Neurological Complications Of Dka

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Here's a quick video tutorial on how to translate ICD-9 codes into ICD-10.

2017/18 Icd-10-cm Codes E13*: Other Specified Diabetes Mellitus

E10.1 Type 1 diabetes mellitus with ketoacidosis E10.10 Type 1 diabetes mellitus with ketoacidosis wi... E10.11 Type 1 diabetes mellitus with ketoacidosis wi... E10.2 Type 1 diabetes mellitus with kidney complica... E10.21 Type 1 diabetes mellitus with diabetic nephro... E10.22 Type 1 diabetes mellitus with diabetic chroni... E10.29 Type 1 diabetes mellitus with other diabetic ... E10.3 Type 1 diabetes mellitus with ophthalmic comp... E10.31 Type 1 diabetes mellitus with unspecified dia... E10.311 Type 1 diabetes mellitus with unspecified dia... E10.319 Type 1 diabetes mellitus with unspecified dia... E10.32 Type 1 diabetes mellitus with mild nonprolife... E10.321 Type 1 diabetes mellitus with mild nonprolife... E10.3211 Type 1 diabetes mellitus with mild nonprolife... E10.3212 Type 1 diabetes mellitus with mild nonprolife... E10.3213 Type 1 diabetes mellitus with mild nonprolife... E10.3219 Type 1 diabetes mellitus with mild nonprolife... E10.329 Type 1 diabetes mellitus with mild nonprolife... E10.3291 Type 1 diabetes mellitus with mild nonprolife... E10.3292 Type 1 diabetes mellitus with mild nonprolife... E10.3293 Type 1 diabetes mellitus with mild nonprolife... E10.3299 Type Continue reading >>

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  1. Eugene

    I HATE being in ketosis. I tried it many many times but it just doesn't feel natural. My sleep gets fucked up, my brain foggy, my motivation suffers, etc etc... And YES I did give enough time for induction period and I did feel better but not perfect. Plus occasionally its impossible to not mess up and you are back to going through induction hell once again.
    I still want the benefits of no grains, no omega 6, etc etc... Without being in Ketosis because I feel much better just out of ketosis then I ever do in full blown ketosis. Also I feel great after accidental fasts like when i go to college without eating anything all day.
    So basically my question is -- what are the best sources of carbs outside of green vegetables like broccoli to get enough carbs to keep the hell out of ketosis, and have enough carbs for weight training. How much carbs from fruits is too much and what fruits are to avoid?
    For now the staples of my diet is broccoli, garlic, onions, avacados, grapefruits, eggs, bacon, beef, cheese.
    Btw, I am by no means fat, but I never seem to go below a certain fat %, even in full ketosis. Like there is slight fat over abbs no matter what I do. I realized recently that i was making a few mistakes in my diet such as eating mayo (omega6) and peanut-butter(legumes with high lectin count and anti-nutrients) so that might explain why. I've heard fasts are good for last stubborn fat; is that true?
    Any opinions? Thanks!
    Also I would like to warn others who eat peanut-butter and peanuts on paleo or keto diet --peanut butter is PEAS not NUTS and thus have their share of anti-nutrients, lectins, etc...
    Is there such thing as almond butter?

  2. prophets

    Click HERE to rent this advertising spot for NUTRITION to support LongeCity (this will replace the google ad above).

  3. oehaut

    Eugene, on Feb 26 2010, 08:30 PM, said:

