Global obesity has reached crisis proportions with more than 2.1 billion people, 30% of the global population, being overweight or obese.1 This number is expected to increase with 50% of the population being overweight or obese by 2030.1 The global economic impact is also staggering costing $2 trillion dollars (2.8% gross domestic product) for managing diabetes and related complications such as cardiovascular disease.1
Some of the causes of such an increase in obesity is likely because we live in an “obesogenic” environment. Urbanization has played a negative role because of sedentary occupations, computerization and mechanization, and improved transportation options. There have also been significant changes in nutrition with the exponential growth of the fast food industry providing highly processed, high fat, sugar, and salt food. Livestock has also been transitioned in that animals are intensely reared with a high omega 6 content with lesser amounts of omega 3. As you may recall, omega 3 has cardioprotective and antiinflammatory benefits and may play a role in the prevention diabetes and certain types of cancer. Grains are also highly processed and are poor sources of fiber, have micronutrients, and phytochemicals.
Australia is experiencing the same trends as other areas in the world regardless of the publicized recommendations for increased fruit and vegetable intake. The NHS, 2011-2012 reported2 that Australians are eating 30% less fruits and vegetables than 15 years ago. In addition, 25% of adults lack any vegetables in their diet while only 7% of the Australian population consumes the recommended 5 servings per day. The consumption of nuts and seeds is also significantly reduced with the average Australian eating 6g of nuts/seeds daily compared to the recommended value of 30 g/day. Of the daily 3 kg intake of food and beverages, 35% of the energy is from high fat, high sugar foods such as cakes, biscuits, alcohol, soft drinks, and chips.
As central adiposity is common in diabetes, these adipocytes produce a variety of cytokines with inflammatory potential. The Mediterranean diet, however, has a high proponent of anti-inflammatory properties therefore providing a defense against these cytokines.
The traditional Mediterranean diet has a favorable ratio of fat, carbohydrates, and protein, all of which are anti-inflammatory and antioxidant rich. The diet has a low environmental footprint and is economically accessible to a wide amount of people. There is a 4:1 plant to animal food ratio and many of the fats are high in omega 3.3 The main 10 items in the traditional Mediterranean diet include the following (Table).
An umbrella meta-analysis reviewed 13 meta-analyses of observational studies and 16 meta-analyses of randomized control trials.4 The total population was close to 13 million subjects and focused specifically on the Mediterranean diet and looked at a total of 37 different health outcomes.4 Findings demonstrated convincing beneficial evidence for Alzheimer’s disease, dementia, overall cancer incidence, and neurodegenerative disease.4 Highly suggestive outcomes were identified for overall mortality, cardiovascular disease, coronary heart disease, myocardial infarction, cancer incidence/mortality, cognitive impairment, and diabetes. Suggestive evidence was also represented in a number of health outcomes as well.4
A systematic review/meta-analysis study focused on the adherence to a Mediterranean diet and the risk of diabetes.5 In the more than 122,800 patients’ data collected from 2007 to 2014, there was a pooled relative risk reduction in type 2 diabetes of 19%.5
In Australia, there is a Greek migrant paradox where Greek-migrants appear to have a lower mortality despite high CVD risk profiles, including prevalence of diabetes. To review this finding in more depth, evidence from the Melbourne Collaborative Cohort Study was reviewed to determine if the Mediterranean diet reduced mortality.6 In more than 40,000 Australian-born and Southern-European-born men and women with type 2 diabetes, there was a modest but significant reduction (males 4%, females 6%) in mortality per unit of the Mediterranean diet score.6
The prevalence of diabetic retinopathy was also evaluated in Greek-born males (22%) compared to Australian-born males (37%) with Greek ethnicity associated with a 68% lower odds of diabetic retinopathy after adjusting for age, duration of diabetes, HbA1c level, and other parameters.7-8 The odds ratio was 0.32 (0.10-0.99); r2 = 0.41, p = 0.047.7-8 The effect of Greek ethnicity was also favorable compared to Australian patients, with Greek-born migrants having a lower risk of diabetic retinopathy.9
Questions remain regarding whether the benefit of a Mediterranean diet can be transferred to a non-Mediterranean population. To research this aspect, a randomized cross-over study was completed using a reconstructed Cretan Mediterranean diet in Australia. After 12 weeks of a Greek-style Mediterranean diet ad libitum vs. the usual diet, there was a clinically significant change in HbA1c (-0.3) equaling a 10% reduction in CHD mortality in type 2 diabetes.10 It is important to note that these finding were independent of weight loss.
When comparing a low-fat diet to a Mediterranean diet, a 6-month study noted improvements in dietary inflammatory index scores in patients with coronary heart disease in patients on the Mediterranean diet. These findings further demonstrate the anti-inflammatory properties of a Mediterranean diet.11
The Mediterranean diet has also shown benefits in improving hepatic steatosis and insulin sensitivity in people with non-alcoholic fatty liver disease. Patients on a Mediterranean diet demonstrated almost a 40% decrease in hepatic lipids compared to 7% of those on a low-fat diet (p = 0.03).12 There was also a greater decrease in the serum insulin concentrations in patients on the Mediterranean diet (35%) compared to those on a low fat diet (0%) (p = 0.008).12
Present disclosure: The presenter has reported that no relationships exist relevant to the contents of this presentation.
Written by: Debbie Anderson, PhD
Reviewed by: Marco Gallo, MD