Proponents of high protein/low-carbohydrate diets have profited from the erroneous assertion that carbohydrates are to blame for the increasing prevalence of Insulin Resistance (IR) leading to obesity and the development of Metabolic Syndrome (a.k.a. Syndrome X).
Metabolic Syndrome is a cluster of symptoms characterized by obesity, insulin resistance, hypertension, and dyslipidemia, leading to an increased risk of cardiovascular disease. Syndrome X is usually associated with obesity (especially abdominal), a high-fat diet and a sedentary lifestyle.[1,2,3,4] A common denominator associated with these factors is high levels of circulating free fatty acids (FFA). In the presence of high FFA concentrations, the body will favor their use as energy, decreasing glucose oxidation, glycogen synthesis, and inhibiting glucose transport. The result of this is hyperglycemia. If blood sugar levels are chronically high, insulin will also be elevated, leading to the conversion of the excess blood sugar to other products such as sugar proteins, and fatty acids.
These facts alone seem to bolster the idea that carbohydrates lead to health problems. However, the truth is that a healthy person would need to eat an extremely high percentage of simple carbohydrates (such as sucrose), a high fat diet, be in an energy excess, or overweight to have chronically elevated blood sugar. Although there is some evidence that there may be a genetic component that contributes to IR, it will not allow for weight gain without an energy intake in excess of expenditure.[5,6] In fact, obesity itself is a risk factor for development of IR, not the other way around.
Excessive eating is the cause of IR
If one constantly overeats, excess calories are stored as fat, increasing the size of the fat cells. The growing fat cell itself becomes insulin resistant and the prevalence of FFA, as mentioned earlier, will cause the body to favor the use of fat for energy, at the expense of glucose. This becomes a viscous cycle that continues to perpetuate itself. The fatness leads to IR, leading to impaired glucose use. Blood sugar (BS) levels rise leading to an increase in insulin secretion. Cholesterol, triglycerides (TG) and blood pressure rise as well. To make matters worse, the impaired ability of glucose to enter muscle cells keeps glycogen stores lower which can increase appetite, motivating the individual to eat more, increasing fat stores, exacerbating IR, round and round we go.
As numerous studies point out, high-fat diets are strongly associated with obesity, thus insulin resistance and diabetes.[8,9,10] Of course eating fat does not make one fat (same with carbohydrate, as explained earlier) unless consumed in excess of energy requirements. However, it is easier to consume excess energy (hyperphagia) on a high-fat diet due to fat's high caloric density, its low satiating ability (per calorie), and its sensory effects (palatability of food).[11,12,13,14,15,16,17] Combine this high intake of dietary fat with excess calories and a sedentary lifestyle and it is easy to envision an abundance of free fatty acids floating around in the blood stream. It is much more likely that a high-fat diet leads to the excess consumption of calories, obesity, insulin resistance and eventually NIDDM than it is that carbohydrates cause insulin resistance and, as a result, obesity. The solution: A diet with the appropriate amount of energy, high in fibrous or minimally processed carbohydrates, and exercise. In fact, a study of type II diabetics, those with insulin resistance and normal weight people found that three weeks of a high-carbohydrate, low-fat diet and exercise significantly lowered insulin levels. Also of interest, researchers following more than 75,000 women aged 38-63 for 10 years found that those eating higher amounts of whole-grain foods were significantly less likely to develop NIDDM. So much for the notion that carbohydrates lead to diabetes.
Perhaps it is convenient to place blame on carbohydrates. Diets such as The Zone, Sugar Busters! and Dr. Atkins New Diet Revolution make the claim that carbohydrate intake leads to high blood sugar and insulin levels, with the inevitable consequence of insulin resistance and weight gain. The solution, according to these diets, is simple. Reduce the intake of those pesky, fat-inducing carbohydrates, insulin levels will fall and everything will be fine. The deception here is brilliant. Since an increase in body fat can lead to IR, lowering body fat by any method can reverse IR.[20,21,22]
By removing carbohydrates obviously one’s calories decline. This leads to a reduction in body weight, causing an improvement in glucose tolerance and insulin sensitivity and a temporary reversal of IR. The authors of these diet books win because you lost weight and became insulin sensitive again. The dieter loses because once they grow tired of protein and are starved for carbohydrate; they will rebound with a vengeance. If you are looking for data proving the long-term success of this type of dieting strategy, there is none.
The American Dietetic Association analyzed the recipes recommended by one such diet book and found that the menus averaged a mere 1,200 calories a day. While this will absolutely lead to weight loss, it is an unrealistic restriction on food intake that cannot be maintained. Keep in mind that weight loss itself reduces the disease symptoms of obesity, not necessarily the method one uses to achieve it.[20,21,22]
With obesity rising, a simple solution to the problem of America's weight gain would be welcomed. Our current environment has created a petri dish ideal for the growth of the human organism. Highly palatable and calorically rich food is readily available and today's work and recreational demands do not encourage physical activity.
The cure for obesity seems simple: move more and eat less.
However, the influence of societal, psychological, and physiological factors make maintaining this simple plan very difficult. All being told, any weight loss solution must ultimately provide a way to increase energy expenditure, decrease energy consumption or a combination of both.
Putting the plan into practice
Everyone is unique, so the best this article can do is offer general guidelines. Also, if a client has the health problems mentioned, they should be under a doctor’s care. The client’s primary care giver (doctor, dietician, etc) should clear recommendations made by the trainer before beginning. In diabetic patients, changes in bodyweight and activity level will affect insulin requirements. With the disclaimer out of the way, here are some general recommendations:
- Appropriate caloric intake to allow for fat loss.
