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Metabolic syndrome natural treatment

Metabolic syndrome can be prevented with a natural treatment.

Metabolic syndrome

The Metabolic Syndrome has been characterised in the United States in 1988 by G.M. Reaven [1].

Metabolic Syndrome, also called Syndrome X, is a serious health hazard worldwide and constitutes a major challenge for healthcare professionals. Clinicians are confronting a rise in obesity of epidemic proportions as a result of sedentary, affluent lifestyles. The rapid increase in the prevalence of the Metabolic Syndrome portends an equally daunting increase in both type 2 diabetes and cardiovascular disease (CVD). Recent prospective studies have confirmed that the Metabolic Syndrome predicts the development of type 2 diabetes and an increased CVD risk emphasising the clinical significance of the Metabolic Syndrome.

Consequently, the identification and treatment of the Metabolic Syndrome become critical in the prevention of both type 2 diabetes and CVD.”

From a pathophysiological point of view, there is a close link between metabolic syndrome, visceral adiposity, insulin resistance, inflammation and endothelial dysfunctions

 

 

Metabolic syndrome natural treatment

Metabolic syndrome can be prevented with a natural treatment. This treatment developed by bioXtract includes use of plant-based actives such as vinyldithiins and allylsulfides.

 

Definition of Metabolic Syndrome

This syndrome, also called syndrome X, is characterised by 5 factors. According to the new IDF definition, for a person to be defined as having the metabolic syndrome they must have:

 

  • Central Obesity: waist circumference ≥ 94 cm ♂and 80 cm ♀ or BMI ≥ 30

 

Plus any 2 of the following 4 factors:

 

High TG

≥ 150 mg/dL (1.7 mmol/L)

Or current treatment for this lipid abnormality

Reduced

HDL cholesterol

< 40 mg/dL (1.03 mmol/L)

< 50 mg/dL (1.29 mmol/L)

Or current treatment for this lipid abnormality

High

Blood Pressure

SystolicBP ≥ 130 or Diastolic BP ≥ 85 mm Hg

Or treatment of previously diagnosed hypertension

Fasting

Plasma Glucose

≥ 100 mg/dL (5.6 mmol/L)

Or previously diagnosed type 2 diabetes.

 

 

Prevalence of Metabolic Syndrome

Comparisons of published prevalence for different populations are difficult despite attempts to reach agreement on the metabolic syndrome.

 

A very consistent finding is that the prevalence of the metabolic syndrome is highly age-dependent. This pattern is clear in the USA where the prevalence of the metabolic syndrome (National Health and Nutrition Examination Survey [NHANES III] [2]) increased from 7% in participants aged 20-29 years to 44% and 42% for those aged 60-69 years and at least 70 years respectively.

 

The prevalence of Metabolic Syndrome in the Malaysian community is 22.9% following IDF definition (40.9% in males and 10.8% in women). Going by age groups, subjects aged 60 years and above exhibited the highest prevalence of Metabolic Syndrome (50.0%) by IDF definition compared to other age groups [3].

 

The prevalence of metabolic syndrome for different populations.

 

 

Pathophysiology of Metabolic Syndrome

Essential Role of Inflammation

 

From a pathophysiological point of view, visceral adipose tissue (abdominal fat close to visceral organs) is particularly incriminated in the genesis of insulin resistance (leading to type 2 diabetes) by its key role in the production of adipocytokines.

 

To summarize, adipocytes produce an excess of inflammatory factors (Cytokines: IL-6, IL-10 and TNF-α; Chemokines: M1P1a, MCP1) that  block the intracellular insulin-signaling pathways at different steps. Moreover, obesity is associated with an inhibition of adiponectin production. Adipose tissue increase in obese individuals leads to an imbalance in the production and secretion of anti-inflammatory and pro-inflammatory factors, in favour of pro-inflammatory factors.

 

These effects lead in time to insulin resistance, with as immediate and logical consequence, an anarchic discharge of free fatty acids (FFA) by adipocytes. These FFA will exert a “toxic” effect at different levels, in particular hepatic and muscular, leading to a certain number of clinical and metabolic abnormalities, characteristic of the metabolic syndrome [4],[5] (hypertension, lipid and glycemic disorders, muscular toxicity,…).

 

Metabolic syndrome pathophysiology.
Pathophysiology of the metabolic syndrome (adapted from [10])

 

Management of Metabolic Syndrome

Metabolic syndrome can be prevented with natural food supplements and a lifestyle change.

 

The presence of the metabolic syndrome carries increased risk for cardiovascular disease[6],[7] and type 2 diabetes [8]. Some affected people are at high or moderately high risk for major cardiovascular disease events in the short term (<10 years); others are at less risk in the short term, but carry fairly high long-term risk [9]. In the latter group, therapeutic lifestyle modification is first-line therapy, but if 10-year risk is high, drug therapy to modify cardiovascular disease risk factors might be required as well [2].

 

As obesity and weight gain in middle age are positively correlated with blood pressure levels, the therapeutic goal is to reach 10% weight loss on the first year, and thereafter to continue weight loss or to maintain weight. This weight loss will also have an incidence on the glucose levels and dislypidemia if correlated with physical activity (30-60 min of moderate-intensity exercise daily) and atherogenic diet. Complete smoking cessation is also recommended.

 

For high risk patients, treatment with LDL-cholesterol drugs, antihypertensive drugs and hypoglycaemic agents can be necessary to achieve goals of therapy.

 

In all cases, a complement to therapeutic lifestyle changes is recommended, for example in the form of food supplement intake.

 

It is important to first reduce the waist circumference, while maintaining normal HDL and TG levels, and limiting hypertension and blood glucose levels. Reduction of systemic inflammation is a key factor in the fight against metabolic syndrome.

 

 

 


[1] Reaven GM. Banding lecture 1988: role of insulin resistance in human disease. Diabetes. 1988; 37: 1595-1607.

 

[2] Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001; 285: 2486-97.

 

[3] Tan BY , Kantilal HK, Singh R. Prevalence of Metabolic Syndrome among Malaysians using the International Diabetes Federation, National Cholesterol Education Program and Modified World Health Organization Definitions. Mal. J. Nutr. 2008; 14: 65-77.

 

[4] Buysschaert M. Le syndrome métabolique: nouvelles définitions et conséquences. Louvain Med. 2006; 125: S79-81.

 

[5] Poitou C, Clément K. Le tissu adipeux: un acteur majeur du syndrome inflammatoire de l’obésité? Cah. Nutr. Diet. 2007; 42: 90-96.

 

[6] Lakka HM, Laaksonen DE, Lakka TA et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 2002; 288: 2709-2716.

 

[7] Hunt KJ, Resendez RG, Williams K, Haffner SM, Stern MP. National Cholesterol Education Program versus World Health Organization metabolic syndrome in relation to all-cause and cardiovascular mortality in the San Antonio Heart Study. Circulation. 2004; 110: 1251–57.

 

[8] Seufert J. Leptin effects on pancreatic beta-cell gene expression and function. Diabetes 2004; 53 (suppl 1): S152–S158.

 

[9] Wilson PW. Estimating cardiovascular disease risk and the metabolic syndrome: a Framingham view. Endocrinol Metab Clin North Am. 2004; 33: 467–81.

 

[10] Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. The Lancet. 2005; 365: 1415-1428