    I HATE being in ketosis. I tried it many many times but it just doesn't feel natural. My sleep gets fucked up, my brain foggy, my motivation suffers, etc etc... And YES I did give enough time for induction period and I did feel better but not perfect. Plus occasionally its impossible to not mess up and you are back to going through induction hell once again.
    I still want the benefits of no grains, no omega 6, etc etc... Without being in Ketosis because I feel much better just out of ketosis then I ever do in full blown ketosis. Also I feel great after accidental fasts like when i go to college without eating anything all day.
    So basically my question is -- what are the best sources of carbs outside of green vegetables like broccoli to get enough carbs to keep the hell out of ketosis, and have enough carbs for weight training. How much carbs from fruits is too much and what fruits are to avoid?
    For now the staples of my diet is broccoli, garlic, onions, avacados, grapefruits, eggs, bacon, beef, cheese.
    Btw, I am by no means fat, but I never seem to go below a certain fat %, even in full ketosis. Like there is slight fat over abbs no matter what I do. I realized recently that i was making a few mistakes in my diet such as eating mayo (omega6) and peanut-butter(legumes with high lectin count and anti-nutrients) so that might explain why. I've heard fasts are good for last stubborn fat; is that true?
    Any opinions? Thanks!
    Also I would like to warn others who eat peanut-butter and peanuts on paleo or keto diet --peanut butter is PEAS not NUTS and thus have their share of anti-nutrients, lectins, etc...
    Is there such thing as almond butter?
    Why are you trying to be that low-carb? Do you have insulin resistance or glycemic control problem? Otherwise just add back quinoa, oat and rice. Just a serving of oat in the morning should keep you out of ketosis. I don't know what is you BF%, but to a certain point you need muscularity to make it come down very low. Do you weight train? Getting rid of the stubborn fat asks for hardcore dieting with a clever training program plan. I don't see what the fat would have to do with it since it all come down to adreno-receptors. Maybe there's a link i'm not aware tho.
    Also, peanut have a fair amount of positive studies for many aspect of health, including weight control.

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Cerebral Accidents In Pediatric Diabetic Ketoacidosis: Different Complications And Different Evolutions

Cerebral Accidents in Pediatric Diabetic Ketoacidosis: Different Complications and Different Evolutions Mozzillo E.a D'Amico A.b Fattorusso V.a Carotenuto B.b Buono P.a De Nitto E.a Falco M.a Franzese A. a I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Diabetic ketoacidosis (DKA) may be associated with neurologic complications: the most common is cerebral edema while the risk of venous and arterial stroke is rare. There is a pathogenetic link between DKA, hypercoagulability and stroke, whose risk is underestimated by clinicians. Our cases present a wide spectrum of cerebral accidents during Continue reading >>

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  1. Edward

    Continued from: http://www.raypeatforum.com/forum/viewtopic.php?f=36&t=2514&start=10#p30662

    SAFarmer said:

