The Functional Effects of Carbohydrate and Energy Underconsumption
Not Eating Enough, 1995
Pp. 303–315. Washington, D.C.
National Academy Press
The physiological effects of energy restriction are wide ranging, and they also depend in part on the mechanism through which the energy deficit is induced. This chapter focuses on the functional effects of caloric and/or carbohydrate restriction in the short and long term and also addresses their potential clinical implications.
In the first half of this century, vigorous debate was waged between nutritionists advocating a high-carbohydrate, low-fat diet for optimum physical
performance and explorers who promoted a high-fat diet as the most compact and practical form of nutrition under adverse conditions. This debate was fueled on the one hand by the experience of trappers, fur traders, and explorers who lived among the native peoples of the North Plains and Pacific Northwest in the United States and throughout Canada. A typical voyageur working for the Canadian Northwest Company was given a daily ration of 1.25 lb (0.6 kg) of pemmican2 as his sole ration. Nourished by this food, these men would paddle and portage loaded canoes across great distances via the lakes and rivers of Canada. The other side of the debate was fueled by the cultural experience of the English, whose empire depended upon a navy fed by salted meat and dried ship biscuits.
Additional information for this debate was derived from the experiences of polar explorers in the latter half of the nineteenth century. Following the disaster of the Royal Navy's Franklin Expedition, debate raged around the issue of food spoilage as a causative factor, while the issue of scurvy was not addressed (Feeney, 1989). This denial of the problem of scurvy probably contributed to the demise of the Scott South Pole Expedition half a century later. In the center of this debate, on the side of high-fat rations, was a unique individual named Vilhjalmur Stefansson, who followed 15 years of living among the Inuit peoples of the far north with 40 years of living among a (not so) different culture at Dartmouth College. In order to salvage his veracity from the attack of more conservative nutritionists, this university professor consented to live under continuous observation for 1 year in the Russel-Sage Research Unit at Bellvue Hospital in New York in 1928. During the year, he ate only meat, fat, internal organs, and bone marrow, without benefit of fruits, vegetables, complex carbohydrates, or supplemental vitamins or minerals. The results of this unique experiment (McClellan and Dubois, 1930) document his continued state of excellent health without any signs of scorbutic symptoms. He had no obvious limitations of physical capability and maintained the ability to vigorously jog around Central Park at a speed that taxed his attendants (McClellan and Dubois, 1930).
As a result of this debate, considerable scientific evidence was assembled on the side of a high-carbohydrate diet. Marsh and Murlin (1928) published data showing improved high-intensity cycling performance on a high-carbohydrate as opposed to high-fat diet. Similar findings were reflected in the famous studies of Christensen and Hanson (1939).
During the Second World War, the issue was again raised as to the potential use of pemmican as a weight-efficient ration for troops under adverse conditions. To test this question, a study was conducted among Canadian troops who were performing winter maneuvers. Soldiers were switched
abruptly from their standard rations to 1.25 lb (0.6 kg) of a dried meat and fat preparation per day as their sole source of calories. In addition to this food ration, soldiers were given tea, matches, and cigarettes. No time was allowed for the troops to adapt to this diet, as they were asked to continue their arctic maneuvers, pulling all of their gear long distances on sleds. By the third day of the experiment, it was determined that the troops were debilitated, and the experiment was halted (Kark et al., 1946).
During the 1960s, elegant work by Bergstrom and Hultman (1972) clearly defined muscle glycogen as the limiting factor in high-intensity physical performances. This work formed the basis for the current dogma that carbohydrate is an obligate nutrient to support both high-intensity aerobic as well as resistance work.
