Dr Dingle's Blog

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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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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Depression caused by inflammation and oxidation. Not a serotonin imbalance

Depression caused by inflammation and oxidation. Not a serotonin imbalance

Depression itself is not a disease, but a symptom of an underlying problem. A new theory called the “Immune Cytokine Model of Depression” holds that depression is a “multifaceted sign of chronic immune system activation,” inflammation. Depression may be a symptom of chronic inflammation. And a large body of research now suggests that depression is associated with a low-grade, chronic inflammatory response and is accompanied by increased oxidative stress—not a serotonin imbalance.

Researchers discovered in the early 1980s that inflammatory cytokines produce a wide variety of psychiatric and neurological symptoms that perfectly mirror the defining characteristics of depression. Cytokines have been shown to access the brain and interact with virtually every mechanism known to be involved in depression[1] including neurotransmitter metabolism, neuroendocrine function, and neural plasticity.

This is now supported by increasing lines of scientific evidence[2] including:

  • Depression is often present in acute, inflammatory illnesses.
  • Higher levels of inflammation increase the risk of developing depression.
  • Administering endotoxins that provoke inflammation in healthy people triggers classic depressive symptoms.
  • One-quarter of patients who take interferon, a medication used to treat hepatitis C that causes significant inflammation, develop major depression.
  • Up to 50% of patients who received the cytokine IFN-alpha therapy to help treat cancer or infectious diseases developed “clinically significant depression.”[3]
  • An experiment involving the administration of a Salmonella typhi vaccine to healthy individuals produced symptoms of fatigue, mental confusion, psychomotor slowing and a depressed mood.[4] These symptoms correlated with the increase in cytokine concentrations.
  • Remission of clinical depression is often associated with a normalization of inflammatory markers.
  • There is now a large body of literature regarding laboratory animals demonstrating that cytokines … can lead to a host of behavioural changes overlapping with those found in depression. These behavioral changes include decreased activity, cognitive dysfunction and altered sleep.[5]
  • All the activities associated with reducing the prevalence of depression and depression symptoms are anti-inflammatory. These include increased sunlight and time spent outside, exercise and physical activity, relaxation and meditation techniques, healthy eating as well as administering anti-inflammatory nutritionals.

There is further support from large epidemiological studies. A number of longitudinal studies have now shown that inflammation in early adulthood predicts depression at a later stage in life. In a large longitudinal study, the risk for depression and psychotic experiences in adolescence was almost two-fold higher in individuals with the highest compared to the lowest levels of inflammation as indicated by interleukin-6 (IL-6) levels in childhood. Children who were in the top third of IL-6 levels at the age of 9 years were 55% more likely to be diagnosed with depression at the age of 18 than those with the lowest childhood levels of IL-6. Children in the highest level of IL-6 levels at the age of 9 were also 81% more likely to report psychotic experiences at the age of 18.[6] A study of more than 73,000 men and women showed increasing inflammation levels were associated with increasing risk for psychological distress and depression. Increasing inflammation (CRP) levels were also associated with increasing risk for hospitalization with depression.[7]

In support of the inflammation depression link, recent studies have found a significant link between the dietary inflammatory index (DII) and risk of depression. In an Australian study of 6,438 middle-aged women, those with the most anti-inflammatory diet had an approximately 26% lower risk of developing depression compared with women with the most pro-inflammatory diet.[8] Similarly, a study in the UK examined the DII and recurrent depressive symptoms over five years in 3,178 middle-aged men and 1,068 women. Researchers found that for each increment of 1 level of DII score (increased inflammation), odds of depression increased by 66% in women, whereas in men the risk increased by only 12%.[9] In a study of 15,093 university graduates in Spain, those on the highest DII (strongly pro-inflammatory diet) had a 47% risk of depression compared with those in the bottom, with a significant dose-response relationship, which means as the diet became more inflammatory it increased the risk of depression. Further analysis also showed the association between DII (the inflammatory diet) and depression was stronger among participants older than 55 years, with an increased risk of 270% and those with cardiometabolic comorbidities (high blood pressure, diabetes, etc.) had an 80% increased risk of depression.[10] In a study of 43,685 women (aged 50–77) without depression at baseline, the risk of developing depression was 41% higher if they were on the highest compared to the lowest Dietary Inflammatory Index diet.[11]

Oxidative stress is closely related to the inflammatory pathway in particular. Pro-inflammatory cytokines are produced in reaction to oxidative stress and oxidative stress in turn amplifies the inflammatory response. High cortisol levels have been associated with increased levels of oxidative damage.[12] Depression has been associated with increased oxidative stress and increased severity of depression is associated with increased systemic oxidatively generated DNA and RNA damage.[13] Severe depression is associated with increased systemic oxidatively generated RNA damage, which may be an additional factor underlying the somatic morbidity and neurodegenerative features associated with depression. In a meta-analysis, 1,308 subjects depressed persons had increased oxidative stress and decreased anti-oxidant defences (as measured by 8-OHdG and F2-isoprostanes).[14] The results indicate that depression is associated with increased oxidative damage to DNA and lipids. The brain is particularly vulnerable to oxidative damage due to its high oxygen consumption and low antioxidant defences. Sustained oxidative brain damage during a depressive episode may make a sufferer prone to developing another depressive episode. Therefore, it has been hypothesized that exposure to oxidative stress could be an explanatory mechanism in the remitting and chronic course of depressive disorders.[15] There is also evidence from post-mortem studies suggesting that in depression oxidative stress is increased[16] and antioxidants are decreased[17] in the brain.

