Entry Level Clinical Nutrition™-Redefining What We Do In A New Age Of Increased Sickness & Increased Scarcity – Part IV

More On The Clinical And Metabolic Foundation Of Entry Level Clinical Nutrition™-The Acute Phase Response

Before I conclude my review of the book chapter by Kushner and Rzewnicki (1) with their fascinating discussion of why the acute phase response (APR) exists in a form that has so many destructive aspects, I would like to thank all of you who took the time to offer comments on the previous installment of this series where I began my in depth exploration of the APR.  I find it gratifying that so many of you now appreciate the fact that this very much under appreciated aspect of all illness, both acute and chronic, plays a major role in creating the chief complaints that bring patients to our offices.  Even more importantly, though, I am gratified that many of you now realize that we must fundamentally revise our approaches to both diagnosis and treatment in a way that seriously considers the APR if we are going to make major inroads into the tremendous challenge of finding cost and time effective ways of dealing with “the tidal wave of chronic illness” that we are now facing in our practices and will continue to face for many years as the baby-boomers age.


Kushner and Rzewnicki (1) finish their excellent book chapter on the APR by delving into a fascinating discussion on why something with so much destructive potential exists in this form.  For, as suggested in the following quote, we have traditionally been inclined to assume that the defensive and adaptive mechanisms we possess always act in totally benevolent and beneficial ways.  Of course, the reality is much different:

“…we presume that acute phase changes play a major role in adaptation and defense because we are inclined to believe that nature tries to accomplish useful purposes.  This is not necessarily true.  The host response may be either protective or destructive; sepsis is a specific example of the latter case.”

Of course, as was suggested from the description of the APR by the authors that appeared in part III of this series, the main entity that is so potentially destructive is inflammation.  The authors point out:

“The term inflammation describes a group of complex, highly orchestrated processes that are initiated in response to various noxious stimuli and then amplified and sustained.  Although the function of inflammation appears to be primarily defensive, an uncontrolled inflammatory response clearly has the potential of causing harm to the host; therefore, the mechanisms that keep inflammation under control (modulate it) and ultimately cause it to resolve are critically important.”

Interestingly, while we tend to be very familiar with the aspects of inflammation that propagate the process such as IL-6, TNFα, and PGE2, we tend to be only superficially familiar with the aspects that mitigate the process.  True, most of us know about the anti-inflammatory prostaglandins PGE1 and PGE3 promoted by omega-6 and omega-3 fats respectively.  However, as noted by Kushner and Rzewnicki (1), there is so much more to the part of the inflammatory process that is involved in retarding inflammation:

“The characterization of molecules as either ‘proinflammatory’ or ‘antiinflammatory’ introduces three problems.  First, it is often forgotten that even purely anti-inflammatory molecules are intrinsic components of the inflammatory process…Second, although some cytokines may only initiate and sustain inflammation and others may only modulate it, many cytokines are multifunctional and play different roles at different points in the process.  Finally, as with hepatocytes, it is likely that cells participating in the localized inflammatory response are rarely exposed to only a single cytokine, arachidonic acid metabolite, neuropeptide, or other molecule capable of influencing inflammation.  Accordingly, the effect of a cytokine on a target cell probably depends on other molecules capable of influencing cell behavior that are present at that point in the evolution of inflammation.”

While this is interesting, what does it mean clinically?  To me, it suggests that the process of inflammation involves many highly integrated processes that involve both stimulation and resolution of the inflammatory process.  In turn, as with so many other aspects of human physiology and biochemistry, balance is key.  What do we know about most chronically ill patients metabolically?  They are imbalanced.  What contributes to this state of imbalance?  As we know, there are many factors such as poor diet, psychological stress, and environmental toxins.  In addition, though, there is one other factor that contributes to this imbalance that is inherent to all chronically ill patients.  However, as I have been trying to emphasize in this series, it is not getting the attention it deserves.  What is this major factor that contributes to inflammatory system imbalance in all chronically ill patients no matter what the symptomatology or clinical presentation?  It has been going on too long!!  The APR is designed to be beneficial only when it is functioning for a short time.  In chronically ill patients, all of whom are experiencing a “chronic phase response,” imbalance and the attendant negative sequelae of this imbalance are inevitable.

