Dr Dingle's Blog / gut

Fasting reverses Type 2 diabetes

Fasting reverses Type 2 diabetes

Despite what we are often told the overwhelming evidence shows that Type 2 diabetes is a diet and lifestyle illness. It also shows that when you reverse the conditions that caused it the disease is also reversible.

Type 2 diabetes (T2D) is a chronic disease closely linked to the epidemic of obesity that requires long-term medical attention to limit the development of its wide range of complications. Many of these complications arise from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. Approximately 10% of the population of the USA and Canada have a diagnosis of T2D, and the morbidity and mortality rates associated with it are fairly high. The economic burden of T2D in the USA is $245 billion and around $20 billion in Australia.

This case documents three patients referred to the Intensive Dietary Management clinic in Toronto, Canada, for insulin-dependent type 2 diabetes. It demonstrates the effectiveness of therapeutic fasting to reverse their insulin resistance, resulting in cessation of insulin therapy while maintaining control of their blood sugars. In addition, these patients were also able to lose significant amounts of body weight, reduce their waist circumference and also reduce their glycated haemoglobin level.

These three cases exemplify that therapeutic fasting may reduce insulin requirements in T2D. Given the rising cost of insulin, patients may potentially save significant money. Further, the reduced need for syringes and blood glucose monitoring may reduce patient discomfort.

Therapeutic fasting has the potential to fill this gap in diabetes care by providing similar intensive caloric restriction and hormonal benefits as bariatric surgery without the invasive and dangerous surgery. During fasting periods, patients are allowed to drink unlimited amounts of very low-calorie fluids such as water, coffee, tea and bone broth. A general multivitamin supplement is encouraged to provide adequate micronutrients. Precise fasting schedules vary depending primarily on the patient’s preference, ranging from 16 hours to several days. On eating days, patients are encouraged to eat a diet low in sugar and refined carbohydrates, which decreases blood glucose and insulin secretion.

This means that patients with T2D can reverse their diseases without the worry of side effects and financial burden of many pharmaceuticals, as well as the unknown long-term risks and uncertainty of surgery, all by means of therapeutic fasting.

 

Source http://casereports.bmj.com/content/2018/bcr-2017-221854.full

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Sugar. Sweet poison for the gut.

Sugar. Sweet poison for the gut.

The incidence of diseases associated with a high-sugar diet has increased in the past years and numerous studies have focused on the effects of high sugar intake on the gut microbiota and its role in obesity, metabolic syndrome, CVD, cancer and other chronic inflammatory diseases.[1] But not all sugars are equal, as a fructose-rich diet appears to be more damaging to the intestinal microbiome than a sucrose-rich diet, which tends to increase weight gain.[2]

Fructose is not absorbed into the small intestine but passed through to the large intestine, where it comes into contact with the microbiome to alter species diversity.[3] Even a small dose of fructose, 0.1% (around 1g /kg), which is found in most modern foods, overwhelms the ability of the small intestine to absorb and clear it, resulting in fructose reaching the large intestine microbiome. However, the microbiome is not designed to process sugar and, as a result, can lead to dysbiosis even when the sugar is added to a normal diet.[4] Microbial diversity significantly decreases, as well as the number of commensal bacteria[5] when consuming a sugar diet—even after one week.[6] Chronic intake of fructose is associated with intestinal inflammation, leaky gut and elevated movement of toxins and other microbial products across the gut wall.[7] Fructose also worsens symptoms in irritable bowel syndrome (IBS);[8] 64% of patients suffering from IBS were not able to absorb fructose properly.[9]

Animal studies show increased liver problems when mice are fed a high-fructose diet[10] and multiple human studies have established that fructose contributes to the progression of NAFLD (non-alcoholic fatty liver disease) by modulating intestinal microbiota. In animal studies, a diet enriched with fructose not only induced NAFLD but also negatively affected the gut barrier and the microbiota, leading to dysbiosis, increased inflammation and oxidation and degrading of the mucosa barrier.[11] The liver is the first organ exposed to gut-derived toxins, receiving 70% of the blood supply from the intestine. So, the liver acts as a first line of defence against bacterial pathogens and toxins. The gut microflora has been shown to stimulate deposits of liver fat contributing to NAFLD.[12] Conversely, supplementation with probiotics and prebiotics has been shown to improve the outcome of NAFLD.[13] The form fructose comes in, whether liquid or solid, has different impacts on the gut microbiota and the integrity of the gut wall.[14]

 

[1] Lambertz et al., 2017.

