MCT oil and daily induced ketosis in my IF

[dtrain]

Here's what I've been doing lately. Its all based around what I've read on suppversity about IF and ampk/mtor (Thx Phys, great stuff)

ramping up AMPK
- 8:30pm 2tbsp MCT oil (to induce ketosis), 7gm fiber (sugar free) + sodium r-ala.
- Wake up 4am... black coffee when I get hungry (to help boost AMPK).
- noon eat meal / break the fast and ketosis, back to gluconeogenesis.
- 2:30 workout (usually lifting)
begin mTOR
- 3:30 40g protein + 10g bcaa powder + 50g dextrose
- 5:00 meal (similar to the noon meal, 30g protein + 10g bcaa powder)
- 6:30 meal (again)
- 8:00 meal (again)
... fast until noon next day (besides mct oil in morning).

What are people's thoughts on inducing ketosis every day? Piss strips show ketosis in the morning (readings taken at 4am, 8, 10), so I think its working. Only problem I'm running into is my hands and feet are cold all day, even though its 70F in the office at work.

Am I doing anything incorrectly or could be improved upon? I'm a 30yr old male with 5 years lifting exp, 185lbs and about 13% bf. I'm up 15 lbs in 10 weeks of this blast with a small decrease in BF. I think I could drop BF faster if I could figure out this cold hands/feet thing. I assume my body is dropping my metabolic rate to compensate for the fast. Thanks in advance guys - d

[IronMind]

How does MCT oil induce ketosis?

Also not sure what the reason is to adding BCAAs to a whey shake?

[Maxximal]

Jesus!!! 50g of Dextrose: (

Sent from my Inspire 4G using Tapatalk

[dtrain]

How does MCT oil induce ketosis? Also not sure what the reason is to adding BCAAs to a whey shake?

http://www.ncbi.nlm.nih.gov/pubmed/15544546 I have assumed MCT oil induces ketosis. Am I missing a step here perhaps? I've heard the key hormones in ketosis are glucagon, and lack of glucose. The ALA I assume is helping me drop glucose levels, and coupled with the ketones formed with the intake of MCT oil, I'm hoping this is jumpstarting me into ketosis. The ketone test piss strips are showing some ketones, but I'm not sure if its just from the MCT oil or if I'm in ketosis. Could I be metabolizing the MCT oil and urinating ketones, but not getting into ketosis?

I have read over the weekend (since the OP) that my ALA is poor, I need the Na-R-ALA. Is the ALA I have still working, just poor bioavailability? Meaning I need to take more, or does it just not work period? I have 3 bottles of 300mg ALA of the non-sodium-R variety, should I toss them, or just take more?

BCAA in addition to whey because leucine is all that's really needed past a certain point from what I've read. Check out this article http://bodybuilding.forum.hu/index.php?topic=769.15 Can't remember where I saw it, but someone did a study with 100g whey ingested post workout, only ~40% didn't end up being burned as energy. I'm thinking at some point the non-essential amino acids and some of the essentials are in abundance and all I need past (say 40g) is leucine (and to a lesser extent isoleucine and valine). 50g dextrose only is 200 calories. I don't see the huge deal. In my binge, I'm shooting for ~2500 calories, so its only 8% of my calories. With my insulin sensitivity increasing in the fast, I would think the insulin surge is synergistic in protein synthesis (addressed in the hungarian bodybuilding forum article linked above)

[TheWon]

This is a interesting study about spiking whey protein with leucine

http://www.ergo-log.com/leucineposttrainingmeal.html

[TheWon]

300mg Na r ala or 600mg rala daily. I forget how much ala = 300mg Na r ala....

[IronMind]

300mg Na r ala or 600mg rala daily. I forget how much ala = 300mg Na r ala....

300mg NA-R-ALA = 210mg R-ala
300mg R-ala = 300mg r ALA
600mg ALA= 300mg r ala

[IronMind]

Some info on ALA
http://www.ralapure.com/?gclid=CKnpi...FUKo4AodbgIGqQ

[intrprtr]

does anybody know if it's okay to have extra virgin coconut oil first thing while on IF and if so, what's the maximum serv size you can get away with i.e. not put your body out of fast

[IronMind]

If your eating food, than your not fasting.

