High Protein Diets


Some of the most frequently asked questions deal with high- protein and  fat  diets that brand  carbohydrates  as evil and the reason for the prevalence of obesity in our society today.  Such diets are not new. They have waxed and waned in popularity over the years, with the previous crescendo occurring in the ’70s. The recent popularity most likely stems from the fact that, in spite of previous dietary recommendations and the prevalence of low-fat and non-fat foods, more and more of the population continues to reach  obesity . This increase in obesity is because people are not following current diet and exercise recommendations. Let’s examine how proponents or marketers of high protein diets trick their patrons. The following are two of the most prevalent claims made in support of these diets:

Claim 1 : People are not getting fat from consuming too many  calories , but from the consumption of carbohydrates, especially high  glycemic index (GI) ones.

Despite the claims of these diets, obesity and weight gain are the result of positive energy balance. If one consumes more calories than they expend, then there will be an increase in mass. One’s genetics and lifestyle determine how easy it is for this to occur. The problem is that society’s caloric intake has increased (by about 300 calories in the last decade) and its caloric expenditure has decreased (due to technology and labor-saving devices).

Claim 2 : Carbohydrates stimulate insulin release, causing the body to store fat. This accompanying insulin production causes insulin resistance (IR) and the development of obesity and NIDDM (type II diabetes).

It is interesting that none of these diet proponents mention that protein also stimulates insulin release. Other than genetic IR, most scientists acknowledge that it is obesity itself (due to an excessive energy intake) that leads to IR, not the other way around.

The truth is that a healthy person would need to eat an extremely high percentage of simple carbohydrates (sweets), a high fat diet, be in an energy excess, or overweight to have chronically elevated blood sugar. The average American eats about 34 percent fat and less than 50 percent carbohydrate in their diet. The consumption of mixed meals with these percentages will not allow blood sugar to be chronically high in a healthy exercising individual. There is some evidence that diets high in sucrose or fructose and fat can lead to insulin resistance and obesity in rats. In either case, the solution is a low-fat diet high in complex carbohydrates.

So, how does one become insulin resistant?

If one constantly overeats, excess calories are stored as fat. Fat cells then increase in size. The growing fat cell itself becomes insulin resistant and the prevalence of FFA will cause the body to favor the use of fat for energy, at the expense of glucose. This becomes a vicious cycle that continues to perpetuate itself. 

  • Increased fat leads to IR.
  • This leads to impaired glucose use.
  • Blood sugar levels rise.
  • Insulin levels rise.
  • Cholesterol, 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…and around and around we go.

As numerous studies point out, high-fat diets are strongly associated with obesity, thus insulin resistance and diabetes. Of course eating fat does not make one fat (same with carbohydrate, as explained later) 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 small volume of food per calorie. Couple the 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 is a diet with the appropriate amount of energy, high in fibrous or starchy carbs, and exercise. In fact, a study of type II diabetics, people with insulin resistance and normal weight people found that three weeks of a high-carbohydrate, low-fat diet, and exercise significantly lowered insulin levels.

Missing the Point

What proponents of low-carbohydrate diets seem to miss is the obvious. Even though CHO and protein stimulate insulin release and lead to storage of substrate as FA, it will not lead to long-term fat accumulation unless caloric intake exceeds caloric expenditure for that day, or week, etc. These proponents take a complex series of events (human metabolism), highlight the portion that supports their claim and ignore the big picture. Because humans are periodic eaters, we will always eat more at a sitting than can be immediately used for energy. This influx of glucose, amino acids, glycerol, and fatty acids stimulate insulin release so that these materials can be used for energy and stored for later use (as glycogen in liver and muscle and fat stores).  As an individual goes through the next several hours without food intake, fatty acids and glucose are liberated from storage depots to fuel metabolic activity that is always occurring.

Some things to remember:

  • In a resting state, fatty acids provide the majority of energy used, regardless of diet composition. We are storing and liberating fat continuously throughout the day. There is absolutely no evidence that a high CHO diet will lead to weight gain if one eats at or below maintenance. In fact, it is impossible. In the end it is caloric intake versus expenditure that determines if one increases or decreases fat stores.
  • If one looks at the energy cost of converting macronutrients to fat, it requires much less energy to convert dietary fat to body fat than to convert CHO to body fat (5 percent of calories vs. 20-25 percent).  A study designed to measure lipoprotein lipase (LPL, a fat storage enzyme) activity in adipose tissue and skeletal muscle on a high carbohydrate or high fat diet inadvertently illustrated this. The study design was to keep participants in calorie balance, so that weight was not gained or lost. Due to the increased thermic effect of food, the participants on the high carbohydrate diet had to eat approximately 300 calories more to maintain body weight than the high fat diet group.
  • One of the biggest concerns associated with high-fat and protein diets, is the impact on health of the individual. High-protein diets are known to increase bone-mineral losses (calcium in particular) and tend to include greater intakes of saturated fats and cholesterol, which contribute to dyslipidemia.
  • Populations that eat diets lower in protein and fat, and higher in carbohydrates, have the lowest incidences of cardiovascular disease.It is when a culture adopts a Western diet, high in calories, fat and sugar and increases their reliance on technology that obesity and its health problems emerge.

A Final Thought

Much time and energy is spent searching for the causes of obesity. Blame is placed on specific foods, classes of macronutrients, and genetics. Obesity is, at its most basic level, an issue of energy imbalance. This imbalance perpetuates itself through a combination of constantly available, palatable food and a society that promotes a sedentary lifestyle.


(1) Zeman, FJ. Clinical Nutrition and Dietetics. 2nd edition. New York, NY: Macmillan Publishing Company; 1991. p 443-444.
(2) Atkins, RC. Dr. Atkins’ New Diet Revolution. New York, NY: Avon Books; 1992. p 64-78.
(3) McArdle, WD, Katch, FI, Katch, VL. Essentials of Exercise Physiology. Philadelphia, PA: Lea&Febiger; 1994. p 35-56.
(4) McArdle, WD, Katch, FI, Katch, VL. Essentials of Exercise Physiology. Philadelphia, PA: Lea & Febiger; 1994. p 35-56.
(5) Hellmich, N. Obesity getting worse, especially in kids. USA Today: 1997 March 7.
(6) Westerturp-Plantenga, MS, Fredix, E, Steffebs, AB [eds]. Food Intake and Energy Expenditure. Boca Raton, Fl: CRC Press; 1994, p.247-250.
(7) Groff, JL, Hunt, SM. Advanced Nutrition and Human Metabolism. 2nd edition. St. Paul, MN: West Publishing Company; 1995. p 327-336.
(8) McGarry, JD. Glucose-fatty acid interactions in health and disease. Amer J Clin Nutr 1998;67(suppl): 500S-4S.

High Protein Diets
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