[2] Volynets et al., 2017.

[3] Jang et al., 2018.

[4] Ferrere et al., 2016.

[5] Zhang et al., 2017.

[6] Sen et al., 2017.

[7] Rosas-Villegas et al., 2017; Lambertz et al., 2017; Volynets et al., 2017.

[8] Melchior et al., 2014.

[9] Goebel-Stengel et al., 2014.

[10] Ferrere et al., 2016.

[11] Jegatheesan et al., 2016; Lambertz et al., 2017.

[12] Mouzaki et al., 2012.

[13] Lambertz et al., 2017.

[14] Mastrocola et al., 2018.

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Sugar. Sweet poison for the gut.

Sugar. Sweet poison for the gut.

The incidence of diseases associated with a high-sugar diet has increased in the past years and numerous studies have focused on the effects of high sugar intake on the gut microbiota and its role in obesity, metabolic syndrome, CVD, cancer and other chronic inflammatory diseases.[1] But not all sugars are equal, as a fructose-rich diet appears to be more damaging to the intestinal microbiome than a sucrose-rich diet, which tends to increase weight gain.[2]

Fructose is not absorbed into the small intestine but passed through to the large intestine, where it comes into contact with the microbiome to alter species diversity.[3] Even a small dose of fructose, 0.1% (around 1g /kg), which is found in most modern foods, overwhelms the ability of the small intestine to absorb and clear it, resulting in fructose reaching the large intestine microbiome. However, the microbiome is not designed to process sugar and, as a result, can lead to dysbiosis even when the sugar is added to a normal diet.[4] Microbial diversity significantly decreases, as well as the number of commensal bacteria[5] when consuming a sugar diet—even after one week.[6] Chronic intake of fructose is associated with intestinal inflammation, leaky gut and elevated movement of toxins and other microbial products across the gut wall.[7] Fructose also worsens symptoms in irritable bowel syndrome (IBS);[8] 64% of patients suffering from IBS were not able to absorb fructose properly.[9]

Animal studies show increased liver problems when mice are fed a high-fructose diet[10] and multiple human studies have established that fructose contributes to the progression of NAFLD (non-alcoholic fatty liver disease) by modulating intestinal microbiota. In animal studies, a diet enriched with fructose not only induced NAFLD but also negatively affected the gut barrier and the microbiota, leading to dysbiosis, increased inflammation and oxidation and degrading of the mucosa barrier.[11] The liver is the first organ exposed to gut-derived toxins, receiving 70% of the blood supply from the intestine. So, the liver acts as a first line of defence against bacterial pathogens and toxins. The gut microflora has been shown to stimulate deposits of liver fat contributing to NAFLD.[12] Conversely, supplementation with probiotics and prebiotics has been shown to improve the outcome of NAFLD.[13] The form fructose comes in, whether liquid or solid, has different impacts on the gut microbiota and the integrity of the gut wall.[14]

 

[1] Lambertz et al., 2017.

[2] Volynets et al., 2017.

[3] Jang et al., 2018.

[4] Ferrere et al., 2016.

[5] Zhang et al., 2017.

[6] Sen et al., 2017.

[7] Rosas-Villegas et al., 2017; Lambertz et al., 2017; Volynets et al., 2017.

[8] Melchior et al., 2014.

[9] Goebel-Stengel et al., 2014.

