Dr Dingle's Blog / asthma
Sleep and weight
Obesity in another disorder linked with insomnia. Research shows that diets that are higher in saturated fats are more susceptible to chronic diseases and disorders which includes insomnia (Novak et al. 1995). This is an alarming fact as 20% of the population of the United States of American are overweight or obese (Patterson et al. 2004).
Many studies, including one spanning twenty years, have tested the hypothesis that sleep and obesity are linked and the majority of results show positive correlations (Gangwisch et al. 2005). Further studies, with over 500,000 total participants via meta‑analysis have supported obesity and insomnia in adults and children (Cappuccio et al. 2008). The trends of increasing BMI and reduced sleep hours appear to go hand in hand, along with sleeping troubles related to Sleep Apnoea often seen in obese patients.
This link between Obesity and the symptoms of its associated diseases demonstrates a common trend towards diminishing an individual’s peak performance. Obesity and many of the health conditions which result from it increase the lower productivity levels associated with lower mental and cognitive functioning.
Obesity is also a serious factor in poor sleep habits. In a number of studies obesity was associated with "reduced sleeping hours " (Ko et al (2007). Obesity, particularly abdominal and upper body obesity, is the most significant risk factor for Obstructive Sleep Apnea (OSA). Patients with sleep apnea often experience daytime sleepiness and difficulty concentrating (Teran-Santos et al, 1999). Studies have also shown a strong association between sleep apnea and the risk of traffic accidents (Terán-Santos et al (1999). In fact, subjects suffering from sleep apnea were at a higher risk than those who had consumed alcohol to be involved in a traffic accident. This has major implications, particularly for overweight and obese workers using any form of equipment of driving vehicles.
This lack in sleep will then leave the employee going to the work already feeling tired, irritable and stressed, therefore making it difficult to concentrate, and highly increasing the chances of being injured or making a mistake which may put fellow workmates in danger (Lynch, 2005) It is situations like this, where the worker comes to work already feeling tired, that the employee is putting his safety and other's safety at risk.
Shift workers are known to be a high-risk group for obesity. In the current study population, rotating-shift workers showed a higher distribution of the highest body mass index compared with daytime workers
In a study of the brains of 24 participants after both a good and a bad night’s sleep. after disturbed sleep, there was increased activity in the depths of the brain, areas which are generally associated with rewards and automatic behaviour. It seems a lack of sleep robs people of their self-control and so their good intentions are quickly forgotten.
What we have discovered is that high-level brain regions required for complex judgments and decisions become blunted by a lack of sleep, while more primal brain structures that control motivation and desire are amplified.”
In other words: lack of sleep robs people of their self-control and so their good intentions are quickly forgotten.
On top of this, the researchers found that after being deprived of sleep, participants displayed greater craving for high-calorie junk food. The more sleep-deprived they were, the greater the cravings. A stufy of 13,284 teenagers found that those who slept poorly also made poor decisions about food. Similarly, a Swedish study found that at a buffet, tired people were more likely to load up their plates.
The link has even been made from poor sleep through to food shopping. A Swedish study found that men who were sleep-deprived bought, on average, 9% more calories than those who’d had a good night’s sleep. These results were likely the result of the poor decision-making. It had been thought that the tendency to eat more after poor sleep was related to the so-called ‘hunger hormone’ ghrelin. But the latest studies suggest that it’s simple self-control that is most important in causing the sleep-deprived to over-indulge.
Obvious symptoms of sleep deprivation constant yawning and the tendency to doze off when not active for a while; for example, when watching television, Grogginess when waking in the morning Sleepy grogginess experienced all day long (sleep inertia) Poor concentration and mood changes (more irritable).
Some of the physical effects found from long term fatigue are heart disease, diabetes, high blood pressure, gastrointestinal disorders and depression (Workplace health and safety QLD, 2008). A study conducted by Andersen involving rats also showed sleep deprivation affects the expression of genes related to metabolic processes, response to stimulus and signalling pathways (Andersen et al, 2009).
Numerous studies have shown that even a little bit of sleep deprivation decreases efficiency and increases risk of disease, including cardiovascular disease, cancer and diabetes. Sleep deprivation has been shown to negatively affect endocrine (hormones) and metabolic functioning as well as nervous system balance (Nilsson, et al., 2004). Sleep deprivation is associated with an increased concentration of cortisol plus other indicators of increased stress such as elevations in pulse rate, body temperature and adrenaline secretion (Vgontzas, et al.,1999). Sleep deprivation also appears to increase blood concentrations of certain chemicals called cytokines and C-reactive proteins (Irwine, 2001 and Vgontzas, et al., 1998), indicating an inflammatory reaction. The effect of unremitting low-grade inflammation may be to damage the inner walls of the arteries, which sometimes leads to vessel narrowing, high blood pressure, stroke, and heart disease (Irwine, 2001). During truncated sleep, your heart might have to work harder, constricting blood vessels and increasing blood pressure even more, which could conceivably result in a heart attack or stroke (Martins, 2003).