    Edward said:
    Babies are in deep ketosis at birth and continue to be so until they are weaned off breast milk. I haven't looked to see how fast that decline out of ketosis happens after babies are weened off breast milk. Scientific reference for this statement of your's please?
    Adam, P. A., Räihä, N., Rahiala, E. L., & Kekomäki, M. (1975).
    Oxidation of glucose and D-B-OH-butyrate by the early human fetal brain. Acta paediatrica Scandinavica, 64(1), 17–24. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1114894
    The isolated brains of 12 previable human fetuses obtained at 12 to 21 weeks’ gestation, were perfused through the interval carotid artery with glucose (3 mM) and/or DL-B-OH-butyrate (DL-BOHB), 4.5 MM, plus tracer quantities of either glucose-6-14C (G6-14C) or beta-OH-butyrate-3-14C (BOHB3-14C). Oxidative metabolism was demonstrated by serial collection of gaseous 14CO2 from the closed perfusion system, and from the recirculating medium. Glucose and BOHB were utilized at physiological rates as indicated (mean plus or minus SEM): G6-14C at 0.10 plus or minus 0.01 mumoles/min g brain (n equal 7) or 17.5 plus or minus 1.9 mumoles/min kg fetus; and BOHB3-14C at 0.16 plus or minus 0.05 mumoles/min g (n equal to 5) or 27.3 plus or minus 7.4 mumoles/min kg. Based on fetal weight, glucose metabolism by brain apparently accounted for about 1/3 of basal glucose utilization in the fetus. On a molar basis BOHB3-14C was taken up at 1.47 times the rate of G6-14C. Both BOHB3-14C and G6 14C were converted to 14CO2. The rate of BOHB3-14C conversion to 14CO2 was equal to its rate of consumption, and exceeded the conversion of glucose to CO2 because 45% of the G6-14C was incorporated into lactate-14C. Accordingly, both substrates support oxidative metabolism by brain; and BOHB is a major potential alternate fuel which can replace glucose early in human development.
    Bon, C., Raudrant, D., Golfier, F., Poloce, F., Champion, F., Pichot, J., & Revol, A. (n.d.). [Feto-maternal metabolism in human normal pregnancies: study of 73 cases]. Annales de biologie clinique, 65(6), 609–19. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/18039605
    From 73 normal pregnancies of gestational age between 17 and 41 weeks of gestation (WG), the concentrations of glucose, pyruvate and lactate, free fatty acids, ketone bodies (aceto-acetate and beta-hydroxybutyrate) and cholesterol were assessed on maternal venous blood (MVB) and umbilical venous blood (UVB), sampled by cordocentesis. The objective of this work was to study feto-maternal metabolism, as well as nutritional exchange between maternal blood and fetal blood during the second and third trimesters of pregnancy. Maternal and fetal glycemias, as well as maternal-fetal glucose concentration gradient, were found stable during the studied gestational period; maternal glucose is always higher than fetal glucose, with a mean concentration delta of 0.69+/-0.34 mmol/L. Maternal lactate level (1.26+/-0.38 mmol/L) is lower than fetal lactate level (1.48+/-0.46 mmol/L), whereas maternal blood pyruvate concentration (0.042+/-0.020 mmol/L) is higher than fetal blood pyruvate concentration (0.025+/-0.010 mmol/L). Consequently, mean lactate / pyruvate ratio is found twice lower in maternal blood (31.77+/-9.89) than in fetal blood (64.10+/-17.12). Free fatty acids concentration is approximately three times higher in maternal blood than in fetal blood (respectively 0.435+/-0.247 mmol/L and 0.125+/-0.046 mmol/L). Maternal venous aceto-acetate (0.051+/-0.042 mmol/L) and beta-hydroxybutyrate (0.232+/-0.270 mmol/L) concentrations are significantly lower than those in UVB (respectively 0.111+/-0.058 and 0.324+/-0.246 mmol/L) and the beta-hydroxybutyrate/aceto-acetate ratio is on average 1.7 times higher in MVB (4.75+/-2.5) than in UVB (2.82+/-1.18). Cholesterol concentration is significantly higher in maternal blood (6.26+/-1.40 mmol/L) than in fetal blood (1.66+/-0.34 mmol/L). Our results show the characteristics of oxidative metabolism of the fetus compared with that of the adult. Blood concentration in energy substrates, measured with glucose and free fatty acids levels, is low in UVB and suggests increased energy needs of the growing fetus. Mean high concentrations in aceto-acetate and beta-hydroxybutyrate in UVB, indicate probably fetal ketogenesis. UVB low cholesterolemia suggests high cholesterol consumption in the fetal compartment for cellular membrane synthesis and steroid biosynthesis.
    Bougneres, P. F., Lemmel, C., Ferré, P., & Bier, D. M. (1986). Ketone body transport in the human neonate and infant. The Journal of clinical investigation, 77(1), 42–8. doi:10.1172/JCI112299
