Dr Dingle's Blog / gut

Roundup is a gut poison

Roundup is a gut poison

Glyphosate is an active ingredient of the most widely used herbicide Roundup. Human exposure to glyphosate among the participants has increased by 500 percent in the past two decades. In the years of 1993-1996, only 12 percent of participants had detectable levels of glyphosate in their urine. By 2013-2016, this number increased to 70 percent. The researchers also found a thirteen-times increase in glyphosate concentrations between the two collection periods.

Although glyphosate was designed to kill weeds, it also kills susceptible bacteria that have biochemical pathways similar to plants and weeds. Glyphosate impacts the intestinal microbiome through the residues from spraying, since glyphosate was shown to have negative effects on the composition of the intestinal flora of glyphosate from contaminated food. Even at incredibly low environmental concentrations (0.1 ppb) glyphosate had an impact on rat gut microbiome composition. In particular, it lowered the diversity of many of the beneficial microorganisms in experimental rats which enabled the proliferation of opportunistic E. Coli strains. These gut microbiome disturbances showed a substantial overlap with those associated with liver dysfunction in other studies. Several studies have also proposed that it may be a cause of autism through its impact on the gut microbiota.

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Probiotics can reduce pain

Probiotics can reduce pain

Treatments for obesity have been shown to reduce pain secondary to weight loss. Intestinal microbiota has been shown to influence obesity and pain sensitivity.
Physiological pain plays a life-essential protective role, while acute or chronic pathological pain indicates a medical problem that needs treatment and imposes a medical challenge. Neurotransmitters, immune cells, and hormones have been demonstrated to contribute in pathogenesis of chronic pain.
Pain threshold is influenced by several factors, including obesity, which alters adipose tissue metabolic and endocrine functions leading to alterations in systemic physiology including an increased release of fatty acids, hormones, and proinflammatory molecules that contribute to obesity associated complications. Studies have demonstrated that obese humans and rats are more sensitive to pain stimuli than normal weighted ones.
Previous studies have demonstrated a relationship between intestinal microbiota and diseases including pain disorders with probiotics having a positive effect.
In this study the mice taking probiotics had a significantly lower sensitivity to mechanical stimulation compared to their corresponding control. The results of this study suggest a protective effect of probiotics on nociception circuits, which propose a direct result of the weight reduction or an indirect result of anti-inflammatory properties of the probiotics.

source

Potential Nociceptive Regulatory Effect of Probiotic Lactobacillus rhamnosus PB01 (DSM 14870) on Mechanical Sensitivity in Diet-Induced Obesity Model

https://www.hindawi.com/journals/prm/2016/5080438/

 

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Mothers milk mycobiome (fungi) - not microbiome

Mothers milk mycobiome (fungi) - not microbiome

Compared to bacterial communities, the human gut mycobiome (fungi) is low in diversity and dominated by yeast including Saccharomyces, Malassezia, and Candida.Studies show they also vary substantially over time and even mice in the same or different cages in the same facility receiving the same feed and treatment also varied in their dominant fungal lineage. Similar results have been shown with humans.

During the last years, human breast milk has been documented as a potential source of bacteria for the newborn. Recently, we have reported the presence of fungi in breast milk from healthy mothers. It is well-known that environmental and perinatal factors could affect milk bacteria; however, the impact on milk fungi is still unknown.

Recent studies report the presence of fungal species in breast milk of healthy mothers, suggesting a potential role on infant mycobiome development. In the present work, we aimed to determine whether the healthy human breast milk mycobiota is influenced by geographical location and mode of delivery, as well as investigate its interaction with bacterial profiles in the same samples. A total of 80 mature breast milk samples from 4 different countries

This study found fungal communities (mycobiota) in breast milk samples across different geographic locations and the influence of mode of delivery. They identified a core of four genera shared across locations, constituted by Malassezia, Davidiella, Sistotrema and Penicillium which have been reported to be present in the infant gut. Our data confirm the presence of fungi in breastmilk across continents and support the potential role of breast milk on the initial seeding of fungal species to the infant gut.

Analysis of bacteria and fungi showed complex interactions that were influenced by geographical location, mode of delivery, maternal age and pre-gestational Body Mass Index. The presence of a breast milk mycobiome was confirmed in all the samples analysed, regardless of the geographic origin.

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Mothers milk mycobiome (fungi) - not microbiome

Mothers milk mycobiome (fungi) - not microbiome

Compared to bacterial communities, the human gut mycobiome (fungi) is low in diversity and dominated by yeast including Saccharomyces, Malassezia, and Candida.Studies show they also vary substantially over time and even mice in the same or different cages in the same facility receiving the same feed and treatment also varied in their dominant fungal lineage. Similar results have been shown with humans.

During the last years, human breast milk has been documented as a potential source of bacteria for the newborn. Recently, we have reported the presence of fungi in breast milk from healthy mothers. It is well-known that environmental and perinatal factors could affect milk bacteria; however, the impact on milk fungi is still unknown.

Recent studies report the presence of fungal species in breast milk of healthy mothers, suggesting a potential role on infant mycobiome development. In the present work, we aimed to determine whether the healthy human breast milk mycobiota is influenced by geographical location and mode of delivery, as well as investigate its interaction with bacterial profiles in the same samples. A total of 80 mature breast milk samples from 4 different countries

This study found fungal communities (mycobiota) in breast milk samples across different geographic locations and the influence of mode of delivery. They identified a core of four genera shared across locations, constituted by Malassezia, Davidiella, Sistotrema and Penicillium which have been reported to be present in the infant gut. Our data confirm the presence of fungi in breastmilk across continents and support the potential role of breast milk on the initial seeding of fungal species to the infant gut.