Sleep is as important to the human body as food and water, but most of us don’t get enough sleep. Insufficient sleep or disruptions to the sleep contribute to adverse health effects. Numerous studies have also shown that even a little bit of sleep deprivation decreases efficiency and increases risk of disease, including cardiovascular disease.
Initial changes to cardiovascular system from insomnia include hypertension, which is a potent co‑morbidity for other cardiovascular diseases. Hypertension has been linked to reduced sleep duration, with the highest correlation shown under 6 hours sleep per night (Gottlieb et al. 2006). However, associations have also been made between sleep of over 9 hours per night and hypertension and obesity. Furthermore this has not been supported at all in some studies and PPI in one older North American population actually showed a reduced risk of hypertension (Phillips, BOková and Enrigh, 2009.).
A study of 71,617 female health professionals found that sleeping fewer than five hours per night was associated with a 39 percent increase in the risk of coronary heart disease; even six hours per night showed an increase of 18 percent compared to sleeping eight hours per night (Najib, et al., 2003). In an analysis of data on more than one million people, the levels of nearly all forms of death were two-and-a-half times higher for people who slept four hours or less compared to those who slept between seven and eight hours on average
A study of 71,617 female health professionals found that sleeping fewer than five hours per night was associated with a 39 percent increase in the risk of coronary heart disease; even six hours per night showed an increase of 18 percent compared to sleeping eight hours per night. In an analysis of data on more than one million people, the levels of nearly all forms of death were two-and-a-half times higher for people who slept four hours or less compared to those who slept between seven and eight hours on average
Experimentally, sleep deprivation has been shown to negatively affect glucose metabolism and to enhance factors associated with Type 2 diabetes (Nilsson, et al., 2004). Research has also shown that people who experience sleep disorders were as much as three times as likely to develop Type 2 diabetes (Kawakami, 2004). Subjects in one study demonstrated impaired glucose tolerance for ten days after four hours of sleep deprivation (Spiegel, et al.,1999). It is also found that sleep deprivation can play a role in obesity. Sleep deficits bring about physiologic changes in the hormonal signals that promote hunger and, perhaps thereby, obesity (Spiegel, et al., 2004). One study found that after two days of sleep curtailment the subjects had reduced levels of the fat-derived hormone leptin and increased levels of the stomach-derived hormone ghrelin. These hormones are responsible for regulating hunger and appetite (Spiegel, et al., 2004). These hormonal differences are likely to increase appetite, which could help explain the relative high BMI in short sleepers.
Part 5 and more coming
Many sleep problems but by far the biggest is sleep deprivation and poor sleep. However too much sleep can also be a problem. Over sleeping may also be a problem. In one study sleeping 10 hours or more also increased the mortality rates by one and a half times.
Sleep is as important to the human body as food and water, but most of us don't get enough sleep. Dysoninia (poor sleep) related sleep disorders alone are broken into Intrinsic, Extrinsic and Circadian‑Rhythm sleep disorders including disorders such as but not limited to: "Psychophysiologic Insomnia, Sleep State Misperception Idiopathic Insomnia, Narcolepsy, Recurrent Hypersomnia, Idiopathic Hypersomnia...Restless Legs Syndrome & Intrinsic Sleep Disorder NOS" (MSM, 2001, pp. 27).
Risk factors for sleep related illness are diet, lifestyle, occupation, stress and grief, amongst many others (Helmanis, 2006 pp. 24‑25).
Almost 90 per cent of Australians suffer from some type sleep disorder at some stage of their lives. Of these, 30 per cent suffer from severe sleep disorders. Very few people regularly enjoy the amount, or quality of sleep that they need. The estimated economic costs to the country from this are between 3 and 7 billion dollars annually. There are also huge, unmeasured physical, psychological, emotional and social costs.
Causative factors for insomnia may be multifaceted but generally include some psycho physiologic hyperarousal or emotional distress. Other precursors may be pain, movement disorders, psychiatric disorders, circadium rhythm dysfunction, medication and substance abuse (Billiard and Bentley, 2004). In some cases, the risk of insomnia is subject to a genetic bias. However, specific physiologic indicators for the familial influence have not been fully identified (Parkes and Lock, 2009).
