Thyroid cancer was negatively associated with tobacco smoking

Guignard, R., Truong, T., Rougier, Y., Baron-Dubourdieu, D., & Guénel, P. (2007). Alcohol drinking, tobacco smoking, and anthropometric characteristics as risk factors for thyroid cancer: a countrywide case-control study in New Caledonia. American journal of epidemiology, 166(10), 1140–9. doi:10.1093/aje/kwm204

Exceptionally high incidence rates of thyroid cancer are observed in New Caledonia, particularly in Melanesian women. To investigate further the etiology of thyroid cancer and to clarify the reasons of this elevated incidence, the authors conducted a countrywide population-based case-control study in this multiethnic population. The study included 332 cases with histologically verified papillary or follicular carcinoma (293 women and 39 men) diagnosed in 1993-1999 and 412 population controls (354 women and 58 men) frequency matched by gender and 5-year age group. Thyroid cancer was negatively associated with tobacco smoking and alcohol drinking, but no inverse dose-response relation was observed. Height was positively associated with thyroid cancer, particularly in men. Strong positive associations with weight and body mass index were observed in Melanesian women aged 50 years or more, with an odds ratio of 5.5 (95% confidence interval: 1.5, 20.3) for a body mass index of 35 kg/m2 or greater compared with normal-weight women, and there was a clear dose-response trend. This study clarifies the role of overweight for thyroid cancer in postmenopausal women. Because of the high prevalence of obesity among Melanesian women of New Caledonia, this finding may explain in part the exceptionally elevated incidence of thyroid cancer in this group.

 

The complaints have been increasing and as administrator I have made the decision to close the doors of the forum to you

You know your doing something right when the folks at the Ray Peat forum ban you.

I received this message from Charlie the administrator (the funny thing about people who claim to be “open-minded”, they always prefix their statements of action with authoritarian language i.e. “as administrator”):

There have been many complaints about you, particularly the number of posts in opposition to Ray Peat and that those type of discussions should be taken elsewhere as this is not the proper forum to continuously initiate such discussion. The forum was created specifically for people to come and discuss the work of Ray Peat – not to debate it, to discuss it, share insights about it and work together to understand it while gaining their health through the practical use of his information. The complaints have been increasing and as administrator I have made the decision to close the doors of the forum to you.

I think accountability is a good thing:

Hi Charlie, receiving complaints does not justify closing the doors on me. You know that I have contributed in depth information to this forum. Further I have the reputation points as evidence that what I write is useful or at least that there is some agreement. I post the the studies in the appropriate sub forum which the description says “A place to post and discuss scientific studies”, I only have ever stated that I disagree with Dr. Peat on some things, and those are more so his abstract concepts, and I am entitled to that opinion especially as a Veteran. It’s not like I don’t think the thyroid isn’t important. So I disagree, and then a user challenges and asks for evidence and I provide evidence which is crystal clear and do not engage in the childish behavior. So complaints about evidence? So what? People who complain about evidence are people who are stuck in dogma.

There is a difference between debates and discussion, discussion is evidence based, debates like in the recent thread are more of personal attacks rather then objective. I don’t participate in that. I just flag it.

Further my points of disagreement have not changed since I became a member of this forum. And like I said most of that has to do with abstract and theoretical implications.

When looking at science you cannot reject evidence, and evidence to the contrary of something does not mean evidence against it necessarily, what it does mean when results conflict is that there is another process at play or even a relationship.

And in the case of thyroid and ketones there is evidence for a relationship that goes back several decades. I’m not really willing to ignore that are you? I want to know the full functionality of the endocrine system.

You can dislike me and my style and so can the users on this forum, but really banning me only takes away from the forum. It’s all too convenient to silence someone who wants to think a little more thoroughly and carefully about things. And then you become no different from the rest of them. It’s not like I spout without presenting a study, how many studies have I provided on this forum for people to download? Hmm.

As I’ve said I’m looking for truth and ways to tie in Dr. Peat’s work with recent evidence. Making ALL your conclusions off of old studies is like saying the earth is flat and rejecting the pictures sent from space showing perfectly clearly the Earth is indeed round.

It’s fine if you want to ban me, ban me, just give me a few days to download the forum and I won’t post anything.

If you change your mind let me know, I will still continue to contribute and still will maintain the same rational and even keeled response I always write. It’s not a pissing contest for me that should be clear for sure through everything I’ve written. Most people argue at least I provide something more to go on than just an opinion.

Also your gums, it’s a sign of inefficient respiration.

Edward

And after I didn’t receive any responses, I responded once more:

Charlie, how about this? What if instead of posting the studies that conflict with Dr. Peat on the “Scientific Studies” portion of the forum I instead post them in the “Ray Peat Debate Forum”, and then the studies that tend to agree with Dr. Peat I post in the “Scientific Studies” portion of the forum. Although I feel that is filtering, it could be a reasonable compromise?

I’m completely willing to post stuff to different parts of the forum if you think it would help.

Edward

Quite frankly this came as a surprise for me. I had contributed a significant amount of time and effort to the forum and I know that my advice has come in handy for several people. I have always given citations when information I provided was counter intuitive.

It becomes apparent after spending a great deal of time on a forum like that the the people there are sick and the evidence of that manifests in their writing. Quite a few people for being healthy seem quite irate. And that is fine. I wish them the best. I made a few good friends while I was on there.

Inhibition of glutamate release via recovery of ATP levels accounts for a neuroprotective effect of aspirin in rat cortical neurons exposed to oxygen-glucose deprivation

De Cristóbal, J., Cárdenas, A., Lizasoain, I., Leza, J. C., Fernández-Tomé, P., Lorenzo, P., & Moro, M. a. (2002). Inhibition of glutamate release via recovery of ATP levels accounts for a neuroprotective effect of aspirin in rat cortical neurons exposed to oxygen-glucose deprivation. Stroke; a journal of cerebral circulation, 33(1), 261–7. doi:10.1161/hs0102.101299

BACKGROUND AND PURPOSE: Aspirin is preventive against stroke not only because of its antithrombotic properties but also by other direct effects. The aim of this study was to elucidate its direct neuroprotective effects. METHODS: Viability parameters, glutamate release and uptake, and ATP levels were measured in cultured cortical neurons exposed to oxygen-glucose deprivation (OGD). In addition, ATP levels and oxygen consumption were studied in isolated brain mitochondria or submitochondrial particles. RESULTS: Aspirin inhibited OGD-induced neuronal damage at concentrations lower (0.3 mmol/L) than those reported to act via inhibition of the transcription factor nuclear factor-kappaB (which are >1 mmol/L), an effect that correlated with the inhibition caused by aspirin on glutamate release. This effect was shared by sodium salicylate but not by indomethacin, thus excluding the involvement of cyclooxygenase. A pharmacological dissection of the components involved indicated that aspirin selectively inhibits the increase in extracellular glutamate concentration that results from reversal of the glutamate transporter, a component of release that is due to ATP depletion. Moreover, aspirin-afforded neuroprotection occurred in parallel with a lesser decrease in ATP levels after OGD. Aspirin elevated ATP levels not only in intact cortical neurons but also in isolated brain mitochondria, an effect concomitant with an increase in NADH-dependent respiration by brain submitochondrial particles. CONCLUSIONS: Taken together, our present findings show a novel mechanism for the neuroprotective effects of aspirin, which takes place at concentrations in the antithrombotic-analgesic range, useful in the management of patients with high risk of ischemic events.

Neonatal ketosis

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.