What are the specific factors in the APR that create the highly integrated, very healthy process of initiation and resolution when working in a balanced manner for a short period of time?  Kushner and Rzewnicki (1) first provide this overview:

“Illuminating data about the differing roles that cytokines may play at various points in the inflammatory process continue to accumulate.  It has long been recognized that TGF-β is both an extremely potent monocyte chemoattractant and activator and an important contributor to wound healing.  We now know that the net effects of TGF-β are anti-inflammatory.  Studies also have indicated that both IL-12 and INF-γ play stimulatory roles in early collagen-induced arthritis but suppress inflammation in late disease; likewise, IFN-α is both proinflammatory and anti-inflammatory.  In addition, some ‘proinflammatory’ cytokines (IL-1 and TNF-α) have been implicated in wound healing.  The ‘antiinflammatory’ cytokines IL-4 and IL-13 upregulate adhesion molecules, and IL-13 can recruit inflammatory cells.  Finally, IL-6 is commonly regarded as proinflammatory, but the argument has been advanced that it is actually anti-inflammatory.  It is likely that both views are correct.”

Of course, I realize that the above quote is a bit nebulous and diffuse in terms of direct clinical application with the chronically ill patients that we typically see.  Therefore, I would like to next point out some key quotes from the Kushner and Rzewnicki (1) chapter that not only discuss key inflammatory mediators more directly but discuss them in a way that will probably have more familiarity and/or clinical applicability.

C-Reactive Protein (CRP)

We tend to think of CRP as an inflammatory marker that we can use to predict the presence of cardiovascular disease that came onto the scene within the last ten years.  However, workers in critical care who deal with the APR have been familiar with CRP for years as a major proinflammatory, acute phase protein that can be upregulated under any circumstance where the APR is activated, which occurs very often in chronically ill patients, as I am suggesting as an underlying principle in Entry Level Clinical Nutrition™.  In turn, as I am also suggesting, CRP is a valuable component of the APR that becomes destructive only when the APR transforms into the chronic phase response that is seen in so many chronically ill patients.  Kushner and Rzewnicki (1) state:

“CRP…can be regarded as a component of the primitive innate, or natural, immune system.  A very large number of binding specificities and biologic effects of CRP are reported, and a major function of CRP is presumed to be ‘proinflammatory,’ related to its ability to specifically bind to phosphocholine and some nuclear components.  Through such binding, CRP could recognize some foreign pathogens, as well as both phospholipids and nuclear constituents of damaged or necrotic cells.  Further, CRP can activate the complement system when bound to one of its ligands and can also bind to phagocytic cells, suggesting that it can initiate elimination of targeted cells by interaction with humoral and cellular effector systems of inflammation.  This argument is supported by the observation that CRP can induce production of inflammatory cytokines and tissue factor, the main initiator of blood coagulation, by monocytes.”

As I hope you can see from this quote, CRP plays an extremely valuable and important role in directing the immune system to optimally do its job, in the short term.  However, as I hope you can also see, what is described in the above quote could be quite destructive when extended without end over a period of years.

Serum amyloid A (SAA)

While I would guess that this acute phase protein may not be familiar to most of you, for those you who know about current information on the formation of coronary artery plaque, what SAA does will be very familiar:

“SAA, the other major human acute phase protein, has been shown to induce adhesion and chemotaxis of phagocytic cells and lymphocytes.  In addition, the findings that macrophages bear specific binding sites for SAA and that SAA-rich HDLs display increased ability to transfer cholesterol to macrophages at inflammatory sites suggest a role of SAA in the transfer of cholesterol to inflammatory cells.  SAA also has been reported to enhance low-density lipoprotein oxidation in arterial cell walls.”