Look into the warrior diet. It is undereating during the day instead if fasting. Seems to be more along the lines of what your tryna do

[intrprtr]

I was following the logic of leangains

[dtrain]

If your eating food, than your not fasting.

Look into the warrior diet. It is undereating during the day instead if fasting. Seems to be more along the lines of what your tryna do

My guess is I'm in gluconeogenesis until the morning when consuming the na-r-ala and MCT oil are switching me over to ketosis until I eat. The ALA dropping my blood sugar and the MCT oil starting ketosis.

I'd like to switch the na-r-ala and MCT oil to right before bed so I operate under ketosis during the night.

[dtrain]

Coconut oil would have some proportion of MCT and LCT. Its not as ideal as MCT oil but will have some MCTs in it. MCT oil is just coconut oil with all but the MCTs extracted.

Abstract
Medium-chain triglycerides (MCT) induce ketosis in several mammalian species including man. To clarify the regulation of this metabolic alteration, we fed rats either MCT or long-chain triglyceride (corn oil) and then attempted to correlate ketosis with changes in (i) concentrations of selected metabolites in plasma and (ii) the synthetic and oxidative capacities of the liver. By 1 hour after MCT feeding, plasma levels of total ketone bodies had increased 18-fold, with a maximum value reached 1 hour later. By contrast, total plasma ketones in rats fed corn oil were increased only about 2-fold at 2 hours after feeding and did not exceed this value at later intervals. Hepatic concentrations of ketone bodies also increased after MCT or corn oil feeding. Although plasma concentrations of glucose decreased and insulin increased in rats fed MCT, they were not affected by corn oil feeding. MCT-induced ketosis was depressed by glucose administration. Neither MCT nor corn oil feeding impaired utilization of glucose by the liver. Hepatic lipogenesis was suppressed 50% and 90% by MCT and corn oil feeding, respectively. A marked increase of long-chain fatty acids in plasma was observed in rats fed corn oil but not in rats fed MCT. The pronounced increase of ketones in MCT-fed rats was closely related to an elevation of octanoate. In liver slices of MCT-fed rats, ketogenesis from octanoate was 10-fold higher than from palmitate, and octanoate was oxidized 4 times more rapidly than palmitate. The ketosis of MCT-fed rats was depressed by administration of 4-pentenoic acid, a potent inhibitor of fatty acid oxidation. These results support the concept that ketosis induced by MCT stems from rapid oxidation of medium-chain fatty acids. Hyperinsulinemia, hypoglycemia and depressed lipogenesis resulting from MCT feeding appear to potentiate but not initiate ketosis.

http://jn.nutrition.org/content/106/1/58.long

[dtrain]

Switching the na-r-ala and mct oil to right-before-bed worked perfectly. After I woke, piss strips indicated ketosis, as did strips later on in the morning.

Only thing is, my workout is 2:30-3:30 (then pwo shake). ~5 hours until 8:30pm to eat. If I want to make sure my system has reached steady state, I'd have to stop at 6:30, assuming it takes 2 hours to get to steady state. 3 hours is only 2 meals and feels like its pushing it (feeding myself before my stomach has completed emptied).

I'm thinking that's not enough time to get in enough meals. Maybe I'll eat from 3:30 to 8:30, then when I get up in the middle of the night to urinate, I'll take the mct oil/na-r-ala. Or I could force myself to stay up until 10:30 and take it then.

[dtrain]

I've decided to back off to only 1 or 2 nights/morning doing IF. I found my gains slowed and nagging injuries wouldn't heal. I think if I didn't have a job, I could make this work at a better level. I think the main flaw in the way I'm doing it is not enough meals after my workout before bed. My workout ends at 4:30 and I'm in bed at 8:30. My ideal would be this:

Workout at 11am. PWO shake/dextrose at noon.
meal 1, 3, 5, 7pm
9pm - na-r-ala and MCT oil.
Fast until 11am next day.

I will try for 1 fast per week, as I saw tremendous benefits in it. Increased energy, increased immune system, helped burn fat (though see below), and its nice not have to prepare a meal every few hours.

