Problems of the Gut and its effects on the hair
I’m unsure how much other practitioners see the links between health, hair loss and a ‘problematic’ gastrointestinal tract (Gut), but I regularly find there is a strong causal association in many Clients.
Around 90% of lymphoid tissue – the body’s immune defences – are located in the gastrointestinal tract (termed ‘GALT’: gut associated lymphoid tissue) – Van Zanden: 2017. If the immune system becomes ‘distracted’ by a dysfunctional Gut (termed: ‘dysbiosis’) – from whatever cause – it may become disorientated & over-stimulated, leading to the production of antibodies to attack the thyroid gland or the skin (of which hair is an appendage).
Hair follicles are normally ‘immune response protected’ skin appendages. The consequences of conditions such as Alopecia areata result when the immune concessions against this tissue-specific autoimmune state are withdrawn.
Common Causes of Gut dysbiosis:
- Insufficient mastication (chewing) of food in the mouth to prepare it for entry in to the stomach. This will be seen as macroscopic food remnants and fibres in the faecal stool. Solid food matter is difficult for the body to break-down and utilise the nutrients from it, but is a continual food source for gut parasites such as Blastocystis hominis and Dientamoeba (Lee: 2018)
- Insufficient stomach acid production: When digestive problems occur, the first two stages of digestion – generous chewing of one’s food and the digestive process within the stomach – are often overlooked. Once food enters the stomach, the hormone Gastrin stimulates the release of hydrochloric acid (HCL) from specialised secretory cells termed ‘Parietal cells’.
The pH of HCL is a very acidic 1.5 to 3.5; vehicle battery acid is pH 1.0. Apart from its role in commencing the breakdown of solid foods, HCL will help destroy pathogens (harmful bacteria) in any contaminated food.
This essential facet of the digestion-absorption process is fundamentally blocked by the taking of prescription medication called PPI’s (Proton Pump Inhibitors) – Somac, Nexium. These drugs are prescribed to assist with gastro-oesophageal reflux (GORD), gastric and duodenal ulcers– often caused by Helicobacter Pylorri infection.
The adverse effects of PPI’s are premature emptying of the stomach before consumed foods have been fully broken down by HCL. This then results in gut dysbiosis further along the gastrointestinal tract; SIBO (small bowel bacteria overgrowth) with resultant nausea, diarrhoea/constipation, bloating/flatulence or abdominal discomfort.
PPI’s increase the risk of Clostridium Difficile Infection (CDI) in the colon (see full description below). Osteoporosis is associated with long term PPI use (> one year); Vitamin B12 absorption is reduced with PPI’s.
- Inadequate beneficial Gut bacteria (termed: microbiota, microbiome, microflora or symbiotes) – The colon (or large intestine) is residence to between 100-650 TRILLION organisms (Percival: 1999), with anaerobic fermentation activity 5000:1 domination over aerobic bacteria. Escherichia Coli (E-Coli), Streptococci, Lactobacillus & Bifidobacterium. E-Coli & Streptococci comprise a significant percentage of the 400-plus species of Gut microbiota; Bifidobacterium numbers can be up to 25% of the total microbiome (ARL Pathology: 2005).
In balanced numbers microbiota aids in digestion of consumed foods, appropriate processing of substances toxic (or unwanted) in the body; decreases inflammation, supports the immune system – as well as the production of certain essential vitamins & metabolites.
It is now recognised the Gut microbiome communicates with our brain to regulate inflammatory responses; dysbiotic microbiome is known to influence neuro-inflammation. (http:www.scientificamerican.com/article/gut-secondbrain/)
When certain micro-organisms (such as Bilophila Wadsworthia or Desulfobacterales) are overly dominant, they tend to increase inflammation and are linked to the onset of Metabolic Syndrome – a pre-diabetic state.
Organisms such as Clostridaceae, Ruminococcus bromii and Agathobacter rectalis tend to have an inflammation decreasing influence on the body. Again – microbiota balance is the key.
Dr. Antony Underwood (Spectrumceuticals founder) revised his company’s probiotic protocol (Underwood: 2017) to commence with a lower CFU count and D-lactate free probiotics:
- Minimises the risk of ‘probiotic toxicity’ in susceptible people.
- When treating people with low gut biome numbers of bifidium and lactobacilli AND where there is concurrent higher count of Streptococci organisms, it is crucial probiotic is D Lactate free if there are D-Lactate producing organisms (such as Streptococci) present on the stool test or a known history of elevated Histamines or Histamine sensitivity (Underwood: 2017).
- Parasites & Pathogens – Clients are often surprised and even shocked when I suggest testing for Gut parasites and pathogens. Most parasites are transmitted through contaminated water, food product or poor personal hygiene, and readily spread to humans. The ‘flood or drought’ inconsistency of the Australian river systems generate a vulnerability to parasite contamination of our waterways (ARCNP: 2005). Infection from these parasites range from the simply bothersome to physical debilitation and life threatening. Some common intestinal parasites found in humans:
- Blastocystis hominis: a protozoan organism more complex than bacteria. B. hominis numbers tend to multiply when gut microbiota is low or unbalanced. B. hominis uses the host’s iron in reproduction resulting in iron malabsorption and deficiency.
