The old way of thinking on obesity and how to fight it has changed in recent times. As much as some of the public like to criticize this as unreliable information in the past, it is really a natural evolution that occurs in all fields.
As society and the scientific community develops new tools to examine data and become more sophisticated in various treatments, we will discover new facts and need to be able to adjust our past way of thinking or get left behind. This will be the first of a three part series looking at different types of obesity, its relationship to other diseases and how to combat it.
The most recent information on obesity or diseases related to obesity and a lack of exercise is now considering the roles of various hormones, neurotransmitters, and cytokines. It is looking beyond just being “bulgy”, and now looking at where those bulges are. Indeed, the old paradigm of exercise more and eat less will still work, but how you exercise more and what you eat does have a significant impact. The new approach toward lowering risk factors is more holistic and integrative in nature- and this change needed to occur!
The Recent Statistics
Most people are familiar with the statistics that 1/3rd of the population fall into the obese category according to the Centers for Disease Control, and that double that (2/3rds) fall into the overweight category on the Body Mass Index. The quick calculation for this is (Wt in lbs * 703)/(Ht in inches2) So, when we look at the categories 18.5-24.9 is normal weight, 25-29.9 is overweight, and over 30 is obese. There are actually 3 categories for obesity and morbid obesity is a BMI over 40. The statistics that are more alarming is the risk of various diseases associated with obesity and the increases in them. According to a new study by Harvard University researchers, the leading preventable risk factors for premature death in the United States are:
1. Smoking- 467,000 deaths (which is 20% of all deaths in the U.S.) ).
2. High blood pressure- 395,000 deaths (which is 17% of all deaths in the U.S.)
3. Overweight-obesity- 216,000 deaths (combined with #4= 20% of all deaths in the U.S.)
4. Inadequate physical activity and inactivity- 191,000 deaths
5. High blood sugar- 190,000 deaths
6. High LDL cholesterol- 113,000 deaths
7. High dietary salt- 102,000 deaths
8. Low dietary omega 3 fatty acids- 84,000 deaths
9. High dietary trans fatty acids- 82,000
10. Alcohol (over)use- 64,000 deaths
11. Low intake of fruits and vegetables- 58,000 deaths 12. Low dietary poly-unsaturated fatty acids- 15,000 deaths
Besides some of the facts in parenthesis (above) are the following:
• High blood pressure kills 5 times as many women as breast cancer, high blood sugar killed 3 times as many people as alcohol
• 2/3rds of deaths attributed to high blood sugar, obesity, and high blood pressure occurred in only 10-33% of the population.
• 1,051,000 deaths can be attributed to poor dietary choices= 45% of all deaths!
So what is going on here? With all the increased knowledge we have on the dangers of obesity, inactivity and dietary issues we are still killing ourselves by poor lifestyle choices. The rest of this article will examine the role of visceral adipose tissue in metabolic syndrome and some of the interrelationships of factors known to causes many of the deaths listed above. Future parts will examine the role of diet, exercise, and some medical treatments. The bottom line is that just being fat is not unhealthy, but it is the diseases that accompany being obese that cause problems and decrease the quality of life.
VAT vs. SCAT: Body Fat Is Not Just Body Fat — Location, Location, Location!
Are you an apple or a pear? This question is common knowledge among those interested in health-related factors. The “apple” being someone who carries there fat higher or toward the chest and abdomen, and the “pear” being someone who carries their fat lower toward the gluteal region and thighs. Well, things have advanced somewhat since those days. Due to instruments such as the DEXA — dual X-ray absorbiometry, magnetic resonance imaging (MRIs), computed tomography (CTs), and ultrasounds — we can now detect the exact amount of adipose tissue in various regions of the body and if it is visceral adipose tissue (VAT) or subcutaneous adipose tissue (SCAT) (1). A major risk factor for metabolic syndrome is central obesity or fat around the abdominal region, sometimes called “belly fat” by the popular press or visceral adiposity by the scientific community (2).
