Bread probably isn’t the first thing that comes to mind when you think about the ketogenic diet because it’s generally full of carbs. But, if you replace your store-bought bread with a homemade keto bread recipe, it can fit seamlessly into your keto low-carb, high-fat diet. How does bread even become keto-friendly? With almond flour, a lot of eggs, cream of tartar, butter, baking soda and apple cider vinegar.

Even when exercising at a submaximal level (for example, biking at a moderate speed), heart rate and adrenaline levels rise more when people are eating a high-fat, low-carbohydrate diet[4] vs. a high-carbohydrate, low-fat diet. This results in those on the high fat diet perceiving that they are working harder to achieve the same pace as the high-carbers, and they have much more difficulty speeding up their pace in sprints or climbs.
Ketosis and the subsequent metabolic state associated with it has been shown to have positive effects on chronic conditions, from PCOS to type 2 diabetes. Just a few weeks of eating keto recipes and keeping your blood sugar stable results in improved energy, elevated mood, and possibly best of all, quick weight loss. It’s not uncommon for people to drop 10 pounds or more in the first couple of weeks while sticking with a keto diet!
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]

Because people with type 2 diabetes are at an increased risk for cardiovascular disease, there’s a specific concern that the saturated fat in the diet may drive up LDL, or “bad,” cholesterol levels, and further increase the odds of heart problems. If you have type 2 diabetes, talk to your doctor before attempting a ketogenic diet. They may recommend a different weight-loss diet for you, like a reduced-calorie diet, to manage diabetes. Those with epilepsy should also consult their doctor before using this as part of their treatment plan.


The ketogenic diet reduces seizure frequency by more than 50% in half of the patients who try it and by more than 90% in a third of patients.[18] Three-quarters of children who respond do so within two weeks, though experts recommend a trial of at least three months before assuming it has been ineffective.[9] Children with refractory epilepsy are more likely to benefit from the ketogenic diet than from trying another anticonvulsant drug.[1] Some evidence indicates that adolescents and adults may also benefit from the diet.[9]
The low glycaemic index treatment (LGIT)[49] is an attempt to achieve the stable blood glucose levels seen in children on the classic ketogenic diet while using a much less restrictive regimen. The hypothesis is that stable blood glucose may be one of the mechanisms of action involved in the ketogenic diet,[9] which occurs because the absorption of the limited carbohydrates is slowed by the high fat content.[5] Although it is also a high-fat diet (with approximately 60% calories from fat),[5] the LGIT allows more carbohydrate than either the classic ketogenic diet or the modified Atkins diet, approximately 40–60 g per day.[18] However, the types of carbohydrates consumed are restricted to those that have a glycaemic index lower than 50. Like the modified Atkins diet, the LGIT is initiated and maintained at outpatient clinics and does not require precise weighing of food or intensive dietitian support. Both are offered at most centres that run ketogenic diet programmes, and in some centres they are often the primary dietary therapy for adolescents.[9]
The idea that ketosis is human beings’ natural state is also contradicted by the heavy dependence of human embryonic and fetal development on glucose. All women become insulin resistant during normal pregnancy[15] as glucose is directed toward the developing baby. Pregnant women deprived of carbohydrates are at high risk of developing ketoacidosis in later pregnancy.[16] This dangerous condition can occur as the nutrient needs of the developing fetus reach their peak and drive up maternal ketone production.
Early studies reported high success rates; in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).[19]

In the 1960s, medium-chain triglycerides (MCTs) were found to produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides).[15] MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system.[16] The severe carbohydrate restrictions of the classic ketogenic diet made it difficult for parents to produce palatable meals that their children would tolerate. In 1971, Peter Huttenlocher devised a ketogenic diet where about 60% of the calories came from the MCT oil, and this allowed more protein and up to three times as much carbohydrate as the classic ketogenic diet. The oil was mixed with at least twice its volume of skimmed milk, chilled, and sipped during the meal or incorporated into food. He tested it on 12 children and adolescents with intractable seizures. Most children improved in both seizure control and alertness, results that were similar to the classic ketogenic diet. Gastrointestinal upset was a problem, which led one patient to abandon the diet, but meals were easier to prepare and better accepted by the children.[15] The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.[10]
Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures, and kidney stones.[18] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About one in 20 children on the ketogenic diet develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in one-seventh of the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]
The Johns Hopkins Hospital protocol for initiating the ketogenic diet has been widely adopted.[43] It involves a consultation with the patient and their caregivers and, later, a short hospital admission.[19] Because of the risk of complications during ketogenic diet initiation, most centres begin the diet under close medical supervision in the hospital.[9]

I actually clicked on the story just to see if they included anything about it’s use in managing chronic migraine. I have chronic migraine, basically intractable. Nothing has helped. I’ve tried medications, meditations, and everything in between including a bunch of dietary changes. Keto is my next consideration. I’m happy to hear it helped you! Thanks for sharing
Reduced hunger. Many people experience a marked reduction in hunger on a keto diet. This may be caused by an increased ability of the body to be fueled by its fat stores. Many people feel great when they eat just once or twice a day, and may automatically end up doing a form of intermittent fasting. This saves time and money, while also speeding up weight loss.
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