I aquired some AICAR, so I'll test that when I do my 1-2x per week IF. I'll post back here or start a new thread when I see what happens

[dtrain]

I'm changing my thoughts on this. I'm thinking the two subtypes of the AMPK make a huge difference in this whole plan. It appears as though AMPK alpha 1 inhibits mTOR and thus protein synthesis. AMPK alpha 2, boosted through exercise (versus starvation in alpha 1) appears to not halt mTOR. This would explain why my gains halted.

[cogrick2]

I'm changing my thoughts on this. I'm thinking the two subtypes of the AMPK make a huge difference in this whole plan. It appears as though AMPK alpha 1 inhibits mTOR and thus protein synthesis. AMPK alpha 2, boosted through exercise (versus starvation in alpha 1) appears to not halt mTOR. This would explain why my gains halted.

Care to say more? Or, could you just say where your diet stabilized? I am experimening with no carbs and little protein until the afternoon with plentiful use of MCT Oil, coconut oil and grass-fed butter (a la Bulletproofexec .com). This works great for me energy-wise. At night, I have not been consistent but I am working towards figuring out if MCT oil helps or hurts my sleep.

[dtrain]

Care to say more? Or, could you just say where your diet stabilized? I am experimening with no carbs and little protein until the afternoon with plentiful use of MCT Oil, coconut oil and grass-fed butter (a la Bulletproofexec .com). This works great for me energy-wise. At night, I have not been consistent but I am working towards figuring out if MCT oil helps or hurts my sleep.

down towards the the bottom http://suppversity.blogspot.com/2011...ittent_09.html cites http://www.ncbi.nlm.nih.gov/pubmed/21799304 I also was reading, I have the link at my computer at home, how insulin prevents fatty acid oxidation and shuttles excess free fatty acids and triglycerides into adipose tissue. It was previously thought that glucagon spurred fatty acid oxidation, or some other hormone, but it appears as though it may be as simple as the presence of insulin inhibits fatty acid oxidation and when its levels decrease, fatty acid oxidation increases. I need to do more research on this. What I do now is workout in the afternoon, eat normally after, and in the morning the next day. After 18hr of so since the workout, I start increasing my time between meals. I eat a meal, let it digest, then about 1.5 hr later, take 1tsp mct oil and a cinnamon/ala pill to lower blood sugar further to facilitate more fat oxidation. I'm not sure what effect mct oil with a regular meal would have, as insulin is released during meals and would counter the mct (which is why I delay taking the mct oil).

[dtrain]