Again, in the short term, the action of SAA is quite important when injury occurs.  However, when chronically active, as I hope you can see, this major acute phase protein plays a key role in the formation of coronary artery plaques.

Of course, with the above in mind, you might wonder whether it would be wise to measure SAA along with CRP to ascertain the presence or future occurrence of CVD.  This question was addressed by Biasillo et al (2) in their recently published paper “Inflammatory biomarkers and coronary heart disease: from bench to bedside and back.”  In terms of assessment of long term CVD risk, unfortunately the authors did not find that SAA measurement would give any additional value over measuring CRP alone:

“SAA is not found to be associated with long-term risk in the ECAT study, and is only marginally associated with long-term risk in a study by Biasucci et al., different from CRP.  This lack of association could be explained in light of a different regulation of SAA and CRP production of cytokines and of a greater variability in SAA levels compared to CRP.”


Many of you may be familiar with ceruloplasmin due to the fact it is a copper containing protein.  However, as you see from the following quote, it is an acute phase protein that has significant destructive potential if increased over a long period of time:

“…ceruloplasmin enhances oxidation of low-density lipoproteins.”


I am sure that many, if not most of you, are aware of the role of fibrinogen in the clotting process.  However, you may not be aware that it is an acute phase protein that, as the quote below suggests, has the potential for causing harm if elevated for a prolonged period of time:

“…fibrinogen, in addition to its participation in the clotting process, can lead to endothelial cell adhesion, spreading, and proliferation, all critical to wound repair.”

Other aspects of the acute phase response (APR) that play an important role but can be detrimental when functioning on a prolonged basis

As I have been suggesting throughout this series, nutrient metabolism is profoundly altered during the APR.  The following quote should require no explanation as to why what happens in the short term is harmful in the long term:

“Decreases in serum levels of iron and zinc may have beneficial effects in defense against bacterial infection and in tissue repair.  It has been hypothesized that decreased zinc concentrations benefit the host by influencing the production of cytokines.”

Finally, consider this quote about two aspects of the APR with which we are all familiar, fever and hypercortisolemia:

“Several acute phase changes such as fever and hypercortisolemia are presumed to provide a systemic environment appropriate for the adaptive requirements of coping with significant tissue injury or infection.”

Again, good short term; bad long term.

Closing comments by Kushner and Rzewnicki (1)

In closing their excellent and informative chapter on the APR, the authors make two important overriding statements.  The first describes what exactly is happening from a metabolic standpoint in many of our chronically ill patients and why we must create diagnostic and therapeutic protocols that enable us to diagnose and treat on an individual basis:

“In a given patient, the APR represents the integrated sum of multiple, separately regulated changes induced primarily by inflammation-associated cytokines and influenced by modulators of cytokine function (cytokine inhibitors, soluble receptors, autoantibodies), some endocrine hormones, and other circulating molecules.  Although many of these changes commonly occur together, clinical experience teaches that not all of them occur in all patients, indicating that they must be individually regulated.  For example, febrile patients may have normal blood levels of CRP and vice versa, leukocytosis does not always accompany other acute phase phenomena, and instances of discordance between levels of the various acute phase proteins are regularly encountered.  These variations may be explained by differences in patterns of specific cytokines or cytokine modulators in the various pathophysiologic states.”

For me, the above quote reaffirms the important reality that while the acute or “chronic” phase response is occurring in virtually every patient, the manifestation of that response will be very unique from patient to patient even though the clinical presentations may be similar.  Therefore, even though a foundational aspect of Entry Level Clinical Nutrition™ is simple, time and cost effective treatment modalities, even more foundational are the types of simple, time and cost effective diagnostic modalities that will allow us to determine how the acute/chronic phase response is specifically “playing out” in any particular patient.

