Dr Dingle Blog

Health Effects of Poor Sleep

Health Effects of Poor Sleep

Sleep is as important to the human body as food and water, but most of us still don’t get enough sleep. We obtain treatment for illness or injury – yet we generally fail to seek help when we aren’t getting enough sleep. The average length of sleep has declined from around 9 hours a hundred years ago to seven hours today. And the depth of sleep has also declined.

Sleep is complicated in the way that there are many different factors that influence the effectiveness of sleep. It’s not just duration that determines the effectiveness of sleep, factors such as quality, frame of mind and deepness all contribute to the maximum desired outcome and even our perception of how we sleep. Many factors can play a part in the quality and quantity of our sleep.     

On average a healthy person will spend around one third of their life sleeping.  Inadequate hours of good quality sleep leads to a disruption to vital biological processes resulting in a decrease in mental and physical health including impaired cognitive function and lower productivity and work performance due to a decrease in attention, judgment and responsible decision making. 

Numerous studies have also shown that even a little bit of sleep deprivation decreases efficiency and increases risk of disease, including cardiovascular disease, diabetes and cancer.  Some of the physical effects found from long term fatigue are heart disease, diabetes, high blood pressure, gastrointestinal disorders, depression eating disorders and weight gain. Sleep deprivation has also been shown to negatively affect endocrine (hormones) and metabolic functioning as well as nervous system balance. A recent meta-analysis which included 122,501 subjects found that insomnia determined an increased relative risk of 45% of developing or dying from cardiovascular disease during the follow-up.

Sleep debt has been found to lead to elevated evening cortisol levels and impaired glucose tolerance and is a risk factors for the development of insulin resistance and perhaps type 2 diabetes.

Obesity is another disorder linked with sleep with sleep deprivation. Many studies, including one spanning twenty years, have shown increasing weight gain with poor sleep. Shift workers for example are known to be a high-risk group for obesity.

While many factors can contribute to insomnia and poor sleep undoubtedly the most important one in the twenty first century is stress. Increasing research shows that there is an activation of the stress-response system and the degree of sleep disturbance experienced correlates with the level of stress-response activation and that insomniacs and others with poor sleep patterns experience more psychological stress.

Unfortunately, there can be a vicious cycle of stress poor sleep and more stress. If you are not getting enough sleep, you have to rely more and more on your alarm clock, and if you oversleep and wake up already fatigued. Thus, a person who is always feeling tired – even after a good night’s sleep – may have overworked adrenal glands.

Cortisol levels are highest in the morning and decrease gradually throughout the day.  The body develops a routine, and cortisol is secreted at roughly the same amounts at a particularly time of day, depending on levels of stress.  If an individual does not receive enough sleep they will produce more cortisol than they would on a normal routine day. Studies also show that stress and elevated levels of cortisol actually inhibit the ability to fall asleep, further exacerbating stress symptoms.

In another study although all subjects reported equivalent numbers of daily stressful events, people with insomnia found the impacts of these events to be more severe. Insomniacs also experienced major life events more intensely, were much more alert before bedtime, viewed their lives as more stressful, and used emotionally-based coping strategies to deal with stress more often than did the normal sleeper group. It appears that although normal sleepers and insomniacs experience similar types of stressful inputs in insomniacs the stress-response is more sensitive to these inputs and its activation leads to lack of sleep.

The effects of sleep deprivation can include fatigue, reduced productivity, slower reflexes and reactions, moodiness and a lack of energy, mimicking many of the characteristics of stress. The more hours we spend awake, the more sluggish our minds become, according to the findings. One night without sleep reduces our brains ability to take in new information by nearly 40 percent, due to a shutdown of brain regions during sleep deprivation. Impaired sleep function decreases the neuroplasticity in the central nervous system resulting in diminished cognitive function as impulse transmission are impaired. Sleep is the regenerative time for the Central nervous system and nerves, without which brain atrophy and weakened conduction can result.

Brains that are sleep deprived aren’t as efficient and have to work harder. Exactly want you don’t want. Studies show the brains of the sleep deprived desperately pumping energy into the prefrontal cortex, trying to overcome the effects of sleep deprivation.

Sleep plays an important role in consolidating memories. While we sleep, our brain orders, integrates and makes sense of things that have happened to us. Not only that, but we seem to consolidate our learning while we sleep. Without sleep the process is badly disrupted, meaning it’s difficult to lay down long-term memories and it’s harder to learn new skills. Sleep deprivation causes many of the powers of focus and attention to decline which partly explains the distracted feeling you get when tired. Sleep deprived people easily get stuck in thinking loops and as a result fall back on the brain’s automated systems, our habits.

Perhaps it is time we valued sleep more and turned off the TV and computer earlier so we can be healthier and smarter the next day. 3 extra steps you can try to reduce stress related poor sleep include;

Meditate a few minutes before you go to sleep;

Try a sleep supplement from your local health food store; and

Don’t eat late and go for a little walk after dinner.

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Fruit is good for you even for diabetics according to a recent very large study.

Fruit is good for you even for diabetics according to a recent very large study.

The study shows the benefits of more fruit to prevent diabetes and reduce diabetic complications for diabetics. Unfortunately, fruit has been put in with all the foods where sugar is added just because it has sugar in it. People are being driven away from consuming more fruit and I have argued against poor advice given to diabetics for years. If it is no bad show me the evidence.

While sugar is a major culprit in diabetes it is not a sugar illness it is a mithochondrial dysfunction brought about by sugar and other poor diet (trans fats, artificial sweeteners etc), microbiome issues and lifestyle including stress, inactivity and loss of metabolic tissue and even toxins in the environment. The difference is that the sugar in fruit comes with a large array of essential nutrients including vitamins, minerals, antioxidants and anti-inflammatory ingredients, fibre, enzymes, water and prebiotics. All of these are potentially involved in repair of the mitochondria.

Of all the studies I have looked at they show that, even for diabetics, fruit is beneficial even when it comes to blood sugar levels. When fruit is consumed the sugar in it does not behave the same way that added sugar does. There are many potential reasons for this but we need to look beyond just basic concepts like if sugar is bad all foods that have sugar in them must be bad. This is naive and does not reflect the complexity of the human body.

This study was of 0.5 million adults in China over 7 years of follow-up. It found that among those without diabetes at baseline, higher fruit consumption was associated with significantly lower risk of developing diabetes with a clear dose–response relationship. That is the more fruit the lower the diabetes. In addition, among those who had diabetes at the beginning of the study, higher fruit consumption was associated with lower risks of all-cause mortality and micro vascular (small blood vessel) and macro vascular (large blood vessel) complications.

"In this large epidemiological study in Chinese adults, higher fresh fruit consumption was associated with significantly lower risk of diabetes and, among diabetic individuals, lower risks of death and development of major vascular complications."

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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.