I should have looked into the method of action of ALA and cinnamon. Apparently alpha lipoic acid activates the insulin receptor and cinnamon prevents its translocation back into the cell (as would happen when glycogen reserves are full). So because of these findings, I'm no longer taking just mct oil + ala + cinnamon, I'm adding ala into meals and backing off cinnamon for now. At this point I'm trying something a little different. I'm going to take MCT oil with every meal. My hopes are this will reduce liver gluconeogenesis and spare muscle protein. I haven't found much yet on this, but it seems as though the brain takes a few days to weeks to adapt fully to utilizing ketones. I will post more as I learn. Anyone have any information to share about this? http://ccforum.com/content/15/2/219 Abstract Although much feared by clinicians, the ability to produce ketones has allowed humans to withstand prolonged periods of starvation. At such times, ketones can supply up to 50% of basal energy requirements. More interesting, however, is the fact that ketones can provide as much as 70% of the brain's energy needs, more efficiently than glucose. Studies suggest that during times of acute brain injury, cerebral uptake of ketones increases significantly. Researchers have thus attempted to attenuate the effects of cerebral injury by administering ketones exogenously. Hypertonic saline is commonly utilized for management of intracranial hypertension following cerebral injury. A solution containing both hypertonic saline and ketones may prove ideal for managing the dual problems of refractory intracranial hypertension and low cerebral energy levels. The purpose of the present review is to explore the physiology of ketone body utilization by the brain in health and in a variety of neurological conditions, and to discuss the potential for ketone supplementation as a therapeutic option in traumatic brain injury. Introduction Ketogenesis is the process by which ketone bodies (KB), during times of starvation, are produced via fatty acid metabolism. Although much feared by physicians, mild ketosis can have therapeutic potential in a variety of disparate disease states. The principle ketones include acetoacetate (AcAc), β-hydroxybutyrate (BHB) and ace-tone. In times of starvation and low insulin levels, ketones supply up to 50% of basal energy requirements for most tissues, and up to 70% for the brain. Although glucose is the main metabolic substrate for neurons, ketones are capable of fulfilling the energy requirements of the brain. Ketones and the brain Glucose is the major fuel for the brain in humans on a balanced diet. More recently it was proposed that other substances such as lactate and pyruvate may be utilized by neurons to sustain their activity [19]. Furthermore, during times of starvation, the brain has the capacity to adapt to the use of ketones as its major energy source (and in the metabolic disease diabetes mellitus). In longstanding starvation, ketones can provide 60 to 70% of the energy needs of the brain [20]. The 1.5 kg human brain utilizes 100 to 150 g glucose per day and 20% of the total body oxygen consumption at rest [7]. Protein catabolism can supply somewhere between 17 and 32 g glucose per day, well below the minimum daily cerebral glucose requirements [21]. In fact, to supply sufficient glucose to support brain metabolic requirements from protein alone would lead to death in about 10 days instead of the 57 to 73 days [22]. Moreover in subjects undergoing total starvation for 30 days, the decrease in hunger coincides with the elevation of blood ketones to 7 mM/l. During periods of ongoing starvation, an average-size person produces about 150 g KB per day [23]. One should note, however, that ketones are incapable of maintaining or restoring normal cerebral function in the complete absence of glucose. Astrocytes may play a significant role in the regulation of brain energy metabolism [24]. Reports suggest that astrocytes can produce KB from fatty acids and leucine and are involved with other pathways of lipid metabolism, such as lipid synthesis and lipoprotein secretion [25-28]. Furthermore, it appears that the production of lactate and KB by astrocytes may increase secondary to neurotransmitters released during enhance synaptic activity [29,30]. Although the implications of ketone body production by astrocytes are still unclear, the fact that astrocytes outnumber neurons approximately 9:1 and occupy at least 50% of the cerebral volume suggests this constitutes a quantitatively important pathway in the brain [31]. Regulation of cerebral ketone uptake As previously noted, humans can achieve very high circulating KB concentrations during prolonged fasting, up to 9 mM/l (range 5.8 to 9.7 mM/l) [20]. The plasma concentration of KB is a significant factor affecting the rate of cerebral uptake. The blood-brain barrier (BBB) is relatively impermeable to most hydrophilic substances, such as KB, unless they are transported by a carrier protein. A family of proteins involved in the transport of monocarboxylic acids such as lactic acid and pyruvate across cellular membranes, called monocarboxylic acid transporters (MCT1 and MCT2), are thought to play an integral role. It is not yet understood how MCTs are regulated. KB are transported at different rates, with the uptake of AcAc being twice that of BHB at a given arterial concentration [12]. Furthermore, prolonged fasting appears to increase the BBB uptake of ketones, with some researchers demonstrating an eightfold increase in the expression of MCT1 [32]. Similarly, Hasselbalch and colleagues reported a 13-fold increase in cerebral uptake of BHB in humans following several days of fasting [33]. In contrast, rapidly increasing plasma ketone concentrations do not lead to such a significant increase in cerebral ketone uptake. Pan and colleagues noted a much smaller increase in cerebral ketone concentrations following a rapid intravenous infusion of BHB as compared with prolonged fasting, implying that MCT upregulation is partly dependent on the length of exposure to increased plasma ketone levels [34,35]. Once across the BBB, KB enter brain cells to support cellular energy requirements. Studies of the uptake of KB by brain cells suggest entry occurs by two mechanisms: diffusion and a carrier-mediated process. MCTs have been demonstrated on neurons and glial cells although their role here appears less significant as compared with that on the BBB. The impact of mitochondrial enzyme activity involved in ketone metabolism is less clear. Certainly, mitochondrial enzymes can be upregulated by increased levels of BHB, as has been demonstrated following exposure to ketones through starvation or a prolonged high-fat diet [12,36-39]. In summary, there- fore, a prolonged high blood ketone concentration leads to an increased rate of cerebral ketone uptake and metabolism.

[dtrain]

wow m+m really messed up my formatting