S., Laker, M.F., Levin, G.E. and Griffin, G.E., 1990. Rapid and simultaneous determination of lactulose and mannitol in urine, by HPLC with pulsed amperometric detection, for use in studies of intestinal permeability. Clinical chemistry, 36(5), pp.797-799.


Grimoud, J., Durand, H., De Souza, S., Monsan, P., Ouarné, F., Theodorou, V. and Roques, C., 2010. In vitro screening of probiotics and synbiotics according to anti-inflammatory and anti-proliferative effects. International journal of food microbiology, 144(1), pp.42-50.


Groeger, D., O’Mahony, L., Murphy, E.F., Bourke, J.F., Dinan, T.G., Kiely, B., Shanahan, F. and Quigley, E.M., 2013. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut microbes, 4(4), pp.325-339.


Laetitia, R., Paul, A., Marinescu, D., Shao, W. and Prakash, S., 2013. Effect of probiotics Lactobacillus and Bifidobacterium on gut-derived lipopolysaccharides and inflammatory cytokines: an in vitro study using a human colonic microbiota model. Journal of microbiology and biotechnology, 23(4), pp.518-526.


Larson, S.D., Li, J., Chung, D.H. and Evers, B.M., 2007. Molecular mechanisms contributing to glutamine-mediated intestinal cell survival. American Journal of Physiology-Gastrointestinal and Liver Physiology, 293(6), pp.G1262-G1271.


Leblhuber, F., Geisler, S., Steiner, K., Fuchs, D. and Schütz, B., 2015. Elevated fecal calprotectin in patients with Alzheimer’s dementia indicates leaky gut. Journal of Neural Transmission, 122(9), pp.1319-1322.


Liu, Y., Chen, F., Odle, J., Lin, X., Jacobi, S.K., Zhu, H., Wu, Z. and Hou, Y., 2012. Fish oil enhances intestinal integrity and inhibits TLR4 and NOD2 signaling pathways in weaned pigs after LPS challenge. The Journal of nutrition, 142(11), pp.2017-2024.


Mo, C., Wang, L., Zhang, J., Numazawa, S., Tang, H., Tang, X., Han, X., Li, J., Yang, M., Wang, Z. and Wei, D., 2014. The crosstalk between Nrf2 and AMPK signal pathways is important for the anti-inflammatory effect of berberine in LPS-stimulated macrophages and endotoxin-shocked mice. Antioxidants & redox signaling, 20(4), pp.574-588.


Moro, C., Palacios, I., Lozano, M., D’Arrigo, M., Guillamón, E., Villares, A., Martínez, J.A. and García-Lafuente, A., 2012. Anti-inflammatory activity of methanolic extracts from edible mushrooms in LPS activated RAW 264.7 macrophages. Food Chemistry, 130(2), pp.350-355.


Paterson, B.M., Lammers, K.M., Arrieta, M.C., Fasano, A. and Meddings, J.B., 2007. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT‐1001 in coeliac disease subjects: a proof of concept study. Alimentary pharmacology & therapeutics, 26(5), pp.757-766.


Skardelly, M., Armbruster, F.P., Meixensberger, J. and Hilbig, H., 2009. Expression of zonulin, c-kit, and glial fibrillary acidic protein in human gliomas. Translational oncology, 2(3), pp.117-120.


Sturgeon, C. and Fasano, A., 2016. Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue Barriers, p.e1251384.


Thomas, C.M. and Versalovic, J., 2010. Probiotics-host communication: Modulation of signaling pathways in the intestine. Gut microbes, 1(3), pp.148-163.


Trent, M.S., Stead, C.M., Tran, A.X. and Hankins, J.V., 2006. Invited review: diversity of endotoxin and its impact on pathogenesis. Journal of endotoxin research, 12(4), pp.205-223.


Wu, Y.H., Chuang, S.Y., Hong, W.C., Lai, Y.J., Chang, G.J. and Pang, J.S., 2012. Berberine reduces leukocyte adhesion to LPS-stimulated endothelial cells and VCAM-1 expression both in vivo and in vitro. International journal of immunopathology and pharmacology, 25(3), pp.741-750.

What is the Selfish Brain Theory?

According to the Selfish Brain theory our brain has a series of (hierarchically ordered) mechanisms in place to maintain constant supply of energy at a certain concentration.