[10] Ferrere et al., 2016.

[11] Jegatheesan et al., 2016; Lambertz et al., 2017.

[12] Mouzaki et al., 2012.

[13] Lambertz et al., 2017.

[14] Mastrocola et al., 2018.

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A short time between eating your last meal and sleep can increase your risk of breast and prostate cancer.

A short time between eating your last meal and sleep can increase your risk of breast and prostate cancer.

Our modern life involves irregular sleeping and eating patterns that are associated with adverse health effects. Studies have shown late eating habits and short periods between sleep and eating are associated with metabolic syndrome, weight gain and altering the gut microbiome and gut health.
 
This study of breast and prostate cancer patients and their controls in Spain found those sleeping two or more hours after supper had a 20% reduction in cancer risk for breast and prostate cancer combined and in each cancer individually. A similar protection was observed in subjects having supper before 9 pm compared with supper after 10 pm.
The effect of longer breaks between eating and sleep was more pronounced among subjects adhering to cancer prevention recommendations and in morning types.
Adherence to diurnal eating patterns and specifically a long interval between last meal and sleep are associated with a lower cancer risk, stressing the importance of evaluating timing in studies on diet and cancer.
 
source
https://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.31649
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Gut Health and our Stomach pH.

Gut Health and our Stomach pH.

One of the most important factors in regulating our gut health, digestion and controlling our microbiome is the pH or acid level.

While often mentioned in terms of the stomach, the pH has a controlling role to play in the health of the entire GI tract from the mouth to the anus; changes in the “normal” pH anywhere in the gut can have major implications on the rest of the GI tract. The pH scale goes from 1, being very acidic, to 14, being very alkaline. The level in our blood and tissues should be constantly around 7.36, neutral, and the level in our GI tract varies from 1 to 8. We cover this a lot more in our book Overcoming Illness, which focuses on the role of inflammation, oxidation and acidosis in illness.

After initial breakdown by chewing, food is churned by the smooth muscles of the stomach and is broken down by hydrochloric acid and stomach juices (enzymes). The pH of the stomach is highly acidic, around 1.5 (1.0 to 2.5) due to the hydrochloric acid that helps to kill harmful micro-organisms, denature protein for digestion, and help create favourable conditions for the enzymes in the stomach juices, such as pepsinogen.[1] Not to mention sending messages along the GI tract that everything is working well in the stomach. If the pH is too high, say 3 or 4 (low acidity and more alkaline), then the system does not work and you end up with poor gut health, digestive and health complications. For example, premature infants have less acidic stomachs (pH more than 4) and as a result are susceptible to increased gut infections.[2] Similarly, the elderly show relatively low stomach acidity and a large number of people, more than 30%, over the age of 60 have very little or no hydrochloric acid in their stomachs.[3]

Similarly, in gastric bypass weight loss surgery, roughly 60% of the stomach is removed. A consequence of this procedure is an increase in gastric pH levels that range from 5.7 to 6.8 (not 1.5) making it more alkaline and, as a result, more likely to experience microbial overgrowth.[4] We see similar patterns in other clinical cases such as acid reflux in which treatment involves the use of proton-pump inhibitors[5] and celiac disease[6] where delayed gastric emptying is associated with reduced acidity and increased disease.

Unfortunately, acid reflux is often wrongly treated as a condition that involves the production of too much acid. It is, in fact, the stomach finding it difficult to digest the foods, most commonly as a result of not having enough acid to complete digestion. Medications (see my other posts) which further reduce stomach acid have serious and sometimes deadly side effects on health, the digestive process and the gut microbiota. Acid reflux affects about 20% of the adult population and is much higher in older people, which is consistent with studies showing lower stomach acid as we age.

 

[1] Adbi 1976; Martinsen et al., 2005.

[2] Carrion and Egan, 1990.

[3] Husebye et al., 1992.

[4] Machado et al., 2008.

[5] Amir et al., 2013.