In the mid-1970s, the work of Blackburn, Bistrian, and Flatt in developing very-low-calorie diets for major weight loss brought renewed interest in ketogenic diets back into the scientific literature (Bistrian et al., 1975a; Blackburn et al., 1973). Because exercise is recognized to be an important component of weight loss and weight maintenance regimens, there were valid concerns that ketogenic diets devoid of carbohydrate would cripple this vital component of multidisciplinary treatment regimens. Empiric observations based upon self-reported physical activity, however, indicated that obese humans on very-low-calorie diets recovered endurance physical performance after a few weeks, and were then able to extend themselves beyond normal daily activities into more purposeful athletic pursuits during the severe calorie-and carbohydrate-restricted phase of such diets. This observation was documented in a number of controlled studies (Phinney et al., 1980, 1988), although the work of Bogardus et al. (1981) suggested that very-high-intensity intermittent activity was still limited by carbohydrate restriction. The other uncontrolled variable in these studies was the contribution of reduced adiposity to changes in cardiopulmonary and muscle dynamics.
To address the question of exercise capacity during ketosis, this laboratory undertook a study of lean, healthy males who were given a diet patterned after the reported food intake of the Inuit people (McClellan and DuBois, 1930). The eucaloric ketogenic diet (EKD) consisted of 15 percent protein and 85 percent calories as fat and provided 1.75 g of protein per kg reference body weight daily. The diet was supplemented with calcium, magnesium, potassium, sodium, trace minerals, and vitamins. Five of the research subjects were highly trained cyclists who were studied both at rest and with exercise (Phinney et al., 1983). Empirically, the cyclists found the first week of the carbohydrate-free diet to be especially difficult, but they still kept up their training schedule of approximately 100 mi/wk (161 km/wk). By the third week of the EKD, their self-reported endurance capability had returned to normal (i.e., two or three of
them could hold a pace line3 at 23 mi/h (37 km/h) for longer than was comfortable for the carbohydrate-fed investigator). In the fourth week of the study, all five subjects underwent repeat testing for peak aerobic power and endurance time to exhaustion. Although the substrate for muscle performance was dramatically shifted away from carbohydrate toward fat (mean exercise respiratory quotient [RQ] declined from 0.83 to 0.72), neither endurance time to exhaustion nor peak aerobic power (5.0 1/min of oxygen consumption) was altered over the baseline values. These observations confirm the prior report by U.S. Army Lieutenant Frederick Schwatka (Stackpole, 1965) that prolonged endurance effort was clearly feasible given 2 to 3 weeks of adaptation to a high-fat diet.
These observations underscore the fact that three critical factors must be met for ketogenic diets to be safe and to allow endurance physical performance: adequate salt, adequate major and trace minerals, and adequate time for adaptation. The study by Kark et al. (1946) ignored all three, achieved the obvious result, but got the wrong answer. A minimum of 3 g of sodium per day is necessary to maintain a euvolemic state in the face of the natriuresis of fasting (or more accurately, the natriuresis of ketosis). The inclusion of salt in the dried meat product or the provision of bouillon as a purposeful supplement is thus necessary to meet sodium needs. With adequate sodium to maintain euvolemia, and increase in aldosterone is avoided, making renal potassium conservation more effective. Nonetheless, the minimum potassium needs of the EKD remain undefined, and potassium intake is best supplemented. In addition, a straight meat and fat diet does not provide adequate calcium or magnesium, and these must also be purposely supplemented to avoid muscle cramps and cardiac dysrhythmias. Importantly, the Recommended Dietary Allowances (NRC, 1989) have not been validated as the appropriate standards for this type of diet. And finally, adaptation to the EKD involves a time lag of 2 to 3 weeks to allow for induction of hepatic ketone production, followed by the suppression of skeletal muscle ketone oxidation to allow optimum ketone provision for central nervous system energy requirements.
