Home » mental health

Tag: mental health

Yogis and Cold exposure

The popularity of cold exposure has increased over the last few years. Whether it is through cryotherapy or cold water immersion more and more people practice and/or hashtag #coldexposure. What are the benefits of cold exposure for the modern yoga practitioner (yogi or yogini)?

 

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 the same state of mind in his 2nd ice bath, with that on the 7th day in a vipassana meditation retreat. Anecdotal evidence like this were confirmed to be valid in a study published in May 2018 titled “Brain over Body” [1].  In this study participants with no previous experience in cold exposure and Wim Hof (a Dutch man with chronic practice in cold environments) 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 To overcome fears

Iyengar’s book “Light on Yoga” has the subtitle: “the yoga journey to wholeness, inner peace and ultimate freedom.” In our yogic journey (our journey to wholeness) we will have to ultimately face our fears. I believe that cold exposure offers a unique opportunity to learn how to do that.

Cold exposure is demanding on many levels; the adrenals, musculoskeletal system, circulation and the brown fat tissue (if existent) 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” [2]. A small area of the brain called amygdala (Greek word for almond) – by activating the HPA (Hypothalamic Pituitary Adrenal) axis – signals a Stress response to the rest of the body. While this initial stage is universal the way one deals with cold thereafter depends on 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 in this process is our breath. Dealing with fear was the focus of a workshop I gave in 2017 to a group of actors. You can see footage from it in the video.

 

Cold exposure to improve Circulation / Cardiovascular Function

The benefits of an asana practice to physical health are far reaching. The improvement of respiratory function, the increase of muscle flexibility and joint mobility are just a few.  Depending though on the style of yoga one practices she may be getting more or less of a cardiovascular workout. Cold exposure is a unique way to strengthen one’s cardiovascular system.

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 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.

 

Conclusion

The list above is not exhaustive of the benefits one can get from cold exposure; controlling pain perception [2], generation of Brown Far [3], strengthening of the immune system [4], improved tolerance to cold [5] are also good reasons for modern yogis and yoginis to practice cold exposure.

 

Future workshops are listed here.

 

References:

  1. Muzik, O., Reilly, K. T., & Diwadkar, V. A. (2018). “Brain over body”–A study on the willful regulation of autonomic function during cold exposure. NeuroImage172, 632-641.
  2. Kanosue, K., Sadato, N., Okada, T., Yoda, T., Nakai, S., Yoshida, K., … & Kobayashi, K. (2002). Brain activation during whole body cooling in humans studied with functional magnetic resonance imaging. Neuroscience letters329(2), 157-160.
  3. van der Lans, A. A., Hoeks, J., Brans, B., Vijgen, G. H., Visser, M. G., Vosselman, M. J., … & Schrauwen, P. (2013). Cold acclimation recruits human brown fat and increases nonshivering thermogenesis. The Journal of clinical investigation123(8), 3395-3403.
  4. Buijze, G. A., Sierevelt, I. N., van der Heijden, B. C., Dijkgraaf, M. G., & Frings-Dresen, M. H. (2016). The Effect of Cold Showering on Health and Work: A Randomized Controlled Trial. PloS one11(9), e0161749.
  5. Vosselman, M. J., Vijgen, G. H., Kingma, B. R., Brans, B., & van Marken Lichtenbelt, W. D. (2014). Frequent extreme cold exposure and brown fat and cold-induced thermogenesis: a study in a monozygotic twin. PloS one9(7), e101653.

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.

 

 

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.

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).

 

 

 

References

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.

What helps Histamine Intolerance?

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

 

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

 

What is Histamine Intolerance?

Histamine is a hormone with varying functions in different tissues.

 

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

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

 

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

 

Histamine’s link with Digestion.

Gastrointestinal problems are very common among those with histamine intolerance.