  1. Shelton and Miller: 2010
  2. Schwarzenberg and Sinaiko: 2006
  3. Taubes 2002
  4. Ridker et al. 1997
  5. Ridker et al. 2000
  6. Dixon et al. 2009
  7. Loppnow et al. 2008
  8. Packard and Libby 2008
  9. Sukhanov et al. 2007
  10. Tracy 2003
  11. Guigliano et al 2006
  12. Vakkila and Lotze
  13. Liu, et al. 2010
  14. Pierce, et al. 2009
  15. Schacter, 2002,
  16. Lin and Karin, 2007
  17. Bunt et at, 2006
  18. Chekhun, 2009
  19. 2004 Prof. Houghton et al
  20. Smith R Cytokines and Depression
  21. Miller et al, 2009,
  22. Berk et al 4
  23. Brydon et al, 2008
  24. Dantzer et al, 2008, p.48
  25. Khandaker et al, 2014


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Triclosan - Deadly Ingredient

Triclosan - Deadly Ingredient

Triclosan is another one of those chemicals that is finally on its way out even though we have known of its toxic effects for decades. After many decades of scientific scrutiny many companies are now removing TCS. Colgate removed triclosan from its Soft-soap liquid hand soaps and Palmolive antibacterial dish liquid in 2011. Unfortunately, the big companies still deny it is a problem but are phasing it out because of public concerns citing “changing consumer preferences and superior formulations”. Interestingly most of the research now shows it is not even effective in what it does.

Triclosan (TCS) is a biocide used as an antibacterial and antifungal agent in a number of consumer products such as toothpaste, mouthwash, disinfectants, soaps, hair products, skin creams (0.1%), feminine hygiene products, and cosmetics (Fang et al 2010, Dhillon et al Int J Environ Res Public Health. 2015). Personal care products and cosmetics are the major source of exposure and studies on human subjects using TCS-containing cosmetics showed variable but significant amounts of TCS in their body fluids (Allmyr et al 2006, Sandborgh-Englund et al 2006) compared to controls.

Triclosan is also used as a preservative, fungicide, and biocide in household cleaning products and is infused into other household items such as kitchen utensils, cutting boards, kitchen wipes, mop heads, computer equipment, clothing, air filters, flooring, toys, bedding, and trash bags (Fang et al 2010). Research suggests that beyond its use in clinical applications (in hospitals) and toothpaste to prevent gingivitis (Gunsolley, 2006) there is questionable evidence that triclosan provides any extra benefit in other consumer products (Tan et al 2002). In 2001, a national survey detected triclosan and triclocarban in 76% of liquid soaps and 29% of bar soaps (Perenceivich et al 2001) whereas now it is likely to be in less than 10-20% of these products. However, as we have already seen many times, what is on the label is not always what is in the products and it has been detected in conventional dish liquid products at low concentrations, although it was not listed on the product labels.

Because of such widespread use in cosmetics, personal care and cleaning products TCS is one of the more frequently detected and highly concentrated contaminants in aquatic and terrestrial environments particularly in drinking water (Dhillon et al Int J Environ Res Public Health. 2015). Triclosan was among the top seven organic wastewater contaminants found in samples from a network of 139 streams across 30 states by the U.S. Geological Survey (Kolpin et al 2002). Looking at the chemical structure of TCS implies that it may have chemical properties related to many toxic compounds, such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), bisphenol A (BPA) and dioxins (Allmyr Sci Total Environ. 2008).

Use of these products, which typically contain 0.1 to 0.3% of the compound, results in absorption through lining of the gastrointestinal tract and mouth, and through the skin (Bhargava etal Am. J. Infect. Control. 1996; Dann and Hontela J. Appl. Toxicol. 2011)

Given the prevalence of triclosan in the environment, it is not surprising that measurable levels have been detected in just about every person even if you don’t use products with it on the label (Casas et al 2011, Philippat et al 2014). TCS absorption and distribution are rapid in humans and detectable levels have been found in body fluids such as amniotic fluid, blood, breast milk and urine (Allmyr et al. Sci Total Environ. 2006, Philippat et al. Environ Health Perspect. 2013) and TCS was detected in 100% of urine and 51% of cord blood samples in pregnant women in 181 expectant mothers from New York (Pycke et al Environ Sci Technol. 2014). TCS was also found in human tissues such as adipose tissue, brain, liver and nails (Geens et al.2012). The high TCS concentrations in the tissues relative to the environmental concentrations suggests that TCS bio-accumulates and is distributed all through human tissues. Other chemicals such as Propylene glycol, which is commonly found in the same product, has been shown to increase skin absorption of TCS (Fang et al. 2014).

Moreover, TCS has been detected in amniotic fluid, indicating that TCS can enter the fetal environment through the placenta (Philippat et al 2013). Fetal life is considered a particularly vulnerable period for exposure to EDC’s because hormonal disturbances during organ development may introduce irreversible changes (MacLeod et al 2010). Studies on pregnant rats have also reported the greatest bioaccumulation of TCS was observed in the placenta and that the hormone disruption might subsequently affect fetal development and growth (Feng et al. 2016).

In the U S, about two-thirds of 90 girls surveyed, aged 6–8 year olds had detectable TCS in their urine (Wolff et al. 2007). Among some Chinese school children aged 3–24 years old, higher TCS levels in urine were reported among females than their male counterparts. 93 % of those between 18 and 24 years had detectable levels (Li et al. 2013). Interestingly, in one study triclosan concentrations were a factor of 2 higher in Australian serum than in the Swedish plasma samples (Allmyr et al. (2008) most probably due to the discouragement to use triclosan containing products by the Swedish government and the lack of concern from the Australian authorities. Samples collected around Australia were remarkably homogenous with little differences between various groups showing they all appear to have a high exposure.

Breastfeeding infants represents a major route of exposure to TCS. In highly industrialized countries elevated concentrations breast milk are common (Dayan 2007). This is a major concern because of their immature metabolizing pathways of infants makes them particularly vulnerable to the negative impact of TCS. Not to mention they may be relying on just one source of food. Moreover, levels of triclosan in breast milk may be increased by underarm cosmetic use, which presents a direct dermal route of exposure to underlying epithelial tissue (Darbre, Best Pract. Res. Clin. Endocrinol. Metab. 2006) and a study of Swedish women who are users of personal care products containing triclosan had higher concentrations in milk and serum than women who use similar personal care products that presumably contain no triclosan (Allmyr et al. (2006) showing that personal care products containing triclosan were the dominant, but not the only, source of exposure to triclosan.

Health effects

Similar to all the research on the other EDC’s the latest science has shown that even small doses of certain chemicals can significantly affect hormone functions, if they are delivered at the wrong moment. The endocrine-disrupting properties of TCS including its effects on estrogen, testosterone activity and disturbance of thyroid hormone action (Arancibia et al.2009, Crofton et al. 2007; Henry and Fair 2013; Jung et al. 2012; Schiffer et al.2014, Paul et al 2010, Rodriguez and Sanchez 2010, Rotroff et al 2010) has been shown to occur at concentrations typically found in the studies on humans and the environment (Foran et al Mar Environ Res. 2000).