- Dientamoeba Fragilis: a ‘flagellate’ amoeba that uses its long cell surface stouthairs for food gathering and mobility.
- Giardia lamblia: a flagellate protozoan with a 1-2 week incubation period before symptoms emerge. In chronic giardiasis the diarrhoea, pain, nausea and bloating may be recurrent over many months.
- Entamoeba histolytica: a protozoan amoeba ranked the third leading cause of death in the 3rd Fever, severe dysentery and chronic colitis typify Entamoeba infestation.
- Cryptosporidium parvum: an intestinal protozoan found in contaminated water. Although C. parvum contamination has caused a major scare to the Sydney water supply some years ago, infants, children, the immune compromised and travel to tropical or developing countries are most ‘at risk’ (Shoery et al: 2000).
- Helicobacter pylorri: not an intestinal pathogen as such, but a bacteria which resides in the stomach and known to be indicated in stomach ulcers and anaemia.
- Enterobacter sp.: is regarded as a leading ‘nosocomial’ infection i.e.: contracted by hospital inpatients. This organism ‘encapsulates’ itself to enhance resistance to antibiotics + adverse gut conditions (for it to thrive). Characteristic mucous colonies reflect the presence of this bacterium.
- Candida Albicans, Yeasts + Moulds: these ‘opportunistic’ pathogens thrive when there is a disturbance in ideal gut microbiota or those with compromised immunity. They aggravate gut lining + cause the host to feel unwell due to toxins they release.
- Clostridium Difficile Infection (CDI): a spore-forming bacterium causing watery diarrhoea, pain, fever and nausea. It’s estimated 20% of this infection is associated with antibiotic or gastric acid suppressant (PPI) drug use. C. difficile can be a fatal disease if severe or left untreated.
Whilst symptoms may vary from mild to severe, all of these parasites are a common cause of diarrhoea, nausea or vomiting, abdominal pain and cramping, fatigue and malaise, bloating, headaches, malabsorption (particularly iron) – and chronic scalp hair thinning.
Important Note: returning the Gut to a state of microbial symbiosis is a multi-step process. Parasite or pathogen overgrowth numbers are regarded as a “marker for gut dysbiosis” (Lee: 2007). Parasites such as Blastocystis or D. Fragilis numbers usually rise when normal gut flora numbers (particularly Bifidobacterium + Lactobacilli) are of low levels, so just seeking to eradicate the parasites without rebuilding the microbiota to ‘push back’ against pathogen numbers will usually results in a return to dysbiosis.
Introducing and maintaining a ‘gut-friendly’ diet high in soluble fibre, vegetables, moderate fruit consumption, and minimise processed foods and hydrogenated fats (trans fatty acids) will aid in optimising good gut microbiota.
- Pancreatic Exocrine Insufficiency – is the term used to describe an under-production of pancreatic enzymes (notably amylase, protease and the various lipases) that are responsible for the break-down of proteins and carbohydrates so they can utilised by the body. This metabolic dysfunction has implications for hair follicle ‘nutrient availability’. Hair is 98% (matrix) protein and grows continuously – so it requires a constant supply. However as a non-essential tissue in nutrient-metabolic-hormonal terms the hair follicle largely receives last supply.
- Intestinal Permeability (‘Leaky Gut Syndrome’) –The small intestine has somewhat enigmatic dual functions in that it’s both an organ of digestion and absorption, with a vital mucosal protection barrier against pathogens (bacteria and parasites), endotoxins and other toxic substances. There is evidence the Gut performs an essential stress-response role when the body undergoes surgery (Wilmore et al: 1988).
Damage to the Gut’s mucosal lining (small and large intestinal tract) is consistently and concurrently found in patients with the following pre-existing conditions:
- Food allergy or sensitivity (including alcohol dependence)
- ‘Irritable’ or inflammatory bowel syndrome; Coeliac and Crohn’s disease or ulcerative colitis.
- Autism; autoimmune thyroiditis – of which scalp hair loss in a primary symptom.
- Inflammatory joint disease; eczema, psoriasis or severe cystic acne (inflammatory skin conditions)
- Exposure to toxic drugs (such as NSAIDs), or gut dysbiosis caused by pathogen infestation or infection (parasites, yeasts/moulds or bacteria).
- Under-producing stomach acid or pancreatic enzymes causing functional dysbiosis.
It’s immediately apparent that most inflammatory disease increases the risk of intestinal permeability (I/P) incompetence, however it appears I/P incompetence is the pre-cursor to developing the inflammatory disease rather than the other way round.
- Disturbance of the Gut’s functioning:
Problems with one’s Gut is usually long apparent to the sufferer before any practitioner suggests testing.