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

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

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

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

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

 

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

 

Histamine Intolerance foods to avoid

 

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

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

 

Histamine Intolerance diet

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

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

 

Blood sugar regulation and Histamine Intolerance

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

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

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

 

How to test for Histamine Intolerance

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

 

Labs that offer this service are:

Smart Nutrition in UK

ImmunoPro in Australia

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

 

23andme results & Histamine Intolerance

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

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

 

Source: Opus23

 

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

 

Source: Opus23

 

How can this information be useful? 

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

 

Source: Opus23

 

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

 

 

References

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

 

 

Mobile phone radiation dangers – myth or fact?

Does mobile phone radiation impose a threat to our health?

A few studies have shown no link between the 2 (1,2,3). Some others though tell a different story (4, 5, 6).

According to a meta analysis published in 2008 (7) brain tumours were positively associated with >= 10 years of mobile use while an earlier study (2006) (8) performed among 2,200 cancer patients in Sweden showed an increased risk for cancer by 10% for every additional year of mobile use. These studies I find them very useful as they test the long term effects of mobile use. Many activities while safe on the short run can impose serious threats on the long run.

 

While the studies referenced above can be useful what they do not do is investigate HOW mobile radiation harms the health. This is partly done in the study published by Volkow et al., in 2011 at The Journal of the American Medical Association (9). In this study, performed among 47 healthy individuals, 50 mins of exposure to mobile radiation increased the glucose metabolism in the brain near the area of exposure! This is not to be taken lightly as disruptions of sugar regulation we know are associated with cell death (10)

Sugarforthebrainpaper

Why mobile radiation affects brain glucose metabolism is unclear. In vivo animal and in vitro experiments have hypothesized the increase of  cell membrane permeability, cell excitability and neurotransmitter release (11).

 

 

 

References:

1. Inskip PD, Tarone RE, Hatch EE,  et al.  Cellular-telephone use and brain tumors.  N Engl J Med. 2001;344(2):79-86

2. INTERPHONE Study Group.  Brain tumour risk in relation to mobile telephone use.  Int J Epidemiol. 2010;39(3):675-694

3. Inskip PD, Hoover RN, Devesa SS. Brain cancer incidence trends in relation to cellular telephone use in the United States.  Neuro Oncol. 2010;12(11):1147-1151

4. Lehrer S, Green S, Stock RG. Association between number of cell phone contracts and brain tumor incidence in nineteen U.S. States.  J Neurooncol. 2011;101(3):505-507

5. Hardell L, Carlberg M. Mobile phones, cordless phones and the risk for brain tumours.  Int J Oncol. 2009;35(1):5-17

6. Myung SK, Ju W, McDonnell DD,  et al.  Mobile phone use and risk of tumors: a meta-analysis.  J Clin Oncol. 2009;27(33):5565-5572
7. 2008: Lennart Hardell; Michael Carlberg; Fredrik Söderqvist; Kjell Hansson Mild
Meta-analysis of long-term mobile phone use and the association with brain tumours.
International journal of oncology 2008;32(5):1097-103.

8. 2006: Lennart Hardell; Michael Carlberg; Kjell Hansson Mild
Pooled analysis of two case-control studies on use of cellular and cordless telephones and the risk for malignant brain tumours diagnosed in 1997-2003.
International archives of occupational and environmental health 2006;79(8):630-9.

9. Volkow N et al. (2011) Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. JAMA;305(8):808-813. doi:10.1001/jama.2011.186.

10. Mergenthaler P et al. (2013) Sugar for the brai: the role of glucose in physiological and pathological brain function. Trends Neuroscience 36(10):587-597.

11. Hyland GJ. Physics and biology of mobile telephony.  Lancet. 2000;356(9244):1833-1836

Gut function and brain health III

This is the 4th of a series of posts demonstrating the link between the brain and other body organs. In the previous 2 we discussed how intestinal permeability and compromised detoxification can affect the brain.

 

The gastrointestinal (GI) track affects the brain through a 3rd pathway; the immune system. The GI track is constantly exposed to foreign substances many of which are pathogenic. While the body has certain mechanisms to neutralise these pathogens (such as saliva and hydrochloric acid) some of them do cause harm. In a similar way that the biggest military force of countries sits near it’s boarders, 70% of the body’s immune system is on the GI track. What does this have to do with the brain?