Because of its widespread environmental contamination many studies have been done on aquatic species show the same type of results. In a study on toads TCS exposure not only resulted in delayed growth and development but also caused birth defects in the animals embryos, and the developmental effects of TCS at high concentrations may be associated with disruption of the thyroid (Chai et al Ecotoxicology. 2016). Another study on tadpoles exposed to TCS developed into smaller froglets and had malformed legs (Helbing et al 2006 Aquatic Toxicology). In humans, recent studies have shown an increasing number of potential birth defects. In a study of 520 male newborns, prenatal triclosan exposure was inversely associated with prenatal growth parameters at week 33 and was statistically associated with reduced head circumference at birth (Philippat et al 2014). In another study prenatal TCS exposure was associated with reduced head and abdominal circumference at birth (Harmer Lassen,et al 2014 Environ Health Perspect)

Increasing evidence suggests that triclosan plays a role in cancer development, perhaps through its estrogenicity or ability to inhibit fatty acid synthesis (Dinwiddle et al 2014, Lee et al. 2012), Rodricks et al. 2010; Winitthana et al.2014; Wu et al.2014; Yueh et al.2014). Including breast cancer (Lu and Archer 2005, Lee et al Chem. Res. Toxicol. 2014) and liver tumours. Numerous studies have now investigated TCS’s estrogenic action in cultured cancer cells, animals and human and have shown estrogen activity. The results of these studies suggest that TCS affects cancer cell proliferation, particularly in the presence of estradiol. In male rats, TCS exposure led to decreases in serum testosterone, sperm production and male reproductive gland weight (Kumar et al Reprod Toxicol. 2009) as well as reduced ability to reproduce.

During the last decade, there has been a remarkable and unexplained increase in the prevalence of asthma. Some have hypothesized that widespread use of antimicrobial ingredients such as TCS may be a contributing factor. This concept is based on the hygiene hypothesis, which proposes that lack of pathogen exposure during development can alter the usual development of the immune system by eliminating or changing the commensal microbiota. But also for the potential of these antimicrobial products to alter the gut microbiome which is so important for the development of the immune system.

There are also increasing evidence of TCS-induced allergic reactions in humans. Dermatitis following prolonged use of TCS-containing hand washes (Wong and Beck 2001) or when further exposed to sunlight after use (Schena et al. 2008) have been recorded. Similarly, blisters were known to have erupted in the mouth and on the lips of human subjects following prolonged use of TCS-containing toothpaste (Robertshaw and Leppard 2007). A study conducted between 2003 and 2006 found a positive association between elevated urinary TCS levels and allergy or hay fever diagnosis, and concluded that TCS may negatively affect the immune system (Clayton et al 2011). A more recent study using data from 860 children obtained from the 2005–2006 National Health and Nutrition Examination Survey found levels of urinary TCS was positively associated with allergies and food sensitization (Savage et al 2012). Another study also found that skin exposure to TCS in the presence of an allergen can augment the allergic response to that allergen (Anderson et al Toxicol Sci 2013).

TCS is known to have a negative impact on β cells in the pancreas which impacts on insulin synthesis and function and ultimately contributing to diabetes (Pi et al.2007). Its negative effect on the power house of the cells, the mitochondria may also be a contributing factor to diabetes (Ajao et al 2015).

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The Health Benefits of Green Spaces

The Health Benefits of Green Spaces

Growing up as a child in the 60’s there was always lots of space to play on the street or out in the big back yards, nearby parks, creeks and the beach. While we have lost a lot of these spaces, research is showing that the more “green” we are surrounded with the the healthier it is for us. Invariably as the suburbs spread out we lose more open space, green and private gardens are either small or non- existent. Globally, the same situation is occurring with a dramatic demographic shift towards urbanization. Between 2000 and 2050, the proportion of people living in urban areas is projected to rise from 46.6 to 69.6% giving less people around the world access to green spaces and their potential health benefits.

Humans exhibit more than just a preference for natural scenes and settings; they suffer health problems when their environment and lifestyle causes them to become nature deficient. Increasing evidence indicates that nature provides restorative experiences that directly affect people's physical, social and mental well-being and health in a positive way. An emerging body of evidence has linked exposure to green spaces with improving both perceived and objective physical and mental health, well-being and decreased mortality. Including living near to, walking in it and even gardening.

Underlying mechanisms of health benefits of green spaces are not well understood, but research suggests that increasing physical activity, reducing psychological stress, anxiety and depression, while increasing social contacts/cohesion and a sense of community belonging 1, reducing noise and air pollution levels, and moderating ambient temperature may underlie such benefits 2,3.

A recent study found that living in more densely vegetated areas was associated with fewer deaths from causes other than accidents. Using data from the Nurses’ Health Study after controlling for factors including socioeconomic status, race, smoking, and whether the women lived in a rural or urban area, the researchers estimated a 12% lower rate of non-accidental death between women who lived in the most densely, versus least densely vegetated areas. When looking at specific causes of death, the researchers estimated a 41% lower rate of kidney disease mortality, a 34% lower rate of respiratory disease mortality, and a 13% lower rate of cancer mortality in the women who lived in the greenest areas, compared with those in the least green areas 4.

A study of adolescents reported lower risk factors associated with cardiovascular disease and diabetes in greener areas 5. In a cross-sectional study of 11,404 adults in Perth Western Australia the odds of hospitalization for heart disease or stroke was 37% lower, and the odds of self-reported heart disease or stroke was 16% lower, among adults with highly variable greenness around their home, compared to those in neighborhoods with low variability in greenness. The odds of self-reported heart disease or stroke decreased by 7% per unit with every 25% increase in the level of greenness 6. In a controlled experiment where 14 children undertook two, 15 min bouts of cycling at a moderate exercise intensity while in one situation viewing a film of cycling in a forest setting and another with no visual stimulus. The systolic blood pressure (SBP) 15 min post exercise was significantly lower following green exercise compared to the control condition 7. The surrounding environment can also significantly impact healing outcomes for patients. Green views from windows have been shown to aid post-operative recovery 8,9

The rise in obesity is well documented and while there are many contributing factors, a systematic review of greenspace research from sixty studies reported the majority (68%) of papers found a positive association between green spaces and obesity-related health indicators 10. One study found that increased vegetation was associated with reduced weight among young people living in high population densities 11 and  across eight European cities, people were 40% less likely to be obese in the greenest areas 12. However, not all spaces are green that can have these benefits. There was also variation by greenspace type, with relationships found only for access to beaches in New Zealand 13 and park playgrounds among children in Canada 14. Overall, the majority of studies found some evidence of a relationship with weight and greenspace 10. In children exposure to greenness has been associated with reduced sedentary behavior and obesity 15,16. In study of 3,178 schoolchildren (9-12 years old) a 25% range increase in residential surrounding greenness was associated with 11-19% lower relative prevalence of overweight/obesity and excessive screen (television and computing) time. Similarly, residential proximity to forests was associated with 39% and 25% lower relative prevalence of excessive screen time and overweight/obesity, respectively 17.

