LDL is the lipoprotein particle that is most often associated with atherosclerosis. LDL particles exist in different sizes: large molecules (Pattern A) or small molecules (Pattern B). Recent studies have investigated the importance of LDL-particle type and size rather than total concentration as being the source for cardiovascular risk [56]. Patients whose LDL particles are predominantly small and dense (Pattern B) have a greater risk of cardiovascular disease (CVD). It is thought that small, dense LDL particles are more able to penetrate the endothelium and cause in damage and inflammation [82–85]. Volek et al. reported that the KD increased the pattern and volume of LDL particles, which is considered to reduce cardiovascular risk [73]. Though we did not show a significant effect on LDL levels for ketone supplements, future chronic feeding studies will investigate the effects of ketone supplementation on lipidomic profile and LDL particle type and size.

MCT Oil is a keto supplement that helps your body make ketones. The oil contains pure medium-chain triglycerides (MCTs), which are types of fatty acids that your body prefers using for immediate energy. Unlike long-chain fatty acids, MCTs don't require enzymes and bile for digestion and they go straight to the liver where they are used for making free fatty acids or ketones. Studies on MCTs show that they promote weight loss [5].


Let’s briefly discuss some organic chemistry. Two molecules that are “the same” but mirror images of each other (like your hands) are known as enantiomers, a type of spatial isomer. Beta hydroxybutyrate comes in two forms, D-β-hydroxybutyrate (“right-handed”) and L-β-hydroxybutyrate (“left-handed”). D-β-hydroxybutyrate is the form that is naturally produced in the body and is most bioavailable when taken exogenously.
Getting into a state of ketosis normally involves eating a ketogenic diet consisting of around 80 percent fat, 15 percent protein, and 5 percent carbs. Over time, the body transitions from burning carbs for fuel to burning ketones—an alternative fuel source that the liver makes by breaking down fat, explains keto diet expert Amy Davis, RD, LDN. Since advocates say that ketosis can help you lose weight fast, think more clearly, and feel more energized, it’s tempting to try.
How to get into ketosis in 24 hours you ask? Can it be done? Yes, it can happen. But only for people who have already been keto-adapted and may have dropped out of ketosis for a short period of time, like after a cheat day. Those people can follow these steps to get back into ketosis quickly. However, if you are just starting keto you have a lot of work to do before your body will let you get into ketosis.
Hi! My question is, how low must my current daily carb count be in order to benefit from taking your exogenous ketones? I am a 33 year old female, keeping total carbs at 100-125 grams per day. My priority is fat loss, and I do HIIT training 4-5 days a week. I’ll soon be adding in heavier strength training. I don’t function well eating less than 100 total carbs a day. Could this even benefit me? And if it will benefit me, would the befits outweigh the sodium content? I keep my sodium at 2,000 mg a day, as I’m trying to avoid water weight.
When our cells undergo the process of autophagy, non-essential parts like damaged proteins are recycled and invading microorganisms and toxic compounds are removed. This means that autophagy plays an important role in stopping the aging process, reversing disease, and preventing cancer, but it doesn’t happen all the time. Fasting, protein restriction, and carbohydrate restriction are the three main ways that can initiate different autophagic processes — all of which are not the same. This is part of the reason why a ketogenic diet has so many positive effects, and it also shows you why intermittent fasting is a way to improve your diet even more.

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.


If the goal is to deplete glucose levels so that we can start producing ketone bodies, then forcibly exerting physical energy through exercise is a great way to go about it. Keeping it relatively low intensity to begin with and working out in the morning is recommended as this helps to keep down your cortisol (stress hormone) levels. This only applies at the beginning of your keto adaptation process, as intense workouts such as HIIT once already keto-adapted will be completely fine.
In addition to the Weir coefficients being potentially off (which impacts EE), the RQ interpretation may be incorrect in the presence of endogenous or exogenous ketones. As a result, the estimation of fat and glucose oxidation may be off (though it’s directionally correct). That said, the current interpretation seems quite plausible—greater fat oxidation when I had to make my ketones; less when I got my ketones for “free.”

The ‘carb-sparing’ effect from BHB suppresses the break down of muscle glycogen. This leads to lower lactate levels. When increasing exercise intensity, fat oxidation (burning) reaches a limit. At that point the muscle burns carbohydrates as fuel. But when consuming Ketone esters, the body does not make this switch. This suggests Ketones are being used instead. 11
Another effect of the ketone drinks was to lower blood glucose, free fatty acids, and triglyceride levels. This sounds great. Elevated levels of all those markers are harbingers of disease, particularly if they remain chronically elevated. But think about what this means. If free fatty acids go down, that means adipose tissue isn’t being liberated for burning.
Again, there are very interesting animal studies plus some single case reports and small uncontrolled trials of humans with neurodegenerative disease and cancer given ketogenic diets and/or exogenous ketones (Murray 2016, Poff 2015, Roberts 2017, Newport 2015, Cunnane 2016). In some cases where the patient does not have the cognitive resources to comply with a well-formulated ketogenic diet, or where target blood levels of BOHB that work in animals are hard to achieve in humans by diet alone, supplemental ketones may have an important role to play in the prevention, management, or reversal of these disease categories.
Whereas ketone esters are 100% D- form, most ketone salts are a 50/50 mix of left and right-handed beta hydroxybutyrate, which is known as a racemic mixture. These beta hydroxybutyrate molecules are linked to a mineral, such sodium (Na), calcium (Ca), potassium (K), or magnesium (Mg). This kind of ketone supplement gets broken down to left and right-handed version of beta hydroxybutyrate along with the mineral.
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Funding. This work supported by an Industrial DPhil Fellowship to BS from the Royal Commission for the Exhibition of 1851. JM was supported by the EPSRC Doctoral Training Centre and Prize Fellowship; Ref: EP/M508111/1. The funding sources were not involved in the design, conduct or analysis of this study. TΔS Ltd. provided the ketone ester, ΔG®, and NTT DOCOMO Inc. provided the acetone meter for the study.
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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