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Dr. Atkins and Ketogenic
Diets
by Hilton Preen CPT
I receive hundreds of calls every
month regarding diet and nutrition. Some of the most frequently asked questions
deal with high-protein and fat diets that brand carbohydrates as evil and as 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 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. 1,2 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). 4,5
Glycemic index refers to the
effect on the blood sugar (BS) level of equivalent amounts of CHO contained in
different foods. 6 In other words, how quickly BS rises and how much insulin is
released in response to a particular food. GI measures a single food source
eaten by itself and on an empty stomach. Several studies have shown that high GI
foods do not have the same glycemic response when given as part of a mixed meal.
7,8 Many, if not most, high GI foods eaten today are refined foods, high in
added sugar, and would not be considered wise food choices by any standard.
We must still face the truth,
which is that high GI foods, while possibly not the wisest use of calories, are
not responsible for weight gain. People get fat when they consume too many
calories in relation to expenditure.
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. 9 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. 2
Insulin resistance is often
accompanied by several other conditions collectively known as "Syndrome X."
Characterized by insulin resistance, hypertension, hyperlipidemia and an
increased risk of cardiovascular disease, Syndrome X is usually associated with
obesity (especially abdominal), a high-fat diet and a sedentary lifestyle.
10,11,12,13 A result of 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. 10 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. 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. 14,15 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 as mentioned earlier will cause the
body to favor the use of fat for energy, at the expense of glucose. 16 This
becomes a viscous cycle that continues to perpetuate itself. The fatness leads
to IR. This leads to impaired glucose use. BS 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, round and round we go.
As numerous studies point out,
high-fat diets are strongly associated with obesity, thus insulin resistance and
diabetes. 16,17,18 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, again, 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. 19
Claim 3. Low-carbohydrate diets are more
effective for weight loss.
If one's goal is simply to lose as much
weight as possible without regard to composition of weight loss, knocking out
carbs may be the way to go. A study comparing short-term weight loss on a
ketogenic (very low CHO and high in fat, leading to ketosis) and nonketogenic
diet illustrate this point quite clearly. Even though total weight loss was
greater on the ketogenic diet, fat loss was essentially equal, water loss was
177 percent greater (due to decreased muscle glycogen and muscle water loss),
and protein loss was 88 percent greater on the ketogenic diet. So, for the goal
of fat loss, there is no benefit to the ketogenic diet. 20
The disadvantages, however, would
likely be a decrease in 24-hour energy expenditure due to dehydration and loss
of lean body mass. Additionally, for most athletes participating in
high-intensity exercise, the decreased muscle glycogen stores would impair
performance significantly and high-protein diets would decrease testosterone
levels when compared with appropriately mixed food intakes, thus having a
negative impact on recovery. Finally, there is increasing evidence that a
high-fat diet may actually promote body-fat storage in genetically predisposed
obese and post obese individuals. 22,23,24,25
Claim 4. A ketogenic diet offers a
"metabolic advantage".
Dr Atkins, in his book Dr. Atkins' New Diet Revolution, states that following
his ketogenic diet will allow one to lose weight on a number of calories that
once led to weight gain. 26 The state of ketosis that Atkins seeks can be
measured by testing for ketones in the urine. This leaves us with the knowledge
that in the production and use of ketones for energy, some is excreted (wasted)
in the urine. Essentially, calories are just eliminated. For those interested in
losing fat while gaining muscle, eating a ketogenic, isocaloric diet sounds very
appealing (i.e., eat the calories your body requires but have some wasted in the
urine, creating a calorie deficit and, therefore, fat loss). However, this
excretion of ketones most likely amounts to only 50 to 60 calories a day, hardly
what would be considered a metabolic advantage. The low glycogen stores that are
an inevitable result of a ketogenic diet would more likely have negative effects
on exercise intensity and appetite, yielding a metabolic disadvantage. 27
Another flaw in the "metabolic advantage" theory is related to the thermic
effect of food (TEF). Thermic effect of food measures the increase in metabolic
rate in response to the ingestion of food. Studies put this contribution at 5-15
percent of basal metabolic rate (BMR), when consuming a mixed diet. The low end
of the range is seen in those eating a high fat diet, and the high end is seen
in those eating a high complex-carbohydrate diet. 3 If a person had an absurdly
low BMR of 1000 calories, this would translate into a TEF of 50 calories on the
high fat diet versus a TEF of 150 calories for a high complex CHO diet. So much
for "metabolic advantage".