    Using a continuous intravenous infusion of D-(-)-3-hydroxy[4,4,4-2H3]butyrate tracer, we measured total ketone body transport in 12 infants: six newborns, four 1-6-mo-olds, one diabetic, and one hyperinsulinemic infant. Ketone body inflow-outflow transport (flux) averaged 17.3 +/- 1.4 mumol kg-1 min-1 in the neonates, a value not different from that of 20.6 +/- 0.9 mumol kg-1 min-1 measured in the older infants. This rate was accelerated to 32.2 mumol kg-1 min-1 in the diabetic and slowed to 5.0 mumol kg-1 min-1 in the hyperinsulinemic child. As in the adult, ketone turnover was directly proportional to free fatty acid and ketone body concentrations, while ketone clearance declined as the circulatory content of ketone bodies increased. Compared with the adult, however, ketone body turnover rates of 12.8-21.9 mumol kg-1 min-1 in newborns fasted for less than 8 h, and rates of 17.9-26.0 mumol kg-1 min-1 in older infants fasted for less than 10 h, were in a range found in adults only after several days of total fasting. If the bulk of transported ketone body fuels are oxidized in the infant as they are in the adult, ketone bodies could account for as much as 25% of the neonate’s basal energy requirements in the first several days of life. These studies demonstrate active ketogenesis and quantitatively important ketone body fuel transport in the human infant. Furthermore, the qualitatively similar relationships between the newborn and the adult relative to free fatty acid concentration and ketone inflow, and with regard to ketone concentration and clearance rate, suggest that intrahepatic and extrahepatic regulatory systems controlling ketone body metabolism are well established by early postnatal life in humans.
    Cotter, D. G., d’Avignon, D. A., Wentz, A. E., Weber, M. L., & Crawford, P. A. (2011). Obligate role for ketone body oxidation in neonatal metabolic homeostasis. The Journal of biological chemistry, 286(9), 6902–10. doi:10.1074/jbc.M110.192369
    To compensate for the energetic deficit elicited by reduced carbohydrate intake, mammals convert energy stored in ketone bodies to high energy phosphates. Ketone bodies provide fuel particularly to brain, heart, and skeletal muscle in states that include starvation, adherence to low carbohydrate diets, and the neonatal period. Here, we use novel Oxct1(-/-) mice, which lack the ketolytic enzyme succinyl-CoA:3-oxo-acid CoA-transferase (SCOT), to demonstrate that ketone body oxidation is required for postnatal survival in mice. Although Oxct1(-/-) mice exhibit normal prenatal development, all develop ketoacidosis, hypoglycemia, and reduced plasma lactate concentrations within the first 48 h of birth. In vivo oxidation of (13)C-labeled β-hydroxybutyrate in neonatal Oxct1(-/-) mice, measured using NMR, reveals intact oxidation to acetoacetate but no contribution of ketone bodies to the tricarboxylic acid cycle. Accumulation of acetoacetate yields a markedly reduced β-hydroxybutyrate:acetoacetate ratio of 1:3, compared with 3:1 in Oxct1(+) littermates. Frequent exogenous glucose administration to actively suckling Oxct1(-/-) mice delayed, but could not prevent, lethality. Brains of newborn SCOT-deficient mice demonstrate evidence of adaptive energy acquisition, with increased phosphorylation of AMP-activated protein kinase α, increased autophagy, and 2.4-fold increased in vivo oxidative metabolism of [(13)C]glucose. Furthermore, [(13)C]lactate oxidation is increased 1.7-fold in skeletal muscle of Oxct1(-/-) mice but not in brain. These results indicate the critical metabolic roles of ketone bodies in neonatal metabolism and suggest that distinct tissues exhibit specific metabolic responses to loss of ketone body oxidation.
    De Boissieu, D., Rocchiccioli, F., Kalach, N., & Bougnères, P. F. (1995). Ketone body turnover at term and in premature newborns in the first 2 weeks after birth. Biology of the neonate, 67(2), 84–93. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7766735
    Using the infusion of D-(-)-3-hydroxy-[1,2,3,4,-13C4]butyrate at tracer doses, we measured total ketone body turnover in 13 premature and 10 at term infants in the first 2 weeks after birth. The premature infants received parenteral and/or oral feeding. The normal newborns were either recently fed or briefly fasting. The premature and the fed at term infants had comparable concentrations of ketone body (476 +/- 86 and 406 +/- 78 mumol/l) and free fatty acids (FFA) (309 +/- 47 and 325 +/- 75 mumol/l). In the premature newborns, ketone body turnover rates (3.2 +/- 0.2 mumol kg-1 min-1) were 74% that of fed newborns at term (4.3 +/- 0.3 mumol kg-1 min-1, p < 0.05), and 18% that of normal newborns during a brief fast (17.3 +/- 1.3 mumol kg-1 min-1, p < 0.01). Ketone body production rates correlated with plasma FFA concentrations in both groups (r = 0.62 and 0.69, p < 0.05). However, for a similar plasma FFA content, ketone production was 2- to 3-fold lower in the premature, indicating an immature hepatic capacity to convert FFA into ketones. Our study therefore shows that ketogenesis is already active in infants born 10 weeks before normal term and continuously fed, but that daily ketone production is lower than at term.