Insomnia is the difficulty initiating or maintaining sleep or both resulting in inadequate quality or quantity of sleep (Tomoda et al, 2009). Insomnia can manifest itself by many symptoms from not being able to sleep at normal hours and low quality and quantity of sleep to sleeping but not finding it refreshing. Other symptoms may include daytime sleepiness, frequent waking, early morning waking and difficulty retuning to sleep (Cureresearch.com, 2005).
Most adults have experienced insomnia or sleeplessness at one time or another in their lives (Straker, 2008). It is estimated that insomnia effects around 30-50% of the general population with 10% experiencing chronic insomnia (Straker, 2008). It has been estimated that in the US that 70 million people suffer sleep problems, and of these, 30 million suffer chronic insomnia (Stahura and Martin, 2006). Recently a survey showed that 1046 of the 2000 adults surveyed experience at least one night of lost sleep due to insomnia symptoms; the survey also concluded that insomnia is a growing issue of concern (Goolsby, 2006).
Insomnia generally affects women more than men and the incidence rate tends to increase with age (Straker, 2008).
There is a clear correlation of age to insomnia (Curless et a!. 1993). A number of surveys have reported between 28% and 64% of post menopausal women suffer from insomnia (Hachul de Campos et al. 2006).
Insomnia can be classified into three categories transient, short-term and chronic insomnia (Tomoda et al, 2009). Transient insomnia are symptoms lasting less than one week, short term insomnia are symptoms lasting between one-three weeks and chronic insomnia are those symptoms lasting longer than three weeks (Tomoda, 2009).
Narcolepsy is a sleep disorder that causes overwhelming and severe day time sleepiness (Retsas et al, 2000). Pathologic sleepiness is characterised by the fact that it occurs at inappropriate times and places (Retsas et al, 2000). These daytime sleep attacks may occur with or without warning and can occur repeatedly in a single day (Edgar et al, 2006). People who suffer from Narcolepsy often have fragmented night time sleep with frequent brief awakenings (Edgar et al, 2006).
Narcolepsy is typically characterised by the following four symptoms:
Excessive daytime sleepiness (90%)
Cataplexy: A sudden and temporary loss of muscle tone often triggered by emotions such as laughter. (75%)
Hallucinations: Vivid dreamlike experiences that occur while falling asleep or upon wakening. (30%)
Sleep paralysis: Paralysis that occurs most often upon falling asleep or waking up. The person is unable to move for a few minutes. (25%) (Retsas et al, 2000)
Interestingly, regular night time sleep schedule and scheduled naps during the day is required for favourable outcomes (Edgar et al, 2006).
Sleep apnoea affects over 12 million Americans with it being more prevalent in men than women (Sjosten et al, 2009). Sleep apnoea not only deprives sleep from the individual but their partners too (Yip, 2001). Sleep apnoea is defined as frequent and loud snoring and breathing cessation for at least 10 second for five or more episodes per hour followed by awakening abruptly with a loud snort as the blood oxygen level drops (Sjorsten et al, 2009). People with sleep apnoea can experience anywhere between 5 apnoeic episodes per hour to several hundred per night (Sjorsten et al, 2009).
Symptoms of sleep apnoea are:
Excessive daytime sleepiness
Obesity is the major cause of sleep apnoea often losing weight is all that is need to treat this disorder (Yip, 2001).
Part 3 and more coming
Inflammation is literally the body "on fire" and is a primary immune mechanism response of the body to a range of noxious stimuli. This can include infectious agents, such as bacteria or virus, oxidation or acidosis, damaged or diseased tissues; however, the inflammatory response can also occur in response to other external or internal cues 1. Inflammation is essentially the body’s first line of defence in common acute conditions 2.
The main function of inﬂammation is a short term response to resolve infection and to repair the damage in order to achieve homeostasis equilibrium balance back to the body. The ideal inﬂammatory response is therefore rapid and destructive, yet speciﬁc and very limited. The release of inflammatory mediators, predominantly from activated leukocytes that migrate into the target area and proteins called cytokines attack the threatening germ and repair damaged tissues. This is the reddening and swelling you see around any infected or injured area. most of us are familiar with: redness, heat, swelling, and pain associated with inflammation. These symptoms are created by the activity of immune cells working to break down injured and dying tissues so that new, healthy ones can replace them.