An important unexplored issue is the optimum composition of the dietary fat that makes up 80 to 85 percent of the energy content of the EKD. It is not clear that all fatty acids are equally preferred by muscles and liver for fuel. Although a high omega-6 polyunsaturated fat intake may be optimum for cardiac health when fats are a minority of total calories, this is probably not true when fat makes up the vast majority of dietary caloric intake. As a first guess, then, one should look to the composition of human adipose tissue for guidance as to "the body's preferred mix of fats as fuel." Human adipose tissue is composed of monounsaturates as the primary class of fatty acids with
only moderate amounts of saturates and polyunsaturates. The Inuit diet, while high in marine lipids, still provided the bulk of calories as monounsaturated fatty acids, because the omega-3 fatty acids that naturally occur in marine sources represent only about 30 percent of total fat. All "native diets" of a ketogenic nature were inherently limited in omega-6 polyunsaturates. Thus any further work with this type of diet should focus on monounsaturates as a primary fuel source and avoid overfeeding either omega-6 or omega-3 polyunsaturates to avoid distorting membrane fatty acid composition and, with it, cellular function.
The majority of recent research involving caloric restriction has been the result of voluntary restriction to induce therapeutic weight loss. Depending on the weight of the individual and the desired degree of loss, reports of voluntary energy deficits have varied from a few hundred kilocalories to total starvation, with deficit durations lasting 6 months or longer (Keys et al., 1950; NIH Technology Assessment Conference, 1992).
Involuntary energy restriction is induced by unavailability of food or the lack of familiar or palatable foods. In addition, a caloric deficit will usually result if the composition of the diet is changed to reduce caloric density or absorbability.
Another method to induce a caloric deficit is to increase physical activity. This increase may not be immediately compensated for by increased food intake (Staten, 1991; Woo et al., 1982; Wood et al., 1988), although other reports indicate that appropriate compensation does occur (Woo and Pi-Sunyer, 1985). The mechanism through which the human system eventually perceives the deficit and compensates by increasing food intake remains poorly understood.
An additional mechanism that results in negative energy balance is the anorexia of illness or injury, with the energy deficit stemming both from reduced intake plus an increase in metabolic rate. This mechanism is probably mediated by tumor necrosis factor (previously called cachectin) and/or interleukin-1 (Moldawer and Lowry, 1988). Besides overt trauma or infection, increases in tumor necrosis factor and the resultant effects on systemic body function can result from muscle injury associated with excessive exercise for which one is not adequately trained. This cytokine response to unaccustomed amounts of exercise may be a factor mediating increased metabolic rate (and thus an energy deficit) following exercise (Phinney and Stern, 1993).
Early Effects of Caloric Deprivation
The early weight loss associated with caloric deprivation represents not just loss of adipose tissue but also loss of lean body mass. Even before this response, however, there is a net loss of body water associated both with glycogen depletion and also a net natriuresis if there is significant restriction of total calories and/or carbohydrate (Sigler, 1975). If the caloric restriction is quite marked (e.g., semistarvation or total starvation), the natriuresis becomes brisk within 2 to 5 days. To compensate, an increased sodium intake is required to maintain euvolemia. Impaired cardiovascular function and work performance result if this compensatory sodium intake is not maintained, because hypovolemia limits circulatory reserve and increased aldosterone leads to accelerated potassium wasting.
Another early effect of hypocaloric feeding is reduced metabolic rate. Depending on the degree of caloric restriction, resting energy expenditure can be reduced as much as 25 percent within the first 2 weeks of restriction (Taylor et al., 1957). Although this effect reduces the net energy deficit, the compensation is incomplete, and weight loss is unavoidable. This result has potential functional importance when severe energy restriction occurs in the context of low-temperature environments.
Effects on Lean Body Mass and Function
Negative nitrogen balance is a common but not obligate early response to reduced food intake. With total starvation in an unstressed adult, lean body mass losses approach 0.5 kg/d, but with adaptation to nutritional ketosis, the daily rate of nitrogen loss is cut by a factor of 4 over 28 days (Cahill, 1970). With lesser degrees of caloric deficit, especially if some protein is provided, the degree of lean body mass wasting is attenuated, but the duration of time necessary for adaptation remains similar (Keys et al., 1950; Phinney et al., 1988).