[6] Usai et al., 1995.

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Antibiotics and “The War on Bacteria”

Antibiotics and “The War on Bacteria”

While antibiotics have been lifesaving, the over-prescription of antibiotics has sparked the evolution of drug-resistant strains of life threatening bacteria, resulting in tens of thousands of deaths each year.[1] The US Centers for Disease Control estimate that up to 50% of antibiotics prescribed in the US are unnecessary.[2] Unfortunately, the use of antibiotics is often prescribed for those groups who are more vulnerable to dysbiosis, including infants born via C-section[3] and in those born preterm, compared to term infants born vaginally,[4] potentially compounding the problems. Micro-organisms such as bacteria, fungi, viruses, and parasites cause many of the world’s diseases, yet only bacterial infections are usually susceptible to treatment with commonly prescribed antibiotics.

However, more subtle side effects of antibiotics on the gut microbiome are only just beginning to be discovered. Broad-spectrum antibiotics can impact up to 30% of the bacteria among the human microbiota, resulting in severe loss of species and function[5] and begins immediately following antibiotic administration. The effects can sometimes last for years after its cessation,[6] and may also lead to the total extinction of some beneficial microbial species. As few as three days of treatment with the most commonly prescribed antibiotics can result in sustained reductions in microbiota diversity.[7] A typical two-week course of high-dose antibiotic treatment, as might be used for an ear infection, can wipe out most of the beneficial gut microbes.

These antibiotic-induced changes in the microbiota have been linked to many disease states including increased infections, metabolic disturbances, obesity, autoimmunity,[8] and mental health conditions. Common outcomes of antibiotics the antibiotic-disturbed gut microbiota are diarrhea and infections with Clostridium difficile,[9] particularly in infants.[10]

Early life exposure to antibiotics presents the greatest risk of long-term damage to the gut microbiota and the more you take, the worse it is.[11] In young children, antibiotics may change the development of the “adult” microbiota, and not allow its normal maturation.[12] It has also been hypothesized to cause a delay in microbial maturation from six to 12 months after birth.[13] Early life exposure is also associated with numerous diseases later in life including IBD,[14] obesity,[15] and asthma, as well as the development of immune-mediated[16] metabolic and neurological diseases.[17]

In a meta-analysis of eight studies including 12,082 subjects, antibiotic use in the first year of life was significantly associated with two-fold (200%) increased chance of the child having asthma.[18] One study reported the use of antibiotics in newborns increased the risk of developing asthma by 24 times. Probiotics during the neonatal period were protective and reduced the risk by as much as 86% for childhood asthma for kids at risk.[19] Studies of mice treated with antibiotics in early life revealed altered microbial populations within the gut microbiota and consequently increased the susceptibility of these mice to asthma.[20]

Antibiotic use has also been shown to have long-term effects on brain neurochemistry and behavior. Such use is known to alter the intestinal microbiome with subsequent changes in microbiota to gut-brain axis[21] and result in poorer neuro-cognitive outcomes later in life.[22]

Even treatment with a single antibiotic course was associated with a 25% higher risk for depression and the risk increased with recurrent antibiotic exposures to 40% for two to five courses and 56% for more than five courses of antibiotics. The higher the rates of antibiotic use, the higher the rates of depression.[23] Animal studies have shown that high doses of a cocktail of antibiotics induced lasting changes in gut microbiota associated with behavioural alterations.[24]

Animal studies of early life exposure to antibiotics show lasting immune and metabolic consequences.[25] Administration of low doses of penicillin to mice early in life increases the risk of weight gain and obesity and promotes lipid accumulation by altering the gut microbiota.[26] Mice treated continuously with low-dose penicillin from one week before birth until weaning exhibited higher body weight and fat mass in adulthood, although the microbial structure returned to normal after four weeks of antibiotics cessation.[27] There is also evidence of antibiotics playing a role in the development of IBD in children[28] and that antibiotic usage during the first year of life was more common in those diagnosed with IBD later in life.[29]