The name “metabolic syndrome” has been called several things in the past including Syndrome X, insulin resistance syndrome, and metabolic obesity. Several risk factors are associated with this syndrome, and actually describe it and about 1 in 4 to 5 people (depending on the country) have it. These risk factors include: insulin resistance, hypertension, glucose intolerance, type 2 diabetes, dyslipidemias including elevated LDL, and triglycerides (3, 4). Intra-abdominal fat is associated with not only metabolic syndrome (4-Carr) but elevated C-peptide levels and the development of Type II diabetes, sometimes known as non-insulin dependent diabetes melitus (NIDDM). Unfortunately, it is hard to tell what is causing what; literally, a chicken or the egg first dilemma. It increases with age as do many of the other risk factors including a lack of exercise. In people who are over 50, 40% of the population of the U.S. and 30% in Europe have metabolic syndrome (5, 6).
Several papers have claimed a low association of insulin resistance to metabolic syndrome. The National Cholesterol Education Program- Adult Treatment Panel (ATP III) does not consider it a significant factor for metabolic syndrome (7) but rather a cardiovascular risk (8).
It really doesn’t matter much, but what does matter is that it is increasing in the U.S. According to the very large and famous longitudinal study- National Health and Nutrition Examination Survey (NHANES-III). its prevalence is at 25% for those above age 20 and rises to 40 by age 60 (9). The ability to tell if someone has high amount of VAT is not so easy. Some people can be lean individuals with normal BMIs but with high VAT. They are known as metabolically obese normal weight (MONW) , and some individuals are high BMIs but relatively little VAT often present with normal metabolic profiles and few risk factors. They are known as metabolically normal obese (MNO) (10, 11). In fact, another group is known as the Fit and Fat group who present with no risk factors but have high BMIs.
So what are some of differences between VAT and SCAT?
Determining Potential Risk in Your Clients
So without all the fancy equipment mentioned, how would a trainer be able to detect the potential for someone high in VAT and thus at higher risk for cardiovascular problems, thus increased likelihood of your risk to train them in cardiovascular activities.
1. Do a waist to hip ratio test. Using a tape measure, measure women’s waist at the narrowest region within proximity to the umbilical, and for men at the umbilical. The hips should be measured at the widest region roughly at the level of the hip joint. (Please note: The below table should be considered along with total body fat %, and blood chemistries if available (below).
2. Determine Android vs Gynoid Obesity Patterns
a. Android-(Apple) BMI >25, Increased WHR, High Body Fat, Screen for Metab. Syndrome, CVD risk factors including- BP, hs-CRP, Glucose & Insulin- both fasting , and 2h post-prandial, HBA1c, homocysteine, fibrinogen, and possible apo-lipoproteins
b. Gynoid-(Pear) BMI >25, Normal WHR, High Body Fat, screen for endocrine imbalance- adrenal, thyroid, estrogen errors, Medical Status Questionnaire if >50, bone density, and rule out insulin resistance.
New Developments in Adipocyte Endocrinology
There have been many recent findings in adipocyte endocrinology, which is a fancy way of saying fat cell secretions and receptor-based activity. The fat cell is actually major endocrine organ. It is responsive to a wide array of hormones, cytokines, and neurotransmitters and it secretes a wide array of substances which affect other organ systems.
(Adapted from Heber, D, PCRI Insights, May 2004, Vol 7, No. 4)
The term adipokines or adipocytokines has been used to describe the many influences of the substances listed above and others including: estrogen, angiotensin II, angiotensinogen, plasminogen activator (PAI-1), agouti protein, resistin, acylation stimulating protein (ASP), bone morphogenic protein (BMP), Insulin-like growth factor (IGF-1), IGF binding proteins, interleukins (including 6- mentioned), transforming growth factor (TGF)-B, and fibroblasts.
Inflammatory adipokines IL-6 and PAI-1 (plasminogen) are more highly secreted by VAT than SCAT; however, leptin- which signals satiety in the body is more highly secreted by SCAT. Apparently VAT secretes its adipokines into the hepatic portal system to directly affect liver function and inflammatory response. Adiponectin is one of the few beneficial adipokines which serves as an anti-inflammatory for vascular walls, adipose tissue, and inhibits vascular smooth muscle proliferation. It protects the endothelium from macrophage adhesion and injury. It may increase fatty acid oxidation in peripheral tissues and has been associated with insulin sensitivity (12,13,14,15).
