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The Ketogenic Diet for Health

We seem to avoid giving up ketosis as long as possible. It seems likely that it facilitated the evolution of our brains, that organ that makes us so different from other animals that we sometimes forget we are animals. Returning to the importance of metabolic switching between glucose and ketone mode, there seems to be a false dichotomy. The absorptive phase on a high carb diet lasts about 4 hours.

Only after that can you start the postabsorptive phase, Marked by using glycogen as your source of blood sugar. But if you are on a protein and calorie sufficient very low carb diet, then even after eating, your glycogen stores don't get that full in the first place.

You can accentuate this by demanding more energy between meals exercise or eating less frequently, for example only once or twice a day. Interestingly, this often naturally happens to ketogenic dieters. In the interest of time, I did not do my usual practice of end-to-end citations. I will probably return to fix that later! According to many plant-eating enthusiasts, we must eat fibre to be healthy for the following reasons:. These are not the only arguments people make for eating fibre.

These are only reasons related to butyrate. Of the above statements, only one of them seems well-justified to me, but it also seems irrelevant. Let's start from the end. This idea a quote from Wikipedia seems to to be an exaggerated interpretation of a study by Donohoe et al.

The authors are studying germ-free mice, who don't, of course, have bacteria synthesising butyrate. They describe what looks to them like impaired colon cell energetics in the mice and ultimately autophagy upregulation, meaning the cells are eating themselves.

They reverse these effects with butyrate. I've already written about some of the curious paradoxes inherent in the study. To summarise, other studies consistently find germ-free mice to be healthier than wild mice by many a measure, including appearing to be more energetic, and living longer.

There seems to have been a conflation of cell energy with mitochondrial energy, by not looking for mitochondrial density changes. So, I'm not convinced the butyrate made things better. Likewise, the reported evidence of autophagy increased autophagosomes attributed to upregulation of AMPK , insofar as it indicates autophagy, could equally be a desirable result, given the role of autophagy in maintaining healthy tissues.

Certainly unrestrained autophagy, with no homeostatic mechanism, should result in total loss of tissue, but that doesn't seem to happen with the germ-free mice. Germ-free rodents have freakishly large caecums, and somewhat reduced small intestines, but so far as I can tell, no colon abnormalities worth mentioning. For an extensive review of the data already available in on germ-free animals, including the structure and function of various organs, see The gnotobiotic animal as a tool in the study of host microbial relationships.

In any case, if the colons of germ-free mice are at any disadvantage there are clearly more differences that might be attributable to than mere lack of butyrate.

Are there other reasons to worry about colon cells that don't get any? If you haven't read my thoughts on the term "preferred" , the point is that what a cell will consume first isn't necessarily the fuel that is the healthiest, though it certainly can be. Other reasons could be to get rid of it, or to access the metabolites. I'm not really suggesting that butyrate is toxic to colon cells. Though as soon as that thought occurred to me I looked for evidence that it can be, which, of course there is [Pen].

Apparently it can accumulate due to maldigestion or bacterial overgrowth and cause serious epithelial damage. All I'm saying is that habitual heavy use doesn't imply something is needed. It's still possible that other fuels are as good or better than butyrate for the colonocyte. Normally, colonocytes do metabolise butyrate, mostly into CO2 and ketone bodies, but this is impaired in ulcerative colitis [Roe] , [Roe] , [Ahm] , such that ketogenesis is is inversely proportional to the severity of the disease [Roe].

This impairment may explain the mixed results in treatments involving butyrate. Some researchers have tried to treat colitis by adding more butyrate for substrate, by enema.

Perhaps unsurprisingly, that has not met with much success. I read a somewhat confusing review [Mal] that has several citations in it that don't appear to line up with the claims preceded by the citations, including citing the same paper that I've cited above Roe , as showing "that restoration of butyrate levels by intracolonic infusion treats UC", which I can find no mention of in the paper, and citing a single paper twice, [Ham] , once to say that enemas had very limited effect which I think is correct and once, later, to say it was a "well demonstrated" "cure".