- Diet composition of 20% protein, 55% CHO, and 25% fat (+/- 5%).
- Choose minimally processed foods, whole grains, fresh fruits and veggies as much as possible.
- Limit junk food (applies to anyone), especially high fat and high sugar items.
- Low on saturated fat, high on monounsaturated and omega 3’s (olive oil, nuts, cold water fish).
- For the sake of compliance, menu must be palatable and realistic.
- Eat at least four times a day and have protein, CHO and fat at each meal.
- Incorporate more movement into daily life.
- Walk more.
- Use fewer machines and gadgets.
- Walk down the hall instead of using the intercom or e-mail
- Take the stairs
- Park farther away
- Walk more quickly
- Exercise 3-5 times a week for 20-60 minutes.
- Watch less TV.
Incorporating better habits consistently is the key. Research and common sense show that the longer one performs the proper habits, the easier it becomes to maintain.
Once your client has lost weight and improved their health, maintenance may become the goal. It is easier to maintain than to obtain. Caloric intake can be raised slightly, assuming that exercise is continued, to maintain current weight. The new lifestyle habits must be continued, forever. If not, then statistically, they will most likely revert to their previous condition.
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- Buemann, B, Tremblay, A. Effects of exercise training on abdominal obesity and related metabolic complications. Sports Med. 1996: 21(3): 191-212.
- Pandolfi, C, Pellegrini, L, Sbalzarini, G, Mercantini, F. Obesity and insulin resistance. Minerva Med 1994: 85(4): 167-71.
- Bloomgarden, ZT. Insulin resistance: current concepts. Clin Ther 1998: 20(2) 216-31.
- Schraer, CD, Risica, PM, Ebbesson, SO, Go, OT, Howard, BV, Mayer, AM. Low fasting insulin levels in Eskimos compared to American Indians: are Eskimos less insulin resistant? Intl J Circumpolar Health 1999 Oct; 58(4):272-80.
- Beck-Nielsen, H. General characteristics of the insulin resistance syndrome: prevelance and heritability. European Group for the study of Insulin Resistance (EGIR). Drugs 1999; 58 Suppl 1: 7-10.
- Pi-Sunyer, FX. Medical hazards of obesity. Ann Intern Med 1993 Oct. 1; 119(7 Pt 2): 655-60.
- Grundy, SM. Multifactorial causation of obesity: implications for prevention. American Journal of Clinical Nutrition. 1998: 67(3S): 563S-569S.
- 139 Vaag, A. On the pathophysiology of late onset non-insulin dependant diabetes mellitus. Current controversies and new insights. Dan Med Bull. 1999; 46(3): 197-234.
- Parekh, PI, Petro, AE, Tiller, JM, Feinglos, MN, Surwit, RS. Reversal of diet-induced obesity and diabetes in C57BL/6J mice. Metabolism. 1998; 47(9): 1089-96.
- Tremblay, A, Lavallee, N, Almeras, N, Allard, L, Despres, JP, Bouchard, C. Nutritional determinants of the increase in energy intake ssociated with a high-fat diet. Am J Clin Nutr 1991 May; 53(5): 1134-7.
- Speechly, DP, Buffenstein, R. Appetite dysfunction in obese males: evidence for role of hyperinsulinaemia in passive overconsumption with a high-fat diet. Eur J Clin Nutr 2000 Mar; 54(3): 225-33.
- Warwick, ZS, McGuire, CM, Bowen, KJ, Synowski, SJ. Behavioral components of high-fat diet hyperphagia: meal size and postprandial satiety. Am J Physiol Regul Integr Comp Physiol 2000 Jan; 278(1):R196-200.
- Prentice, AM. Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake. Am J Clin Nutr 1998 Mar; 67(3): 535S-541S.
- Blundell, JE, MacDiarmid, JI. Fat as a risk factor for overconsumption: satiation, satiety, and patterns of eating. J Am Diet Assoc 1997 Jul; 97(7 Suppl): S63-9.
- Astrup, A. Obesity and metabolic efficiency. Ciba Found Symp 1996; 201:159-68; discussion 168-73, 188-93.
- Warwick, ZS. Probing the causes of high-fat hyperphagia: a mechanistic and behavioral dissection. Neurosci Biobehav Rev 1996; 20(1): 155-61.
- Barnard, RJ, Ugianskis, EJ, Martin, DA, Inkeles, SB. Role of diet and exercise in the management of hyperinsulinemia and associated atherosclerotic risk factors. American Journal of Cardiology. 1992; 69(5):440-4
- Liu S, Manson JE, Stampfer MJ, Hu FB, Giovannucci E, Colditz GA, Hennekens CH, Willett WC. A prospective study of whole-grain intake and risk of type-2 diabetes mellitus in US women. Am J Public Health 2000 Sep;90(9):1409-15.
- Su, HY, Sheu, WH, Chin, HM, Jeng, CY, Chen, YD, Reaven, GM. Effect of weight loss on blood pressure and insulin in normotensive and hypertensive obese individuals. Am J Hypertens 1995 Nov; 8(11): 1067-71.
- Ikeda, T, Gomi, T, Hirawa, N, Sakurai, J, Yoshikawa, N. Improvement of insulin sensitivity contributes to blood pressure reduction after weight loss in hypertensive subjects with obesity. Hypertension 1996 May; 27(5): 1180-6.
- Fagerberg, B, Berglund, A, Andersson, OK, Berglund, G. Weight reduction versus antihypertensive drug therapy in obese men with high blood pressure: effects upon plasma insulin levels and association with changes in blood pressure and serum lipids. J Hypertens 1992 Sep; 10(9):1053-61.