Antibiotics and pregnancy

In human studies, mother’s use of antibiotics during pregnancy is consistently associated with cow’s milk allergy,[30] wheeze, asthma,[31] and atopic dermatitis,[32] with the strongest association for antibiotic use in the third trimester of pregnancy.[33] A study of 306 children with asthma showed that mother’s use of antibiotics during pregnancy increased the risk by a whopping four times (390%).[34] Low-dose penicillin in late pregnancy and early postnatal life in the offspring of mice resulted in lasting effects on gut microbiota, increased brain inflammation, and resulted in anxiety-like behaviours and displays of aggression.[35] Similar results have been shown for antibiotic exposure through breastfeeding.[36]

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[1] Fleming-Dutra et al., 2016.

[2] Fleming-Dutra et al., 2016.

[3] Penders et al., 2006.

[4] Forsgren et al., 2017.

[5] Francino, 2016.

[6] Jakobsson et al., 2010.

[7] Shira et al., 2016.

[8] Francino, 2016.

[9] Ng et al., 2013.

[10] Rousseau et al., 2011.

[11] Fouhy et al., 2012; Tanaka et al., 2009.

[12] Bokulich et al., 2016.

[13] Ibid, 2016.

[14] Hviid et al., 2011.

[15] Azad et al., 2014.

[16] Metsälä et al., 2013.

[17] Arrieta et al., 2014.

[18] Marra et al., 2006.

[19] Zhang et al., 2017.

[20] Russell et al., 2012.

[21] Rogers et al., 2016; Tochitani et al., 2016.

[22] Russell et al., 2013.

[23] Lurie et al., 2015.

[24] Bercik, P. et al., 2011; Desbonnet, L. et al., 2015; Fröhlich, E. E. et al., 2016; Wang, T. et al., 2015.

[25] Russell et al., 2013; Cox et al., 2014.

[26] Cox et al., 2014.

[27] Ibid, 2014.

[28] Shaw et al., 2010;  Ortqvist et al., 2017.

[29] Shaw et al., 2010.

[30] Chu et al., 2015.

[31] Stensballe et al., 2013; Kashanian et al., 2017; Mulder et al., 2016; Murk et al., 2011.

[32] Timm et al., 2017.

[33] Zhao et al., 2015; Wang et al., 2017.

[34] Zhang et al., 2017.

[35] Leclercq et al., 2017.

[36] Kummeling et al., 2007.

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Proton pump inhibitors (PPIs) and increased illness

Proton pump inhibitors (PPIs) and increased illness

The human stomach, when healthy, is not a suitable host for micro-organisms, but in pathological conditions such as gastritis, when gastric acid secretion is impaired, microbial overgrowth can be observed. The use of gastric acid suppression drugs has been shown to have profound effects on the microbiome.[1] Acid-blocking drugs, or proton pump inhibitors (PPIs) used for gastroesophageal reflux disease (GERD) to reduce gastric acid secretion, are among the most commonly prescribed medications in the world with approximately 6%–15% of the general population receiving acid suppression therapy.[2] Once initiated, they are often used for long periods of time without question,[3] despite the guidelines saying “for short term use only.”

PPIs increase the stomach pH to make it less acidic,[4] which is what they are designed to do, and as a result, change the composition of the intestinal microbiota[5] and impact the pH of the rest of the gut. They are associated with a decrease in small bowel beneficial Bifidobacteria and increase in the toxic gram-negative bacteria, as well as being associated with a significant decline in microbial diversity within seven days of beginning therapy.[6]

PPIs dramatically increase the risk of stomach bacterial overgrowth (SBO) and small intestinal bacterial overgrowth (SIBO), with increased risk of these bacteria getting into the blood[7] and the potentially fatal infection, Clostridium difficile.[8] Bifidobacteriaceae, important and beneficial bacteria of human gastrointestinal microbiota, can over-colonise the stomach of people with low stomach acid. Bifidobacteriaceae species, typically found in the oral cavity, readily colonise the low acid stomach[9] and become good bacteria but in the wrong place as a result of altered pH.