These are probably just simple citation errors on my part or theirs. There have been some successes using enemas, but the results are mixed [Ham]. Insofar as there are successes, it is worth noting that the butyrate was taken in by rectal cells, not colon cells, and so the effect was post-absorptive.

In other words, it must have come systemically. In fact, when the butyrate is applied directly to impaired cells it seems to worsen the situation. These points are noted in the review, and motivates their own contribution.

The researchers used intraperitoneal injections of butyrate to apparently almost completely restore colonocyte integrity in rodent models of colitis.

At face value, this would suggest that it is not the butyrate that helped, but a metabolite of butyrate, i. If it's systemic ketone bodies we want, we know how to do that! Also, this method is rarely used in humans, so it may not be easy to make any practical use of.

In any case, none of this would suggest that eating plant fibre will help colitis in any way, given that the issue appears to depend on inability to use the butyrate. There is not clear evidence that fibre intake helps with IBD, and in fact, "low residue" or "low fibre" diets are usually recommended see below. In case you were wondering, "residue" means anything that survives digestion, and comes all the way through the intestines.

That includes fibre , but also microorganisms, and secretions and cells shed from the alimentary tract. While there are studies that support the benefit of fibre in IBD, there are others showing harm. The evidence is mixed enough to be called weak and inconclusive [Kap].

Anecdotes such as the " Crohn's Carnivore " suggest a different solution might hold for some:. That experience runs both with and possibly against current dietary guidelines for IBD. In a review [Bro] , the authors show that most guidelines advise low fibre intake, especially during flares.

Some also advise low fat intake, and in particular, to eat lean meat. I'm not sure whether the Crohn's Carnivore was eating lean or fatty meat during his year of healing. At first blush, the low fat advisory looks like just another "extra-mile" kind of recommendation, in which guideline writers are throwing in other ideas about healthy diet for good measure. However, they state that it comes from the reported reactions of some patients. One wonders if there are conflations. Later, the authors specifically say that there is little to support or refute a low fat recommendation.

Another anecdote, this time elevated to "case study" level, because physicians penned it, comes from the Evolutionary Medicine Working Group, in Budapest, Hungary [Tot]. They report complete resolution of symptoms in a child with Crohn's and cessation of medications from an essentially meat-only diet.

The exception was that patient was allowed some honey, but it was low enough that ketosis was maintained. This was a 2: The child had previously tried low fat, low fibre, and several medications without improvement.

It is interesting to note that even one dose of "paleo approved" fibre caused a flare up. In other words, a fibre-free ketogenic diet appears help IBD more than a diet including fibre, even a ketogenic diet including fibre.

The idea that butyrate might be protective of colon cancer seems to have started in the s see, e. This area of research is extensive, and I am by no means an expert. If you haven't guessed, that butyrate has a protective effect on colon cancer is the one statement I think is entirely defensible. For example butyrate's histone deacelytase HDAC inhibition is considered an important mechanism [Hin] , [Blo]. Gpra receptor activation is a recently identified mechanism [Sin]. In fact, the argument behind the relevance of the Gpra discovery is just as strong an argument for a ketogenic diet as for eating fibre!

This sentence is incorrect. That is, the researchers demonstrated that butyrate could substitute for niacin in activating these receptors, and that just as niacin activation of Gpra in fat cells is protective of cardiovascular disease, it may also be in diseases of the colon, and this argues for eating fibre to substitute for pharmalogic doses of niacin. From a press release:. Their search for other activators identified butyrate, which led Ganapathy to find that not only is the Gpra receptor expressed on the surface of colon cells, but that with sufficient fiber intake, butyrate levels in the colon can activate it.

A critic pointed out that the cell receptors for SCFAs are facing the lumen, and therefore argued that beta-hydroxybutyrate from the portal side would be irrelevant. Indeed, the researchers using niacin also assume that the extremely high dose of niacin does not act sytemically, but rather reaches the lumen because of the super-high doses.

So the statement I made above, about the argument for beta-hydroxybutyrate being equal to that for niacin is not correct. The argument still stands that the beta-hydroxybutyrate metabolites activating targets inside could be where the majority of the benefits of butyate come from. That is where the HDAC inhibition occurs and where the immune cell receptors are. At least one research group agrees with my speculation that the interior metabolites may be important for the effect [Siv].