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). 5 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.
By the way, 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.
Also, 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). 28 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 TEF, the participants on the high
carbohydrate diet had to eat approximately 300 calories more to maintain body
weight than the high fat diet group.
Lastly, 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. 29,30 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. 31,32,33
If the preceding information is
not convincing enough that high-protein diets are not the answer for long-term
fat loss in exercising individuals, consider this: of the 438 initial enrollees
of the National Weight Control Registry (having lost an average of 66.0 lbs. for
over five years), none were successful by following a low-carbohydrate, high-fat
diet. In fact, the common denominator for success dietarily was a low-fat diet
with a macronutrient profile of approximately 20 percent protein, 25 percent fat
and 55 percent carbohydrate. 34
This information, from a study
published in the Journal of the American Dietetic Association, is the most
comprehensive study of its kind to date. Data from many other studies support
this. 35,36,37,38,39
Before concluding, consider these
real-world examples: Endurance athletes, who typically consume between 60-75
percent of their calories from CHO, are some of the leanest people on the
planet. Conversely, Inuit Eskimos, who consume only protein and fat, comprise
the fattest culture in the world.
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. Adding to the
confusion is the erroneous belief that the obese maintain very high bodyweights
despite low caloric intakes. Many studies show that as body weight increases,
reported caloric intake decreases. A recent study showed that self reported
energy intakes in American women are approximately 750-1000 calories below
energy expenditures as calculated by the doubly labeled water method. 40 This
discrepancy increases as body mass index (BMI) increases. This is more proof
that 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 Brody, T. Nutritional Biochemistry. 2nd
Edition. San Diego, Ca: Academic Press; 1999. 1006 p. (pp.274).
2 Jensen,MD. Diet effects on fatty acid metabolism in lean and obese humans.
American Journal of Clinical Nutrition. 1998(67 suppl):531-534.
3 Westerterp-Plantenga, MS, Fredix, E, Steffens, AB [editors]. Food Intake and
Energy Expenditure. Boca Raton, Fl. CRC Press; 1994. 408 p. (pp. 139-140).
4 Agricultural research service. Fat intake continues to drop; veggies, fruits
still low in the US diet. Res News 1996.
5 Hellmich, N. Obesity getting worse, especially in kids. USA Today 1997 March
7.
6 Zeman, FJ. Clinical Nutrition and Dietetics. 2nd edition. New York, NY.
Macmillan Publishing Company; 1991. 854 p. (pp. 443-444).
7 Coulston, AM, Hollenbeck, CB, Swislocki, ALM, Reavan, GM. Effect of source of
dietary carbohydrate on plasma glucose and insulin responses to mixed meals in
subjects with NIDDM. Diabetes Care, 1987; 10(395).
8 Bantle, JP, Laine, DC, Castle, GW, Thomas, JW, Hoogwerf, BJ, Goetz, FC. Post-prandial
glucose and insulin responses to meals containing different carbohydrates in
normal and diabetic subjects. New England Journal of Medicine. 1983;309(7).
9 Spector, MC. Biochemistry: A Case-Oriented Approach. 5th Edition. St. Louis,
MO. The C.V. Mosby Company; 1990. 905 p. (pp.771).
10 Epstein F [Editor], Shepherd PR, Kahn BB. NEJM 1999 July 22;341(4):248-257.
11 Buemann, B, Tremblay, A. Effects of exercise training on abdominal obesity
and related metabolic complications. Sports Med. 1996: 21(3): 191-212.
12 Pandolfi, C, Pellegrini, L, Sbalzarini, G, Mercantini, F. Obesity and insulin
resistance. Minerva Med 1994: 85(4): 167-71.
13 Bloomgarden, ZT. Insulin resistance: current concepts. Clin Ther 1998: 20(2)
216-31.
14 Grimditch GK, Barnard RJ, Sternlicht E, Whitson RH, Kaplan SA. Effect of diet
on insulin binding and glucose transport in rat sarcolemmal vesicles. Am J
Physiol 1987 Mar;252(3 Pt 1):E420-5.
15 Berger JJ, Barnard RJ. Effect of diet on fat cell size and hormone-sensitive
lipase activity. J Appl Physiol 1999 July;87(1):227-232.
16 Grundy, SM. Multifactorial causation of obesity: implications for prevention.
American Journal of Clinical Nutrition. 1998: 67(3S): 563S-569S.
