In Summary, I think it’s important to do your own research and draw your own conclusion about the long term risks of ketosis. For some people, a ketogenic diet may be a necessity given their health situation. For those of us who do not suffer from such health conditions I would present the question ‘why do you want to follow a strict ketogenic diet for an extended period’, and then follow this up with ‘are the potential risks and sacrifices worth the benefits?’
One thing to remember here is that even if your calculated daily ‘keto approved’ protein allowance is (let’s say) 150g, that doesn’t mean you can eat 150g in one meal and still be in ketosis. You may find that you can’t eat more than 40g of protein at a time, otherwise you will drop out of ketosis. OR, you may find you can eat 50g of protein but you need a LOT of fat. Whereas a small serve of 15g of protein without fat might knock you out of ketosis.
Now that you have fasted for quite a long time, you can break your fast at around 4 to 5 pm. Try having some good fat for this purpose, such as coconut oil or MCT oil, butter, or any other healthy fat. MCT oil might come in as a better option in this case since it gets quickly absorbed by the body. It swiftly bypasses the gallbladder and reaches the liver where it is transformed to ketones rapidly.
Instead of being bound to a mineral (like ketone salts), the ketone molecule (BHB or AcAc) is bound to a ketone precursor (e.g. butanediol or glycerol) via an ester bond. While there aren't as many esters on the market as salts, there is still some variance–especially when looking at the ketone molecule in these products. Before selecting the best one for you, it's important to gather all the necessary information to make your decision.
The CNS cannot use fat as an energy source; hence, it normally utilizes glucose. After 3–4 days without carbohydrate consumption the CNS is ‘forced' to find alternative energy sources, and as demonstrated by the classic experiments of Cahill and colleagues4 this alternative energy source is derived from the overproduction of acetyl coenzyme A (CoA). This condition seen in prolonged fasting, type 1 diabetes and high-fat/low-carbohydrate diets leads to the production of higher-than-normal levels of so-called ketone bodies (KBs), that is, acetoacetate, β-hydroxybutyric acid and acetone—a process called ketogenesis and which occurs principally in the mitochondrial matrix in the liver.6
Selective attention involves focusing only on relevant information while suppressing the impulse to pay attention to irrelevant distractions. A v-shaped flock of birds are displayed. The center (target) bird points in one direction and is surrounded by birds that either match the target’s direction or do not. The task is to rapidly identify which direction the target bird is pointing.
For whatever reason, many patients won’t attempt a ketogenic diet—even if the evidence is clear that it could help. Doctors are often hesitant to recommend dramatic dietary shifts—even if they believe in their efficacy—to patients who are already dealing with difficult health issues. If you’ve got a picky kid with epilepsy, a pickier adult with Alzheimer’s, or a cancer patient who refuses to give up the familiar-yet-non-ketogenic foods that give him some small manner of comfort in this trying ordeal, exogenous ketones could make a big difference.
Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. – Glucose is the brain’s principal energy substrate. In Alzheimer’s disease (AD), there appears to be a pathological decrease in the brain’s ability to use glucose. Neurobiological evidence suggests that ketone bodies are an effective alternative energy substrate for the brain. Elevation of plasma ketone body levels through an oral dose of medium chain triglycerides (MCTs) may improve cognitive functioning in older adults with memory disorders. On separate days, 20 subjects with AD or mild cognitive impairment consumed a drink containing emulsified MCTs or placebo. Significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) were observed 90 min after treatment (P=0.007) when cognitive tests were administered. beta-OHB elevations were moderated by apolipoprotein E (APOE) genotype (P=0.036). For 4+ subjects, beta-OHB levels continued to rise between the 90 and 120 min blood draws in the treatment condition, while the beta-OHB levels of 4- subjects held constant (P<0.009). On cognitive testing, MCT treatment facilitated performance on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog) for 4- subjects, but not for 4+ subjects (P=0.04). Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy. (http://www.ncbi.nlm.nih.gov/pubmed/15123336)
We’ve all been taught that high sodium intake is bad for us, similar to how we’ve been told for decades that fat is the driver of coronary heart disease, and consuming large amounts will kill us. Sodium has been thought to increase blood pressure, and therefore increase the risk of heart disease, kidney disease, stroke, osteoporosis, and stomach cancer. Thus, many of us tend to avoid consuming foods or supplements with labels that have high amounts of sodium.
Do you need carbs to train? No. Again this is an anecdote only, but I have done numerous training sessions in a carb deprived state. Heck some of my best training sessions where done in a fasted, carb deprived state. And there are a lot of endurance athletes who are using a ultra-low carb/ketogenic diet and putting up some great times (more on this below).
The metabolic phenotype of endogenous ketosis is characterized by lowered blood glucose and elevated FFA concentrations, whereas both blood glucose and FFA are lowered in exogenous ketosis. During endogenous ketosis, low insulin and elevated cortisol increase adipose tissue lipolysis, with hepatic FFA supply being a key determinant of ketogenesis. Ketone bodies exert negative feedback on their own production by reducing hepatic FFA supply through βHB-mediated agonism of the PUMA-G receptor in adipose tissue, which suppresses lipolysis (Taggart et al., 2005). Exogenous ketones from either intravenous infusions (Balasse and Ooms, 1968; Mikkelsen et al., 2015) or ketone drinks, as studied here, inhibit adipose tissue lipolysis by the same mechanism, making the co-existence of low FFA and high βHB unique to exogenous ketosis.
