October 12, 2014

Live well or Die Young – Professor Tieraona Low Dog 

  • We all want to be as healthy for as long as possible and compress any period of morbidity – there is so much we can do to help ourselves do this.
  • Medicine today is very adept at preventing and managing disease but often does not address ways in which we can promote health. Each of us must take responsibility and ownership of our own health.
  • What are the determinants of health or disease? 70-90% of chronic disease is influenced by lifestyle, environment, and physiology/biochemistry, with the balance being driven by genetics. But even there, genetics loads the gun while environment pulls the trigger.
  • If the American public embraced a healthier lifestyle (appropriate exposure to a clean environment, no smoking, no or moderate alcohol consumption, no or limited exposure to toxic chemicals, healthy nutrition, balance of exercise and rest, stress management, and social integration) we could prevent 93% of diabetes, 81% of heart attacks, 50% strokes and 36% of cancers. (Ford 2009)
  • There are two unifying themes driving most disease – inflammation and insulin resistance.
  • Inflammation is important to life, allowing for a rapid defense and repair mechanism, however, chronic inflammation is ultimately damaging to the organism.
  • Coronary artery disease was formerly considered a lipid accumulation-mediated disease; it has now been clearly shown to involve an on-going inflammatory response (Christodoulidis 2014). Many of the benefits of statins may be due to their anti-inflammatory activity, not simply their lipid lowering capabilities.
  • Inflammation and cancer – NFκβ – central mediator of inflammatory responses and activation of this is mechanism of host defense occurs in response to infection and stress. If inflammation remains active it causes havoc e.g. suppresses the types of genes that keep cancer growth under control (e.g. p53).
  • Central adiposity is more important than BMI when considering risk of cardiovascular disease (Coutinho 2013).
  • Excess weight, excessive carbohydrate intake, sedentary lifestyle and genetics are all driving insulin resistance.
  • Insulin like growth factors drive the growth of cells and have been linked to cancer.
  • Obesity is associated with many factors that cause an increased risk for cancer and cancer related mortality including insulin resistance, high blood sugar and insulin growth factors.
  • Factors that drive inflammation and insulin resistance – sedentary lifestyle, lack of exercise, pattern of central obesity, western dietary pattern, high fructose diet, prolonged psychosocial stress, environmental exposures, as well as alterations in gut flora and permeability.
  • Stress and its impact on the gut, the stress response is immediate in the gut, mast cell degranulation and release of histamine allows movement of luminal bacteria into mucosa triggering inflammation and increasing intestinal permeability. Lipopolysaccharides (LPS) from the membrane of gram-negative bacteria can then enter the bloodstream, binding to toll-like receptors and inciting systemic inflammation and altering insulin sensitivity. Chronic exposure to LPS may be contributing to weight gain and type-2 diabetes. This is one hypothesis for explaining the significant negative effects persistent stress has on health.
  • Social isolation and health – 148 studies including more than 300 000 people found that when people self identify as socially isolated – it can be as dangerous to one’s health as smoking 15 cigarettes/day, being an alcoholic, never exercising, and twice as dangerous as being obese (Lancet 2004).
  • Loneliness turns on the same genes that lead to heart disease, diabetes, cancer and possibly depression. Social isolation increases stress response, drives systemic inflammation and reduces immune response.
  • Having four close social contacts seems to be the magic number for most people!
  • Developing resiliency is important! The ability to bounce back – can be taught and enhanced.
  • There is no question that much of the chronic disease we are seeing at younger ages is due to the way we live our lives. An integrated approach that focuses on areas of diet, movement, stress management and resiliency can dramatically improve health and compress morbidity.
  • Do this for yourself and translate it to your family and those patients you care for. The motivation of being healthy should always be there. Invest in yourself.

Run For Your Life, Exercise and Health – Professor Manfred Lamprecht 

  • Appropriate physical exercise and a balanced diet complement each other for a healthier life.
  • The myokine concept helps to explain the anti-inflammatory effects of physical exercise training. There are a number of cytokine signalling pathways and mechanisms involved. E.g. IL-6 derived from muscle contraction improves glucose uptake and fat oxidation and muscle contraction inhibits TNF-alpha production.
  • Physical inactivity contributes to chronic inflammation and disease. However, it is also important to remember that false physical exercise (high intensity training) may exert pro inflammatory effects and can result in oxidative stress.
  • The key determinants of the anti-inflammatory effects of exercise include the duration, intensity, level of fitness and environmental conditions (ozone, air pollution, heat stress, altitude).
  • The key determinants of the anti-inflammatory effects of diet include hydration, balanced nutrition profile, plant food content and environmental conditions.

“Floss or Die” Revisited – Professor Thomas Dietrich 

  • Scandinavia studies linked oral disease to adverse health outcomes 25 years ago.
  • Associated systemic diseases linked with periodontitis – cardiovascular disease, diabetes, pre-term low birth weight, rheumatoid arthritis, chronic kidney disease, pancreatic cancer and cognitive impairment.
  • Is this relationship casual? Can we make a difference as a periodontist?
  • Patients with periodontal disease have a higher risk of certain systemic diseases. These associations exist independent of established risk factors.
  • 50% periodontal disease is determined by genetic factors but we don’t know specifically which genetic factors these are. We need to take into account pro-inflammatory genetic factors that influence pro-inflammatory susceptibility.
  • The inflammatory or infectious load that patients with periodontitis carry in the mouth is significant. A periodontal pocket can be seen as an ulcerated wound area in contact with a biofilm. The size of this can be compared to the palm of a hand if the disease is generalised. It is therefore not surprising we consider the systemic effects.
  • The ‘wound area’ differs between patients. If the patient is edentulous then the wound area is zero. Extraction may be a good answer after all?
  • Many mechanisms have been proposed to explain the association between periodontitis and systemic disease (Kebschull 2010).
  • Observational studies support association but currently no convincing evidence for causative relationship – AHA scientific statement (Lockhart 2012).
  • There is evidence from (some) RCTs indicating that non-surgical therapy of periodontitis may lead to improvement in surrogate cardiovascular endpoints and systemic inflammatory biomarkers. But studies are not always consistent and are relatively small
  • The effect of non surgical periodontal therapy on haemoglobin A1c levels in persons with type 2 diabetes and chronic periodontitis – a null result. Perhaps the treatment hadn’t worked? (Engebretson 2013)
  • Does periodontal therapy improve systemic health outcomes? We don’t know is the real answer to the question of causality, but it doesn’t look encouraging if we look at recent large phase III studies in the fields of adverse pregancny outcomes and diabetes. However, the results and limitations of these trials also demonstrate how little we know about the effectiveness of periodontal therapy in the general population, or in medically compromised patients. We should take this positively and say we have to do a lot of work in the periodontal arena to understand treatment better and the efficacy of what we are doing.
  • Problems epidemiological studies – susceptible to confounding. RCTs – problems of feasibility and a practical challenge due to the sample size and time needed, in terms of recruitment of patients with severe periodontal disease, question success of periodontal treatment and maintenance, external validity, expensive and difficulty in trying to answer a very specific question.


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