Helping the Bloated Gut

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Helping the Bloated Gut

Health and Disease Begin in the Gut – Part Two: A Practical Approach

In Part One of Health and Disease Begin in the Gut we explored the central function of the small intestinal duodenum:

  • how inflammation hampers duodenal controls and functions
  • how an inflamed duodenum plays a significant role in a wide array of disorders from
  • how we can recognize an inflamed gut.

Once we have recognized inflammation and its effects, it is time to identify causes and solutions to any particular set of health challenges. There is no good-for-all solution to gut inflammation and its many secondary disorders. When it comes to true healing we all require an individualized, carefully planned approach.

 

Establishing the Cause

Diseases such as diabetes or heart disease are not the initial cause of GI health issues but the result of underlying factors and dysfunctions. Therefore, while acknowledging their presence and need to be addressed, we must dig deeper. As we have seen in Part I, the duodenum very frequently is that control center that has gone awry.

As in the case of autoimmune reactions such as non-celiac and/or celiac gluten sensitivity[1] or lactose/casein intolerance[2] an individual’s genetic makeup may play the determining role when it comes to formulizing the best approach to bloating and duodenal inflammation.

Given particular patterns, many health professionals today have their patients gene tested (HLA-DQ 2/DQ8 with specific subtype and alleles) for potential non-celiac and/or celiac gluten sensitivity[3] to asses a possible risk along with stool IgA titers for gliadin, casein, ovalbumin (eggs), and soy (legumes) as indicators of present inflammatory reaction levels.

"…HLA-DQ genotype allows to establish clinically relevant genetic risk profiles."[4]

and

"…Considering 1:100 disease prevalence, we obtained a risk gradient ranging from 1:7 for DQ2 and DQ8 individuals down to 1:2518 for subjects lacking all predisposing factors. The DQB1*02 and DQB1*0302 concurrence (p = 9 x 10(-4)), besides the DQB1*02/*02 homozygosity, had an additional role in disease genetic determination. The CD prevalence rose to 17.6% in sisters, 10.8% in brothers, and 3.4% in parents. In the three groups, the subjects carrying high-risk HLA molecules were 57%, 71%, and 58%; among them, 29%, 15%, and 6% respectively had CD. Those siblings and parents with no susceptible factors were not affected. These findings indicate the impact of the HLA test for CD in clinical practice."[5]

 

Establishing the Triggers

Some of the most obvious food related conditions impacted by a compromised duodenum include metabolic disease, heart disease, thyroid disease, diabetes, non-celiac and/or celiac gluten sensitivity, respiratory challenges, skin diseases, muscular and bone disorders, mental-emotional disorders and more.

Because food allergies and intolerances often are the main cause of metabolic and gastro-intestinal inflammation, food is also the first and safest go-to when it comes to relieving inflammation and achieving better health.

Therefore, among the causes and triggers that need to be considered are:

  • Food
  • Environment (includes soil, air and water)
  • Toxins (such as aluminum-borne[6] causes)
  • General lifestyle, sleep.

The reason behind this is simple and straight forward: We don’t put diesel fuel into the tank of a gasoline driven car without clogging up and killing its engine. Similarly, we cannot put foods into a body that it is not designed to digest without causing cell, function, and organ damage.

 

Address the Underlying Cause   

Increasingly, research is looking into genetic links between different disorders from vascular and mucous conditions to metabolic issues, thyroid or endocrine disorders, and mineral imbalances to behavioral and mental challenges.

Together with the knowledge of a patient’s underlying risk factors and conditions the ability of genetic linking allows a knowledgeable health practitioner to zoom into a specific and individualized approach.

It is important not to simply treat individual conditions but troubleshoot the potential underlying component and start there. Here is where HLA-DQ2/DQ8 testing becomes particularly helpful where bloating or abdominal flaccidity are concerned.

Once tested, certain of the genetic subtypes and alleles directly point to possible "exposure" spots; for instance, genetic gluten sensitivity with a concurrent casein, lactose or legume allergy, or a birch pollen allergy with a reaction to salicylic acid containing foods and an aspirin allergy, and so on.

 

Understanding the Healing Process    

LESSON NUMBER ONE, therefore, is to eliminate triggers in order for the body to clear acute and chronic inflammation.

  • Stick to non-allergenic, "clean" and unprocessed, fresh foods that don’t add additional "fire" to the inflammation (see below).
  • Adjust your lifestyle to allow for the "cleanest" possible and least toxic physical and emotional environment (see following chart). 

LESSON NUMBER TWO: Be persistent and be patient! Healing rarely progresses in a linear fashion.

  • Any healing process breaks down into several phases.
  • Detoxification must be controlled and induced gently and in baby-steps only once the acute inflammation levels have been reduced.—In severely ill individuals a radical detox approach may have long-lasting negative consequences and may jeopardize a positive healing outcome.
  • Regression more frequently takes place in the initial phases and, if suppressed, may delay healing indefinitely. Regression must never be suppressed!

With the right food choice, initial improvements may be felt in as little as a couple of weeks. Yet, because of their complex tissues and functions, a previously leaky gut or a villi-stripped duodenum may take two to five years for more thorough healing.