17 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.
18 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.
19 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.
20 Yang, MU, Van Itallie,TB. Composition of weight lost during short-term weight
reduction. Metobolic responses of obese subjects to starvation and low-calorie
ketogenic and nonketogenic diets. J Clin Invest, 1976; 58(3): 722-30.
21 Volek, JS, Kraemer, WJ, Bush JA, Incledon, T, Boetes, M. Testosterone and
cortisol in relationship to dietary nutrients and resistance exercise. Journal
of Applied Physiology. 1997 Jan; 82(1):49-54.
22 Astrup, A, Raben, A. Obesity: an inherited metabolic deficiency in the
control of macronutrient balance? European Journal of Clinical Nutrition. 1992
Sep. 46(9): 611-20.
23 Astrup, A, Buemann, B, Western, P, Toubro, S, Raben, A, Christensen, NJ.
Obesity as an adaptation to a high-fat diet: evidence from a cross-sectional
study. American Journal of Clinical Nutrition. 1994 Feb. 59(2): 350-5.
24 Raben, A, Anderson, HB, Christensen, NJ, Madsen, J, Holst, JJ, Astrup, A.
Evidence for an abnormal postprandial response to a high-fat meal in women
predisposed to obesity. American Journal of Physiology. 1994 Oct. 267(4 part 1):
E549-59.
25 Dalton, S. Overweight and Weight Management. Gaithersburg, MD. Aspen
Publishers Inc. 1997. p. 615 (pp.405-438).
26 Atkins, RC. Dr. Atkins' New Diet Revolution. New York, NY. Avon Books. 1992.
417 p (pp. 64-78).
27 McArdle, WD, Katch, FI, Katch, VL. Essentials of Exercise Physiology.
Philadelphia, PA. Lea&Febiger. 1994. 563 p. (pp. 35-56).
28 Westerturp-Plantenga, MS, Fredix, E, Steffebs, AB [editors]. Food Intake and
Energy Expenditure. Boca Raton, Fl. CRC Press; 1994, 408 p. (pp.247-250).
29 Groff, JL, Hunt, SM. Advanced Nutrition and Human Metabolism. 2nd edition.
St. Paul, MN: West Publishing Company; 1995. 575 p. (pp. 327-336).
30 McGarry, JD. Glucose-fatty acid interactions in health and disease. The
American Journal of Clinical Nutrition. 1998;67(suppl): 500S-4S.
31 Seidell, JC. Dietary fat and obesity: an epidemiological perspective. The
American Journal of Clinical Nutrition. 1998; 67 (suppl): 546S-50S.
32 McGarvey, ST. Obesity in Samoans and a perspective on its etiology in
Polynesians. American Journal of Clinical Nutrition. 1991; 53(suppl): 1586S-94S.
33 Price, RA, Charles, MA, Pettitt, DJ, Knowler, WC. Obesity in Pima Indians:
large increases in post-World War II birth cohorts. American Journal of Physical
Anthropology. 1993; 92: 473-9.
34 Shick, MS, Wing, RR, Klem, ML, McGuirre, MT, Hill, JO, Seagle, H. Persons
successful at long-term weight loss and maintenance continue to consume a
low-energy, low-fat diet. Journal of the American Dietetic Association. 1998:
98: 408-413.
35 Harris,JK, French, SA, Jeffery, RW, McGovern, PG, Wing, RR. Dietary and
physical activity correlates of long-term weight loss. Obesity Research. 1994:
2: 307-313.
36 Pronk, NP, Wing, RR. Physical activity and long-term maintenance of weight
loss. Obesity Research. 1994:2:587-599.
37 Kayman, S, Bruvold, W, Stern, JS. Maintenance and relapse after weight loss
in women: behavioral aspects. American Journal of Clinical Nutrition.
1990:52:800-807.
38 Colvin, RH, Olson, SB. A descriptive analysis of men and women who have lost
significant weight and are highly successful at maintaining the loss. Addictive
Behavior. 1983:8:287-295.
39 Klem, ML, Wing, RR, McGuire, MT, Seagle, HM, Hill, JO. A descriptive study of
individuals successful at long-term maintenance of substantial weight loss.
American Journal of Clinical Nutrition. 1997:66:239-246.
40 Seidell, JC. Dietary fat and obesity: an epidemiologic perspective. American
Journal of Clinical Nutrition. 1998: 67(3S): 546S-549S. |
