Identifying Metabolic Syndrome: What to Look For

Metabolic syndrome is a growing problem in the United States, perpetuated by the standard American diet that includes excess carbohydrates and sugar.

With massive sugar consumption comes consequences: metabolic syndrome affects more than 47 million people in the US, while approximately 16.2 million US adults have developed type 2 diabetes.

It is estimated that some form of dysglycemia affects more than 30% of US adults, with a rapidly increasing number of children and adolescents affected as well. ^[6]

Luckily, research supports lifestyle change and nutraceutical support strategies that may offer extensive benefits and healing to those with, or at risk for metabolic syndrome and related conditions.

Metabolic Syndrome’s Conditions

Metabolic syndrome is a unifying theme for a variety of pro-inflammatory conditions.

This major health issue is characterized by the presence of three or more of the following conditions:

• abdominal adiposity
• a waist to hip ratio greater than 1
• insulin resistance
• hypertriglyceridemia
• low HDL cholesterol
• hypertension
• high fasting glucose^[6]

Co-morbid conditions with metabolic syndrome include:

• type 2 diabetes
• atherosclerosis
• hypertension
• stroke
• cancer
• gall bladder disease
• hormone imbalance

Testing blood sugar and insulin levels is a well-known method of detecting and managing insulin resistance and metabolic syndrome.

However, it is essential to consider these when on the lookout for metabolic syndrome:

• chronic stress
• sugar consumption
• vitamin D levels
• the hormones leptin and ghrelin

Stress and the HPA Axis

Stress activates the sympathetic nervous system, inducing excitatory neurotransmitters norepinephrine and epinephrine.

Chronic stress may be a cause of metabolic syndrome, as research indicates that there is reactive cardiac sympathetic dominance in metabolic syndrome. ^[7]

Furthermore, patients with metabolic syndrome may have higher levels of insulin and norepinephrine, suggesting that insulin and norepinephrine contribute independently to the development of metabolic syndrome. ^[11]

Research also shows that increased BMI and total caloric intake are independently associated with increased norepinephrine. Mean norepinephrine excretion has been shown to be higher in subjects with high blood sugar and/or insulin levels than the mean norepinephrine of subjects with normal blood sugar and insulin levels. ^[16]

Stress and Metabolic Syndrome

The link between stress and metabolic syndrome is supported in practice, as a typical pattern seen on a neurotransmitter and adrenal assessment for a person with metabolic syndrome or insulin resistance will show high norepinephrine, usually with low epinephrine. This often indicates decreased medullary activity and low adrenal function.

This may be due to years of increased blood sugar with the body using epinephrine and cortisol to stabilize blood sugar. The adrenals get worn out and patient is “running on norepinephrine,” along with anxiety, sleep difficulty, and/or hypertension.

Metabolic Syndrome and Fructose

Fructose is a type of sugar that can have dire consequences to health if consumed in excess. Fructose is found in agave nectar, honey, fruits, and fruit juices.

High fructose corn syrup is another source of fructose, found in foods we consume such as sodas and other beverages, condiments, yogurt, breads, cereals, and many other packaged goods.

Fructose consumption is associated with oxidative stress, which may be implicated in many cardiovascular, neurodegenerative, and other chronic diseases. Increased inflammatory markers have also been noted in high fructose diets.

High fructose consumption in combination with magnesium deficiency induces:

• insulin resistance
• hypertension
• dyslipidemia

– all of which are risk factors for metabolic syndrome.

High fructose has also been associated with a rapid increase in reactive oxygen species (ROS), which may cause cell damage.

Fructose also lowers the plasma vitamin E to triglycerides ratio, resulting in an increase in triglyceride-rich lipoprotein susceptibility to lipid peroxidation. This peroxidation can alter cellular metabolism, accelerating oxidative stress and causing cell damage. ^[13]

Taking antioxidants reduces ROS production, and improves both mitochondrial function and insulin sensitivity. ^[8]

Metabolic Syndrome and Vitamin D

Low vitamin D is strongly associated with coronary heart disease and metabolic syndrome.

Vitamin D increases insulin secretion, improves glucose tolerance, lowers levels of free fatty acids, and regulates renin gene expression, which can lead to hypertension when upregulated.

Increasing vitamin D intake improves insulin sensitivity by 60%. ^[12] Vitamin D may also help lower blood pressure and inflammatory cytokines. ^[10]

Fat, Leptin, and Ghrelin

Leptin, a hormone produced by adipose tissue, plays a key role in metabolic syndrome. Leptin is a crucial regulator of energy intake and expenditure, including appetite and metabolism.

Leptin travels through the bloodstream to the “appetite center” in the hypothalamus, signaling to the brain that the body has had enough to eat, or satiety. ^[1] In general, people with obesity have unusually high leptin levels, suggesting that they have developed leptin insensitivity. ^[5] This can lead to a vicious cycle of increasing hunger and weight gain.

Additionally, ghrelin, an appetite-stimulating hormone, can contribute to obesity. Ghrelin is increased by weight loss and insufficient sleep. Research supports around 8 hours of sleep for optimal control of appetite and obesity. ^[2]

Metabolic Syndrome Interventions

Physical activity is essential in optimal wellness, and is extremely advantageous as an intervention in metabolic syndrome.

Exercise increases glucose transport into skeletal muscles, where 80% of insulin receptors are located. This indicates the need for increased lean muscle mass, especially as we age and tend to lose muscle. Resistance training will help increase muscle mass, improving insulin resistance.