The lower prevalence of obesity, adverse health and improved health outcomes may be attributable to higher levels of physical activity, such as neighborhood walking which is positively influenced by the natural environment. Walking is the most popular physical activity 18, and levels of recreational walking have been linked the distance to and attractiveness of local parks and ovals 19.  Many studies have reported that adults with access to a large high-quality park within walking distance (within 1600 m) from home have elevated levels of walking 20 and and in general live longer 21. In a review of 50 studies twenty studies (40%) reported a positive association between greenspace and physical activity, including children and older people.

Being around vegetation can lead to better mental health and less stress 22,23, positive emotions 24,25, focus and attention 26, as well as reduced stress 27. While walking itself can reduce stress, walking in a natural setting provides greater stress-relieving benefits 28.  There is also evidence that exposure to natural settings can lower blood pressure, reduce mental fatigue, reduce negative feelings, increase attentional capabilities, and enhance effectiveness in dealing with major life issues.  The most preferred parkland settings have repeatedly been shown to be those where human influences do not dominate the natural elements 29. Accessible green spaces are ‘escape facilities’, and lack of access to green space contributes to poor mental health 30. Some of the more potent restorative effects of nature relate to being able to ‘get away’ from everyday settings and immerse oneself in an extensive natural setting that creates a sense of being in a ‘whole other world.’ A “quiet fascination, characterized by a moderate level of effortless attention coupled with aesthetic beauty in the setting, will foster a more deeply beneficial restorative experience” 31. In one study after a 40 minute test to exhaust their directed attention capacity participants were randomly assigned 40 minutes walking in a local nature preserve, walking in an urban area, or sitting quietly while reading magazines and listening to music. Those who had walked in the nature preserve performed better than the other participants on a standard proof reading task. They also reported more positive emotions and less anger.

Green spaces have been associated with improved mental health in children. Neuropsychiatric problems including behavioral problems occur in 10–20% of children worldwide. The most commonly diagnosed behavioral disorder among children and adolescents is attention deficit/hyperactivity disorder (ADHD). In one study investigating ADHD symptoms they found a statistically significant inverse associations between green space playing time and total difficulties, emotional symptoms, and peer relationship problems; between residential surrounding greenness and total difficulties and hyperactivity/inattention and ADHD total and inattention scores; and between annual beach attendance and total difficulties, peer relationship problems, and prosocial behavior 32. In another study results indicate that children with ADD function better than usual after activities in green settings and that the “greener” a child’s play area, the less severe his or her attention deficit symptoms  33. Thus, contact with nature may support attentional functioning in a population of children who desperately need attentional support.

And the benefits do not seem to end there. Recent research suggests an association between increased residential greenness and improved birth outcomes. The researchers assessed the relationship between birth weight, preterm birth, and residential greenness among 64,705 births recorded and reported that increases in greenness were associated with higher birth weight for babies born at term (37 weeks or later) and decreased likelihood of having a moderately or very preterm birth, or a small-for-gestational-age baby 34. In a study of 2,393 pregnant women, on average, babies born to mothers living in "greener" areas had higher birth weights and slightly larger head circumference compared to babies whose mothers lived in areas with lower plant cover. The effects were strongest in babies born to moms with lower education, suggesting that increasing green space may have the most benefit in socioeconomically deprived areas 2.

Unfortunately, as the urban expansion and infill continues we are no longer getting our daily exposure to green environments. Increasing housing density can contribute to urban sustainability, but the loss of private garden space must be compensated for the availability of quality public open space and ‘green infrastructure’ throughout urban areas. While the health of the populations is important nature provides critical ‘ecosystem services’ essential for our long term survival.  These include filtering air and water, absorbing wastes, maintaining beneficial insect and bird populations, and nutrient cycling.  There is also evidence that green spaces in urban areas help to moderate the urban climate and in some cases could offset the heatwaves associated with global warming. Perhaps we need to rethink our building incorporating more green and our ever increasing encroachment on our green spaces?



  1. Hartig T, et al. 2014
  2. Dadvand et al. 2012
  3. Lee and Maheswaran 2011
  4. James P, et al.2016
  5. Dengel et al. 2009
  6. Gavin Pereira et al 2012
  7. Duncan, et al 2014.
  8. Hartig et al, 2003
  9. Kaplan, 2001
  10. Lachowycz and Jones 2011
  11. Liu GC, 2007
  12. Ellaway et al 2005
  13. Witten K 2008
  14. Potwarka 2008
  15. Bell et al. 2008
  16. Wolch et al. 2011
  17. Dadvand et al 2014
  18. McCormack et al, 2003
  19. Giles-Corti et al, 2005
  20. Sugiyama T, et al 2010
  21. Takano 2002
  22. Ward Thompson et al 2012,
  23. Taylor MS, et al.2015
  24. Hartig et al 1991,
  25. Hartig et al. 2003
  26. Berman 2008
  27. Marselle et al 2014
  28. Gidlöf-Gunnarsson & Öhrström, 2007
  29. Bjerke et al, 2006
  30. Guite, Clark & Ackrill, 2006
  31. Herzog, Maguire & Nebel, 2003
  32. Amoly, 2014
  33. Taylor and Kuo 2001
  34. Hystad P, et al. 2014


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Was Being Active in the New Year Your New Years Resolution - Find out the benefits

Was Being Active in the New Year Your New Years Resolution - Find out the benefits

In the new year, with all the mention of healthy foods it is also important to put the role of physical activity in perspective and perhaps make that one of our top goals for 2017. Up until 10,000 years ago, humans were still living a nomadic, hunter-gatherer lifestyle, scouting the landscape in the search for food, which placed a high level of physical stress on the body. Even going back just 200 years, humans were much more physically active than they are today, living a predominantly agrarian life, running farms and crop fields.

The genetic and physical make up of humans has not changed significantly since those days, but our levels of physical activity have. In addition, with each subsequent generation, levels of physical activity have reduced - the highest participation in physical activity occurs amongst school-aged children and adolescents, but this tends to decrease with age. A study of 1032 participants, found that after age 9, physical activity decreased by 38 minutes per year, while weekend physical activity decreased by 41 minutes per year. Additionally, at around 13.1 years in girls and 14.7 years of age in boys, the level of physical activity went below the recommended 60 minutes of physical activity per day 1.

In Australia, conservatively more than 8000 deaths occur annually due to lack of physical activity, costing not only lives and suffering, but also millions of dollars to the health care system. Increased physical activity has been associated with increased life expectancy, as well as reduced risk of heart disease, stroke, hypertension, obesity, diabetes, cognitive decline and Alzheimer’s disease 2,3 and much more. The single biggest killer in Australia today is cardiovascular disease (CVD) and an individual who undertakes regular physical activity, is half as likely as his sedentary counterpart to contract cardiovascular disease (CVD) 4,5,6.