Despite weighing only ~2% of body weight, the brain consumes a disproportionate high amount of energy: ~20%. Knowing that, it should come as no surprise that many physical symptoms linked with poor metabolism (incl. muscular fatigue, obesity, taxed liver function possibly due to alcoholism) are linked with compromised brain function (i.e. migraines, forgetfulness, irritability).

The Selfish Brain theory was put forward by scientist at University of Luebeck in Germany in 2004 and is likely to bring a swift in the way we understand and treat metabolic & personality disorders in the future. [ The theory has its roots in some earlier research in 1997 on addiction (DuPont RL 1997) ]

In clinical practice I consider 3 qualitative markers as a sign of good health: Energy, Mood & Appetite (EMA). When all 3 in are balance the body is 95% of the time thriving. The Selfish Brain theory offers a “simple” model of their intimate relationship.

1. The brain’s unique role in energy management

How the human body manages energy supply to different organs is key for treating chronic illness including: obesity, PCOS, cardiovascular disease & cancer. Energy metabolism is dependent on:
i. energy supply
ii. energy allocation

The brain plays a key role in this process. What gives the brain a unique role in body’s metabolism?

i. It carries important functions for the rest of the body.
Together with the heart the brain is responsible for processes that run on an ongoing basis. Shortage of energy supply to these 2 organs can be life threatening.

ii. It consumes a lot of energy.
Despite its small weight (~2% of total body weight), it consumes a disproportionate high amount of energy ~20%, partly due to the energy needs of neurotransmitter transmission (Attwell D and Laughlin S 2001).

iii. It has low energy storage capacity.
In contrast to most other organs it depends almost entirely on glucose for energy but has limited capacity to store glucose. The liver and (to a lesser extent) the muscles are the body’s main glucose reserves (in the form of glycogen).

iv. It’s access to the blood supply is controlled.
The brain comes in contact with the blood (cardiovascular system) in 2 areas only: the Blood Brain Barrier (BBB) where astrocytes (neuron cells) serve as a filter wall and the Hypothalamus. Due to the high amounts of toxins and pathogens circulating in the blood there may be an evolutionary benefit in this physical protection of the brain.

v. It is able to monitor other organs and affect their function.
Through the Peripheral Nervous System (PNS) the brain is able to record information from other organs as well as control their function.

Accounting for the above idiosyncratic functions, the Selfish Brain theory suggests that the brain:

i. Prioritises its own energy supply before other organs by using the stress system when there is an energy deficit (Allocation)

ii. It subsequently alters appetite to alleviate stress and return to balance (Appetite -> Food intake)

The model has the shape of a fishbone to illustrate the hierarchically structure of the pathway.

2. How does the brain sense if it has enough energy?

Cells in the brain as well as skeletal muscles (Lazdunski M. 1994) sense the levels of energy intracellularly through: ATP-sensitive potassium (Katp) channels. ATP & ADP (the body’s energy currencies) bind on these channels and this way signal availability or lack of energy. In an excitatory neutron adequate levels of ATP (by binding on Katp channels) will trigger the release of glutamate or brain-derived neurotrophic factor (BDNF) while elevated ADP will silence it.

A key feature of the Selfish Brain theory is that the brain has 2 types of Katp channels: high & low affinity. When a cell has relatively low ATP concentrations, high affinity Katp channels are still occupied. On the other hand low affinity Katp channels require high ATP concentration to get occupied. The high affinity Katp channels are found mostly in excitatory neurones (releasing glutamate & Brain-Derived Neurotrophic Factor (BDNF)) while low affinity ones are in inhibitory neurones (releasing γ-amino-butyric acid / GABA) (Ohno-Shosaku T et al., 1993). Both types of are found in the human neocortex (Jiang C et al., 1997).

With low ATP concentrations the glutamateric neurones are dominantly active while at high ATP concentrations the GABA-eric neurones predominate.

It is worth mentioning that at critically reduced ATP both excitatory & inhibitory neurones are inactive – a phenomenon referred to as “global silencing” (Mobbs CV et al., 2001).

3. How does the brain maintain a constant energy level?

The brain according to the Selfish Brain theory has 2 ways to maintain a set energy level. One via moderating the allocation on the currently available energy from the peripheral tissue to itself and a 2nd by demanding more energy from the environment by controlling eating behaviour.

