Sugar & Health

Metabolic Syndrome

The Rise of Metabolic Syndrome 

  • Metabolic Syndrome is the name for a group of risk factors that raise your risk of heart disease, diabetes and stroke.
  • The Syndrome is becoming more common due to a rise in obesity rates.
  • Lifestyle modification associated with weight loss, including increased physical activity and appropriate dietary measures, are a key component to managing Metabolic Syndrome.


Defining Metabolic Syndrome

Metabolic Syndrome is the name for a group of risk factors that can raise a person’s risk of heart disease, diabetes and stroke (1). It may also be referred to as Dysmetabolic Syndrome, Insulin Resistance Syndrome, Obesity Syndrome or Syndrome X.

Risk factors for Metabolic Syndrome include:

  • Hyperglycaemia
  • Insulin resistance
  • Central obesity
  • Raised blood pressure
  • Dyslipidemia (increased triglycerides, predominance of small dense LDL particles or a low HDL-cholesterol)
  • Increased uric acid and gout
  • Increased plasminogen activator inhibitor (PAI-1)
  • NASH (non-alcoholic steatohepatitis)
  • Endothelial dysfunction
  • Increased pro-inflammatory cytokines
  • Increased homocysteine

The clinical usefulness of the term, Metabolic Syndrome has been debated over the years. Some argue that making a diagnosis is no more useful than an assessment of the individual risk factors alone. However, others believe it can be a useful clinical tool to help identify people who may be at higher risk of cardiovascular disease and diabetes, and to encourage them to seek regular follow up and treatment.

Diagnosing Metabolic Syndrome - Criteria suggested by different international organisations (2)

WHO (1999)

NCEP, ATP111 (2001)

IDF (2006)

Hyperglycaemia or insulin resistance,

Plus two of:

WH> 0.9 (M, 0.85 (F) or BMI > 30kg/m2

Triglyceride ≥ 1.7mmol/L or
HDL < 0.9mmol/L (M), 1.0mmol/L (F)

Blood pressure ≥ 140/90mmHg


Three or more of:

Central obesity: Waist > 102cm (M), 88cm (F)

Fasting glucose ≥ 6.1mmol/L

Triglyceride ≥ 1.7 mmol/L
Low HDL < 1.0mmol/L (M), 1.3mmol/L (F)

Blood pressure ≥ 135/85 mmHg or treatment

Central obesity: Waist (ethnic specific)
Europeans ≥ 94 cm (M), ≥ 80cm (F)
South Asians/ Chinese ≥90cm (M), ≥ 80cm (F)

Plus two of:

Fasting glucose ≥ 5.6mmol/L

Treated dyslipidemia:
Raised triglyceride ≥ 1.7mmol/L
Reduced HDL ≥ 1.03mmol/L (M),
≥ 1.29 mmol/L (F)

Treated hypertension:
Raised blood pressure: >130 systolic or > 85 diastolic

ATP= adult treatment panel; BMI = body mass index; F = female; HDL = high-density lipoprotein; IDF = International Diabetes Federation; LDL low-density lipoprotein; M = male; NCEP = National Cholesterol Education; W/H = waist/hip ratio; WHO = World Health Organisation

Prevalence and causes

While the concept of Metabolic Syndrome has been around for decades, there has been much debate over its definition, making it difficult to gauge the true global prevalence. In 2012, it was predicted in many affluent and some developing countries, that approximately a quarter of all adults would fit the criteria for Metabolic Syndrome set by WHO and the NCEP, and a higher proportion if the criteria suggested by the International Diabetes Federation was used (2).

Since this time, Metabolic Syndrome has become more prevalent due to rising obesity rates. New Zealand and Australia currently rank in the top five most obese nations in the OECD , with obesity continuing to climb in both countries, increasing across all age groups and both genders in the last decade (3, 4). We can therefore expect that our countries are also disproportionately affected by Metabolic Syndrome (5).

Differences in diet, lifestyle, age, genetic background and level of physical activity can all influence the prevalence of Metabolic Syndrome. While some factors cannot be controlled, including age and genetics (family history and ethnicity), other factors such as excess body weight, lack of physical activity, insulin resistance and diet can be moderated through lifestyle intervention.

Investigations into specific dietary factors that may increase risk of Metabolic Syndrome continue. While research indicates that asides from sugar’s contribution to energy, there is no direct relationship between sugar intake and obesity. There is some evidence that in excess amounts during states of energy surplus, fructose in particular may be linked to other Metabolic Syndrome risk factors via raised uric acid concentrations (6, 7). In animal studies, it has been shown that lowering uric acid concentrations could largely prevent features of Metabolic Syndrome induced by fructose including weight gain, insulin resistance and hypertension (8). In humans however; despite being unable to consume the volumes of fructose prescribed in animal studies; the levels of fructose consumed may play a small role in obesity, insulin resistance, dyslipidemia and hypertension. However these conditions all have complex and multi-factorial origins and therefore more research is required to see conclusive results (6).

Treatment and prevention

There are two general approaches to managing Metabolic Syndrome.  Treat Metabolic risk factors in isolation or target the root causes of the Syndrome, including high BMI, physical inactivity, and insulin resistance. While pharmacological modification of the associated risk factors has seen the most success in clinical practice, by far the greatest potential for both prevention and management of Metabolic Syndrome lies in reversing its root causes through lifestyle modification (9).  Weight loss associated with increased physical activity and the appropriate dietary measures provides the only means of favourably influencing the broad range of abnormalities associated with the Syndrome (2). A weight loss of just 5-10% is often enough to make a difference. Adequate sleep and stress management may also play an important role in management (10-12).

NEXT: Glycemic index and glycemic load

Key References

  2. Page 340-341, Essentials of human nutrition 3rd Ed.
  3. Statistics New Zealand. (2015). NZ Social Indicators: Obesity. Retrieved from
  4. Australian Bureau of Statistics. (2001-2013). Profiles of Health, Australia: Overweight and Obesity. Retrieved from
  5. Gentles D, Metcalf P, Dyall L, Sundborn G, Schaaf D, Black P, Scragg R, Jackson R. MetabolicSyndrome prevalence in a multicultural population in Auckland, New Zealand. N Z Med J. 2007 Jan 26;120(1248):U2399.
  6. Stirpe F, Della Corte E, Bonetti E, Abbondanza A, Abbati A, De Stefano F. Fructose-induced hyperuricaemia. Lancet 1970;2:1310 –1.
  7. Stavric B, Johnson WJ, Clayman S, Gadd RE, Chartrand A. Effect of fructose administration on serum urate levels in the uricase inhibited rat. Experientia 1976;32:373– 4.
  8. Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced MetabolicSyndrome. Am J Physiol Renal Physiol, 2006;290:F625–31.
  10. AlDabal L, BaHammam AS. 2011. Metabolic, Endocrine and Immune Consequences of Sleep Deprivation. Open Respir Med J. 5:31-43.
  11. Lappalainen R, et al., The effectiveness and applicability of different lifestyle interventions for enhancing wellbeing: the study design for a randomized controlled trial for persons with MetabolicSyndrome risk factors and psychological distress. BMC Public Health. 2014; 14: 310.
  12. Chandola T, Brunner E, Marmot M. 2006. Chronic stress at work and the MetabolicSyndrome: prospective study. BMJ 2006;332:521.




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