A large number of studies have reported that physical activity not only reduces the risk of, but also protects against coronary heart disease 7,8,9. Additionally, in a cohort study of 743,498 men, aerobic fitness in late adolescence was a good predictor of a heart attack later in life. However, obese men with high aerobic fitness had a higher risk of heart attack than lean men with low aerobic fitness. Therefore, it is important to be physically active and maintain a healthy weight to keep the risk of heart attack at it's lowest 10.

High Blood pressure, or hypertension, is characterised as any blood pressure over 140/90, with the optimal being 120/80. Exercise resulting in weight loss, has been shown to have significant benefits in reducing blood pressure. Numerous large population-based studies 11,12,13 have demonstrated an inverse relationship between physical activity and blood pressure. In addition, interventional studies where individuals were trained to do more physical activity, demonstrated that increased exercise works to lower blood pressure 14,15.  Furthermore, a randomized, controlled trial, found exercise training is effective in lowering blood pressure in overweight, sedentary patients with high-normal or mildly elevated blood pressure, and that weight loss is of added benefit when combined with aerobic training 16.

Physical activity has been shown to decrease mortality and increase life expectancy. In a study of 252,925 men and women, those doing moderate activity (at least 30 minutes on most days of the week) decreased mortality risk by 27%, whereas those who met recommendations for vigorous activity, at least 20 minutes, three times per week- not much if you really think about it, had a 32% reduction of mortality risk 17 a finding consistent with many other studies 18,19,20. And it is not too late to start now no matte how old you are. In a 4.9 year longitudinal study of 9,777 men, it was discovered that those who improved from unfit to fit, reduced their all-cause mortality risk by 44% and cardiovascular mortality by 52%, compared to those who remained unfit 21.

Inflammation and Triglycerides

Inflammation is the underlying condition in many chronic illnesses, including CVD and cancer. Physical activity decreases inflammation and additionally, those with higher cardio fitness levels, have lower circulating levels of inflammation markers such as of IL-6, CRP and fibrinogen 22. Physical activity and fitness are also associated with improved plasma lipid (fat) profiles, including the ratio of high-density lipoproteins (HDLs) to low-density lipoproteins (LDLs), and plasma triglycerides. Triglycerides decrease by 24%, while HDLs increase by about eight percent, in response to regular physical activity 23,24. Studies have also shown similarly favourable findings in diabetes 25.

Low levels of physical activity and cardio-respiratory fitness, are associated with the development of metabolic syndrome and type 2 diabetes. In one study, older men and women, who were in the lowest third of cardio-respiratory fitness, had a 10-fold higher risk of developing metabolic syndrome than those who were in the highest third. There was a strong inverse association between fitness and metabolic syndrome, as well as a significant relationship to all the components of metabolic syndrome 26.

Additionally, a low fitness level has been found to be an important risk factor for incidence of type 2 diabetes - men with the lowest 25% of fitness had a relative risk of diabetes that was four times higher compared to those in the highest 25% 27. It seems that both physical activity and fitness are separately and independently associated with metabolic risk profile 28 i.e., they are both contributing factors to reducing the risk of metabolic syndrome.

Incorporating more exercise to the day-to-day routine, is crucial for sufferers of type 2 diabetes. In type 2 diabetes, insulin is in short supply, or is difficult for the body to utilize – exercise, has been shown to improve the body's sensitivity to insulin. Not only does exercise help improve the diabetic condition, it can also help reduce the risk of developing type 2 diabetes altogether. A Harvard University study examining the exercise habits of more than 70,000 women, showed that a 40 minute walk every day reduced type 2 diabetes risk by 40%, and with a longer walk the risk could be decreased by an even larger percentage.

Exercise also helps to increase blood flow, which is important to help reduce the risk of neuropathy, a common neurological disorder associated with type 2 diabetes. In addition, studies have shown that a short-term reduction in daily physical activity, negatively affects insulin sensitivity.

One small step for diabetes. Just as important as the amount of exercise for diabetes is the timing. Much of the damage done in diabetes is done by the circulating sugar and or high insulin levels causing oxidation, inflammation and acidosis. Going for a walk 10 or so minutes after eating, particularly after a large dinner can have a direct and rapid impact on lowering blood sugar and subsequently the amount of insulin required to control the sugar. It is very important to bear in mind that this small change to a days routine can make a big difference in managing diabetes.

Immune System

The immune system may be enhanced or depleted, depending on the intensity of physical activity 29 - both too little and too much exercise is proven to be detrimental to the immune system. For example, there is a high incidence of upper respiratory tract infections (URTI) in professional athletes (50-70% getting an infection in the 2 weeks following a marathon), which suggest that too much exercise can act as an immunosuppressant. Similarly, longitudinal studies have shown that moderate exercisers can overcome URTIs in half the time that an elite athlete does. Studies have also demonstrated similar findings with a decrease in mucosal (salivary etc) immunity with excessive exercise 30. Whilst excessive exercise may have a detrimental effect to the immune system, research has suggested that moderate levels of exercise can be beneficial to the immune system. Blood lymphocyte concentrations of a sedentary person are comparable to that of a high performance athlete, whereas the lymphocyte count is higher in a person who undertakes regular moderate exercise. Research suggests that regular, but not excessive exercise, improves the immune system 31,32.

Osteoarthritis (OA) is the second most common cause of disability in the developed countries and Rheumatoid Arthritis (RA), has also become a major health concern 33,34. Both are degenerative diseases of the joints, which can be improved with the implementation of moderate aerobic and weight bearing exercise. Research shows that short term gains of muscle strength, and a range of movement can increase the functionality of patients suffering from OA or RA. In addition, improved fitness levels have been shown reduce the risk of gout, another form of arthritis, in physically active men 35.

Different forms of activity have shown to have important impacts on our hormones and  endocrine system. In the period prior to, during and after exercise, the endocrine system reacts in order for the body to function effectively and at optimum levels. Simultaneously, hormones governing the body's regulation, such as epinephrine and norepinephrine, are produced in greater quantities to assist the body in operating efficiently.

Additionally, physical activity has demonstrated positive effects on mental health, and has been shown to be more effective than drug therapy without any deadly side effects and works well alongside counselling therapy for depression and anxiety. It has been shown to improve individuals’ mood, reduce anxiety and stress, and increase self-esteem. Physical activity has been demonstrated to bring about positive structural brain changes and plasticity, as well as alter the production of neurotransmitters including Gamma-Aminobutyric acid (GABA). If you want to be smarter make sure you get enough exercise.

On the other side of the equation a number of medications can have a negative impact on the level of physical activity. For example, the most prescribed drug worldwide, statins, which are used to lower cholesterol, reduce the effectiveness of exercise. A recent study found the statin previously sold under the brand name "Zocor," hindered the positive effects of exercise for obese and overweight adults by 85%. The study also found that this statin, decreased the effectiveness of the mitochondria (power house) in the muscles.

