Are you an apple or a pear?
The pear shape is the shape most frequently associated with ladies, and hormonal influences that lead to fat deposits on the buttocks, hips and thighs. This fat is referred to as ‘subcutaneous fat’ and located under the surface of the skin. A well-known cereal manufacturer used this in their advertisements some years back as “can you pinch more than an inch?” So subcutaneous fat located under the skin can frequently be pinched between finger and thumb.
The apple shape develops fat in the upper and lower abdominal area, giving a more rotund or distended appearance. This apple shape is referred to as ‘central obesity’, and whilst you will see a layer of subcutaneous fat under the skin’s surface, there is also an accumulation of fat located under the muscle layer and around the organs of the body called ‘visceral fat’. Post menopausal women can see a change in the fat deposits and a change from pear to apple.
Still unsure if you are an apple or pear? Research using latest imaging has found that the waist measurement is an accurate reflection of abdominal fat. A waist measurement deemed to reflect lower health risks is under 37 inches/94 cm for men and 32 inches/81 cm for women. (1)
Visceral fat is considered contributory to insulin resistance, glucose intolerance, dyslipidaemia (abnormal levels of cholesterol and/or triglycerides), hypertension and coronary artery disease. (3) It is possible to have excess visceral fat whilst remaining a normal body weight. In this situation, the visceral fat is stored internally, around the organs.
Is it a simple case of eat less?
For many, excess food is the reason behind weight and obesity: equally, it may be poor food choices. However, it also appears that there are genetic predispositions which can play a factor. (4) Lack of exercise and dietary factors, however, remain a vital part of weight, obesity and visceral fat.
Did you know that when you lose weight your fat cells shrink, but you never decrease the number? This goes some way to explaining the weight loss and rapid gain often found by frequent dieters.
If all the diets that you’ve tried that state “eat less, exercise more” have resulted in only meagre weight loss, should you be considering other reasons for not losing weight?
Insulin, a hormone that carries glucose into the cells of the body, is produced in the pancreas. Insulin resistance is found in both obesity and type 2 diabetes. In both of these conditions, fat cells become desensitised to the effects of insulin, resulting in an increased demand on the pancreas to produce greater insulin supplies. Eventually, the pancreas fails to keep up with the need by the body for insulin, leading to the development of type 2 diabetes. (Type 2 diabetes refers to non-insulin-dependent, or ‘adult onset’ diabetes).
The World Health Organisation’s definition, and that of a paper published in the Lancet, defines the metabolic syndrome as the presence of ‘visceral obesity, dyslipidaemia, hyperglycaemia and hypertension’. (3) (Dyslipidaemia is defined as higher total cholesterol and/or triglycerides and/or lower high-density lipoprotein).
Individually, these conditions are considered to increase the risk for cardio vascular disease: together they increase the risk substantially, particularly in those with type 2 diabetes. It is considered that the major factor in metabolic syndrome is central obesity, with visceral fat being the most significant factor. (2)
The stress factor can play a major role in central obesity. For some time, there has been a known association between elevated cortisol levels, insulin resistance and central obesity. Cortisol is produced by the adrenal glands, which are located one above each kidney. Salivary cortisol measurements have shown that stress-related cortisol levels are frequently elevated in metabolic syndrome. (7)
A study of long-term stress, carried out during a sailing race around the world found that after five months, a weight gain, mainly consisting of body fat, was recorded and this was located in the abdominal region. (8) An additional long term study of civil servants found that those with chronic work stress were more than twice as likely to have the presence of metabolic syndrome than those not subject to stress. (9)
Lack of exercise appears strongly implicated in not only obesity but the presence of visceral fat, and appears to be particularly relevant in the sedentary and overweight, with studies confirming inactivity leading to significant gains in visceral fat in a study of men and women aged between 40 and 65 years. The study recorded that ‘moderate exercise resulting in an increased calorie expenditure was found to prevent significant increases in visceral fat’. (12)
What should we be doing?