The last concluding statement by Kushner and Rzewnicki (1) reaffirms the dualistic nature of the APR that cannot be emphasized too often:

“It is widely held that components of the APR influence the inflammatory response or enhance adaptation to noxious stimuli.  Although this probably is true most of the time, it is not invariably true.  The host response may be either protective or destructive…”

Before moving on, I would like to elaborate on another “big picture” issue suggested by Kushner and Rzewnicki (1) that I feel has tremendous clinical implications whenever increased protein and/or amino acid ingestion is recommended to chronically ill patients.  As I hope you noticed in the preceding review, increases in the production of primarily pro-inflammatory acute phase proteins such as CRP and many others are an overriding force in making the acute/chronic phase response a catabolic phenomena that leads to so many of the signs and symptoms that we very often encounter in our chronically ill patients.  Of course, given that this catabolic physiology, to a large extent, involves converting amino acids to glucose via gluconeogenesis, it would seem inherently logical that mere supplementation with protein and amino acids could easily and predictably compensate for the gluconeogenesis-induced protein/amino acid losses.  However, is it really that simple in terms of reliable clinical improvement?  Any of you who have only employed protein/amino acid supplementation as a sole intervention with chronically ill patients know the answer to this question.  Why does a therapeutic modality that, on the surface, seems so logical and predictable, in reality, not “deliver the goods” as often as we would like?  Many would, with good reason, bring up issues of digestion and absorption.  However, there exists another, incredibly important, but little recognized or appreciated reason that I have been emphasizing in this series and forms an underlying principle in Entry Level Clinical Nutrition™:

The acute/chronic phase response profoundly alters macro- and micronutrient metabolism in ways that can often make stimulation of tissue repair with nutrient supplementation difficult, if not impossible.

As you will see from the following quote, this is certainly true in situations where you desire to give protein and/or amino acid supplementation in order to build key tissues such as muscle.  According to Tisdale (3):

“Although protein synthesis in skeletal muscle is depressed in patients with cachexia, liver protein synthesis is enhanced due to acute phase protein (APP) synthesis.  Thus liver protein synthesis shifts from the synthesis of albumin to APP such as C-reactive protein (CRP), fibrinogen, serum amyloid A, 2-macroglobulin and α-1 antitrypsin.”


“It is possible that enhanced APP synthesis in the liver inhibits synthesis of myofibrillar proteins in muscle by reducing the pool size of critical amino acids.”

As I hope you can see, if your chronically ill patient is inflamed with elevations in key inflammatory indicators such as CRP, it is very likely that the protein/amino acid supplementation you are providing with intention of restoring muscle mass will, in reality, lead to production of more acute phase proteins such as CRP and fibrinogen.  How can the probability of this outcome be reduced?  Concurrently or beforehand, make efforts to reduce inflammation via supplementation of fish oil, anti-inflammatory herbs, etc. and rule out food sensitivities.

Before closing this discussion, I would like to address another key clinical point brought up by Kushner and Rzewnicki (1).  Recall that production of phase I detoxification enzymes is profoundly altered during the APR.  Extending the points made above by Tisdale (3), when you provide a protein-based detox product to a patient with the desire to increase production of key detoxification enzymes, and the patient experiences flu-like symptoms that we typically associate with “detox reactions,” could it be that the supplemented proteins are, in fact, increasing production of pro-inflammatory acute phase proteins?  It seems to me that this is a very realistic possibility.  In turn, I am of the opinion that, when chronically ill patients demonstrate elevated levels of CRP or other signs and symptoms consistent with chronic inflammation, we should proceed cautiously with protein/amino acid based approaches to detox until the inflammation has been reduced.