It seems that statins block the ability of exercise to improve the fitness levels of the individual that takes them. Participants in the exercise-only group increased their cardio-respiratory fitness by an average of 10% compared to a 1.5% increase among participants also prescribed statins. Additionally, skeletal muscle mitochondrial content, the site where muscle cells turn oxygen into energy, decreased by 4.5 percent in the group taking statins while the exercise-only group had a 13 percent increase, a normal response following exercise training.

With the new year upon us it is time to get serious about our physical activity. There are just far too many benefits. It doesn’t have to be much just a little bit every day is enough to get you started on a better health journey.

  1. Nader, et al., 2008
  2. Lindsay et al., 2002
  3. Kohl 2001; Kujala 2004
  4. Berlin and Colditz 1990
  5. Miller, Balady and Fletcher 1997
  6. Rastogil et al., 2004
  7. Sundquist, Malmstrom and Johansson 1999
  8. Fletcher et al., 1996
  9. Kiess et al., 2001
  10. Hogstrom et al. 2014
  11. Criqui et al.,1982
  12. Hickey et al., 1975
  13. Miall and Oldham, 1958
  14. deVries, 1980;
  15. Jennings et al., 1986
  16. Blumenthal et al., 2000
  17. Leitzmann et al., 2007
  18. Manini et al., 2006
  19. Reis et al., 2009
  20. Heinzelmann and Bagley 2009
  21. Blaire et al., 1995
  22. Kullo et al., 2007
  23. Anderson and Anderson 1998
  24. Durstine et al., 2002
  25. Sigal et al., 2006
  26. Hassinen et al., 2008
  27. Sawada et al., 2003
  28. Steele et al., 2008
  29. Bruunsgaard and Pedersen 2000
  30. Pyne and Gleeson 2000
  31. Kendall, et al., 1990
  32. Rhind, et al., 1994
  33. Cote, 2001
  34. Kettunen and Kujala, 2004
  35. Williams, 2008



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Are your medications making you (Pharmaceutical) fat?

Are your medications making you (Pharmaceutical) fat?

Most people don't realise that a large number of pharmaceutical agents, including many over-the-counter and prescription drugs, are linked with weight gain and obesity. Drug-induced weight gain is a serious side effect of many commonly used drugs. The weight gain can be extremely high in a relative short time: sometimes more than 10 kg over 12 months. Some medications can increase appetite, cause fluid retention, or slowly lead to weight gain over a period of time due to fatigue and lower activity.
The best know impact, however, is the role of antibiotics in weight gain. The growth (fat) promoting effects of antibiotics were first discovered in the 1940s. Since then, antibiotics administered in low doses have been widely used as growth promoters in the agricultural industry worldwide. As a result, the largest use of antibiotics and related antimicrobial substances is on farms, with low doses fed to large numbers of animals used for food production, to increase weight gain by as much as 15%. If antibiotics are so effective in causing weight gain in farm animals, similar results are likely to occur in human populations. Unfortunately, antibiotic use in humans has increased markedly, often for the wrong reasons, now approximating one antibiotic course per year for the average child and most of them for the wrong reason. Antibiotics can cause many problems and we do overuse them. For a bacterial, not viral, infection always listen to you health professional; the gut microbiome can be rebuilt after the treatment finishes with super probiotics and prebiotics.
Blood pressure lowering medications such as Beta blockers reduce metabolic rate and slow utilization of nutrients, thus resulting in weight gain. Obesity and hypertension contribute to metabolic syndrome, which could further complicate the patient’s situation. Many of the diabetes medications can lead to weight gain. These agents may increase insulin production, which can lower blood sugar levels and result in an elevated appetite. Injectable insulin itself can also lead to weight gain, possibly due to periods of low blood sugar that stimulate appetite. Other drugs used in the treatment of type 2 diabetes can lead to weight gain and fluid retention.
Many psychotropic drugs, including antipsychotics, antidepressants and mood stabilizers, are also linked with significant weight gain. In a study of three antipsychotic drugs over 12 months, at three months haloperidol added 3.8 kg, risperidone 5.9 kg and 8.4 kg for olanzapine. After one year, all participants had gained between 9 and 11 kg. Some antidepressant drugs induce significant body weight gain, which may amount to 20 kg over several months of treatment. The older antidepressants, known as tricyclic antidepressants (TCAs) are notorious for increasing appetite and causing weight gain.
Commonly prescribed oral glucocorticoids like prednisone can also cause significant weight gain, especially when taken over prolonged durations, by causing fluid retention, stimulating appetite and increasing deposits of fat in the upper part of the body and the abdomen. Antihistamine drugs that are used to treat allergies can result in weight gain through blocking of a chemical called histamine in the brain. Weight gain is a common side effect of drugs used for headache prevention.
Statin drugs used to lower cholesterol have now been shown to be ineffective in prevention of heart disease. However, they are associated with an increase in diabetes and weight gain.
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Sleep is Important

Sleep is Important


Sleep has been shown to be as important to the human body as food and water, but most of us still don’t get enough sleep. We obtain treatment for illness or injury – yet we generally fail to seek help when we aren’t getting enough sleep. The average length of sleep has declined from around 9 hours a hundred years ago to seven hours or less today. And the depth of sleep has also declined.

Sleep is complicated in the way that there are many different factors that influence the effectiveness of sleep. It’s not just duration that determines the effectiveness of said sleep, factors such as quality, frame of mind and deepness all contribute to the maximum desired outcome and even our perception of how we sleep. Many factors can play a part in the quality and quantity of our sleep and to maximize our sleep time an understanding of this is essential.     

On average a healthy person will spend around one third of their life sleeping.  Sleep is considered a natural periodic state of rest for the mind and body, in which the eyes will usually close and consciousness is completely or partially lost resulting in a decrease in bodily movements and responsiveness to external stimuli. Inadequate hours of good quality sleep leads to a disruption to vital biological processes resulting in a decrease in cognitive function mental and physical health including impaired work performance due to a decrease in attention, judgment and responsible decision making. 

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Fluoride Lowers Kids Intelligence

Fluoride Lowers Kids Intelligence

There is increasing evidence emerging from the scientific community which suggests that mass-medication in the form of water fluoridation is in fact having a serious and adverse effect on the public’s health. A recent report from the US National Research Council 1 concluded that adverse effects of high fluoride concentrations in drinking-water may be of concern. Animal studies have shown Fluoride may cause neurotoxicity, including effects on learning and memory 2,3. Recent experiments where the rat hippocampal neurons were incubated with various concentrations of sodium fluoride showed that fluoride neurotoxicity may target hippocampal neurons.