An active immune system produces chemicals (called cytokines) in order to destroy the foreign pathogens. Many of these chemicals cross the blood brain barrier (BBB) causing inflammation in the brain. Although it’s the lymphatic system’s job to control inflammation, other processes (such as thyroid and reproductive function) controlled by the brain are altered when the immune system is active.

 

The compound effect:

When the immune system is activated the gut-blood barrier gets also compromised, compounding the problem. All the issues discussed in the previous 2 articles then become relevant.

What can you do to prevent activation of the immune system in the GI track?

1. Avoid foods you are allergic to.

2. Stay away from highly processed foods and trans-fats.

3. Eat a diet high in antioxidant foods.

Gut function and brain health I

This is the 2nd of a series of posts demonstrating the link between the brain and other body organs.

Even if you haven’t heard the gut been called as the 2nd brain, you must be at least familiar with the expression “gut feeling”. What’s the basis though of this link? and while we discussed in last week’s post how the brain can affect the gut is the relationship reciprocal?

The gastrointestinal (GI) track similar with the nervous system (NS) contains a high amount of neuron cells. Neurotransmitters produced in the brain are also produced in the GI track. Serotonin is one example:

– In the brain it functions as a mood thermostat. Calms us down when “hyper” and cheers us up when “low”.

– In the gut serotonin is responsible for the muscle contractions necessary for digestion and food transport through the GI track.

 

How does gut function then affect brain health?

1. The intestines (mainly small but also the large one) is the area in the body where the food is transported into the blood. As you would expect this is a very controlled process. Who controls it? 3 things:

– structure. The structure of the GI wall is such to allow only for small molecules to enter the blood stream.

– bacteria.

– enzymes.

 

When this process is compromised nutrients and toxins which are not supposed to enter the blood cause havoc. The most straight forward way on how the brain can be affected is: A toxin crosses the gut-blood barrier → circulates in the blood stream → crosses the blood-brain barrier.

I hope it has become obvious how important it is to keep the integrity of the GI track healthy. What can we do to support it?

– avoid foods we are allergic to. While many lab tests can help us finding out, the elimination challenge test is an inexpensive good starting point.

– Support your diet with pre and probiotic foods.

– Reduce your exposure to toxics.

 

Healthy brain and overall body health

This is the 1st of a series of post demonstrating the link between the brain and other body organs.

The brain is responsible for autonomously (unconsciously) running many functions in the body. Nerve cells passing through the brainstem control the breath digestion heart beat. These nerve cells are called vagal nuclei and branch out to the vagus nerve.

Without getting too technical, do you see how a healthy brain and overall body health are linked? When the vangus nerve is in good shape messages from the brain are transmitted to the different organs in the body resulting in enzyme production, bowel movement, decrease of heart rate when it’s time for bed and so on.

How can you keep the vangus nerve is good shape then?

1. Gargle water (bringing it as deep down your throat as possible)

2. Singing loudly

3. Gag by pressing a tongue blade at the back of your tongue

 

Reference: Why isn’t my brain working? by Datis Kharrazian

A seahorse in your brain that likes sex

 

If we were to draw a parallelism between parts of the brain and a night club, hippocampus is the dj! This seahorse like part of the brain is responsible for controlling many functions in our body among which are:

👉🏻 our body temperature

👉🏻 our circadian rhythm

👉🏻 memory storage.

Hippocampus though hates stress. High cortisol (a stress hormone) levels have been shown to shrink its size and contribute this way to the development of Alzheimer’s.

On the other hand though the seahorse in your brain likes sex. A 2010 study conducted by Leuner B et al. from Princeton University tested the impact of sexual experience in the hippocampus of 14 rats. The researchers found that chronic sexual experience not only decreased corticosterone levels (initially released due to the mating process) but also led to production of new neurons in the hippocampus.