In spite of the fact that the rate of nitrogen wasting is most pronounced early in a period of restriction, the physiologic effects are generally the result of cumulative losses over time rather than the absolute rate (Keys et al., 1950). Thus brief periods of even severe restriction have relatively little immediate effect on body structure and health, while the effects on physical performance are more likely due to depletion of muscle glycogen (resulting in impaired high-intensity activity) than due to effects on lean body mass (Davis and Phinney, 1990). With infection or trauma, however, the rate of nitrogen loss can reach such a magnitude that host defense against infection and wound healing are affected (Blackburn et al., 1973).
Energy Deficits Induced by Exercise
As noted above, an abrupt increase in exercise energy expenditure is frequently undercompensated by dietary intake. Although this increase results in weight loss, it is usually not accompanied by loss of lean body mass as long as protein intake remains adequate (greater than 1 g/kg reference body weight) (Wood et al., 1988). In this setting, early weight loss is attributable to loss of glycogen-associated water and body fat, but it appears to be well tolerated in even quite lean individuals (Taylor et al., 1957; Wood et al., 1988).
Energy Deficits and Immune Function
Advanced protein calorie malnutrition is associated with impaired immune function (Bistrian et al., 1975b). This effect does not occur as a linear response with total body nitrogen loss, however, as even significant losses of lean tissue appear to be well tolerated without a reduction in the delayed hypersensitivity response as long as the rate of loss is modest (Keys et al., 1950). However, after significant lean tissue reserves are lost (e.g., lean body mass is reduced to 80 percent of normal), it takes less injury or stress to induce host compromise (Blackburn and Thorton, 1979). Thus, both resistance to infection and recovery from injury may be impaired if nitrogen losses are allowed to accumulate.
An additional effect of dietary restriction on immune function can result if intakes of vitamins and minerals (such as vitamin A and zinc) are reduced. Starting with a well-nourished adult, vitamin and mineral deficiencies take months to develop, but if they are allowed to occur, they contribute to impaired host defense independent of protein depletion.
SUMMARY AND RECOMMENDATIONS
Calorie underconsumption generally has negative effects on lean body mass, physical performance, and host defense against infection. These effects can be forestalled by attention to protein, mineral, and vitamin intakes. Severe calorie or carbohydrate restriction can result in natriuresis, requiring sodium supplementation. Eucaloric ketogenic diets have some potential as a weight-efficient ration for humans. They can support prolonged endurance performance once subjects become adapted to them; however, intense anaerobic work is necessarily very limited on this type of regimen. Due to lack of experience with such diets, further research is needed to determine the proper fatty acid composition and the mineral and vitamin intakes that should accompany such a regimen.
Bergstrom, J., and E. Hultman 1972. Nutrition for maximal sports performance. J. Am. Med. Assoc. 221:999–1006.
Bistrian, B.R., G.L. Blackburn, J.P. Flatt, J. Sizer, N.S. Scrimshaw, and M. Sherman 1975a. Nitrogen metabolism and insulin requirements in obese diabetic adults on a PSMF. Diabetes 25:494–504.
Bistrian, B.R., G.L. Blackburn, N.S. Scrimshaw et al., and J-P. Flatta 1975b. Cellular immunity in semi-starved states in hospitalized adults. Am. J. Clin. Nutr. 28:1148–1155.
Blackburn, G.L., and P.A. Thornton 1979. Nutritional assessment of the hospitalized patient. Med. Clinics of No. Amer. 63:103–115.
Blackburn, G.L., J-P. Flatt, G.H.A. Clowes, T.F. O'Donnell, and T.E. Hensle 1973. Protein sparing therapy during periods of starvation with sepsis and trauma. Ann. Surg. 177:588–594.
Bogardus, C., B.M. LaGrange, E.S. Horton, and E.A.H. Sims 1981. Comparison of carbohydrate containing and carbohydrate restricted hypocaloric diets in the treatment of obesity. J. Clin. Invest. 68:399–404.
Cahill, G.F., Jr. 1970. Starvation in man. N. Engl. J. Med. 282:668–675.
Christensen, E.H., and O. Hanson 1939. Zur methodik der respiratorischen quotient bestimmung in Ruhe und bei Arbeit. Scand. Arch. Physiol. 81:160–171.