Orthodox medicine tends to assess the Gut via colonoscopy and/or endoscopy procedures. These are essential investigative measures without question, and much is gained by visual inspection of the intestinal walls, clearing of polyps or biopsy to confirm Coeliac Disease, Crohn’s Disease, Diverticulitis, Ulcerative Colitis or bowel malignancy.
Gastroenterologists consider microscopic histopathology and visually assess intestinal wall integrity – but rarely is any evaluation of gut functioning (through testing) considered.
All of the above conditions will tend to adversely affect health due the maldigestion, malabsorption or blood loss (in Ulcerative Colitis). Follicle hair growth is consistently one of first areas to reflect reduced nutrient absorption.
Evaluating actual Gut function is achieved by faecal sampling:
- Complete Digestive Stool Analysis (CDSA)* which assesses total gut function including protein, carbohydrate and fat malabsorption, pancreatic enzyme adequacy, faecal pH, microbiota balance or the presence of excessive pathogen/parasite numbers.
- Faecal PCR** which only indicates the pathogen or parasitic activity in the Gut (and no other causes for dysbiosis).
The most relevant markers of interest for practitioner are:
- Faecal pH: pH is a vital biochemical parameter to consider because out-of-range pH may indicate maldigestion/malabsorption, poor diet or general Gut dysbiosis. The reference range for faecal pH is 6-7.2 to optimally absorb nutrients. A low (acidic) pH may indicate an elevated (n)–Butyrate, whereas a high pH reflects diminished (n)-Butyrate and/or a ‘putrefactive’ gut resulting in increased ammonia levels (smelt on the breath)
- Valeric acid (Valerate): is an absorption marker for undigested proteins. This is most significant to follicle hair growth and hair shaft integrity as hair is 98% matrix protein, but as a non-essential tissue in nutrient resource terms receives last supply after skin and muscle repair. Protein starved hair shafts are thin, dry and prone to fracturing***
- Butyric Acid: Butyric acid (aka Butanoic acid) is an essential short-chain fatty acid, with Butyrate being the measurement of Butyric acid percentages. (N)-Butyrate reflects the total amount of Butyric acid and the marker for carbohydrate metabolism, and measures the UNDIGESTED portion of Carbohydrate intake. Butyric anion is readily absorbed by enteric cells and used as a preferred source of energy for the colonic epithelium (Zaleski et al: 2013). Decreased (n)-Butyrate is known to linked to colon malignancy (Healthscope Functional Pathology: 2015. Elevated (n)-Butyrate suggests excess dietary carbohydrate intake or over-compensation, or Amylase deficiency****.
- ‘Starch’ cells: is a marker for Amylase deficiency and indicates pancreatic exocrine insufficiency, i.e.: the under-production of pancreatic enzymes. Elevated Starch Cells are generally found in 1:10 patients tested.
- Fat Globules (Total Fat): a marker for fat malabsorption termed: Mal-absorption of one’s dietary fats often indicate Vitamin D malabsorption and pancreatic exocrine insufficiency – particularly the Lipases (Chan: 2017; Lee: 2007). Odorous, pale stools that are difficult to ‘flush’ characterise fat malabsorption.
- Faecal Cholesterol (+ Triglycerides): Faecal cholesterol is derived from both dietary sources and mucosal epithelial cell breakdown. Faecal cholesterol levels tend to remain constant despite fluctuating dietary intake. Elevated cholesterol may indicate malabsorption or increased mucosal epithelial cell mitosis. Elevated triglycerides suggests hypochlorhydria, pancreatic exocrine or bile salts insufficiency (Australian Clinical Labs: 2017).
The importance of a well-functioning Gut on overall well-being cannot be understated. This particularly applies to (scalp) follicle hair growth due its metabolically-active status*****. The hair follicle as a vehicle for continuous hair production, requires a consistent, stable environment of nutrient, metabolic and hormonal support, as well as constant body homeostasis.
Illness, fevers, extreme emotional stress, blood loss, surgery, vomiting, diarrhoea or chronic constipation can all adversely impact and potentially interfere with follicle anagen (growth) cycles.
Copyright – Anthony Pearce 2017 (Revised July 2018)
* Complete Digestive Stool Analysis (CDSA) is one company’s name for assessing Gut function via faecal testing.
** Faecal PCR: I use this test to assess for pathogens or parasites interfering with iron absorption and/or causing iron deficiency anaemia.
***’Split ends’, Trichorrhexis nodosa – the most common hair shaft defect where the shaft fractures and breaks away. The hair shaft cuticle is a resilient keratin that may be degraded by poor quality or insufficient protein supply.
****’Malabsorption Carbohydrate Syndrome’ – a common condition associated with Amylase insufficiency in Cystic Fibrosis sufferers (Lee: 2007).
*****Hair growth is considered the 3rd most metabolically-active cell reproduction process in the human body.