Proton pump inhibitors also promote progression of both alcoholic and non-alcoholic fatty liver disease in mice and contribute to the increasing incidence of chronic liver disease as a result of dysbiosis.[10] The list of side effects for PPIs is extensive, serious and even life-threatening and they are all mediated through the gut.

A growing number of studies are showing connections between autoimmune conditions linked with dysbiosis, including antibiotics and the use of protein pump inhibitors (PPIs) in controlling gastric reflux.[11] The use of PPIs can potentially create far greater problems in the long run.

 

[1] Krezalek et al., 2016; Mackenzie et al., 2017.

[2] Johansen et al., 2014.

[3] Reimer and Bytzer, 2009.

[4] O’May et al., 2005.

[5] Bajaj et al., 2014; Imhann et al., 2016; Jackson et al., 2016.

[6] Seto et al., 2014; Wallace et al., 2011.

[7] Choung et al., 2011.

[8] Lo and Chan, 2013; Janarthanan et al., 2012.

[9] Mattarelli, 2014.

[10] Llorente et al., 2017; Reveles et al., 2017.

[11] Andresson et al., 2016.

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Stress linked to weight gain and diabetes type 2.

Stress linked to weight gain and diabetes type 2.

Another study shows that the stress around you increases your risk of putting on weight, increases your risk of diabetes2 and reducing the stress helps with weight loss. The stress this time was living in a poorer environment. But many studies have shown multiple forms of stress works the same way.

Persistently elevated cortisol levels have been closely tied to weight gain, increased abdominal fat, and other aspects of metabolic syndrome, a collection of things that includes obesity and pre-diabetes.

When cortisol is released in response to stress, it signals the body to shift energy production into overdrive. It’s a signal for organs and various tissues in the body to accelerate production of glucose, the sugar that fuels our muscles, by breaking down carbohydrates and protein. As part of its role in freeing up energy, chronic exposure to cortisol also increases cravings for high-sugar, high-fat foods, and increases the body’s resistance to insulin, the hormone that signals the body’s cells to absorb sugar.

In support of this in mice, stress increases cravings for energy-dense foods; in people, comfort- or stress-eating is a familiar phenomenon.

in addition consistent exposure to cortisol may re-wire the brain, for example, shrinking the pre-frontal cortex and bulking up the amygdala. Over time cortisol can increase the risk for depression and mental illness.

 

http://nautil.us/issue/61/coordinates/why-living-in-a-poor-neighborhood-can-change-your-biology-rp?utm_source=EHN&utm_campaign=13e26bbadf-Science_saturday&utm_medium=email&utm_term=0_8573f35474-13e26bbadf-99011233

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Gut Dysbiosis. A dysfunctional gut microbiome

Gut Dysbiosis. A dysfunctional gut microbiome

While we have an idea on what a healthy gut looks like we are also aware of what constitutes a dysfunctional gut that contributes to adverse health. This condition is called “Dysbiosis” where the microorganisms in the gut including the bacteria do not live in mutual accord, when the “good”, microorganisms are not successfully controlling the “bad” ones or disturbing the balance between “protective” versus “harmful” intestinal microorganisms.[1] It can also mean where an overgrowth of “pathobionts,” i.e., normally good bacteria[2], could negatively affect important functions of the microbiome ecosystem. Even lactobacillus in high concentrations are good for the large intestine and urogenital tracts of females but becomes a pathobiant if there are too many of them in the stomach (SBO) or small intestine where an overgrowth is linked with Small Intestinal Bacterial Overgrowth (SIBO). So even the so called “good bacteria” can become problematic and lead to dysbiosis if they are out of balance or in the wrong place.