Unfortunately, we have created a situation in our lives where we now suffer from chronic low level inflammation over decades of our lives as a result of our unhealthy and unbalanced lifestyles and diet. Chronic inflammation is being shown to be involved in the onset and the development of most if not all chronic illness that are now at epidemic proportions in our society. These include atherosclerosis (damaged and blocked arteries), heart disease, stroke, obesity, neurodegenerative diseases, depression, Alzheimer’s, Parkinsons Disease, thyroid disorders, diabetes, asthma, autism, arthritis, celiac disease, eczema, psoriasis, Multiple Sclerosis, lupus, migraines, periodontal disease, sleep apnoea, chronic kidney failure and cancer. It is a long list but it is only the main ones I have mentioned.
Even though chronic inflammation in the body is hard to detect there are some common symptoms to look out for. These include the following:
Chronic pain in the joints and/ or muscles
Allergies or asthma
Elevated blood pressure
Fluctuations in blood sugar levels
Gut issues (constipation or diarrhoea)
To judge the level of inflammation in individuals, a number of markers have been identified that are directly associated with inflammatory processes 3.4.5. C‑reactive protein (CRP), interleukin‑6 (IL‑6), fibrinogen, and tumor necrosis factor‑alpha (TNF‑a) are the most common markers that the medical system uses, with CRP leading in terms of assessing risk. Each marker has a different role in the inflammatory process and the development of chronic illness and are also often linked to each other. For example, IL6 plays a central part in the inflammatory process and is known to be linked to the production of C-reactive protein (CRP) in the liver. CRP is commonly used to monitor inflammatory states as it is secreted by the liver in response to a variety of inflammation, trauma and infection and decreases rapidly with the resolution of the condition. If the person has high C reactive protein and does not have an infection of some sort, then they probably have chronic inflammation. It is like the body is trying to fight off an illness all the time rather than just short term acute situations. It becomes exhausting for the body and is also likely to result in some long term damage.
The inflammatory process is driven by the immune system in your body. Therefore, in order to reduce the incidence of disease you must reduce inflammation, and to reduce inflammation you must identify and eliminate the immune system trigger(s). The typical approach of allopathic medicine is to treat the symptoms of the disease itself or the immune system (immune-suppressive drugs) or inflammation (anti-inflammatory drugs) directly without addressing the underlying cause of the disease. But not dealing with the underlying causes. Sustainable health looks at identifying and eliminating the sources of the inflammation to address the situation at its cause. While I will leave much more of the detail to the next months edition some good examples of anti inflammatory nutrients include turmeric, probiotics, vitamin C and D and Magnesium. While physical activity, meditation and strategies to de-stress are all anti inflammatory. Get the idea.
Inflammation and Cardio Vascular Disease (CVD)
CVD is no longer considered a disorder of lipid (fat) accumulation or elevated cholesterol, but rather a disease process characterized by low-grade inflammation of the vascular (artery) lining and an inappropriate wound healing of the blood vessels 5. It is similar to a low-grade wound on your skin that does not heal, but it is on the inside. There is now extensive and rapidly growing evidence that inflammation, which is what you get with every wound, plays a critical role in all stages of CVD 6,7,8,9. That is why if you treat the cholesterol you are treating the symptoms, yet if you treat the inflammation you are treating the underlying cause of the disease. To highlight the direct link in one study weekly injections of the cytokine (inflammation protein) given to mice caused a 2.5 fold increase in atherosclerotic lesions, that is 250% 10.
Since half of all myocardial infarctions (heart attacks) occur in individuals that display normal plasma lipid (cholesterol) levels, using markers of inflammation is much more effective to detect those at risk of CVD before its onset 4,5,11. Atherosclerosis (arterial plaque build up also known as artheriosclerotic vascular disease or ASYD) is a chronic inflammatory disease occurring in the innermost layer of the artery, the intima, where it thickens resulting from a build up of plaque. An injury or oxidation (free radicals) activity damages the blood vessel lining and induces an inflammatory response resulting in the adhesion of platelets and build up of macrophages (a type of white blood cell that swallows and destroys damaged tissue and infectious agents) and white blood cells at the site of injury. The inflammatory response, is mediated by activated T cells, macrophages and mast cells and produces cytokines (chemical messengers). Modified (through oxidation or enzymes) low‑density lipoproteins in the arterial intima initiate an inflammatory response in the arterial wall that leads to a cascade of inflammatory responses. As arteries lose flexibility and lesions occur, IL‑6 increases leading to further inflammation.