    Herrera, E. (2000). Metabolic adaptations in pregnancy and their implications for the availability of substrates to the fetus. European journal of clinical nutrition, 54 Suppl 1, S47–51. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10805038
    During the first two-thirds of gestation, the mother is in an anabolic condition, increasing her fat depots thanks to both hyperphagia and enhanced lipogenesis. During the last third of gestation, the mother switches to a catabolic condition. Glucose is the most abundant nutrient crossing the placenta, which causes maternal hypoglycemia despite an increase in the gluconeogenetic activity. Adipose tissue lipolytic activity becomes enhanced, increasing plasma levels of FFA and glycerol that reach the liver; consequently there is an enhanced production of triglycerides that return to the circulation in the form of very low density lipoproteins (VLDL). Glycerol is also used as a preferential gluconeogenetic substrate, saving other more essential substrates, like amino acids, for the fetus. Under fasting conditions, fatty acids are converted into ketone bodies throughout the beta-oxidation pathway, and these compounds easily cross the placental barrier and are metabolized by the fetus. An enhanced liver production of VLDL-triglycerides together with a decrease in adipose tissue lipoprotein lipase (LPL) and an increase in plasma activity of cholesterol ester transfer protein causes both an intense increment in these lipoproteins and a proportional enrichment of triglycerides in both low and high density lipoproteins. Maternal triglycerides do not cross the placenta, but the presence of LPL and other lipases allows their hydrolysis, releasing fatty acids to the fetus. Under fasting conditions, the maternal liver uses circulating triglycerides as ketogenic substrates. Around parturition there is an induction of LPL activity in the mammary glands, driving circulating triglycerides to this organ for milk synthesis, allowing essential fatty acids derived from the mother’s diet to become available to the suckling newborn.
    Herrera, E., & Amusquivar, E. (n.d.). Lipid metabolism in the fetus and the newborn. Diabetes/metabolism research and reviews, 16(3), 202–10. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10867720
    During late gestation, although maternal adipose tissue lipolytic activity becomes enhanced, lipolytic products cross the placenta with difficulty. Under fasting conditions, free fatty acids (FFA) are used for ketogenesis by the mother, and ketone bodies are used as fuels and lipogenic substrates by the fetus. Maternal glycerol is preferentially used for glucose synthesis, saving other gluconeogenic substrates, like amino acids, for fetal growth. Placental transfer of triglycerides is null, but essential fatty acids derived from maternal diet, which are transported as triglycerides in lipoproteins, become available to the fetus owing to the presence of both lipoprotein receptors and lipase activities in the placenta. Diabetes in pregnancy promotes lipid transfer to the fetus by increasing the maternal-fetal gradient, which may contribute to an increase in body fat mass in newborns of diabetic women. Deposition of fat stores in the fetus is very low in the rat but high in humans, where body fat accretion occurs essentially during the last trimester of intra-uterine life. This is sustained by the intense placental transfer of glucose and by its use as a lipogenic substrate, as well as by the placental transfer of fatty acids and to their low oxidation activity. During the perinatal period an active ketonemia develops, which is maintained in the suckling newborn by several factors: (i) the high-fat and low-carbohydrate content in milk, (ii) the enhanced lipolytic activity occurring during the first few hours of life, and (iii) both the uptake of circulating triglycerides by the liver due to the induction of lipoprotein lipase (LPL) activity in this organ, and the presence of ketogenic activity in the intestinal mucose. Changes in LPL activity, lipogenesis and lipolysis contribute to the sequential steps of adipocyte hyperplasia and hypertrophia occurring during the extra-uterine white adipose tissue development in rat, and this may be used as a model to extrapolate the intra-uterine adipose tissue development in other species, including humans.
    Koski, K. G., Lanoue, L., & Young, S. N. (1995). Maternal dietary carbohydrate restriction influences the developmental profile of postnatal rat brain indoleamine metabolism. Biology of the neonate, 67(2), 122–31. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7539298
