Dr Dingle's Blog / inflammation
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.
Despite the increases in technology, life style changes and the promise of more free time, it is becoming apparent that stress is becoming one of the greatest health concerns of the Western World. Recent statistics indicate that between 70 ‑ 80 percent of all health related problems are either precipitated or aggravated by stress. Although the way we live, and the situations we face everyday have changed over thousands of years, our modern brain still has the ability (as it has had for thousands of years) to give us the same feelings and responses to stress. This is because these are deeply instinctive responses of protection and survival.
‘Distress’ is stress that arises from a negative situation such having an argument, being under too much pressure at work, or being called into the bosses office. ‘Eustress’ on the other hand, is stress that results from a positive situation, such as getting married or receiving an award . A mild amount of pressure can be beneficial; making a person more motivated to increase performance. However, the major difference between the positive eustress and the negative distress is how you perceive them. To one person public speaking creates eustress but to another it creates distress and high pressure for one individual in the work environment may not be experienced by another, being instead seen as more of a personal challenge. They both place the same physiological demands on the body, but are processed mentally and emotionally in different manners.
However, too much pressure or pressure for a long period of time can lead to excessive stress, a state of distress, which is unhealthy for both the mind and body. Stress can also be looked at from being acute and chronic stress.The evolutionary explanation behind stress is that ancestor’s perceived reaction to threats and dangers has survival value. When hunter-gathers would risk their lives in hunting for food or defending their community they would experience dangers that would trigger the bodies stress response, preparing them for action, to either fight or flee from the threat. In today’s society, stress experienced is not usually life threatening but still triggers the same stress response.
The reason I call it the blood pressure smoothie is all of the ingredients have been shown in many scientific studies to reduce blood pressure. By no way is this meant to replace advice from you GP but you can share it with them and see if they are interested in preventing the problem rather than just treating it with pharmaceuticals. Remember also that I am not a GP I am just the guy who does all the research which is why I have a PhD.
4 ingredients in order of importance
Almonds (soaked for at least 8 hours)
Filtered re-mineralised ionized water.
Extras for taste and minerals
Start by grinding the linseed and the almond in the smoothie maker.
Add the beetroot and the filtered water to make up to the constituency you need.
If you want to make it a bit sweeter add some ripe banana, dates or coconut water (and coconut meat if you have the whole coconut) as they are rich in Potassium (and other minerals) which is essential for muscle relaxation and tastes great. But wait till the banana is ripe for the best taste. You can also cold green tea instead of water to add to the antioxidant mix.
The properties that make this smoothie such a potent blood pressure mix is all of the ingredients have excellent antioxidant properties, rich in minerals and other nutrients liked with lowering blood pressure in scientific studies.
High blood pressure or hypertension is having a blood pressure reading of above of around 90mm Hg on 140mm Hg. Hypertension itself is not a disease but a condition or as an indicator of ‘increased risk’ of cardiovascular disease. Patients who are hypertensive have an increased risk of heart attack and stroke due to the direct correlation between the two. Hypertension also contributes significantly to the increased risk of kidney failure and other chronic illness.
In healthy people the cells of blood vessels produce the substance called nitric oxide (NO) which instructs smooth muscles surrounding arteries to relax. If they cant relax they stay rigid and you end up with high blood pressure. The NO is produced in a single layer of cells that line the inside of the arteries called the endothelium. If this tissue is damaged in the case of too much pressure, oxidation or through other means it stops producing NO and blood pressure rises.
Many of the beneficial actions of nutrition on lowering blood pressure results both directly and indirectly through improving endothelial tissue and NO production and release from this tissue. Two major pathways to increase NO are increase the rates of nitrates in the diet, the building block for NO, and L-Arginine which stimulate the enzyme to manufacture NO. Endothelial-derived NO also inhibits platelet adhesion, activation, secretion, and aggregation and promotes platelet disaggregation so you are less likely to have a stroke. A third mechanism that is absolutely critical is to protect and repair the endothelium, remember it is only one cell thick and very susceptible to damage. Vitamin C and antioxidants are essential for this part.