3.1 Brain’s “energy on demand”

In order for the brain to access glucose (energy) available in the blood it needs to “open” the blood-brain barrier (BBB). Glutamate activates the glucose receptors (GLUT1 in the astrocytes) of the BBB and sequentially the glucose enters the brain (Magistretti PJ et al., 1999). GABA on the other hand does not have the same impact in the BBB (Chatton JY et al., 2003).

Glutamate* was also shown to activate the limbic-hypothalamic-pituitary-adrenal (LHPA) axis (Yousef KA et al., 1994). LHPA axis is commonly referred to as the stress or the flight or flight response. By activating the LHPA axis glutamate is able to restrict glucose supply to other organs and preserve it for the brain. The steps are as follows:

Glutamate signals the limbic system that the body is in a stressful state. The limbic system stimulates the sympathetic nervous system (NS) through the Ventromedial part of the Hypothalamus (VMH) resulting in the release of CRH & vasopressin hormones. In this way it tells the pituitary to release ACTH hormone. ACTH is released in the blood and stimulates the production of cortisol from the adrenals. Cortisol finally inhibits the production of insulin from pancreatic β cells and thus the uptake of glucose for certain organs making it available for the brain (Jansen AS et al., 1997). In the Selfish Brain model the allocation of energy takes place in the VMH.

In a state of high energy GABA (a calming neurotransmitter) is also released counteracting glutamate’s excitatory effects. The sympathetic system is not activated and the junctions in the BBB remain tightly closed.

In summary the brain can moderate the allocation on the currently available energy from the peripheral tissue to itself as follows:

When there is low energy in brain, glutamate is released in relatively higher levels than GABA causing 2 effects:
1. the BBB opes and increases the intake of glucose from the blood stream to the brain
2. the Limbic Hypothalamic Pituitary Adrenal (LHPA) axis is activated restricting the supply of glucose in peripheral tissue.

3.2 Requesting energy from the environment

Lateral Hypothalamus (LH) is a key area of the brain where appetite is controlled (Anand BK, Brobeck JR. 1951), although not the only one. Glutamate can stimulate the LH to increase appetite [13]. With the increase of food intake, energy from the environment is enters the body (Stanley BG et al., 1993)

According to the Selfish Brain theory the Neocortex acts at the primary regulatory system for energy and the LHPA axis functions as a secondary. xxx Many more hormones (i.e. Leptin hormone signals the hypothalamus that energy has been stored in the fat tissue (Spanswick D et al., 1997)) can be added to the graph without affecting its hierarchy.

The Selfish Brain theory demonstrates how the brain manipulates the stress response mechanism to moderate energy supply. That’s worth keeping in mind when dealing with mental or eating disorders.




* in particular through glutamate receptors of N-methyl-D-aspartate (NMDA) subtype (Molina PE, Abumrad NN 2001).





Anand BK, Brobeck JR. Hypothalamic control of food intake in rats and cats. Yale J Biol Med 1951;24:123–46.

Attwell D, Laughlin SB. An energy budget for signaling in the grey matter of the brain. J Cereb Blood Flow Metab. 2001;21:1133-45.

Chatton JY, Pellerin L, Magistretti PJ. GABA uptake into astrocytes is not associated with significant metabolic cost: Implications for brain imaging of inhibitory transmission. Proc Natl Acad Sci USA 2003;12456–61.

DuPont RL. The selfish brain: learning from addiction. Center City, Minnesota: Hazelden; 1997.

Jansen AS, Hoffman JL, Loewy AD. CNS sites involved in sympathetic and parasympathetic control of the pancreas: a viral tracing study. Brain Res 1997;766(1–2):29–38.

Jiang C, Haddad GG. Modulation of K . channels by intracellular ATP in human neocortical neurons. J Neurophysiol 1997;77(1): 93–102.

Magistretti PJ, Pellerin L, Rothman DL, Shulman RG. Energy on demand. Science 1999;283(5401):496–7.

Mobbs CV, Kow LM, Yang XJ. Brain glucose-sensing mechanisms: ubiquitous silencing by aglycemia vs. hypothalamic neuroendocrine responses. Am J Physiol Endocrinol Metab 2001;281(4):E649–54.