As I pointed out in the last installment of this series, the APR involves all the ways the body responds metabolically to physiologic, biochemical and psychological stressors.  Interestingly, though, most of the researchers writing on the APR tend to focus on the inflammatory aspects, as demonstrated by the  chapter I have just reviewed by Kushner and Rzewnicki (1).  Nevertheless, while I felt it was important to begin this discussion of the APR/metabolic response to stress by addressing the major and still under appreciated role of inflammation in its initiation and progression, thereby emphasizing our need to address reduction of inflammation as a central prerequisite in all chronically ill patients, I also recognize the fact that we, as nutritional practitioners, tend to primarily think of chronically ill patients from a nutritional perspective.  In turn, I would now like to review “The metabolic response to stress and alterations in nutrient metabolism” by Martindale et al that appears in the book Nutritional Considerations in the Intensive Care Unit (4).  While there is, admittedly, some overlap with the information discussed from the Kushner and Rzewnicki (1) book chapter, I hope you will welcome it given both the complexity of some of the information and the relative unfamiliarity it has for many nutritional practitioners.  However, with that being stated, it is my hope that the more direct and detailed discussion on nutrition that is to follow will further clarify and convince you that one of the biggest limitations to more predictable, cost effective outcomes in higher percentages of chronically ill patients when employing nutritional modalities is the fact that we need to have a better understanding of both the unique metabolism of chronic illness and how this metabolism affects macro- and micronutrient metabolism.

Martindale et al (4) begin their discussion by presenting an overview of something that cannot be overemphasized – what happens metabolically when the body is subjected to stress of any type:

“These stress responses are generally characterized by hypermetabolism, hypercatabolism, persistent lean body mass wasting, hyperglycemia, and fluid retention.”

As I hope you can realize, the above statement emphasizes why Entry Level Clinical Nutrition™ so strongly focuses on the idea that the place to begin with chronically ill patients incorporates optimization of fluid and electrolyte/acid-alkaline balance, protein/amino acid intake, and insulin/glucose metabolism.  However, is this enough to create predictable, cost effective outcomes?  The next quote points out why we need to address still other factors, especially inflammation:

“The metabolic response to injury is a complex interaction of numerous mediators, including nervous system input, hormones, and cytokine messengers.”

How important is nutritional intervention in correcting the imbalances mentioned in the above quotes?  The authors state:

“The importance of nutritional intervention for the metabolically stressed patient cannot be overstated.  For the past 3 decades, physicians have begun to understand the molecular and biological effects of nutrients in supporting the response and maintaining homeostasis in the metabolically stressed population.”

What follows are two charts from the Martindale et al (4) chapter that I feel provide an excellent summary of many of the nutritionally related changes that occur when the body is under stress.  In particular, please notice many of the key aspects of Entry Level Clinical Nutrition™ such as fluid and electrolyte balance, potassium and magnesium deficiency, increased protein/amino acid need, insulin/glucose imbalances, increased inflammation (“Hypercoagulability; increased coagulation”), and gut dysfunction (“Shunting of blow flow to control organ, away from gut”).

Table 2.Table 2.2

Next, consider this somewhat lengthy description of what happens metabolically with stressful conditions, with emphasis on nutrient metabolism.  According to Martindale et al (4):

“In simplest terms, these responses are activated to liberate stored nutrients and substrates to support the healing process and endogenously nourish the organism.  These nutrients are utilized as oxidative fuels and for the synthesis of building blocks essential for the stabilization of organ function, maintenance of immunocompetency, and repair of injured tissue.  The byproducts of these efforts are the commonly encountered derangements of critical illness including fluid and sodium overload, hypermetabolism, hypercatabolism, and glucose intolerance.