The most important aspect of dysbiosis is that a loss of total microbial diversity which represents the first link in the chain of events leading to the development of local and body wide inflammation. Multiple human conditions have been associated with dysbiosis, including autoimmune and auto inflammatory disorders, such as allergies, cardio vascular, metabolic disorders (diabetes, obesity and non-alcoholic fatty liver disease), various cancers and inflammatory bowel disease such as Crohn's and ulcerative colitis (UC)[3], celiac disease[4], and neurological disorders including autism[5].

Once inflammation starts it appears that these opportunistic microorganisms are able to exploit the inflamed environment and expand their numbers[6] to become an even bigger problem.

There appear to be three types of dysbiosis that more often than not, occur together to create the problem. These include (i) loss of beneficial microbial organisms perhaps through the use of antibiotics, (ii) expansion of pathobionts or potentially harmful microorganisms as a result of too much processed foods and (iii) loss of overall microbial diversity. It is likely that dysbiosis encompasses all three of these manifestations at the same time to influence disease.[7]

The challenge is that the Dysbiotic microbial ecosystem can become resilient over time and may become hard to alter. In one study while dieting rapidly reversed the metabolic problems associated with a high fat diet, the dysbiosis in mice after a 4-week high fat diet persisted up to 21 weeks after returning to normal chow diet.[8] It did however change after 21 weeks.

 

[1] Milani et al., 2016.

[2] Chow et al., 2011.

[3] Baumler and Sperandio, 2016.

[4] Del Chierico et al., 2012.

[5] Konig et al., 2016.

[6] Spees et al., 2013.

[7] Petersen and Round, 2014.

[8] Thaiss et al., 2016.

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Gut health, gut integrity and your health

Gut health, gut integrity and your health

The integrity of our gut and our gut health is so important to our health but has largely been ignored until recently. The mucous membrane absorbs and assimilates foods and serves as a barrier to pathogens and other toxic substances. When this integrity is compromised the permeability of the gut may be altered, gut function erodes and we end up with many health conditions associated with inflammation and leaky gut.

The gut lining is composed of close fitting, thin cells separated by tight junctures, like a thin protein mortar. When the barrier is disrupted the intestines permeability increases allowing larger particles, bacteria, undigested foods or toxins to cross the barrier. This intestinal permeability, called leaky Gut, is linked with virtually all the gut related disorders including ulcerative colitis, Crohn’s disease, celiacs disease, and auto immune conditions including inflammatory joint disease, ankylosing spondylitis, juvenile onset arthritis, psoriatic arthritis, diabetes mellitus type one and primary biliary cirrhosis.

To maintain integrity and normal function of intestine, a delicate equilibrium must be reached between the microbiota and intestinal immune system.[1] In a healthy body the immune system protects us against invasion and controls the commensal microorganisms. In return the beneficial bacteria provide essential nutrients to the gut cells and promote healthy immune responses in the gut.

A healthy microbiome contributes to the maintenance of intestinal epithelium barrier integrity maintaining the tight junctures, promoting intestinal cell repair, and even ensuring a healthy rate of cell turnover. It does this by maintenance of local cell nutrition and circulation and protection against pathogenic microorganisms.

Unlike most other cells in the body that get their energy and nutrients from the blood supply, more than 50% of the energy needs of the small intestine and more than 80% of the energy of the large intestines (where most of our microbiome is) comes directly from the food in the gut. This is not just a one off but with each turning over of gut cells which is over a period of just days, the barrier has to be continually re-established. The end result of this mutually beneficial co-habitation is a symbiotic relationship between the two partners, us and our microbiome. Any change in the relative proportions of the different bacteria alters the subsequent nutrients available and maintenance and protection for the digestive tract. If the right food and conditions are not there for a healthy microbiome then the nutrients are not available for the gut wall and the cells are damaged leading to damage to the integrity of the gut wall and leaky gut. This highlights the importance of eating the right foods for the microbiome to do their job and to maintain optimal gut health.

[1] Magalhaes et al., 2007.

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