    Dietary glucose restriction during pregnancy can retard fetal brain development, lower term brain glycogen levels and adversely affect the serotonergic neurotransmitter system in the fetus. To study if the postnatal profile of brain indoles continues to respond to these diet-induced changes, pregnant rats were fed graded levels (0, 12, 24, 60%) of glucose from impregnation to day 15 postpartum, and neonatal brain measurements were made. A steady decrease in tryptophan levels, a steady increase in 5-hydroxytryptamine (5-HT) levels and a U-shaped change in 5-hydroxyindoleacetic acid (5-HIAA) were observed during the first 15 postpartum days. Superimposed on these development profiles was a temporary surge in the concentrations of all three indoles 24 h after birth, which was dramatic for tryptophan and more modest for 5-HT and 5-HIAA. The level of carbohydrate in the maternal diet significantly influenced the magnitude of this increase in tryptophan, 5-HT and 5-HIAA at 24 h: the values were significantly higher in the carbohydrate-restricted (12 or 24%) rat pups when compared with control or carbohydrate-free (0% glucose) offspring. No effects of dietary treatment were apparent by day 6. However, the reemergence of a significant difference in brain 5-HT content at day 15 postpartum indicates that even when energy intake is adequate the level of carbohydrate in the maternal diet may continue to play a role in modulating serotonergic neurotransmitter levels later in development.
    Shambaugh, G. E. (1985). Ketone body metabolism in the mother and fetus. Federation proceedings, 44(7), 2347–51. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3884390
    Pregnancy is characterized by a rapid accumulation of lipid stores during the first half of gestation and a utilization of these stores during the latter half of gestation. Lipogenesis results from dietary intake, an exaggerated insulin response, and an intensified inhibition of glucagon release. Increasing levels of placental lactogen and a heightened response of adipose tissue to additional lipolytic hormones balance lipogenesis in the fed state. Maternal starvation in late gestation lowers insulin, and lipolysis supervenes. The continued glucose drain by the conceptus aids in converting the maternal liver to a ketogenic organ, and ketone bodies produced from incoming fatty acids are not only utilized by the mother but cross the placenta where they are utilized in several ways by the fetus: as a fuel in lieu of glucose; as an inhibitor of glucose and lactate oxidation with sparing of glucose for biosynthetic disposition; and for inhibition of branched-chain ketoacid oxidation, thereby maximizing formation of their parent amino acids. Ketone bodies are widely incorporated into several classes of lipids including structural lipids as well as lipids for energy stores in fetal tissues, and may inhibit protein catabolism. Finally, it has recently been shown that ketone bodies inhibit the de novo biosynthesis of pyrimidines in fetal rat brain slices. Thus during maternal starvation ketone bodies may maximize chances for survival both in utero and during neonatal life by restraining cell replication and sustaining protein and lipid stores in fetal tissues.
    Yeh, Y. Y., & Sheehan, P. M. (1985). Preferential utilization of ketone bodies in the brain and lung of newborn rats. Federation proceedings, 44(7), 2352–8. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3884391
    Persistent mild hyperketonemia is a common finding in neonatal rats and human newborns, but the physiological significance of elevated plasma ketone concentrations remains poorly understood. Recent advances in ketone metabolism clearly indicate that these compounds serve as an indispensable source of energy for extrahepatic tissues, especially the brain and lung of developing rats. Another important function of ketone bodies is to provide acetoacetyl-CoA and acetyl-CoA for synthesis of cholesterol, fatty acids, and complex lipids. During the early postnatal period, acetoacetate (AcAc) and beta-hydroxybutyrate are preferred over glucose as substrates for synthesis of phospholipids and sphingolipids in accord with requirements for brain growth and myelination. Thus, during the first 2 wk of postnatal development, when the accumulation of cholesterol and phospholipids accelerates, the proportion of ketone bodies incorporated into these lipids increases. On the other hand, an increased proportion of ketone bodies is utilized for cerebroside synthesis during the period of active myelination. In the lung, AcAc serves better than glucose as a precursor for the synthesis of lung phospholipids. The synthesized lipids, particularly dipalmityl phosphatidylcholine, are incorporated into surfactant, and thus have a potential role in supplying adequate surfactant lipids to maintain lung function during the early days of life. Our studies further demonstrate that ketone bodies and glucose could play complementary roles in the synthesis of lung lipids by providing fatty acid and glycerol moieties of phospholipids, respectively. The preferential selection of AcAc for lipid synthesis in brain, as well as lung, stems in part from the active cytoplasmic pathway for generation of acetyl-CoA and acetoacetyl-CoA from the ketone via the actions of cytoplasmic acetoacetyl-CoA synthetase and thiolase.