 

The Seven Phases of Healing    

SEVEN PHASES OF HEALING    (with a few basic "fix-it" ideas)

The Four

CLEARING Phases

 

Avoidance

and

Removal

  1. Identification Phase:

identify main trigger(s)

Tests: CBC, HbA1C, HLA genetic testing + IgA stool titers, etc.  

gluten, casein, ovalbumin, legume (soy), Rx, environmental, parasites[7]

  1. Avoidance Phase:

avoid and eliminate main trigger(s)

Diet: "package-free" paleo-type,[8] fresh foods and non-chlorinated H2O

Lifestyle: eliminate toxic cleaning and personal care products

Exercise: Tai Chi, ballroom dancing, fencing, horseback riding, ping pong, swimming, walking, etc.  

  1. Retox Phase:

remove old toxins stored in body tissue

Diet: fine-tune and trouble shoot for hidden toxins

Detox: old toxins re-enter blood and lymph system

  1. Reassessment Phase:

find and remove remnant triggers

Repeat IgA stool titers

Ask your health professional about adding glutenfree vitamin D and orally absorbable vitamin C

The Three

BUILDING

Phases

 

Support

and

Supplement

  1. Calcium Metabolism:

assess and (re-)establish proper balances

Remember, an inflamed gut does NOT absorb traditional supplements!

Along with the specific diets we recommend anti-homotoxic, homeopathically prepared and orally absorbed compounds individually balanced (e.g. Ca/Mg/Mo or Zn/Cu, etc.)  

Consult with your knowledgeable health professional for biochemical balance – avoid "band-aid" approaches.

  1. Electrolyte and Nutrient[9] levels:

balance, (re-)establish

  1. Hormone levels:

fine-tune

All of us who have gone this route to better health sooner or later discover how difficult a "clean food" approach is in today’s processed food driven environment. Since we have so been conditioned that food only becomes edible if processed, a switch in food choices quickly turns into a change in lifestyle.

 

The Most Common Long Time Fail Approach

Many patients experience a wide variety of concurrent challenges and often present with a long list of prior disorders and diagnoses in addition to abdominal bloating or flaccidity. Let us repeat: A bloated gut is not normal!

Mainstream and natural health practitioners quickly fall prey to bombarding such a body with additional "magic pills" – an enzyme here, a vitamin or mineral concoction there, an anti-inflammatory or elixir – often with initial improvements but rarely with long-term results.

Such complex interactions do not allow for a trial and error approach and, in most cases, require close interaction with a knowledgeable health professional. Here the problem starts.

Change is difficult. In our addiction or lifelong conditioning to repeating the same behavior over and over while expecting a different outcome we are looking to what (else) we can take (i.e. devour) to fix our food-intake induced problem.

More is not always better. Neither are there any magic pills. Yet, this kind of thinking is being happily supported and nurtured by a billion dollar health food and supplement industry that promotes what I call the "this is good for this—that is good for that" band-aid attitude.

Instead, we must shift our consciousness to avoiding triggers, not to cover them up. Furthermore, in an attempt to avoid genetic typing, many practitioners recommend following an elimination diet. This is a long road and, while it will allow to narrow down possible triggers, in the end a food elimination diet is still only guess work.

Worst, knowing the human mind, sooner or later (after successfully having gone through the elimination diet approach), the little devil pokes us to try a forbidden food again, "we need proof!" And if, by chance, we get away without our system collapsing, we will happily return to our previous inflammation causing habits.

 

In Summary

Start with genetic typing and change what you can change: your food intake and environment.



[1] http://www.ncbi.nlm.nih.gov/pubmed/22649918 J AOAC Int. 2012 Mar-Apr;95(2):349-55.  Gluten and celiac disease--an immunological perspective.

[2] http://www.ncbi.nlm.nih.gov/pubmed/22086322 Rev Gastroenterol Peru. 2011 Jul-Sep;31(3):278-81.  [Celiac disease and intestinal obstruction by T cell lymphoma].

[3] http://www.ncbi.nlm.nih.gov/pubmed/11068484 Rev Med Brux. 2000 Sep;21(4):A303-8.  [Lactose and gluten intolerance: which to suspect?].

[4] http://www.ncbi.nlm.nih.gov/pubmed/22662777 Rev Esp Enferm Dig. 2012 May;104(5):248-254.  HLA-DQ typing in the diagnostic algorithm of celiac disease.

[5] http://www.ncbi.nlm.nih.gov/pubmed/19027045 Hum Immunol. 2009 Jan;70(1):55-9. Epub 2008 Nov 21.  HLA-DQ and risk gradient for celiac disease.

[6] http://www.ncbi.nlm.nih.gov/pubmed/22235058 Lupus. 2012 Feb;21(2):231-8. Aluminum as an adjuvant in Crohn's disease induction.

[7] http://www.ncbi.nlm.nih.gov/pubmed/22617359 Eur J Gastroenterol Hepatol. 2012 May 20. [Epub ahead of print]  Celiac disease and giardiasis: a case report.

[8] http://www.ncbi.nlm.nih.gov/pubmed/22262579 Am J Hum Biol. 2012 Mar-Apr;24(2):110-5. doi: 10.1002/ajhb.22218. Epub 2012 Jan 19.  Paleolithic diets as a model for prevention and treatment of Western disease.

[9] http://www.ncbi.nlm.nih.gov/pubmed/22606367 Nutrients. 2012 Apr;4(4):243-57. Epub 2012 Mar 27.  Celiac disease, inflammation and oxidative damage: a nutrigenetic approach.

 

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