SCFAs are low-affinity agonists for these receptors, and the normal luminal concentrations of these bacterial metabolites are in the millimolar levels, sufficient to activate these receptors from the luminal side. However, some of the molecular targets for these metabolites are either inside the cells e. Therefore, concentrations of these metabolites inside the colonic epithelial cells and in the lamina propria are relevant to impact these molecular targets.

The intracellular target HDAC is inhibited by butyrate and propionate at low micromolar concentrations. There are effective transport systems for SCFAs in the apical membrane of colonic epithelial cells e. Even though the luminal concentrations of SCFAs are in the millimolar range, it is unlikely that they reach lamina propria at significant levels to activate the cell-surface receptors present on the mucosal immune cells.

These metabolites are present only at micromolar levels in the portal blood [57], indicating that they undergo robust metabolism inside the colonic epithelial cells. This raises the question as to the physiological relevance of these bacterial metabolites to the activation of the cell-surface SCFA receptors in immune cells located in the lamina propria.

This ketone body is released from the cells into portal blood. Interestingly, as in the case of colitis, colorectal cancer appears to involve a dysfunction in ability to use butyrate.

Specifically, there are detrimental changes in membrane transport that reduce its entry into the cell [Gon]. Therefore, it's unclear that once the disease process has begun, increased fibre intake will be of any use. Beta-hydroxybutyrate in the bloodstream, however, might. There is at least some preliminary evidence that butyrate in the bloodstream has similar effects on intestinal tissue as butyrate coming from the colon itself [Kor] , [Rol] , [Bar] , as does infusion of glutamine and acetoacetate, another ketone body [Rom].

Ketogenic diets do increase blood acetoacetate. These common mechanisms suggest that much or even all of the benefits obtainable by butyrate are equally achievable simply through ketogenic diets, making additional butyrate in the context of a ketogenic diet potentially superfluous. Even though it seems likely that a fibre-free ketogenic diet is not only sufficient for colon health, but better for treating colon disease, we might feel cautious about going without the butyrate from fibre, given the dire pronouncements from nutritional scientists.

Is there any other way to get butyrate? The most significant food source, butter, doesn't give much. That would take about a pound of butter! Stepping back, it should be obvious that carnivores such as felines and canines provide an important source of data relevant to this question. Carnivores have colons, and they are not normally in ketosis unless food is scarce. Either their colons don't need butyrate, or they are getting sufficient butyrate from some other source.

As it happens, there are microbes that ferment amino acids in to short chain fatty acids SCFAs , including butyrate. Carnivores are known to get "animal fibre" from their prey. That is, amino acids from incompletely digested animal parts reach their colons and are fermented. In particular, in cheetahs, casein, collagen, and glucosamine have been shown to result in butyrate production comparable to fructo-oligosaccharides [Dep].

Beyond poorly digested animal sourced fibre, many amino acids are fermented into SCFAs, including butyrate [Ras] , and these amino acids are abundant in human intestines and colons and are fermented there [Vit] , [Dai] , [Nei] , [Wie]. I was unable to determine how much butyrate this would account for. I did find research comparing the SCFA levels produced in dogs under conditions of high fibre vs. This idea is supported by these observations:.

Colonocyte butyrate metabolism was investigated in experimental colitis in mice. Colonocytes isolated from colitic and normal control mice were incubated with [ 14 C]butyrate or glucose, and production of 14 CO 2 , as well as of intermediate metabolites acetoacetate, beta-hydroxybutyrate and lactate , was measured. The effect of different substrate concentrations on oxidation was also examined.

Production of beta-hydroxybutyrate was decreased and production of lactate increased in DSS colitis compared with controls. Increasing butyrate concentration from 10 to 80 mM enhanced oxidation in DSS colitis 0. Surface and crypt epithelial cells showed similar ratios of butyrate to glucose oxidation. When 1 mM DSS was added to normal colonocytes in vitro, it did not alter butyrate oxidation.