Davis, P.G., and S.D. Phinney 1990. Differential effects of two very low calorie diets and aerobic and anaerobic performance. J. Obes. 14:779–787.
Feeney, R.E. 1989. Food technology and polar exploration. Food Technol. 43:70–82.
Kark, R., R. Johnson, and J. Lewis 1946. Defects in pemmican as an emergency ration for infantry troops. War Med. 8:345–352.
Keys, A., J. Brozek, A. Henschel, O. Michelsen, and H.G. Taylor 1950. The Biology of Human Starvation, 2 vols. Minneapolis: University of Minnesota Press.
Marsh, M.E., and J.R. Murlin 1928. The muscular efficiency of high carbohydrate and high fat diets. J. Nutr. 1:105–137.
McClellan, W.S., and E.F. Dubois 1930. Clinical calorimetry XLV. Prolonged meat diets with a study of kidney function and ketosis. J. Biol. Chem. 87:651–668.
Moldaver, L.L., S.F. Lowry, and A. Corami 1988. Cachectin: Its impact on metabolism and nutritional status. Annual Rev. Nutr. 8:585–609.
NIH (National Institutes of Health) Technology Assessment Conference Panel 1992. Methods for voluntary weight loss and control. Ann Intern. Med. 116:942–949.
NRC (National Research Council) 1989. Recommended Dietary Allowances, 10th ed. Report of the Subcommittee on the Tenth Edition of the RDAs, Food and Nutrition Board, Commission of Life Sciences. Washington, D.C.: National Academy Press.
Phinney, S.D., and J.S. Stern 1993. The thermogenic role of exercise in the treatment of morbid obesity. Am. J. Clin. Nutr. 57:454.
Phinney. S.D., E.S. Horton, E.A.H. Sims, J. Hanson, and E. Danforth, Jr. 1980. Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric ketogenic diet. J. Clin. Invest. 66:1152–1161.
Phinney, S.D., B.R. Bistrian, W.J. Evans, and G.L. Blackburn 1983. The human metabolic response to chronic ketosis without caloric restriction: Preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 32:769–776.
Phinney, S.D., B.M. LaGrange, M. O'Connell, and E. Danforth, Jr. 1988. Effects of aerobic exercise on energy expenditure and nitrogen balance during very low calorie dieting. Metabolism 37:758–765.
Sigler, M.H. 1975, The mechanism of the natriuresis of fasting. J. Clin. Invest. 55:377–387.
Stackpole, E.A., ed. 1965. The Long Arctic Search. The Narrative of Lieutenant Frederick Schwatka. Mystic, Conn.: The Marine Historical Society.
Staten, M.A. 1991. The effect of exercise on food intake in men and women. Am. J. Clin. Nutr. 53:27–31.
Taylor, H.L., E.R. Buskirk, J. Brozek, J.T. Anderson, and F. Grande 1957. Performance capacity and effects of caloric restriction with hard physical work on young men. J. Appl. Physiol. 10:421–429.
Woo, R., and F.X. Pi-Sunyer 1985. Effect of increased physical activity on voluntary intake in lean women. Metabolism 34:836–841.
Woo, R., J.S. Garrow, and F.X. Pi-Sunyer 1982. Effect of exercise on spontaneous caloric intake in obesity. Am. J. Clin. Nutr. 76:470–477.
Wood, P.D., M.L. Stefanick, D.M. Dreon, B. Frey-Hewitt, S.X. Garay, P.T. Williams, H.R. Superko, S.P. Fortmann, J.T. Albers, K.M. Vranizan, N.M. Ellworth, R.B. Terry, and W.L. Haskell. 1988. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N. Engl. J. Med. 319:1173–1179.
RONALD SHIPPEE: Dr. Phinney, what do you think the protein is doing under conditions of severe water excretion? In other words, in providing an amount of protein, how much of it is being used as protein, and what would probably be used as amino acids, the main body musculature, and what percent of it simply is oxidized?