It appears there are some steps we can all undertake which will have an impact on our visceral levels.
- Take chronic stress seriously, and try to reduce exposure to long-term stress.
- Eat healthily; research reported in 2003 demonstrated that a diet high in saturated fat increases the amount of abdominal fat, whilst fish oil and olive oil in the diet have been shown to modify the quality and distribution of the body fat. (10)
- Reduced intake of processed and refined foods and carbohydrates and an increase of unprocessed and fibre-rich, low glycaemic foods, with a moderate intake of mono-unsaturated fats was considered beneficial when considering the optimal diet. (11) (Mono-unsaturated fat sources are olive oil, peanut oil, rapeseed oil, avocados, nuts and seeds)
- We know exercise to be beneficial to many aspects of health, with all body fat shown to respond. (12,13)
2. ES Freeland. “Role of Critical Visceral Adipose Tissue Threshold (CVATT) in Metabolic Syndrome: Implications for Controlling Dietary Carbohydrates: A Review”. Nutrition & Matabolism 05 November 2004. http://www.nutritionandmetabolism.com/content/1/1/12
3. KGMM Alberti, P Zimmet, J Shaw, for the IDF Epidemiology Task Force Consensus Group “The Metabolic Syndrome – A New Worldwide Definition”. The Lancet, Vol 366, issue 9491 pg 1059-1062. Sep 2005
4. M Dragan “The Impact of Abdominal Obesity”. Institute of Endocrinology, Diabetes and Diseases of Metabolism, Belgrade, Serbia. Endocrine Abstracts (2008) 16ME1.
5. MS Winzell, R Nogueiras, Dieguez, B Ahern (2004) “Dual Action of Adiponectin on Insulin Secretion in Insulin-resistant Mice”. Biochemical and Biophysical Research Communications 321-154-60
7. P Björntorp, R Rosmond. “The Metabolic Syndrome – A Neuroendocrine Disorder?” British Journal of Nutrition (2000), 83:S49-S57.
8. S Branth, G Ronquist, M Stridsberg, Hambraeus, E Kindgren, R Olsson, D Carlander, B Arnetz. “Development of Abdominal Fat and Incipient Metabolic Syndrome in Young Healthy Men Exposed to Long-Term Stress”. Nutrition, Metabolism and Cardiovascular Diseases. Volume 17, Issue 6, July 2007, pages 427-435.
9. T Chandola, E Brunner, M Marmot. “Chronic Stress at Work and the Metabolic Syndrome: Prospective Study”. BMJ, doi:10.1136/bmj.38693.435301.80 (published 20 January 2006) BMJ.com accessed 29/3/09.
10. F Soriguer, F Moreno, G Rojo-Martý’ nez, F Cardona, F Tinahones, JM Gomez-Zumaquero, E Garcý’ a-Fuentes & S Morcillo. “Redistribution of Abdominal Fat after a Period of Food Restriction in Rats is Related to the type of Dietary Fat”. British Journal of Nutrition (2003), 89, 115-122.
11. R Riccardi and AA Rivellese. “Dietary Treatment of the Metabolic Syndrome – The Optimal Diet”. British Journal of Nutrition (2000) 83:S143-S148
12. CA Slentz, LB Aiken, JA Houmard, CW Bales, JL Johnson, CJ Tanner, BD Duscha, WE Kraus. “Inactivity, Exercise and Visceral Fat. STRIDE: A Randomized, Controlled Study of Exercise Intensity and Amount”. J Appl Physiol 99: 1613-1618, 2005
13. EL Thomas, AE Brynes, J McCarthy, AP Goldstone, JV Hajnal, N Saeed, G Frost, JD Bell. “Preferential Loss of Visceral Fat Following Aerobic Exercise, Measured by Magnetic Resonance Imaging”. Lipids. 2000 Jul:35(7)769-76.