Both alone and in combination with diet, exercise is effective in improving impaired glucose regulation and delaying or preventing type 2 diabetes.

Long term exercise is associated with improvements in the dyslipidemic profile by raising HDL-C and lowering triglycerides – even in the absence of clinically significant weight loss. Exercise also reduces hypertension. ^[3] Exercises such as interval training are associated with improved weight loss and health outcomes. ^{[9, 14, 15]}

Preventative Behavior for Metabolic Syndrome

It is essential to regulate eating behaviors for treatment and prevention of metabolic syndrome:

• Overall caloric intake should be controlled and tailored to the individual’s energy needs.
• Alcohol, trans fats, sugar—especially fructose—should be avoided.
• Transform eating habits to an insulin-sparing diet of whole foods and complex carbohydrates low on the glycemic index. ^[4] When selecting fruits for example, apples, apricots, pears, plums, and peaches are preferred, while tropical fruits such as bananas, pineapples, and mangoes are high on the glycemic index.
• Consider supplementing the diet with vitamin D and nutraceuticals such as:
  • alpha lipoic acid
  • magnesium
  • chromium
  • cinnamon
  • fish oil
  • fiber
• Identifying and managing stressors and lifestyle factors such as diet, exercise, and caffeine intake may help control sympathetic overstimulation and thus help control metabolic syndrome.
• Rebalancing the HPA axis can also be beneficial for people with, or potentially at risk for metabolic syndrome. This can be achieved through assessing hormone and neurotransmitter levels, and supplying the body with necessary amino acid precursors and cofactors for optimal HPA function.

Metabolic syndrome and other pro-inflammatory conditions such as obesity and insulin resistance are prevalent in the US and often bring poor health outcomes to those affected. Fortunately, lifestyle interventions of diet and physical activity, combined with balancing the HPA axis, can prevent the progression of these conditions, empowering people to take control of their wellness, improve their quality of living, and even avoid many of the degenerative diseases of aging!

Resources

1. Arora, S. (2008). Leptin and its metabolic interactions–an update. Diabetes, Obesity and Metabolism, 10(11), 973-993.
2. Cappuccio, F. P., Taggart, F. M., Kandala, N., Currie, A., Peile, E., Stranges, S., & Miller, M. A. (2008). Meta-analysis of short sleep duration and obesity in children and adults. SLEEP-NEW YORK THEN WESTCHESTER-, 31(5), 619.
3. Carroll, S., & Dudfield, M. (2004). What is the relationship between exercise and metabolic abnormalities?. Sports Medicine, 34(6), 371-418.
4. Chiu, C. J., Liu, S., Willett, W. C., Wolever, T. M., Brand-Miller, J. C., Barclay, A. W., & Taylor, A. (2011). Informing food choices and health outcomes by use of the dietary glycemic index. Nutrition reviews, 69(4), 231-242.
5. Considine, R. V., Sinha, M. K., Heiman, M. L., Kriauciunas, A., Stephens, T. W., Nyce, M. R., … & Caro, J. F. (1996). Serum immunoreactive-leptin concentrations in normal-weight and obese humans. New England Journal of Medicine, 334(5), 292-295.
6. Ford, E. S., Giles, W. H., & Dietz, W. H. (2002). Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. Jama, 287(3), 356-359.
7. Juneja, M., Shipley, M. J., Kumari, M., Andrew, R., Seckl, J. R., Papadopoulos, A., … & Marmot, M. G. (2002). Adrenocortical, Autonomic, and Inflammatory Causes of the Metabolic Syndrome. Circulation.
8. Kim, J. A., Wei, Y., & Sowers, J. R. (2008). Role of mitochondrial dysfunction in insulin resistance. Circulation research, 102(4), 401-414.
9. Mazurek, K., Krawczyk, K., Zmijewski, P., Norkowski, H., & Czajkowska, A. (2014). Effects of aerobic interval training versus continuous moderate exercise programme on aerobic and anaerobic capacity, somatic features and blood lipid profile in collegate females. Annals of Agricultural and Environmental Medicine, 21(4).
10. Michos, E. D., & Melamed, M. L. (2008). Vitamin D and cardiovascular disease risk. Current Opinion in Clinical Nutrition & Metabolic Care, 11(1), 7-12.
11. Pergola, G., Giorgino, F., Benigno, R., Guida, P., & Giorgino, R. (2008). Independent influence of insulin, catecholamines, and thyroid hormones on metabolic syndrome. Obesity, 16(11), 2405-2411.
12. Rammos, G., Tseke, P., & Ziakka, S. (2008). Vitamin D, the renin-angiotensin system, and insulin resistance. International urology and nephrology, 40(2), 419-426.
13. Rayssiguier, Y., Gueux, E., Nowacki, W., Rock, E., & Mazur, A. (2006). High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnesium Research, 19(4), 237-243.
14. Talanian, J. L., Galloway, S. D., Heigenhauser, G. J., Bonen, A., & Spriet, L. L. (2007). Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women. Journal of applied physiology, 102(4), 1439-1447.
15. Tjonna, A. E., Lee, S. J., Rognmo, O., Stolen, T. O., Bye, A., Haram, P. M., … & Kemi, O. J. (2008). Aerobic interval training versus continuous moderate exercise as a treatment for the metabolic syndrome: a pilot study. Circulation, 118(4), 346-354.
16. Troisi, R. J., Weiss, S. T., Parker, D. R., Sparrow, D., Young, J. B., & Landsberg, L. (1991). Relation of obesity and diet to sympathetic nervous system activity. Hypertension, 17(5), 669-677.

Clinical Contributor

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