The duration and severity of these responses are quite variable.  Numerous factors will determine the extent of the metabolic responses.  These include the degree of insult, the persistence of the insult, the host response, the nutritional status of the host, and the timing in relation to previous insults.  For simplicity, the metabolic responses to infection, injury, and catabolic illness can be divided into local responses and systemic responses.  The local responses to insult yield a predictable neurohormonal response that increases metabolic activity and increases local cellular work.  The increases in energy consumption by the inflammatory cells and fibroblasts allow for collagen synthesis, matrix protein synthesis, and wound repair.  The systemic response is manifested by the elevation of the ‘counter-regulatory hormones’ such as cortisol, epinephrine, and glucagons, as well as the elaboration of the cytokine cascade.  This systemic response results in a myriad of effects including altered protein synthesis, increased nitric oxide synthase, and an increase in leucocyte endothelial cell adhesion molecules.  When the systemic insult becomes overwhelming, distinct remote organ and tissue injury can occur.  In addition to the hormonal and cytokine response, other mediators propagate the responses including reactive oxygen metabolites, nitric oxide, and arachidonic acid products.”

Before continuing, please note again the phrase “…an increase leukocyte endothelial cell adhesion molecules.”  This is not only part of the metabolic response to stress but a major component in the formation of coronary artery plaques.  In turn, as with the changes in total cholesterol, HDL cholesterol, and LDL cholesterol discussed in my review of the Kushner Rzewnicki (1), could it be that these plaques that we regard as “disease” are actually a coordinated effort on the part of the body to deal with a stressful situation but have become harmful because the process has gone on too long?  This is exactly what an ever growing body of research is demonstrating.

The authors continue:

“The net effect of these metabolic pathways is the liberation of peripherally stored substrates to meet the energy and substrate requirements of the major organ systems.  Each substrate plays a vital physiologic role in the stress response.  Glucose is an important fuel for the central nervous system, the wound, and the immune system, all of which are metabolically active during stress.  The fatty acids provide a readily available energy source for cardiac and skeletal muscle, the liver, and many other tissues.  Although some liberated amino acids are utilized for gluconeogenesis, the majority are required for the synthesis of the acute phase proteins, for thermogenesis, and as the precursors for tissue repair.”

As I hope you can see from this detailed description, what we have tended to regard as isolated entities, i.e., stress hormones, reactive oxygen metabolites, nitric oxide, arachidonic acid byproducts, cytokines, wound repair, gluconeogenesis, insulin resistance, and on and on and on, that are typically treated on an isolated basis are, in fact, part of a well coordinated process that the body is using to cope with a stressful situation.  In turn, they are not what we have conventionally considered them: Evidence of “disease” where the body is being “attacked” by noxious agents.  Why, then, do they demonstrate the harmful effects that we have traditionally tried to defeat with “weapons” such as antioxidants, etc.?  They are designed to be helpful for only a short period of time because, teleologically, there is an implicit assumption that stress will end, one way or another, soon, i.e., the caveman either escapes the sabertoothed tiger quickly or is eaten.  Either way, it only lasts a short time.  For, when the stressful situation ends, physiology is designed to return to the healthy, anabolic state.  Martindale et al (4) elaborate:

“Recovery, should it occur, leads to a decrease in the metabolic rate, a replenishing of the depleted body energy stores and a rebuilding of the lost lean body mass.  Catabolic, metabolic rates, fluid status and insulin sensitivity all return to pre-injury levels and homeostasis is renewed. Anabolism becomes the predominant event.”

The central problem, then, with chronically ill patients is they never recover and never die; they never escape the sabertoothed tiger nor are eaten.  Because of this, a process designed to be helpful inevitably becomes destructive and creates the clinical picture of pain, fatigue, obesity, and tissue destruction we see so often. 

One final thought: While I realize this way of considering chronic illness may seem quite complicated because it is so different from what we have learned over the years, I hope you can also see, from a clinical management standpoint, it can be quite liberating.  Using our conventional way of regarding patients and treating them, we would give one product to deal with oxidant stress, one to deal with nitric oxide, one to deal with arachadonic acid metabolites, one to deal with insulin resistance, one to deal with stress hormones, one to deal with…well I think you get the point.  Wouldn’t it be nice to first understand how all these seemingly isolated entities fit together and then address them all with a few foundational modalities such as hypoallergenic, whole foods diets, alkalizers, anti-inflammatory agents, amino acid/protein supplements, etc.?  Don’t you think that it might be more enjoyable for you not only because the programs are simpler but because simplicity leads to lower costs for the patient and, in turn, better compliance and better outcomes?  Hopefully, the answers to these questions are obvious.