The initial histological lesion of DSS administration was very patchy and involved crypt cells. Abnormal butyrate oxidation became apparent only after six days of DSS administration, at which time histological abnormalities were more widespread. Histological abnormalities preceded measurable defects in butyrate oxidation. It was logical to assume that liver and muscle glycogen could serve as the fermentable substrate for lactate production in the stomach, but most of this should have been digested and absorbed by the small intes tine.

Another possible source of ferment able substance which could survive passage through the small intestine is the protein- polysaccharides of the connective tissue ground substance found in abundance in the meat by-products and whole ground chicken.

The ground substance is made up of chondroitin sulfates and hyaluronic acid. The polysaccharide portion of these substances is composed of long chains of disaccharide units consisting of glucosa- mine or galactosamine and glucuronic acid. The linkages of these polysaccharides are not such that they can be cleaved by the endogenous digestive enzymes found in the gut but they could be split by microbial enzymes.

However, the ability and timing of SCFA to augment adaptation in the neonatal intestine is unknown. Furthermore, the specific SCFA inducing the intestinotrophic effects and underlying regulatory mechanism s are unclear.

Within each group, piglets were further randomized to examine acute 4, 12, or 24 hours and chronic 3 or 7 days adaptations. Indices of intestinal adaptation, including crypt-villus architecture, proliferation and apoptosis, and concentration of the intestinotrophic peptide, glucagon-like pepide-2 GLP-2 , were measured.

Indicative of an antiapoptotic profile, jejunal Bax: The intestinotrophic mechanism s underlying butyrate's effects may involve GLP Ultimately, butyrate administration may enable an infant with short-bowel syndrome to successfully transition to enteral feedings by maximizing their absorptive area. The question of whether or not to use probiotics continues to be debated. It may be important to communicate to IBD patients that high-fiber foods are not recommended, especially for those with CD, during flares or in the presence of active disease states, fistulas or strictures.

There appears to be a tendency among the dietary guidelines to restrict foods such as raw fruits, raw vegetables, beans, bran, popcorn, seeds, nuts, corn hulls, whole grains, brown rice and wild rice. Although not mentioned, raw salads would also fall into this category. Few research studies are available to support or refute such a recommendation. The topic needs further investigation because patients with malabsorption may be at risk of not obtaining their necessary essential fatty acids.

Perhaps saturated fats should be limited, with more of an emphasis on more healthy fat intakes. The abundance of the AA-fermenting bacteria in the large intestine is very high and their number can reach up to per gram dry feces Smith and Macfarlane, Using the traditional plate counting technique, the authors have also reported that the dominant bacterial species for the utilization of single AA or pairs of AA are very different.

For instance, Clostridium bifermentans is the predominant bacteria for the utilization of lysine or proline, and pairs of AA e. Many species of bacteria utilize the same AA as substrates for growth Smith and Macfarlane, Overall, bacteria belonging to the Clostridium spp. The FOS and collagen showed comparable acetate production. Collagen not only had a high production of total SCFA but also resulted in a greater acetate to propionate ratio relative to all other substrates 8.

Considerable variation in BCFA ratios was observed among substrates. So, knowledge on the mechanisms involved in its membrane transport is relevant to both its physiological and pharmacological benefits. Also, changes in transporter expression or function will have an obvious impact on the effect of BT, and therefore, knowledge on the regulation of its membrane transport seems particularly important. More specifically, BT is transported into normal colonic epithelial cells by both MCT1 and SMCT1, but its intracellular concentration is kept low because it is efficiently metabolized and effluxed from these cells by BCRP-mediated transport.

In these cells, BT accumulates intracellularly because it is inefficiently metabolized due to the fact that glucose becomes the primary energy source of these cells and because there is a reduction in BCRP expression. Butyrate is thought to exert its cellular effects through the induction of histone hyperacetylation.

We sought to determine the effects of a variety of the SCFA on colon carcinoma cell growth, differentiation and apoptosis. HT or HCT wild-type and pdeleted cells were treated with physiologically relevant concentrations of various SCFA, and histone acetylation state was assayed by acid-urea-triton-X gel electrophoresis and immunoblotting. Growth and apoptotic effects were studied by flow cytometry, and differentiation effects were assessed using transient transfections and Northern blotting.