Analysis of bacteria and fungi showed complex interactions that were influenced by geographical location, mode of delivery, maternal age and pre-gestational Body Mass Index. The presence of a breast milk mycobiome was confirmed in all the samples analysed, regardless of the geographic origin.

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Our Acid Stomach

Our Acid Stomach

The intestinal microbiome is a plastic ecosystem that is shaped by environmental and genetic factors, interacting with virtually all of our organs, tissues and cells. One of the most important factors in regulating 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 whole GI tract from the mouth to the anus and changes in the normalpH anywhere in the gut can have large 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 trace varies from 1 to 8. We cover this a lot more in our book Overcoming Illnesswhich 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 (1.0-2.5) due to the hydrochloric acid which helps to kill harmful microorganisms, denature protein for digestion, and help create favorable 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 (more alkaline) then the system does not work and you end up with 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 percent 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) to making it more alkaline and as a result are 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 which 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 not having enough acid to complete digestion and why medications (see later) which further reduce stomach acid have serious and 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 the 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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A brief history of Gut Health

A brief history of Gut Health

Research into the gut microbiome has ramped up over the past decade thanks to high investments over 100 million dollars by the US Governments in the Human Microbiome Project in 2007 as well as large sums from companies and private sources not wanting to be left behind as its importance for our health has become more widely recognised and understood by the mainstream. There is now a tsunami wave of information coming through on the gut microbiome, literally thousands of new studies and increasing each year.

Until recently the positive effects of the gut microbiome on our digestive system and health has been severely under rated. Wisdom of Chinese doctors from centuries ago, who somehow knew that the intestines were not merely a digestive organ, but the centre of health and well being. Hippocrates was recoded as saying that all illness begins in the gut. Throughout history from the Egyptians till around 80 years ago medicine and the bowels were frequently mentioned in the same sentence.

Even today the nomadic Maasai tribes in Africa attribute most illnesses to the effect of “pollutants” that block or inhibit digestion. In these communities the plants are used to cure diseases served mainly as strong purgatives and emetics; they "cleanse" the body and digestive system from polluting substances.[1] While studies of the great apes show they self-medication to control intestinal parasite infections and gut problems across Africa.[2] Chimpanzees (Pan troglodytes) for example, swallow the leaves of certain plant species whole, without chewing to aid expulsion of certain parasites. Swallowing rough or bristly leaves increases gut motility causing expulsion of adult worms, which disrupts the nematodes life cycle and likely reduces worm burdens.[3] Even carnivores first eat the guts of their kill and get all the intestinal bacteria. We seem to be the only ones who have forgotten the importance of the gut.

We now know the gut is the cornerstone of health and inflammation in the body. The first theory to explain the link between the gut and inflammation, which underlies all the chronic diseases we suffer from, was put forward in 1907, when Elie Metchnikoff proposed that tissue destruction (disease) and senescence (ageing) throughout the body were consequences of chronic systemic inflammation, which occurred as a result of increased permeability in the colon and the escape of bacteria and their products into the blood. He believed that these bacterial products activated our immune response (macrophages) and that the resulting inflammatory response caused deterioration of surrounding tissues and that this macrophage “intoxification” had systemic effects and led to deterioration of even distant tissues. And he was right.

[1] Bussmann et al., 2006.

[2] MCLennan and Huffman, 2012.

[3] Huffman and Caton, 2001.

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The healing power of raw cabbage

The healing power of raw cabbage

Another reason to add some of the cabbage family to your daily diet, preferably raw is because of their gut healing properties and how they promote gut health through the gut microbiome. The Brassica family including cabbage, broccoli, brussel sprouts, kale, arugula (rocket), bok choy, cauliflower, collard greens, radish, turnip and others have been recognized for their gut healing and gut health properties for hundreds of years and modern epidemiologic studies have shown a frequent consumption of cruciferous vegetables is associated with lower risk of cancer, especially cancers of the digestive tract, bladder, breast, prostate, and lung. However, only now are we recognizing that many of these benefits are mediated through the microbiome and that their frequent consumption alters the composition of the microbiome.

Cruciferous vegetables are a rich source of glucosinolates a precursor to the Isothiocyanates (ITC), which exhibit powerful biological functions in fighting cancers, cardiovascular, neurodegenerative diseases and gut healing. The Isothiocyanates are a by product of specific plant enzymes (myrosinase) active during chewing or crushing when broccoli is consumed raw or lightly steamed, however, like all enzymes myrosinase is deactivated by cooking and ingestion of cooked broccoli typically provides only about one tenth the amount of isothiocyanates as that from raw broccoli. So to maximize the gut healing, gut health and overall benefits of these foods they are best eaten raw or just lightly steamed.

Instead when cooked cruciferous vegetables are consumed, gut bacteria are mainly responsible for ITC production in the gut. This is highlighted after taking oral antibiotics, the ITCs availability and uptake decreases after eating cooked cruciferous vegetable. It also appears that there is considerable difference in the ability of individuals, due to individual differences in gut microbial community, to produce the isothiocyanates. Although, the gut communitys ability is altered over just 4 days. In one study feeding raw or cooked broccoli for four days or longer both changed the microbiota composition and caused a greater production of isothiocyanates. Interestingly, a three-day withdrawal from broccoli reversed the increased microbial metabolites suggesting that the microbiota requires four or more days of broccoli consumption and is reversible.

The lactic acid bacteria appear to have myrosinase-like activity and the fermented Brassica food products, such as sauerkraut and kimchi, are particularly rich in Lactobacillus, and a diet rich in Brassica may promote Lactobacillus growth in the colon.

 

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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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