STEPHEN PHINNEY: To people who didn't hear the question in the back, the question was, how much of the extra protein that I count here, 1.5 is being used just for oxidation.
If someone is at 0 nitrogen balance, and they are eating 75 g of protein a day, then 75 g of protein were provided, then 75 g of protein, somewhere, depending on what they ate or what they had, is being oxidized.
If it takes 1.5 g of protein per kilo, it has to go to about twice that level to nitrogen balance. A severe flow of restrictions obviously has greater protein metabolism going on. And my guess is that at least part of that is used for gluconeogenesis to maintain brain function.
Now, in the studies I showed you an adaptation of ketosis. There may be an uncomfortable thing. We might say, rather than giving that extra 75 g of protein, let's give 75 g of carbohydrate.
So, what you do in that is, you pull the rug out from under the ketoadaptive state. And you may not get the same ability to do that for prolonged exertion, but intermediate intensity of performance that I showed you we could do.
So, I am not sure that we are living on a perfect continuum there, in terms of having a wonderful substitution of carbohydrate and protein.
The way I am reading now is that when you get up to a level of 1.5 g of protein per kilo, some people begin to feel a little uncomfortable with that as being unnecessary. But it is well within the envelope of what the average adult American male typically eats.
ELDON W. ASKEW: In addition, in your weight-loss study, they maintained and actually increased performance capacity.
Did you have an activity monitoring during that? In other words, did they gradually become more active as they lost more weight and basically got more into shape, so to speak, and that had something to do with it?
STEPHEN PHINNEY: Again, the question is, in the weight-loss studies where we saw the improvement in endurance time, was there some improvement in activity? People lived within the metabolic research wards. They were allowed to leave the metabolic research ward on their own for employment or school.
We had people who agreed that they would not increase their exercise. We saw no increase in their peak aerobic power during the course of the studies. So, I don't think there was a training effect, but I can't absolutely rule that out.
WILLIAM BEISEL: A lot has been made well known that the advantage of intake is the declining protein efficiency goes down, but there are also a lot of studies out there that show that increased protein intake increased the efficiency of energy.
STEPHEN PHINNEY: It is always interesting to me, mostly I sit with Mary and Karl over a cup of coffee. I wish that they could stand up and show the data, but first of all, in the Ranger study, that we would ever be able to see a protein deficiency base.
But also, Mary and I have had a lot of discussions about this. Mary has the ability to sock it up, sock it up. So, when I look at her tests I have got a little problem. But you can't tell the immune systems to sock it up.
And Dr. Crane, who is an immunologist, in both studies, he had always had a problem, that we couldn't publish. If you look at human spots(?), they go down. So, they eat and it starts to come back up. Body weight is still going
down. Body composition is still going down, and our measures are still going down. So, we look at this adaptive measure and that is looking a—looking at the slide with some increase, and now at your data in which there is some kind of flow—
KARL FRIEDL: Again, this is purely speculative, but back to one of my early slides, and that is, we have very little knowledge about the acute effects of changing exercise patterns.
We talk about sending people out there, and troops function in bursts. But again. I haven't seen it published, but Bill Evans told me a year ago that he has data showing that with the acute imbalance in exercise, during which people unaccustomed are resulting in muscle stiffness, they see an increase in circulating IL-1.
Bet we know that, among other things, that the effect of IL-1, and TNF is in part impacting the immune system.
So, acute injury effects, not gunshot wounds, not crush injuries, but maybe the rather subtle injury that comes from stiff muscles and sore muscles may be enough to down-regulate some of the things for our sensitive tests of immune function and therefore work.
And those might be the result of why you see some of those changes in immune function. But eventually, once you put them back in a garrison situation with adequate calories, these guys come back and respond.
The immune system sees the whole body all the time.
ELDON W. ASKEW: One thing that you made mention of, Dr. Phinney, about the secondary anorexia, due to cytokine production, we are beginning to think that there is a change in immune function, just like going to the field, because it is non-specific stress, perhaps, of going to the field.