A study of 37 patients with bipolar disorder showed that bipolar disorder is associated with increased oxidatively generated damage to nucleosides, which could be contributing to the increased risk of medical disorders, shortened life expectancy, and the progressive course of illness observed in bipolar disorder.[18] Another study showed increased oxidative stress as indicated by increased nitric oxide (NO) and lipid peroxidation, measured by thiobarbituric acidic reactive substance (TBARS) assay in patients with bipolar disorder.[19]

There is evidence suggesting that antioxidants are decreased in depression, illustrated by lower antioxidant levels,[20] including carotenoids,[21] and antioxidant enzymes.[22] There is some evidence to suggest that antidepressants have antioxidant properties and may act through reducing pro-inflammatory cytokines and ROS production and improving levels of antioxidants such as superoxide dismutase.[23]

 

[1] Miller et al. 2009.

[2] Berk et al. 2011.

[3] Miller 2009.

[4] Brydon et al. 2008.

[5] Dantzer et al. 2008.

[6] JAMA Psychiatry 13, 2014.

[7] Wium-Anderson et al. 2013.

[8] Nitin Shivappa et al. 2016 British Journal of Nutrition.

[9] Akbaraly et al. Clinical Psychological Science 2016.

[10] Sanchez-Villegas A et al. British Journal of Nutrition 2015.

[11] Lucas et al. 2014.

[12] Joergensen et al. 2011.

[13] Jorgensen et al. 2013; Pandya et al. 2013.

[14] Black et al. 2014; Palta et al. 2014.

[15] Moylan et al. 2013.

[16] Wange et al. 2009; Michel et al. 2012.

[17] Gawryluk et al. 2011.

[18] Munkholm et al. 2015.

[19] Andreazza et al. 2008.

[20] Palta et al. 2014.

[21] Milaneschi et al. 2012.

[22] Sarandol et al. 2007.

[23] Khanzode et al. 2003; Lee et al. 2013.

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Time to rethink what we put on our skins

Time to rethink what we put on our skins

Claiming our power as consumers means we need to challenge assumptions we have about these products, the companies that manufacture them and the government bodies that regulate them.

Common Consumer Fallacies

  • I can trust in the safety of the products I use.
  • The products I use do not affect my health.
  • Labels are accurate and consistent and list all of the chemical ingredients in the products I use.
  • The government adequately regulates these products and in the process protects me from chemicals known to harm my health.
  • I can trust the companies making the products I use because they put my health before dollars and cents.

If you believe any of the above statements, it is time to arm yourself with new knowledge. Next time you shop, take your awakened awareness and your new consumer power with you.

Know that:

  • Just because products are sold over the counter doesn’t mean they won’t harm you.
  • Just because these products aren’t making you sick right now doesn’t mean they aren’t affecting your health in the long term.
  • If products don’t have all the ingredients listed, the manufacturer isn’t giving you information that could affect your decisions and your health.
  • Current government legislation is incomplete and doesn’t protect you from a huge range of chemicals that are known to harm your health.
  • The cosmetics and personal care industry is first and foremost a business. It is driven by the principle of maximising economic gain. History confirms that profit-driven interests are likely to take precedence over safety and health considerations.

We also need to ask ourselves an essential question: “Can we consume less, rather than more?” It is well recognised that when tested, the majority of cosmetics and personal care products do not have the correct molecular weights, potency, or combinations of ingredients required to benefit the consumer in a measurable way. The gains are psychological—we feel better, feel more attractive or think we have greater sex appeal.

Simplifying your lifestyle can bring a better quality of life. Using fewer personal care products is one of the easiest (and the most economical) ways to reduce your exposure to chemicals. If you must buy certain products, after reading this book you will at least be able to choose those with lesser or lowest toxicity. And, once you know the facts, there are some products that you will choose not to use at all.

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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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Improving Your Sleep: Stimulus Control and Stress Reduction

Improving Your Sleep: Stimulus Control and Stress Reduction

Stress is an essential part of a lifestyle; however, it is also a major precursor to insomnia, probably the most important contributing factor. Studies have shown that a reduction of stress could lead to a 53% decline in insomnia rates. Stress and insomnia are tricky to control because if the stress is not removed and the insomnia persists it is also creating a stress on the body, and increasing the insomnia; this quickly becomes a vicious cycle.

Stimulus control is generally used in conjunction with sleep restriction, as a method of reducing time in bed. It is particularly useful in subjects who have conditioned themselves to become mentally active when they get into bed. If sleep initiation takes more than 10 minutes to achieve, the subject should then get out of bed, leave the room and do something unstimulating until they feel drowsy. This should be repeated as required. The objective of this is to disassociate bed with stimulating activity, therefore bed is strictly for sleep only (sex is permitted) so that they become conditioned to sleep in bed and nothing else. Even though sleep debt and daytime fatigue may initially increase, stimulus control (particularly in partnership with sleep restriction) can effectively decrease sleep latency. The degree of impact is significantly higher than that associated effectively decrease sleep latency. The degree of impact is significantly higher than that associated with hypnotic use.

 

In one study a group of self-selected subjects all reporting to be suffering from stress, insomnia and various other health issues (excessive drinking, smoking cigarettes, and the use of tranquillizers and hypnotics) met for an hour and a half a week over eight weeks to undergo stress management training. The training consisted of learning about stress theory, low-stress lifestyle principles, techniques for handling stressful events and relaxation methods. At a follow-up check twelve months after receiving the treatment there was a seventy-eight percent improvement in the insomnia.

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