1) Kim SK, Kim HJ, Hur KY, Choi SH, Ahn CW, Lim SK, Kim KR, Lee HC, Huh KB, Cha BS: Visceral fat thickness measured by ultrasonography can estimate not only visceral obesity but the also risks of cardiovascular and metabolic diseases. Am J Clin Nutr 2004, 79: 593-599.
2) Lamarch B: Abdominal obesity and its metabolic complications: implications for the risk of ischaemic heart disease. Coron Artery Dis 1998, 9:473-481.
3) Blair D, HabrichtJP, Sims EA, Slyvester D, Abraham S: Evidence for an increased risk for hypertension with centrally located body fat and the effect of race and sex on this risk. Am. J. Epidemiol 1984, 119: 526-540.
4) Carr DB, Utzschneider KM, Hull RL, Kodama K, Retzlaff BM, Brunzell JD, Shoefer JB, Fish BE, Knopp RH, Kahn SE: Intra-abdominal fat is a major determinate of the National Cholesterol Education Program-Adult Treatment Panel III Criteria for metabolic syndrome. Diabetes 2004, 53:1195-1200.
5) Cameron AJ, Shaw JE, Zimmet PZ: The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin North Am 2006; 28: 629-636
6) Ford ES, Giles WH, Mokdad AH: Increasing prevalence of the metabolic syndrome amount U.S. adults. Diabetes Care 2004; 27: 2444-2449.
7) McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G: Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med, 2003, 139: 802-809.
8) Reaven GM: Insulin resistance, cardiovascular disease, and the metabolic syndrome: how well do the emperor’s clothes fit? Diabetes Care, 2004, 27: 1011-1012.
9) Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among US adults- Findings from the Third National Health and Nutrition Examination Survey. J Am Med Assoc 2002,287: 356-359.
10) Katsuki A, Sumida Y, Urakawa H, Gabazza EC, Murashima S, Maruyama N, Morioka K, Nakatani K, Yano Y, Adachi Y: Increased visceral fat and serum levels of triglycerides are associated with insulin resistance in Japanese metabolically obese, normal weight subjects with normal glucose tolerance. Diabetes Care, 2003, 26: 2341-2344.
11) Ruderman N, Chisholm D,Pi-Sunyer X, Schneider S: The metabolically obese, normal weight individual revisited. Diabetes 1998, 47: 699-713. Skinny on Fatness 6
12) Fain JN, Madan AK, Hiler ML, Cheema P, Balhouth SW: Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissue of obese humans. Endocrinology 2004, 145: 2273-2282.
13) Pantanetti P, Garrapa GG, Mantero F, Boscaro M, Faloia E, Venarucci D: Adipose tissue as an endocrine organ? A review of the recent data related to cardiovascular complications of endocrine dysfuctions. Clin Exp Hypertens 2004, 26: 387-398.
14) Minnoci A, Savia G, Lucantoni R, Berselli ME, Tagliaferri M, Calo G, Petroni ML, de Medici C, Viberti GC, Liuzzi A: Leptin plasma concentrations are dependent on body fat distribution in obese patients. Int J Obese Relat Metab Disord 2000, 24: 1139-1144.
15) Fain JN, Balhouth SW, Madan AK: TNF alpha release by the nonfat cells of the human adipose tissue. Int J Obese Relat Metab Disord 2004, 28: 615-622.
Mark P. Kelly has a doctorate in Exercise Physiology and Education Administration, he has specialties in kinesiology, exercise and nutritional biochemistry, weight management, and endurance athletic physiology. He was a nationally ranked duathlete, body building contest winner, trainer of professional athletes, and personal trainer for 20 years. He is a primary writer for the NFPT certification programs, a teacher in universities, and runs Principle Centered Health Human Performance Services, which specializes in assessments and corporate wellness. He can be reached at [email protected].