The most science-backed performance-boosting supplements, such as creatine monohydrate, beta-alanine, and caffeine, are all A-OK on the ketogenic diet. So, if you take a pre-workout, you should be able to continue without issue. I would also recommend gulping down some bouillon before your session to ensure your sodium and magnesium levels are on point.
keto almond flour keto asparagus keto avocado keto bacon keto baking keto beef keto bread keto Brussels sprouts keto cakes keto cauliflower keto cheesecake keto chicken recipes keto chocolate keto cocktail keto coconut flour recipes keto cookies keto donuts keto green beans keto muffins keto mug cakes keto nuts keto pancakes keto pecans keto pie keto pizza keto pork keto pudding keto pumpkin spice keto seafood keto veggies
2) Now you need to do a little learning before we move any further. Start by learning a bit more about ketosis itself, and the pitfalls you may experience. I love Bodybuilding.com and think that this article on the Keto Diet is perfect for beginners, so go check it out. Unless you are planning to start bodybuilding part, 2 of the post will not apply to you. 😉
Anticonvulsants suppress epileptic seizures, but they neither cure nor prevent the development of seizure susceptibility. The development of epilepsy (epileptogenesis) is a process that is poorly understood. A few anticonvulsants (valproate, levetiracetam and benzodiazepines) have shown antiepileptogenic properties in animal models of epileptogenesis. However, no anticonvulsant has ever achieved this in a clinical trial in humans. The ketogenic diet has been found to have antiepileptogenic properties in rats.[56]
Normal dietary fat contains mostly long-chain triglycerides (LCTs). Medium-chain triglycerides (MCTs) are more ketogenic than LCTs because they generate more ketones per unit of energy when metabolised. Their use allows for a diet with a lower proportion of fat and a greater proportion of protein and carbohydrate,[18] leading to more food choices and larger portion sizes.[4] The original MCT diet developed by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil.[15] Consuming that quantity of MCT oil caused abdominal cramps, diarrhea, and vomiting in some children. A figure of 45% is regarded as a balance between achieving good ketosis and minimising gastrointestinal complaints. The classical and modified MCT ketogenic diets are equally effective and differences in tolerability are not statistically significant.[9] The MCT diet is less popular in the United States; MCT oil is more expensive than other dietary fats and is not covered by insurance companies.[18]
The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.[7]
Another difference between older and newer studies is that the type of patients treated with the ketogenic diet has changed over time. When first developed and used, the ketogenic diet was not a treatment of last resort; in contrast, the children in modern studies have already tried and failed a number of anticonvulsant drugs, so may be assumed to have more difficult-to-treat epilepsy. Early and modern studies also differ because the treatment protocol has changed. In older protocols, the diet was initiated with a prolonged fast, designed to lose 5–10% body weight, and heavily restricted the calorie intake. Concerns over child health and growth led to a relaxation of the diet's restrictions.[19] Fluid restriction was once a feature of the diet, but this led to increased risk of constipation and kidney stones, and is no longer considered beneficial.[18]
Urine Strips: When tested in urine, these strips will elicit a color change based on the level of ketones, namely acetoacetate, which is present in the urine. It is important to note that acetoacetate is different than the ketones present in the blood, namely, beta-hydroxybutyrate (βHB). Due to its nature, urine ketone testing may be a sufficient initial method to test ketone production; however, it is not the ideal method for determining the utilization of these ketone bodies, especially once “keto-adapted.”
Constipation: As mentioned above, the elimination of carbohydrates coupled with the increased release of water may lead to constipation. If this occurs, simply increasing water consumption as well as incorporating more fiber into the diet can alleviate these symptoms. Additionally, some electrolytes like magnesium can also assist with this in higher amounts.
Variations on the Johns Hopkins protocol are common. The initiation can be performed using outpatient clinics rather than requiring a stay in hospital. Often, no initial fast is used (fasting increases the risk of acidosis, hypoglycaemia, and weight loss). Rather than increasing meal sizes over the three-day initiation, some institutions maintain meal size, but alter the ketogenic ratio from 2:1 to 4:1.[9]

Diabetic Ketoacidosis: Diabetic ketoacidosis (DKA) is the variation of ketosis that is responsible for deterring society from considering the adoption of a keto diet for beginners. DKA occurs primarily in those suffering from Type 1 diabetes. The inability to secrete insulin prevents ingested carbohydrates (glucose) from entering our insulin-dependent cells (i.e., muscle and adipose tissue) as a substrate for energy production. Due to this induced cellular starvation, the body will begin to produce ketones at an uncontrolled rate.


Variations on the Johns Hopkins protocol are common. The initiation can be performed using outpatient clinics rather than requiring a stay in hospital. Often, no initial fast is used (fasting increases the risk of acidosis, hypoglycaemia, and weight loss). Rather than increasing meal sizes over the three-day initiation, some institutions maintain meal size, but alter the ketogenic ratio from 2:1 to 4:1.[9]
Thanks for trying to stick to the evidence! So often these “newer” diets and therapies are not fully researched and are of peoples opinions. As a physical therapist I try to keep up on what will help my patients. This article and website will be added to my resource list. It’s not possible to be the expert on everything, so thanks for putting out quality information.
So question….what if you are watching your sodium intake due to high blood pressure? From what I read here, there is a lot of salt/sodium involved (more than my normal intake), how do I deal with this issue if doing keto? I do not take any medications. About three years ago I found that my thyroid levels were on the low end of the normal range and it affected my blood pressure. So I lowered my sodium intake and increased my iodine/iodide intake. This has worked for me for the past three years, in the sense that after a month of being on bp meds, I no longer needed those meds and my thyroid levels have stayed around the mid-range of normal. I have always eaten healthy with some junk foods here and there, but apparently being pregnant kicked off a thyroid issue and weight gain. What are my sodium options with keto? How do I balance it so my bp doesn’t take a freefall nor a significant increase?
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