Diets high in dietary nitrate such as beetroot are associated with reduced blood pressure increased exercise performance as a result of vasodilation (expansion) of the blood vessels and a decreased incidence in cardiovascular disease. 100-200mg of beetroot per day has been shown to produce immediate effects of lowering blood pressure by around 15 mm of Hg. Beetroot is also rich in vitamins, phytochemicals and contains large amounts of iron and folic acid Mg, Na and Ca. Apart from the nitrates the major bioactive molecules in beet are polyphenols, flavonoids, betalains, therapeutic enzymes, ascorbic acid, and dehydroascorbic acid (DHAA). So they not only provide the ingredients for NO production but also help in repair and protection of the endothelium.
Almonds have one of the highest sources of L-Arginine (most nuts have lots of L-Arginine so you can substitute the almonds if you want) which stimulates NO synthesis. Studies of almonds have shown reductions of 5-6 mm of blood pressure. It is important to soak the almonds as they (all nuts and seeds) have enzyme-inhibiting factors in them which stop them from germinating until they have enough water. These enzyme inhibitors also stop the absorption of some nutrients, particularly minerals. When you soak the nuts many of the nutrients also become more available for digestion.
Flaxseed is rich in Omega 3 fatty acids, L Arginine (about 20% less than almonds), lignans, antioxidants and fiber that together probably provide benefits to patients with cardiovascular disease. Studies on consuming 30g of flaxseed have been shown to reduce blood pressure by up to 15 mm Hg.The great thing about this smoothie is that you can add just about anything else you want to it and it will make it even tastier and better for you.
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. The US Centers for Disease Control estimate that up to 50% of antibiotics prescribed in the US are unnecessary. Unfortunately, the use of antibiotics is often prescribed for those groups who are more vulnerable to dysbiosis, including infants born via C-section and in those born preterm, compared to term infants born vaginally, 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 and begins immediately following antibiotic administration. The effects can sometimes last for years after its cessation, 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. 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, and mental health conditions. Common outcomes of antibiotics the antibiotic-disturbed gut microbiota are diarrhea and infections with Clostridium difficile, particularly in infants.
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. In young children, antibiotics may change the development of the “adult” microbiota, and not allow its normal maturation. It has also been hypothesized to cause a delay in microbial maturation from six to 12 months after birth. Early life exposure is also associated with numerous diseases later in life including IBD, obesity, and asthma, as well as the development of immune-mediated metabolic and neurological diseases.
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. 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. 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.
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 and result in poorer neuro-cognitive outcomes later in life.
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. Animal studies have shown that high doses of a cocktail of antibiotics induced lasting changes in gut microbiota associated with behavioural alterations.
Animal studies of early life exposure to antibiotics show lasting immune and metabolic consequences. 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. 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. There is also evidence of antibiotics playing a role in the development of IBD in children and that antibiotic usage during the first year of life was more common in those diagnosed with IBD later in life.
In human studies, mother’s use of antibiotics during pregnancy is consistently associated with cow’s milk allergy, wheeze, asthma, and atopic dermatitis, with the strongest association for antibiotic use in the third trimester of pregnancy. 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%). 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. Similar results have been shown for antibiotic exposure through breastfeeding.
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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 including neurotransmitter metabolism, neuroendocrine function, and neural plasticity.
This is now supported by increasing lines of scientific evidence 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.”
- 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. 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.
- 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. 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.
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. 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%. 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. 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.
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. Depression has been associated with increased oxidative stress and increased severity of depression is associated with increased systemic oxidatively generated DNA and RNA damage. 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). 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. There is also evidence from post-mortem studies suggesting that in depression oxidative stress is increased and antioxidants are decreased 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. 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.
There is evidence suggesting that antioxidants are decreased in depression, illustrated by lower antioxidant levels, including carotenoids, and antioxidant enzymes. 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.
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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.
- 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.
- 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.
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.
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), celiac disease, and neurological disorders including autism.
Once inflammation starts it appears that these opportunistic microorganisms are able to exploit the inflamed environment and expand their numbers 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.
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. It did however change after 21 weeks.
 Milani et al., 2016.
 Chow et al., 2011.
 Baumler and Sperandio, 2016.
 Del Chierico et al., 2012.
 Konig et al., 2016.
 Spees et al., 2013.
 Petersen and Round, 2014.
 Thaiss et al., 2016.
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. 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.
 Magalhaes et al., 2007.