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The effects of physiological levels of 3-hydroxybutyrate on noradrenaline binding to rat erythrocyte membranes were studied. The binding of noradrenaline to membranes was determined by measuring the union of 3H-noradrenaline in the presence of varying concentrations of 3-hydroxybutyrate. Scatchard plots of the results were used to determine that 3-hydroxybutyrate provoked a loss of affinity of the 2-adrenergic receptors for adrenaline. Thus high (but physiological) 3-hydroxybutyrate levels can lower the binding of the catecholamine, thus diminishing the extent or intensity of adrenergic-driven responses

http://www3.interscience.wiley.com/...ETRY=1&SRETRY=0

It makes sense for the ketogenic diet to cause an increase in adrenaline, noradrenaline and cortisol. These hormones encourage lipolysis and fat burning and an increase in ketones. It makes equal sense for ketones to be involved in a feedback mechanism that decreases the action of those hormones, to keep lipolysis and ketone formation from going beyond what is actually necessary for the body's present needs. Physiologic hormone resistance.
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http://www.ncbi.nlm.nih.gov/pubmed/7719390

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The aim of this work was to investigate the changes of cardiac performance by both electrocardiography (ECG) and echocardiography (ECHOc), in addition to anthropometric and hormonal variables before, during and after prolonged total fasting (TF) and re-feeding in an overweight adult man. Physical examination, laboratory and hormonal measurements, ultrasonographic study of body fat distribution, ECG and ECHOc study were performed before during and after 34 days of TF and after 17 days of isocaloric re-feeding. The subject was a 52-year old Caucasian who was overweight with increased abdominal fat content (BMI: 28.6; W/H ratio: 0.95) and increased levels of arterial systolic and diastolic blood pressure (SBP, DBP). HPLC measurements of urinary catecholamine levels (HPLC), ECHOc study of cardiac performance, ultrasonographic study of body fat distribution were performed. The subject starved for 34 days losing 22kg, but after that time he was compelled to re-feed because of nausea and severe vomiting. A marked ketosis (ketonuria > 1200mg/day) was already present after 6 days of TF. After 17 days of TF norepinephrine (NE) and epinephrine (EPI) urinary levels showed a two-fold and nine-fold increase respectively, but they became undetectable at the end of TF. After 17 days of re-feeding catecholamine urinary levels were similar to those measured after 17 days of TF. After both TF and 17-day isocaloric re-feeding we found a decrease of visceral fat content and W/H ratio reached the normal values for age-matched subjects (W/H ratio after TF: 0.80, after re-feeding: 0.80)

Just working from the abstract again here. Peter commented on the red letters;

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So increased sympathetic tone seems to be a feature of both fasting as well as ketogenic eating. It does look as if the effect is transient during fasting, so this may also be the case in ketogenic eating, but I have no data on that. The fact it may well be transient is no consolation if you have been admitted to a cardiology ward via A&E due to severe palpitations!

Urinary levels of adrenaline and noradrenaline were high half way through the fast at seventeen days; but the fast wasn't stopped then. The real concern came at the end of thirty four days, when the subject got nauseous and these hormones were undetectable in the urine. If this guy was six feet tall, at a bmi of 28.6 then he started at 211 pounds, if the online calculator I'm using works right. 22 kg is 48.4 pounds, so that's 162.6 pounds the guy was down to at the end of the fast. If he was six feet. If he was any shorter, it's worse. And he'd have to be awfully tall to make 48.4 pounds a reasonable amount of weight to lose in a total fast at that starting bmi.

I need to know more about these hormones, they seem to tie in with stage fright, social anxiety and all that. Weren't we looking at a study about a month ago dealing with ketones and post traumatic stress disorder?

Okay. Propranolol is sometimes used for stage fright. Propranolol is a beta blocker, it blocks the action of adrenaline and noradrenaline. So I guess ketones are a beta blocker too? I know which medicine I'd choose.

In this study here,

Blood pressure and norepinephrine spillover during propranolol infusion in humans

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Arterial plasma norepinephrine levels rose from 183 +/- 20 to 250 +/- 29 pg/ml during propranolol (P less than 0.001), suggesting increased sympathetic vasoconstrictor tone. However, isotope dilution studies using tritiated norepinephrine infusion showed that arterial plasma levels of tritiated norepinephrine rose from 743 +/- 78 to 1,002 +/- 101 dpm/ml during propranolol (P less than 0.001), indicating a reduction in the rate of norepinephrine clearance from plasma. The calculated fall in clearance from 1.90 +/- 0.13 to 1.42 +/- 0.11 1/min (P less than 0.001) entirely accounted for the rise in plasma norepinephrine, since the calculated rate of norepinephrine spillover into plasma remained at the base-line level of 340 +/- 40 ng/min during propranolol.

norepinephrine in the serum increases, as its uptake is blocked. Because its uptake is blocked.

I wish they'd just stick to the word ''adrenaline.'' Epinephrine doesn't have the same oomph.