Propionate C3 and valerate C5 caused growth arrest and differentiation in human colon carcinoma cells. The magnitude of their effects was associated with a lesser degree of histone hyperacetylation compared with butyrate. Acetate C2 and caproate C6 , in contrast, did not cause histone hyperacetylation and also had no appreciable effects on cell growth or differentiation.

Butyrate also significantly increased apoptosis, whereas the other SCFA studied did not. The growth arrest induced by the SCFA was characterized by an increase in the expression of the p21 cell-cycle inhibitor and down-regulation of cyclin B1 CB1.

These data suggest that the antiproliferative, apoptotic and differentiating properties of the various SCFA are linked to the degree of induced histone hyperacetylation. Furthermore, SCFA-mediated growth arrest in colon carcinoma cells requires the p21 gene. Since butyrate is expected to impact cellular metabolic pathways in colon cancer cells, we hypothesize that it could exert its antiproliferative properties by altering cellular metabolism.

We show that although Caco2 colon cancer cells oxidized both butyrate and glucose into CO2, they displayed a higher oxidation rate with butyrate as substrate than with glucose. Furthermore, butyrate pretreatment led to an increase cell capacity to oxidize butyrate and a decreased capacity to oxidize glucose, suggesting that colon cancer cells, which are initially highly glycolytic, can switch to a butyrate utilizing phenotype, and preferentially oxidize butyrate instead of glucose as energy source to produce acetyl coA.

Butyrate pretreated cells displayed a modulation of glutamine metabolism characterized by an increased incorporation of carbons derived from glutamine into lipids and a reduced lactate production. The butyrate-stimulated glutamine utilization is linked to pyruvate dehydrogenase complex since dichloroacetate reverses this effect.

Furthermore, butyrate positively regulates gene expression of pyruvate dehydrogenase kinases and this effect involves a hyperacetylation of histones at PDK4 gene promoter level.

Our data suggest that butyrate exerts two distinct effects to ensure the regulation of glutamine metabolism: As a product of fermentation within the human colon, it serves as the most important energy source for normal colorectal epithelium. It also promotes the differentiation of cultured malignant cells. A switch from aerobic to anaerobic metabolism accompanies neoplastic transformation in the colorectum. The separate functional roles for n-butyrate may reflect the different metabolic activities of normal and neoplastic tissues.

Relatively low intracolonic levels of n-butyrate are associated with a low fibre diet. Deficiency of n-butyrate, coupled to the increased energy requirements of neoplastic tissues, may promote the switch to anaerobic metabolism.

The presence of naturally occurring differentiating agents, such as n-butyrate, may modify the patterns of growth and differentiation of gastrointestinal tumours. This study aims to assess the effects of butyrate on inflammation and oxidative stress in subjects with chronically mildly elevated parameters of inflammation and oxidative stress.

Before and after the intervention feces, blood and colonic mucosal biopsies were obtained. Parameters of antioxidant defense and oxidative damage, myeloperoxidase, several cytokines, fecal calprotectin and CRP were determined. Although in general butyrate did not affect colonic glutathione levels, the effects of butyrate enemas on total colonic glutathione appeared to be dependent on the level of inflammation.

The current article adds to this discussion but does not definitively answer the question. Overall, the data suggest that in the absence of a known fibrostenotic stricture with obstructive symptoms, a high fiber diet is likely safe in patients with IBD and may impart a weak benefit. Yet, answering these clinically relevant questions with more confidence and detail is within our grasp. The advent of e-cohorts offers the potential to transform research in the future by allowing investigators to design cost-efficient Web-based clinical studies, particularly for interventional environmental clinical trials.

Short-chain fatty acids SCFAs are produced in the colon by the fermentation of dietary carbohydrates and fiber polysaccharides and have been shown to stimulate mucosal-cell mitotic activity in the intestine. This study compared the effects of an intravenous and an intracecal infusion of SCFAs on the small-bowel mucosa.

Standard TPN produced significant atrophy of the jejunal and ileal mucosa. The intravenous and intracolonic infusion of SCFAs were equally effective in inhibiting small-bowel mucosal atrophy. Since then, butyrate enemas have popularly been used as medicaments stemming from their potential to impart beneficial attributes to the colon.