Inflammation and cancer
The link between chronic inflammation and cancer has long been recognized since the 19th century German pathologist Rudolph Virchow first hypothesized that the origin of cancer was at sites of chronic inflammation. Now it seems that modern science has caught up with the observations of the 19th Century. Considerable advances in cancer research relates to the role of inflammation in the development of cancer. Research in 2003 demonstrated that there is a link between inflammation and tumour growth 12. In 2010 several piece of the puzzle came together when researchers reported they could definitively show that inflammation in the breast is key to the development and progression of breast cancer 13. In an earlier study, women with high levels of two markers of inflammation―C-reactive protein and serum amyloid A―were two to three times more likely to die early or have their cancer return than women with lower level 14.
Now there is a large body of evidence that chronic inflammation is involved in all stages of cancer development. Generally inflammatory white blood cells (leukocytes such as neutrophils; monocytes, macrophages and eosinophils) mediate the growth of inflammation associated cancer, although other cells including cancer cells are also involved 15,16. Animal testings provide strong evidence that chronic inflammation contributes to the promotion of cancer 15 and through suppression of the immune system it allows the outgrowth and proliferation of malignant cells 17. Inflammation affects the micro environment of the cancer; it increases malignant growth 17; may alter blood flow processes; and the cancers response to remedial substances and hormones 18.
There is now convincing evidence that carcinogenesis often evolves as a progressive series of highly specific cellular and molecular changes in response to induction of constitutive over-expression of COX-2, an enzyme responsive for inflammation, and the prostaglandin cascade in the ‘inflammation of cancer’. Molecular studies reveal that over expression of COX-2 is a prominent feature of virtually every form of cancer while the expression intensifies with stage at detection, cancer progression and metastasis. It appears that COX-2 expression is not only an early event in the genesis of cancer, but is required throughout the entire evolutionary process of cancer development
In support of this back in 2005 Prof. Houghton 19 and her colleagues found that an infection with Helicobacter felis (a bacterium related to infectious Helicobacter pylori in humans) which causes a large amount of inflammation leads to an influx of bone marrow-derived stem cells (BMDCs), as the body tries to repair the injury caused by the infection. They were able to show that this transformation of BMDCs is the event that actually sparks malignant tumors of the stomach. They showed that bone marrow-derived stem cells attempt to participate in repair but, under conditions of inflammation and oxidation, are unable to behave normally and instead progress towards cancer. BMDCs have other cancer-like properties, including: the capacity for unlimited growth and the ability to avoid apoptosis (programmed cell death) signals. These properties give them a significant growth advantage making them difficult to control once they have mutated. the BMDCs, depending on environmental cues for development and differentiation, encounter an abnormal environment of conflicting growth signals. There follows a downward spiral of metaplasia (the conversion of normal to abnormal tissue); dysplasia (emergence of a precancerous growth); and finally carcinoma (frankly malignant cancer, capable of metastasizing). It appears that cancers are just the body trying to adapt to a toxic internal environment of inflammation and oxidation.
Inflammation depression and mental health
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 not a disease itself, but instead a “multifaceted sign of chronic immune system activation”, inflammation. Instead 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 which perfectly mirror the defining characteristics of depression 20. Cytokines have been shown to access the brain and interact with virtually every mechanism known to be involved in depression 21 including neurotransmitter metabolism, neuroendocrine function, and neural plasticity.
This is now supported by increasing lines of scientific evidence 22 including:
- Depression is often present in acute, inflammatory illnesses.
- Higher levels of inflammation increase the risk of developing depression.
- Administering endotoxins that provoke inflammation to 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” 21.
- 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 23. 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 in laboratory animals demonstrating that cytokines … can lead to a host of behavioural changes overlapping with those found in depression. These behavioural changes include decreased activity, cognitive dysfunction and altered sleep 24.
- 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 2-fold higher in individuals with the highest vs the lowest levels of 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 tertile of IL-6 levels at the age of 9 were also 81% more likely to report psychotic experiences at the age of 18 25.
Perhaps this is a message that we need to start acting now and early with children to avoid the epidemic of inflammation and chronic illness including depression everyone is predicting for the future.
- Shelton and Miller: 2010
- Schwarzenberg and Sinaiko: 2006
- Taubes 2002
- Ridker et al. 1997
- Ridker et al. 2000
- Dixon et al. 2009
- Loppnow et al. 2008
- Packard and Libby 2008
- Sukhanov et al. 2007
- Tracy 2003
- Guigliano et al 2006
- Vakkila and Lotze
- Liu, et al. 2010
- Pierce, et al. 2009
- Schacter, 2002,
- Lin and Karin, 2007
- Bunt et at, 2006
- Chekhun, 2009
- 2004 Prof. Houghton et al
- Smith R Cytokines and Depression
- Miller et al, 2009,
- Berk et al 4
- Brydon et al, 2008
- Dantzer et al, 2008, p.48
- Khandaker et al, 2014