  2. Edward

    Hawdon, J. M., Ward Platt, M. P., & Aynsley-Green, A. (1992). Patterns of metabolic adaptation for preterm and term infants in the first neonatal week. Archives of disease in childhood, 67(4 Spec No), 357–65. Retrieved from http://www.pubmedcentral.nih.gov/articl ... e=abstract
    There have been few comprehensive accounts of the relationships between glucose and other metabolic fuels during the first postnatal week, especially in the context of modern feeding practises. A cross sectional study was performed of 156 term infants and 62 preterm infants to establish the normal ranges and interrelationships of blood glucose and intermediary metabolites in the first postnatal week, and to compare these with those of 52 older children. Blood glucose concentrations varied more for preterm than for term infants (1.5-12.2 mmol/l v 1.5-6.2 mmol/l), and preterm infants had low ketone body concentrations, even at low blood glucose concentrations. Breast feeding of term infants and enteral feeding of preterm infants appeared to enhance ketogenic ability. Term infants had lower prefeed blood glucose concentrations than children but, like children, appeared to be capable of producing ketone bodies. This study demonstrates that neonatal blood glucose concentrations should be considered in the context of availability of other metabolic fuels, and that the preterm infant has a limited ability to mobilise alternative fuels.
    Ferré, P., Pégorier, J. P., Williamson, D. H., & Girard, J. R. (1978). The development of ketogenesis at birth in the rat. The Biochemical journal, 176(3), 759–65. Retrieved from http://www.pubmedcentral.nih.gov/articl ... e=abstract
    In the suckling newborn rat, blood ketone bodies begin to increase slowly 4h after birth and then rise sharply between 12 and 16h, whereas the major increase in plasma non-esterified fatty acids and liver carnitine occurs during the first 2h of life, parallel with the onset of suckling. In the starved newborn rat, which shows no increase in liver carnitine unless it is fed with a carnitine solution, the developmental pattern of the ketogenic capacity (tested by feeding a triacylglycerol emulsion, which increases plasma non-esterified fatty acids by 3-fold) is the same as in the suckling animal. This suggests that the increases in plasma non-esterified fatty acids and liver carnitine seen 2h after birth in the suckling animal are not the predominant factors inducing the switch-on of ketogenesis. Injection of butyrate to starved newborn pups resulted in a pattern of blood ketone bodies which was similar to that found after administration of triacylglycerols, but, at all time points studied, the hyperketonaemia was more pronounced with butyrate. It is suggested that, even if the entry of long-chain fatty acids into the mitochondria is a rate-limiting step, it is not the only factor controlling ketogenesis after birth in the rat. As in the adult rat, there is a reciprocal correlation between the liver glycogen content and the concentration of ketone bodies in the blood.
    Ward Platt, M., & Deshpande, S. (2005). Metabolic adaptation at birth. Seminars in fetal & neonatal medicine, 10(4), 341–50. doi:10.1016/j.siny.2005.04.001
    After birth, the neonate must make a transition from the assured continuous transplacental supply of glucose to a variable fat-based fuel economy. The normal infant born at term accomplishes this transition through a series of well-coordinated metabolic and hormonal adaptive changes. The patterns of adaptation in the preterm infant and the baby born after intrauterine growth restriction are, however, different to that of a full-term neonate, with the risk for former groups that there will be impaired counter-regulatory ketogenesis. There is much less precise linkage of neonatal insulin secretion to prevailing blood glucose concentrations. These patterns of metabolic adaptation are further influenced by feeding practices.
    Wells, M. A. (1985). Fatty acid metabolism and ketone formation in the suckling rat. Federation proceedings, 44(7), 2365–8. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3884393
    Rat milk triacylglycerols contain 35% medium-chain length fatty acids. About 70% of ingested medium-chain fatty acids are released from milk triacylglycerols in the stomach and small intestine and are absorbed directly into the portal venous system. Based on studies with the perfused suckling rat liver and in vivo studies with 2-tetradecylglycidic acid, an inhibitor of long-chain fatty acid oxidation, it is estimated that medium-chain fatty acids provide 75-80% of the substrate for ketogenesis. The preferential use of medium-chain fatty acids for ketogenesis spares long-chain fatty acids for complex lipid and membrane biosynthesis during this period of rapid growth. Although medium-chain fatty acids are the major substrate for ketogenesis, this pathway accounts for only 15% of the utilization of ingested medium-chain fatty acids, the rest presumably being oxidized directly in extrahepatic tissues.
    Girard, J., Duée, P. H., Ferré, P., Pégorier, J. P., Escriva, F., & Decaux, J. F. (1985). Fatty acid oxidation and ketogenesis during development. Reproduction, nutrition, development, 25(1B), 303–19. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3887527
    Fatty acids are the preferred oxidative substrates of the heart, skeletal muscles, kidney cortex and liver in adult mammals. They are supplied to these tissues either as nonesterified fatty acids (NEFA), or as triglycerides after hydrolysis by lipoprotein lipase. During fetal life, tissue capacity to oxidize NEFA is very low, even in species in which the placental transfer of NEFA and carnitine is high. At birth, the ability to oxidize NEFA from endogenous sources or from milk (a high-fat diet) develops rapidly in various tissues and remains very high throughout the suckling period. Ketogenesis appears in the liver by 6 to 12 hrs after birth, and the ketone bodies are used as oxidative fuels by various tissues during the suckling period. At the time of weaning, the transition from a high-fat to a high-carbohydrate diet is attended by a progressive decrease in the ketogenic capacity of the liver, whereas other tissues (skeletal muscle, heart, kidney) maintain a high capacity for NEFA oxidation. The nutritional and hormonal factors involved in changes in fatty acid oxidation during development are discussed.