This potential involves an increase in mechanical strength of injured colonic mucosa to hasten the healing process Bloemen et al. Much as butyrate tends to impart a protective effect, several authors have indicated failures or limited success of butyrate to relieve IBD patients Harig et al. This is done mainly through intrarectal administration of enemas that contain butyrate. The procedure is one of the earliest approaches to treat UC even in patients who had been unresponsive to or intolerant of standard therapy Scheppach et al.

The intrarectally administered butyrate needs to be absorbed before it works. Normally butyrate absorption mainly occurs in proximal colon whose function is impaired during UC. This hinders absorption of topically administered butyrate and may not benefit UC patients. However, butyrate absorption in the colon can be increased by manipulating electrolyte composition in the rectal lumen Holtug et al. Thus, topical butyrate, given intrarectally in form of SB, plays a double role; firstly by employing sodium ions, it accelerates rectal absorption of SB and secondly, the absorbed butyrate imparts healing to the colonocytes.

The end result is epithelial proliferation to restore the damaged epithelium, especially the lost colonic epithelial continuity. To the best of our knowledge, this finding has not been reported before. However, the systemic effect of butyrate to other body systems and organs has been reported. All these facts and our own study affirm that butyrate has a potential to impart protective roles to various body organs and systems through systemic administration.

Consistent with this theme, we recently reported that in mice, compositionally defined diets that are made with purified ingredients and lack fermentable fiber promote low-grade inflammation and metabolic syndrome, both of which could be ameliorated by supplementation of such diets with the fermentable fiber inulin.

However, in contrast to the case of low-grade inflammation, addition of inulin, but not the insoluble fiber cellulose, further exacerbated the severity of colitis and its associated clinical manifestations weight loss and bleeding in both low- and high-fat diets. However, the purpose of autophagy is not the simple elimination of materials, but instead, autophagy serves as a dynamic recycling system that produces new building blocks and energy for cellular renovation and homeostasis.

Here we provide a multidisciplinary review of our current understanding of autophagy's role in metabolic adaptation, intracellular quality control, and renovation during development and differentiation. We also explore how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.

These amino acids can subsequently be used by the microbiota in the colon, or transported from the lumen into the portal blood stream. In addition, the host itself produces substrates such as glycoproteins e. This higher rate of bacterial protein fermentation has been related to high pH and low carbohydrate availability in the large intestine [22].

The preferred amino acid substrates of colonic bacteria include lysine, arginine, glycine, and the BCAA leucine, valine, and isoleucine [32], resulting in the generation of a complex mixture of metabolic end products including among others ammonia, SCFA acetate, propionate, and butyrate , and branched-chain fatty acids BCFA; valerate, isobutyrate, and isovalerate.

Intestinal barrier function is significantly less developed in full-term newborn piglets receiving total parental nutrition compared with those receiving enteral nutrition 7.

Production of SCFA in the bowel may be crucial for gastrointestinal adaptation and maturation in the early stage of postnatal life 8. To test the hypothesis that SCFA may originate from polypeptides as well, the production of these acids from albumin and specific amino acids was examined in a faecal incubation system.

Albumin was converted to all C2-C5-fatty acids, whereas amino acids generally were converted to specific SCFA, most often through the combination of a deamination and decarboxylation of the amino acids, although more complex processes also took place.

This study indicates that a part of the intestinal SCFA may originate from polypeptides, which apparently are the major source of those SCFA isobutyrate, valerate, and isovalerate only found in small amounts in the healthy colon. Moreover, gastrointestinal disease resulting in increased proteinous material in the colon exudation, mucosal desquamation, bleeding, and so forth may hypothetically influence SCFA production.

The present study was undertaken to assess the metabolic performance of the mucosa in UC and especially to explore whether a metabolic abnormality could be detected.

To facilitate this approach a method of preparing suspensions of colonocytes was devised. Mucosa of the distal colon depended metabolically mostly on n-butyrate, whereas the proximal colonic mucosa depended mostly on glucose and glutamine for respiratory fuel. Production of 14C02 was linear whenever this could be tested for 60 min. Parenteral nutrition objectives for very low birth weight infants: Standardised neonatal parenteral nutrition formulations- an Australasian group consensus Effect of a neonatal standard aqueous parenteral nutrition formulation on aseptic unit capacity planning.