Fluoride readily crosses the placenta exposing the developing brain, which is much more susceptible to injury caused by toxicants than is the mature brain, may possibly lead to damage of a permanent nature 4

In a study conducted by Tianjin Medical University in China, a comparison in the Intelligence Quotient (IQ) was measured between 60 children living in a high fluoride area and 58 children living in a low fluoride area. The IQ of the 60 children living in the high fluoride area was lower than that of the 58 children living in the low fluoride area. 21.6% of the children in the high fluoride area were retarded compared to 3.4% of retarded children living in the low fluoride area 5.

In a study at Tokyo University Medical School, water fluoridation was linked to Down syndrome. The study found that - as well as the aging of mothers - the number of excess Down syndrome births caused each year by water fluoridation was estimated to be several thousand cases throughout the world 6.

In the most recent meta analysis of 27 eligible epidemiological studies found that children in high fluoride areas had significantly lower IQ scores than those who lived in low fluoride areas 7. The conclusions of the study “support the possibility of an adverse effect of high fluoride exposure on children’s neurodevelopment.”

Some of the other adverse health effects of fluoride include lowered levels of collagen synthesis, depleted energy reserves and lowered immunity, irritable bowel syndrome,thyroid disorders, Skeletal fluorosis, Osteosarcoma, Osteoporosis and bone fractures as well as Alzheimer's disease.

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Supplements for the Heart

Supplements for the Heart

Vitamins for the heart

The science is overwhelming. We can reverse heart disease, unblock arteries and lower blood pressure with good nutrition and lifestyle changes and it can be improved even further with supplementation. There are now thousands of articles in all levels of scientific journals—on the benefits of supplementing, not only for the general population but also for cardio vascular disease conditions. Unfortunately, these do not seem to get media attention despite the fact that they may show dramatic reductions in the incidence and severity of diseases such as heart attack, stroke, and diabetes. However, we may need to re-evaluate our expectations when investigating nutrients used to treat serious chronic disease because it is unrealistic to expect a vitamin to undo a lifetime of unhealthy behaviours on there own and in a short period of time.

In fact, most people do supplement, especially those who know the most. Our own research shows us that people who supplement are usually people who have higher levels of education, enjoy a healthier diet and lifestyle and are more interested in health; these are people who are taking responsibility for their own health. The increasing use of dietary supplements in general is one example of better health through preventative measures, which is a result of consumers wishing to take charge of their wellbeing.

Far too much credit is given to the Recommended Daily Intakes (RDIs) of nutrients, the information on the side of your breakfast food box, as a guide to healthy nutrition. These guides are based on precluding acute nutrient shortages, not preventing or treating modern day chronic disease epidemics. There has been a big shift in thinking from the concept of “adequate nutrition,” being all that is required, to “optimal nutrition” needs, the nutrients that help us flourish and be free of disease. Our early nutrition models were great for preventing scurvy and pellagra but not for the chronic illnesses that afflict so many now. Current evidence suggests that optimising nutrition and metabolism will delay ageing and the diseases of ageing in humans, including CVD. The proof however is in the pudding. I have seen so many people, literally in the hundreds, who have told me how they have personally benefitted from supplementing. Most commonly though, I see people who have a new lease on life: they feel better and have more energy and libido both good indicators of cardiovascular health.

A 2010 Swedish study of 31,671 women found that multivitamin use was associated with a reduction in the rate of heart attack (myocardial infarction), especially long-term use among women with no CVD. During an average of 10 years of follow-up, the women without any history of CVD who took multivitamin supplements had 27% fewer heart attacks over the period. That is better than any drug to lower cholesterol and has no negative side effects. The use of multivitamins over a five-year period—that is, those who took them the longest—saw a reduction of 41%.

Vitamin C supplementation has been shown to benefit many of the underlying mechanisms of the development of atherosclerosis (plaque build up) and hypertension, including preventing oxidation of cholesterol and improving endothelial dysfunction in patients with proven artery disease.[1] A 2011 study found that adequate intake of vitamin C was associated with longer survival in patients with heart failure.[2] The study of 212 patients, average age of 61, found that heart failure patients with low levels of vitamin C had the highest levels of inflammation markers and had more major heart attacks and higher death rates. The heart failure patients in the study with low vitamin C were also about twice as likely to die from heart disease within one year of follow-up.

A meta-analysis of 29 clinical trials with a median dose of 500 mg per day for eight weeks showed a reduction in systolic blood pressure of 3.84 mm Hg and 1.48 mm Hg for diastolic blood pressure. In trials in hypertensive participants, corresponding reductions in SBP and DBP were 4.85 mm Hg and 1.67 mm Hg [3] and higher doses of vitamin C also produced greater reductions in blood pressure. In a meta-analysis of 29 randomised, controlled, clinical trials investigating vitamin C intake, researchers found that taking an average of 500 milligrams of vitamin C daily reduced blood pressure by 3.84 mm Hg in the short term.[4] Among those diagnosed with hypertension, the drop was nearly 5 mm Hg. Patients who take blood pressure medication such as ACE inhibitors or diuretics can expect a roughly 10 millimetre of mercury reduction in blood pressure.

A number of studies have demonstrated that high dosages of vitamin E or supplementation are associated with a significant reduction in cardiovascular diseases [5] with relative risk reductions up to 65%. The Cambridge Heart Antioxidant Study (CHAOS) examined the effects of vitamin E supplementation on 2,002 patients suffering from coronary atherosclerosis, the buildup of arterial plaque, over a period of three years. Patients with advanced coronary heart disease were able to significantly reduce their risk of suffering a heart attack if they supplemented with vitamin E at the levels of 400 international units (IU) to 800 IU per day.[6] Patients receiving supplementation of vitamin E were less than half as likely to suffer a heart attack than those receiving the placebo. Two additional large prospective studies also found that persons who supplement with vitamin E for at least two years display approximately 40% lower incidence of coronary heart disease than those not taking vitamin E supplements.[7]

In a study of 39,910 US male health professionals 40 to 75 years of age who were free from coronary heart disease, diabetes and high cholesterol, researchers found a lower risk of coronary disease among men with high intakes of vitamin E. Researchers found that men who took at least 100 IU per day for at least two years had a risk reduction for coronary disease of 37%. The maximal reduction in risk of around 40% was seen among men consuming 100 to 249 IU per day with no further decrease at higher levels. In a study of 87,245 female nurses followed for up to eight years, both vitamin E supplements and multivitamins were associated with a lower risk of major coronary disease and the relative risk from multivitamins was a result of the vitamin E content.[8] The use of vitamin E for two or more years was associated with a 41% decreased risk. Researchers found that a dose of less than 100 IU per day was associated with little or no apparent benefit.

Vitamin D is a pro-hormone that plays an essential role in the vasculature and in kidney function not to mention dozens of other functions including immune health. Low vitamin D concentrations appear to significantly associate with left ventricular hypertrophy, increased arterial stiffness, hypertension, endothelial and renal dysfunction [9] in normal subjects and in patients with chronic kidney disease and type 2 diabetes. Low vitamin D reduces calcium levels in the blood, causing weak heart muscle contraction and strength. Arteries become stiff and blood flow is poor. D3 allows the immune system to address infection that creates build up of plaque in arteries. Large recent populations studies have shown that up to 75% of people are D3 deficient and 40% are severely depleted.