  3. Edward

    I think these studies demonstrate clearly that not only are babies in ketosis but are able to rapidly decline into ketosis with short fasting, whereas in adults it takes a few days. Not only are babies in ketosis but the mother's milk enhances ketogenesis. So whether the baby is fasted or being breast fed they are still in ketosis. This makes logical sense given the high fat content of breast milk. Breast milk also contains short and medium chain fatty acids which are similar to those in coconut oil. Which we of course know stimulate ketogensis.
    As far as optimal, no one has said that being ketogenic is optimal. Remember there are various degree of ketosis, the question is what degree of ketosis is optimal. Instead of trying to have this idea that there is this one size fits all diet for every stage of life (when that clearly isn't the case) we need to look at things like this to give clues.
    When a baby is born, the transistion to breathing oxygen is stressful, ketones are superior fuels and so are short chain fatty acids (SCFAs are preferentially oxidized over glucose), that is why in babies they are produced at such high levels. They are protecting the baby. There is this idea that somehow ketosis is stressful, it is when you are starving. But a baby that is fed is not starving, they are not producing ketones out of stress, they are producing ketones because the types of fatty acids in the mothers milk is stimulating ketogenesis. When you eat coconut oil and produce ketones you are not under stress.
    There are a lot of interesting things to think about here.

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=================================================== PLEASE SUBSCRIBE TO OUR CHANNEL https://www.youtube.com/channel/UCHvQ... =================================================== =================================================== Google Plus Profile : Google Plus Profile : https://plus.google.com/u/0/111392267... =================================================== How to Check Feet for Complications of Diabetes Part 1 : Looking for Changes in Foot Sensations 1.Be aware of numbness in your feet. One of the initial and most common symptoms of peripheral neuropathy that diabetics notice is that their feet lose sensation and become numb. 2.Be alert to tingling and burning sensations. Another common symptom is uncomfortable sensations, such as tingling, pins and needles and/or burning pain. 3.Take note of increased sensitivity to touch, called hyperesthesia. Another alteration of foot sensations that develops in a minority of diabetics is an increase in sensitivity to touch. 4.Pay attention to cramps or sharp pains. As the peripheral neuropathy progresses, it starts to affect the muscles of the feet. 5.Be mindful of muscle weakness. As high glucose goes into nerves, water follows glucose

Complications Of Diabetes Mellitus

Natural History Of Diabetic Nephropathy In Persons With Insulin The 1982 publication of The Prevention and Treatment of FiveComplications of Diabetes: A Guide for Primary Care Practitionerswas an initial attempt to provide straightforward and practicalinformation that primary care practitioners could immediately applyin their practice in the diagnosis and prevention of complicationsof diabetes. In the eight years since that publication wasreleased, over 200,000 copies have been distributed. The emphasison early application of currently available preventive measures ortreatments has resulted in the widespread use of the document. The scope of the present revised edition has been broadened tocover nine complications of diabetes, and the recommendations forthe previous five. We anticipate continued widespread use of thisguide in assisting practitioners in the care of their patients withdiabetes. The recommendations are clear, practical, and based uponscientific evidence, and they can be generally implemented in anoffice practice. We believe that they are conceptually consistentwith the American Medical Association's new emphasis on practiceparameters. Although this publication is mea Continue reading >>

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Popular Questions

  1. SnowPetal

    Per week weightloss that is.

  2. thepapillon

    I've done this a few times while trying to lose weight... and am doing it now. I would say the first week you lose a lot. (5-7 pounds or so) After the first week I found it reduces to more like 3-4 pounds. I think it also depends on your weight. If you have extra weight, it'll come off easier than someone trying to get those last few pounds off. Good luck!

  3. SnowPetal

    That's good to know, thanks.
    I am also doing a lower calorie ketogenic diet as well. I'm hoping I can lose a pound a day like the hcg diet. But I will see.

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