And it occurs to me that if the anorexia that we see in soldiers who are going to the field might possibly be mediated or tied in to cytokine production and secondary effect on appetite and so forth. I don't know at this point in time.
STEPHEN PHINNEY: Since I have no knowledge, it is very easy for me to speculate that it could be very important and really deserves study.
JOËL GRINKER: There was an article in The New England Journal of Medicine that looked at the antibody side, and also showing it a couple of months later, by work done at the University of Michigan. So, there is a lot of the IL-1 and the others that these cytokines can cause the anorexia that is associated with disease and other situations where cytokines are related.
EILEEN THOMPSON: I was struck by comments that people made yesterday, that we are in a situation where people are going out into the field
more often, and yet the studies that we have looked at so far seem to be sort of one-time semistarvation or some sort of—I know the same thing that yo-yo dieting issue, the fact that yo-yo dieting is shown to have a negative health effect in the Framingham study.
Is anybody doing anything to look at the impact of episodes like this on health issues? There are a lot of people doing it.
MARY MAYS: I mean, if you are asking if people are investigating that in an epidemiological compilation?
EILEEN THOMPSON: No, I meant in terms of these Army studies. You know, has anybody done a follow-up with the Rangers when they actually go out and do their thing?
MARY MAYS: I don't think there is a consensus that there is a real phenomenon.
STEPHEN PHINNEY: They supposedly do it only once. They pass the course, and they don't go through that again.
EILEEN THOMPSON: But then, if they are out there in Somalia or wherever, they are probably doing this underconsumption that you guys have been talking about.
So, in general, the sense is that this is probably only happening—this is not happening to these people on a regular basis and that it isn't a health issue.
MARY MAYS: I think I don't find that entirely valid because the types of folks that are going our on a repetitive and prolonged period field deployment, or are your support troops, they are not your combat troops—the Rangers and special forces—but it is the CSS community that is—it is a smaller trail.
I mean, the reconfiguration in the military over the last 15 and 20 years, the tail has shrunk. So, the support base for all these other folks is the same population.
So, when all these other lead elements go out, the same support element trails with them, although A, B, and C on the maneuver units, the Ranger units, if you will, those guys will rotate. But the guys who are supporting those people are the ones that are going out on very short-term functions and stuff. And we are seeing this particularly in the European community where these guys are going out to the major training centers, spending months upon months upon months, coming back for a 5 and 6 day break, bringing your laundry, balancing their checkbooks, and then going out again. And it is the same support troops, but not the same fighter population that is in training there.
And these folks, these support folks, are not the focus of any of the major efforts in terms of reactions.
STEPHEN PHINNEY: Their food intake opportunities are different than what you would have in your line forces. I think they are very different. They usually have the vehicles, and they will pack them full of all kinds of stuff that they want.
KARL FRIEDL: At least they have the opportunity for doing a lot more. I think that we do need some more information on that.
MARY MAYS: The CSS community probably has more repetitive actions in terms of endurance type activities as opposed to short burst high peak activity. These are the guys doing the truck off-loads, the truck on-loads, the warehousing operation.
Yes, they perhaps—perhaps and not always—perhaps have more access to latrines and showers and so forth, those other things in terms of a stabilized group.
But I think there is too often a conclusion that there are performance requirements that are not as demanding. And I think that is a very untrue statement. I think in terms of total energy expending, I think that you are probably going to see this as the support troops are expending as much as the—
ELDON W. ASKEW: My comment was not to say that they are not working, that they have the opportunity, I think, for—I think that that is an area that needs to be looked at.
MARY MAYS: But those populations other than the Ranger group, because that is specialized training, has the inability to receive sufficient calories, because we are very good at delivering sufficient calories throughout the battlefield. It is the pattern that permeates the battlefield that we are talking about.
STEPHEN PHINNEY: To return to Eileen's original question, I do think that soldiers who go out in the field and come back, there is much yo-yo dieting going on. You know, they lose 5 pounds and 10 pounds. It is not the big yo-yo dieting. We don't know how that is happening.