Dr Dingle's Blog

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]

"Gut Secrets" the book
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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.

 

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