The next aspect of this metabolic response to stress I would like to discuss is its chronology.  It has been well defined for years that it can be divided into two distinct phases called the “ebb phase” and the “flow phase.”  Martindale et al (4) elaborate on this aspect of the metabolic response to stress:

“The classical description of the stress response by Cuthbertson employed a two-phase theory.  The ebb phase occurs immediately after injury and lasts approximately 24 to 48 hours.  During this short-lived period, there is an increase in sympathetic activity and a stimulation of the hypothalamic-pituitary axis.  This period is characterized by marked hypometabolism and decreased oxygen consumption.”

Next comes the flow phase:

“In contrast to the ebb phase, the second phase, called the acute or flow phase, is one of hypermetabolism, catabolism, and increased oxygen consumption.  These mechanisms are known to be mediated by cytokines, hormones, and the afferent nervous signals from the injured tissues.  It is during this phase that there is an active liberation of endogenous substrates such as glycogen-derived glucose, skeletal muscle-derived and labile amino acids, and adipose tissue fatty acids.  Since glycogen stores are limited, this source of glucose is rapidly depleted.  The need for readily available glucose will then be met by enhanced muscle protein breakdown to provide amino acids for hepatic gluconeogenesis.”

Why is knowledge of this somewhat complicated two stage process important to us clinically?  It demonstrates why, even though the clinical presentation may be similar, the acute patient is very different from the chronic patient metabolically.  Specifically, the acute patient in the ebb phase has experienced relatively limited metabolic changes beyond the area of the chief complaint.  In contrast, the chronic patient with a similar chief complaint is in the flow phase and, therefore, is not only experiencing dysfunction in the area of the chief complaint, but is experiencing tremendous destructive/catabolic changes throughout the entire body.  In turn, it should be no surprise that a reparative supplemental protocol that worked so well in the patient with a back injury that occurred two days ago is a miserable failure in the patient with similar symptoms due to an identical back injury that occurred five years ago.  Does this mean that the reparative protocol for back pain is worthless for chronic patients who have been spending years in the flow phase?  Not at all.  In contrast, I feel this protocol can be very beneficial if proceeded with an effort to deal with the destructive/catabolic physiology that makes up the flow phase with a foundational approach such as that advocated in Entry Level Clinical Nutrition™

In part V of this series I will continue my review of the Martindale et al (4) book chapter, which, for me, makes it unmistakably clear that, when used with a good understanding of the metabolic issues involved, clinical nutrition is absolutely essential to lasting improvements in health for chronically ill patients who have undergone years of physiologic, biochemical, and/or psychological stress plus the inevitable well-meaning, but highly destructive catabolic efforts of the body to deal with it.

Moss Nutrition Report #232 – 04/01/2010 – PDF Version


  1. Kushner I & Rzewnicki. Acute phase response. In: Gallin JI & Snyderman R, ed. Inflammation: Basic Principles and Clinical Correlations, 3rd Edition. Philadephia: Lippincott Williams & Wilkins; 1999:317-329.
  2. Biasillo G et al. Inflammatory biomarkers and coronary heart disease: from bench to bedside and back. Intern Emerg Med. 2010;Published online February 25, 2010.
  3. Tisdale MJ. Protein metabolism in cachexia. In: G M, ed. Cachexia and Wasting: A Modern Approach. New York: Springer; 2006:185-190.
  4. Martindale RG et al. The metabolic response to stress and alterations in nutrient metabolism. In: Shikora SA et al, ed. Nutritional Considerations in the Intensive Care Unit. Dubuque, IA: Kendall/Hunt Publishing Co.; 2002:11-19.