In a study of 12,644 US civilians, systolic BP was inversely and significantly correlated with 25(OH)D levels.[10] Other large international studies have reported similar results.

A growing number of studies suggest that exposure to sunlight improves health overall, because the benefits of reducing blood pressure far outweigh the risk of developing skin cancer. Heart disease and stroke linked to high blood pressure are estimated to lead to around 80 times more deaths than those from skin cancer in the UK. Production of nitric oxide rises after exposure to sunshine. In a study of the blood pressure of 24 volunteers who sat beneath tanning lamps for two sessions of 20 minutes each, the results showed that blood pressure dropped significantly for one hour following exposure to UV rays, but not after the heat-only sessions.

Coenzyme Q10 (CoQ10) is an essential cofactor (helper) of enzymes involved in the process of energy production. Coenzyme Q10, or ubiquinone, helps to convert fats, carbohydrates and protein into energy. Coenzyme Q10 is an obligatory member of the respiratory chain in the mitochondria of all cells. Cells that make up tissue with higher energy demand, such as muscles, have a higher number of mitochondria present. These tissues include the tissues of the heart, where CoQ10 plays an important role in protecting the heart. Coenzyme Q10 has been extensively researched for its ability to strengthen the heart muscle, specifically in patients with heart failure. Coenzyme Q10 (CoQ10) is naturally produced in the body and is the only antioxidant that humans synthesise in the body, but levels drop off as we age.

In a controlled study, researchers found that supplementing with CoQ10 (100mg twice a day) and selenium (200 mg) reduced heart attack risk in the elderly by around 50%.[11] In the study, researchers gave 433 people, aged from 70 years upwards, the supplements or placebo pills every day for five years. Other heart failure medications block, rather than enhance, cellular processes and may have side effects. Supplementation with CoQ10, which is a natural and safe substance, corrects a deficiency in the body and blocks the vicious metabolic cycle in chronic heart failure called the “energy starved heart.”

B vitamins have been associated with a 24% reduction in heart disease risk in women who take four to seven multivitamins a week.[12] There was a significant inverse relation between dietary intake of folate and vitamin B6 and mortality and morbidity from cardiovascular disease in the Nurses’ Health Study of 80,082 women over 14 years.[13] Each 100-microgram-per-day increase in folate was associated with a 5.8% lower risk of coronary heart disease. In a retrospective cohort study of 5,056 men and women aged 35 to 79 years, there was a 69% increase risk of coronary mortality among those in the lowest levels compared with the highest blood levels of folate.[14]

In a study of 38 patients with atherosclerosis of the carotid arteries, supplementation with folic acid pyridoxine and vitamin B12 was associated with regression of the arterial plaque—that is, reversing the plaque in the arteries.[15] WOW. The benefits of folic acid supplementation are further emphasised by a 1996 meta-analysis that calculated that around 56,000 deaths due to heart disease could be prevented yearly with adequate folic acid supplementation alone.[16]

One study reported a folate intake of 400 micrograms per day reduced total homocysteine (a major risk factor for heart disease) to the lowest level.[17] A controlled study of 46 people (42 men, average age 73) found that even a low-dose folic acid supplement (400 micrograms) could lead to significant reductions in hyperhomocysteinemic elderly people.[18] The researchers report that, while the low-dose folic acid supplements had no significant effect on homocysteine concentrations in the general study population, levels did significantly decrease in hyperhomocysteinemic subjects by 1.8 micromoles per litre.

Vitamin K is a fat-soluble vitamin also known as phylloquinone or phytomenadione. Increased intake of vitamin K reduces the buildup of calcium in arteries that leads to hardening of the blood vessels. A study found that higher intake of vitamin K2 (menaquinone), but not K1, was associated with a 20% reduction in calcification of the arteries (atherosclerosis). On the other hand, another study found that supplements of K1, also known as phylloquinone, might slow hardening of the arteries in people already suffering from the condition.[19] In support of the clinical human studies, in a study of rats high doses of vitamin K led to reduced arterial calcification.[20] The study found that high vitamin K intake not only prevents calcification but also even regresses arterial calcification. After six weeks of treatment with warfarin (supposed to reduce risk), researchers reported that the rats showed signs of significant arterial hardening. However, in both high-dose groups (K1 and K2) no continued calcification occurred, and the existing hardening was found to be reversed by about 40% after six weeks of supplementation. The reduced calcification was also accompanied by improved arterial elasticity in the high vitamin K groups to a similar level as in the control rats. Similar results have been shown on improving elasticity and reversing calcification of the skin with vitamin K supplements.[21]

Time to look at supplementing with more vitamins to lower your risk of heart disease.


1        Gokce et al. 1999; Vinta et al. 1998; Ting et al. 1997; Huang et al. 2000; Fonorow and Till 2003; Sakuma et al. 2001; Fernandez 2001.

2        Song et al. 2011.

3        Juraschek et al. 2012.

4        Miller et al. 2012.

5        Stampher et al. 1993; Rimm et al. 1993; Knekt et al. 1994; Kushi et al. 1996.

6        Stephens et al. 1996.

7        Stampher and Rimm 1995.

8        Stampher et al. 1993.

9        Liu et al. 2013.

10      Reis 2007.

11      International Journal of Cardiology (2012).

12      Harvard Heart Letter 1998.

13      Rimm et al. 1998.

14      Morrison et al. 1996.

15      Peterson et al. 1998.

16      Boushey et al. 1995.

17      Selhub et al. 1993.

18      Journal of Nutrition Research Vol. 26.

19      American Journal of Clinical Nutrition (2009).

20      Schurgers 2006.

21      Gheduzzi et al. 2007

[1] Gokce et al. 1999; Vinta et al. 1998; Ting et al. 1997; Huang et al. 2000; Fonorow and Till 2003; Sakuma et al. 2001; Fernandez 2001.

[2] Song et al. 2011.

[3] Juraschek et al. 2012.

[4] Miller et al. 2012.

[5] Stampher et al. 1993; Rimm et al. 1993; Knekt et al. 1994; Kushi et al. 1996.

[6] Stephens et al. 1996.

[7] Stampher and Rimm 1995.

[8] Stampher et al. 1993.

[9] Liu et al. 2013.

[10] Reis 2007.

[11] International Journal of Cardiology (2012).

[12] Harvard Heart Letter 1998.

[13] Rimm et al. 1998.

[14] Morrison et al. 1996.

[15] Peterson et al. 1998.

[16] Boushey 1995.

[17] Selhub et al. 1993.

[18] Journal of Nutrition Research Vol. 26.

[19] American Journal of Clinical Nutrition (2009).

[20] Schurgers 2006.

[21] Gheduzzi et al. 2007.

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