European e-Journal of Clinical Nutrition and Metabolism ;5: Parenteral nutrition in neonatology — to standardize or individualize? Safe parenteral nutrition and the role of standardised feeds.

Standardised versus pharmacist-monitored individualised parenteral nutrition in low-birth weight infants. Pharmacist monitoring of parenteral nutrition: Standardized versus individualized parenteral nutrition in very low birth weight infants: Standard two-compartment formulation for total parenteral nutrition in the neonatal intensive care unit: Assessment of implementation of a standardized parenteral formulation for early nutritional support of very preterm infants.

Evaluation of standardized versus individualised total parenteral nutrition regime for neonates less than 33 weeks gestation. Standardized parenteral nutrition in preterm infants: Catch-up growth and head circumference of very low birthweight, small for gestational age preterm infants and mental development to adulthood.

Randomised trial of early diet in preterm babies and later intelligence quotient. First-week protein and energy intakes are associated with month developmental outcomes in extremely low birth weight infants. Postnatal head growth in preterm infants: Increased protein intake decreases postnatal growth faltering in ELBW babies. Aggressive nutrition of the very low birthweight infants.

Rigo J, Senterre T. Intrauterine-like growth rates can be achieved with premixed parenteral nutrition solution in preterm infants.

Iron, minerals and trace elements. However, in a papal allocution, Pope John Paul II stated that clinicians are obligated to provide nutrition and hydration to most patients in a persistent vegetative state.

What an individual believes vs. Therefore, healthcare providers must communicate with patients and families to determine preferences. Guidelines for Approaching Nutrition Support Nutrition and hydration are life-sustaining medical therapies that, like other medical therapies, can be legally initiated or ceased. Conversations about end-of-life issues should be initiated early in the diagnostic and treatment stages rather than waiting until the dying process has begun.

The sequence is often based on physician bias rather than patient goals and desires. Clinical practice guidelines for determining who should be considered for HPN have been published and include the following:. Futility or ineffectual therapy may be hard to quantify for the patient and family, and it may behoove the clinician to discuss the overall appropriateness or the minimal benefit of the therapy for the patient.

If therapy is stopped abruptly, it could be perceived as lack of caring or abandonment. Communication among the patient, his or her family, and healthcare providers is essential. Ongoing evaluation of benefit vs. She has served on the American Society for Parenteral and Enteral Nutrition board of directors and is currently on the American Dietetic Association board of directors.

She has published peer-reviewed journals and textbooks and given numerous professional presentations on topics related to nutrition support.

Barry and his wife should be encouraged to discuss what to do if the therapy is unsuccessful. Barry has severe nausea, vomiting, and diarrhea. Pharmacotherapy reduces but does not alleviate his symptoms. He and his wife are told that the weight loss is a consequence of his therapy and will improve when his cancer is in remission. Weight loss is often considered an inevitable consequence of cancer therapy. Nutrition intervention at this point may prevent ongoing nutritional and physical deterioration.

Barry finishes chemotherapy, but dumping syndrome continues to cause diarrhea and nausea, resulting in poor dietary intake and continued weight loss. At his six-month checkup, Barry is diagnosed with recurrent cancer that is not resectable and is causing a partial small-bowel obstruction.

Over the next six weeks, his health deteriorates, and he is bedridden with an increased requirement for pain management, resulting in impaired mental acuity and an inability to tolerate solid food. She does agree to hospice but wants her husband to be fed. Barry is admitted to hospice. Ten days later, he dies. This case exemplifies the misunderstanding and miscommunication that can hinder providing nutrition support at the end of life.

Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. Ethical issues in artificial nutrition and hydration. Klein S, Koretz RL. Nutrition support in patients with cancer: What do the data really show? Tube feeding in patients with advanced dementia: A review of the evidence. Does artificial enteral nutrition prolong the survival of institutionalized elders with chewing and swallowing problems?

B. Nutritional assessment