The term “metabolic syndrome” smacks of new age mumbo-jumbo. In reality, metabolic syndrome is a clutch of symptoms, including obesity, hypertension, and high blood sugar, which can lead to diabetes and heart disease. As causes and effects of these major killers find common ground, it is evident that metabolic syndrome demands attention.
First, a bit of backstory. For a much fuller explanation, consult Frank B Hu’s amazing textbook Obesity Epidemiology published by Oxford University Press in 2008.
In the late 1980s, several researchers spoke of the relationships between symptoms and conditions such as obesity, hypertension, lipid disorders and insulin resistance, treated separately up until then. The “deadly quartet” and “Syndrome X” didn’t stick.
Metabolic syndrome was coined by the World Health Organization (WHO) in 1998.
The WHO definition:
Impaired glucose tolerance with at least two of the following: dyslipidemia, hypertension, obesity or microalbuminuria.
Next, the Adult Treatment Panel (ATPIII) took a stab:
Three or more of the following: abdominal obesity, high triglycerides, low HDL cholesterol, hypertension, high fasting blood sugar
By 2005, the International Diabetes Foundation (IDF) thought these conditions would better define metabolic syndrome:
Central obesity plus any two of these four risk factors constitute a diagnosis of metabolic syndrome:
- raised triglycerides
- reduced high- density lipoprotein (HDL) cholesterol
- raised blood pressure
- raised fasting blood sugar
A rose by any other name is still a rose. Definitions may vary but the importance is clear; all of these conditions intersect.
Fatness, and particularly abdominal fat (also called visceral fat), appears to be the match which sets the metabolic dysfunction in motion. Substances secreted by excess adipose tissue interfere with metabolism and cause insulin resistance.
Turns out adipose tissue is packed with more than just excess energy. Inside this dynamic mass are several types of cells including immune cells and stem cells, which may become either fat cells or immune cells. Most people would vote for additional immune cells but alas, the all too prevalent menu of fatty, sugary foods casts that choice in the other direction.
- Which numbers are cut-off points? For example, ATPIII uses a fasting blood sugar above 119 mg/dL but IDF2005 uses 109 mg/dL.
- Does diagnosis lead to better treatment?
Meanwhile, microbiologists have discovered that gut microbes play no small part. When germ-free mice receive microbes from obese mice they get fatter than when transplanted with those from lean mice—all on the same chow and exercise schedule. Bariatric surgery has an immediate effect on blood sugar metabolism and changes in microbes are thought to be one reason. Read Gut microbiota and metabolic syndrome by Davide Festi and colleagues for a 2014 review of studies exploring the pathogenic role of gut microbiota in the development of metabolic syndrome.
This excerpt is a good summary: “An impairment of the fine balance between gut microbes and host’s immune system could culminate in the intestinal translocation of bacterial fragments and the development of “metabolic endotoxemia”, leading to systemic inflammation and insulin resistance… Manipulation of gut microbiota through the administration of prebiotics or probiotics could reduce intestinal low grade inflammation and improve gut barrier integrity, thus, ameliorating metabolic balance and promoting weight loss.”
Probiotic research shows promise in rolling back some of the mess left behind by metabolic syndrome.