There are enticing anecdotes of supplemental ketones being used to boost human physical performance in competitive events, notably among elite cyclists. Given that BOHB can deliver more energy per unit of oxygen consumed than either glucose or fatty acids (Sato 1995, Cox 2016, Murray 2016), this makes sense. But what we do not know is if there is any required period of adaptation to the use of exogenous ketones, and thus how to employ them in training. It is clear that exogenous ketones decrease adipose tissue lipolysis and availability of fatty acids, the exact opposite to what happens on a well formulated ketogenic diet. This distinction between exogenous ketones and ketogenic diets on adipose tissue physiology and human energy balance underscores an important reason why these two ketone-boosting strategies should not be conflated.
Increased calcium levels in the bloodstream may contribute to the hardening of arteries (atherosclerosis), which in turn can lead to a heart attack. Calcium from supplements enters the bloodstream in one bolus, whereas we usually tend to get calcium from foods in small doses from the breakdown process. This might explain why calcium from food doesn’t create the same risk that is introduced by calcium supplements. At first glance, it seems to be the case that high calcium intake –at least from supplements–may not be ideal.
Hi Rob thanks so much, many people experience inconclusive results from the pee strips, as the ketone concentration in our pee is a measure of ketones not being used by the body. Basically the overflow or unused ketones. As our body becomes more adapted to using ketones, there will be less in our urine. It’s tough to keep the variable constant of how hydrated you are across many pee tests. Don’t be discouraged by pee test results. We have had many times where our blood tests show 1-3mmol/dl BHB but our pee test showed no results. Definitely keep testing (consider using a precision Xtra) and changing the dose to suit your needs. Hope this is helpful!
Over the years, we have seen and heard many different things about the effects and benefits of Raspberry Ketone supplements. Be it capsules or sprays, the discussion around them actually working always had opposing sides. So, we decided the best solution was to do our own research by conducting our own reviews on the most talked about products, to find out exactly how good they were as a "top-rated" ketone supplement.
If you are trying to lose weight, following a ketogenic diet can help you burn fat fast. However, trying to get into ketosis can be a frustrating experience. Am I eating too many carbs, not enough fat, too much protein? Getting into ketosis usually takes 3 to 5 days at least, and can take people up to two weeks. Recently I have discovered a simple and easy way to get into ketosis very quickly. I went from eating lots of carbs one night, to in ketosis 24 hours later.
Task switching is the process of adapting to changing circumstances (switching from one goal to another). Two cards are shown one above the other, and a combination of letter and a number (i.e., “A4”) will appear on one of the two cards. If it appears on top, the task is to indicate whether the number is an even number, and if on the bottom the task is to indicate whether the letter is a vowel.
Hi Acadia, just want to clear up a few things you noted in your post: The manufacture of BHB salts involves ionic bonding of an anion (beta-hydroxybutyrate) with a cation (Na+, K+, Ca+, Mg+). At least one of the exogenous ketone products you listed does in fact contain potassium ions. People taking potassium-sparing drugs need to know this and that raises concerns about leaving it off your chart. Some people are genuinely sodium sensitive even to small amounts of salt added to otherwise healthy foods. This can hold true even for those following ketogenic diets. The term you’re looking for… Read more »
Relationship between blood ketone and glucose levels: a BMS + MCT (5 g/kg) supplemented rats demonstrated a significant inverse relationship between elevated blood ketone levels and decreased blood ketone levels (r2 = 0.4314, p = 0.0203). b At week 4, BMS + MCT (10 g/kg) and MCT (10 g/kg) showed a significant correlation between blood ketone levels and blood glucose levels (r2 = 0.8619, p < 0.0001; r2 = 0.6365, p = 0.0057). Linear regression analysis, results considered significant if p < 0.05
This was a big surprise. We were at the very least expecting that drinking a ketone supplement would cause blood ketones to rise, but an average increase of 0.33 mmol/L is very small. The supplement associated with the highest average increase in blood ketones was Prüvit’s Keto-OS Max, but it was only an increase of 0.6 mmol/L. Brianna Stubbs, the ketone researcher I consulted with, agrees that an increase of below 2.0-3.0 mmol/L is unlikely to be of much use.
This research is a good reminder to discuss with your doctor before taking any supplements. Given the widespread use of calcium supplements, more research is required before any final conclusions can be drawn. Several ketone companies have tried to avoid the large sodium loads but instead relied on a bump in the calcium content from the BHB ketone salts, seemingly without consideration for the aforementioned results. Calcium BHB will likely absorb slower compared to sodium BHB due to digestion and absorption kinetics. For those looking to optimize brain uptake of ketones, this probably isn’t the best strategy (as uptake is directly proportional to the levels in the blood). Be cautious of supplements running from the sodium and chasing the calcium BHB instead, and make sure you factor that into your overall daily needs.
Glucose and BHB went down slightly throughout the effort and RQ fell, implying a high rate of fat oxidation. We can calculate fat oxidation from these data. Energy expenditure (EE), in kcal/min, can be derived from the VO2 and VCO2 data and the Weir equation. For this effort, EE was 14.66 kcal/min; RQ gives us a good representation of how much of the energy used during the exercise bout was derived from FFA vs. glucose—in this case about 87% FFA and 13% glucose. So fat oxidation was approximately 12.7 kcal/min or 1.41 g/min. It’s worth pointing out that “traditional” sports physiology preaches that fat oxidation peaks in a well-trained athlete at about 1 g/min. Clearly this is context limited (i.e., only true, if true at all, in athletes on high carb diets with high RQ). I’ve done several tests on myself to see how high I could push fat oxidation rate. So far my max is about 1.6 g/min. This suggests to me that very elite athletes (which I am not) who are highly fat adapted could approach 2 g/min of fat oxidation. Jeff Volek has done testing on elites and by personal communication he has recorded levels at 1.81 g/min. A very close friend of mine is contemplating a run at the 24 hour world record (cycling). I think it’s likely we’ll be able to get him to 2 g/min of fat oxidation on the correct diet.
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