Molina PE, Abumrad NN. Contribution of excitatory amino acids to hypoglycemic counter-regulation. Brain Res 2001;899(1–2): 201–8.

Lazdunski M. ATP-sensitive potassium channels: an overview. J Cardiovasc Pharmacol 1994;24(4):S1–S5.

Spanswick D, Smith MA, Groppi VE, Logan SD, Ashford ML. Leptin inhibits hypothalamic neurons by activation of ATP-sensitive potassium channels. Nature 1997;390(6659):521–5.

Stanley BG, Ha LH, Spears LC, Dee MG. Lateral hypothalamic injections of glutamate, kainic acid, D,L-alpha- amino-3-hydroxy- 5-methyl-isoxazole propionic acid or N-methyl-D-aspartic acid rapidly elicit intense transient eating in rats. Brain Res 1993; 613(1):88–95.

Ohno-Shosaku T, Sawada S, Yamamoto C. ATP-sensitive K . channel activators suppress the GABAergic inhibitory transmission by acting on both presynaptic and postsynaptic sites in rat cultured hippocampal neurons. Neurosci Lett 1993;159(1–2):139–42.

Yousef KA, Tepper PG, Molina PE, Abumrad NN, Lang CH. Differential control of glucoregulatory hormone response and glucose metabolism by NMDA and kainate. Brain Res 1994; 634(1):131–40.

The ROSE Method

Do you care about your body composition?

Although I cannot see your face I can guess your response: “WHAT A STUPID QUESTION? OF COURSE I…” and some of you will say “DO” and some will say “DON’T”. For me to ask this question and have developed a method for it I obviously consider it a significant one. Not because I think that everyone needs to look like the cover model of a fashion magazine but because body composition is a great indication of health.

Science has shown body composition to be linked with the development of certain diseases (cancer been one [1]) but not others (like inflammatory bowel disease [2]). So if you are health conscious you should be only partly concerned if you have low muscle tone or excess fat, correct?

OK I suggest we keep it real. Low muscle tone and/or excess body fat is as bad for health as it is for self esteem. The view of a person with a low % of muscle mass and high % of body fat is almost the opposite of a sick one!


What can you do to improve your body composition then?

You want to learn more?

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?



Underactive thyroid and weight management – part III

According to the American Thyroid Association 12% of Americans will develop hypothyroidism at some point in their life, while 60% of those with an underactive thyroid are undiagnosed. Given the pandemic of inflammatory conditions now present and the link between the adrenal, immune and digestive system with the thyroid I believe that the above numbers are an underestimate. One of the most common manifestations of an underactive thyroid is challenges with weight management.

The link thyroid has with the adrenals and digestion described in the previous 3 posts will have an indirect impact on weight management. In this post I will discuss how thyroid directly affects body weight and body composition.

1. When someone is hypothyroid his/her liver and gallbladder will become sluggish (1,2) having 2 implications:
i. the body will store fat faster than burn it.
ii. the fat cells’ ability to uptake LDL diminishes (3) causing the Triglycerides, cholesterol and LDL in the blood to increase.

2. An underactive thyroid slows down the absorption of glucose both from the gut to the bloodsteam and from the blood to the cells. This is very important to keep in mind as blood tests may return normal blood sugar levels while the person may suffer from hypoglycemia or/and insulin resistance.


Knowing about the link between underactive thyroid and weight management what can you do?

First and foremost, you should not assume that only overweight people can have an underactive thyroid. This is a very common misconception. Second remember that symptoms are more valuable than tests. If you feel crap there is something wrong in your body no matter what the tests say. Last you need to find the route cause of the underactive thyroid. In an earlier post I referred to the chemicals that can disrupt thyroid function. Work with a Naturopath or Nutritional Therapist.



1. Possible chronic thyroiditis revealed by [18F]-FDG-PET/CT scan in a euthyroid patient with recurrent gallblader carcinoma. Thyroid 2007 17:1157-1158.

2. Is bile flow reduced in patients with hypothyroidism? Surgery 2003, 133: 288-293.

(3) Oge A, Sozmen E, karaoglue AO (2004) Effect of thyroid function on LDL oxidation in hypothyridism and hyperthyroidism. Endocr Res; 30: 481-489.