Noakes petition

(Sybella) #21

They will get him on appeal

(Rob) #22

Exactly. The petition was founded 2 days ago to address this new issue.

(Bunny) #23

The petition signing numbers go up by the seconds!

Wow!

(Rob) #24

The goalpost moved from 2500 to 7500 in one day and that is now almost done… I would look at 25000 at least for the next goal. Keto/paleo must be big enough to get 6 figures really…

(CharleyD) #25

Signed, will hit 7500 any moment.

(Rob) #26

Over 17,000 now :smiley:

(Rob) #27

BUMP - if you haven’t signed it… it’s at 34,000 but has slowed right down. Wouldn’t it be great to get it to 50K?

https://www.change.org/p/health-professions-council-of-south-africa-stop-the-harassment-of-prof-tim-noakes

Pass it on…

(Runs on bacon) #28

BUMPING AGAIN - for newbies like me!

Nearing the goal of 50,000 signatures!

Status of the petition from the page:
“Prof. Noakes was actually acquitted last April, but the medical board is appealing its own decision. Although there are many disturbing ethical issues surrounding the HPCSA’s treatment of Prof. Noakes, this petition will only focus on the fact that his advice IS evidence based and that this evidence is acknowledged by a group of physicians, other health care providers, scientists, and researchers.”

(Bunny) #29

Some interesting reading on the subject:

  1. KETOSIS – KEY TO HUMAN BABIES’ BIG BRAINS?
  1. Babies thrive under a ketogenic metabolism
  1. Babies in Ketosis
  1. Obligate Role for Ketone Body Oxidation in Neonatal Metabolic Homeostasis 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
  1. Ketone-body metabolism during the neonatal period It is reasonable to assume that [malonyl-CoA] is very low a long time before ketogenesis becomes active. Therefore the neonatal period is ideal to test whether factors other than [malonyl-CoA1] regulate hepatic ketogenesis. Among these factors the large increase in gluconeogenesis after birth (Ballard, 1971; Girard et al., 1975) could influence the fate of intramitochondrial acetyl-CoA by channeling oxaloacetate toward glucose synthesis, thus decreasing citrate synthesis and favouring ketogenesis.
  1. Ketone Body Transport in the Human Neonate and Infant As in the adult (21, 23), ketone levels in our infants were directly correlated with outflow transport (Fig. 1) and inversely correlated with metabolic clearance rate (Fig. 2). However, both outflow transport and clearance rates were about two times greater in newborns and young infants than in adults having similar ketone body levels (14, 21, 23). This increased capacity for taking up ketone bodies from the blood stream in the neonate is consistent with its large brain size in relation to total body weight, and the fourfold increase in neonatal cerebral ketone body uptake compared with the adult (6,9). The close agreement between the regression equation for ketone body production and FFA levels in our patients and the regression calculated from data presented in adult studies (14, 21, 23, 28) (Fig. 3) is supported by the similar fraction (=301%) ofthe FFA flux, which is converted into ketones (35). These similar relationships, taken together with the ability of the neonate to produce large amounts of ketones, suggest that ketogenesis is already mature in humans on the first day of life, and that the intrahepatic and extrahepatic regulatory systems controlling the conversion of FFA into KB are well established by this early postnatal age.
  1. The Pattern of Blood Lipids, Glycerol and Ketone Bodies during the Neonatal Period, Infancy and Childhood The importance of neurogenic, hormonal and nutritional factors in the regulation of FFA metabolism is discussed. When the values for glucose tolerance (obtained from a previous study) are compared to the fasting FFA levels of corresponding age groups, there is a relationship: with decreasing FFA values there is an improvement of the carbohydrate tolerance.
  1. Ketone Body Metabolism Preserves Hepatic Function during Adaptation to Birth and in Overnutrition Abnormal lipid and carbohydrate metabolism occur in and contribute to obesity, diabetes, and NAFLD. In liver, fluxes of carbohydrate and fatty acid metabolism are tightly linked to ketogenic flux. Nonetheless, ketogenesis has largely been overlooked as both a driver and as a modifier of metabolic disease states. My work is the first to mechanistically identify insufficient ketogenesis as a driver of hyperglycemia and NASH. Prospectively, ketonemia may serve as a predictive biomarker of fatty liver disease and diabetes progression. Future studies may reveal that therapeutic augmentation of hepatic ketogenesis can mitigate hyperglycemia and ameliorate fatty liver disease. Final thought. My most sincere hope is that this body of work will vitalize interest in ketone body metabolism as a prospective diagnostic biomarker and therapeutic target in metabolic disease states.