Studies assessing the efficacy of the MAD reported seizure freedom rates of up to 25% and seizure reduction rates of up to 60% in children. One study used a simplified MAD (sMAD) and reported seizure freedom rates of 15% and seizure reduction rates of 56% in children. One study utilised a MAD in adults and reported seizure reduction rates of 35%, but no patients became seizure free (GRADE rating low).
Researchers also observed that the size of VLDL particle size did not change in either of the groups. However, they noted that the total number of VLDL particles decreased by 19% from 76.2 nmol/L to 61.7 nmol/L.  More specifically, large VLDL particles reduced by 40.2% from 3.33 nmol/L to 1.74 nmol/L, medium VLDL particles decreased by 4.8% from 46.2 nmol/L to 44 nmol/L. 
Another hypothesis regarding the function of the KD is related to changes in neuronal metabolism, mitochondrial function and energy reserve, and the environment. In normal conditions, the usual substrate for the neurons is glucose. To facilitate its diffusion through the brain-blood barrier, glucose transports are present in the brain capillary endothelial layer (Greene et al., 2003). The glucose metabolism produces the rapidly available energy that is necessary for seizure activity. Therefore, in patients on the KD, the blood glucose energy levels are low, and the brain begins to use KB for energy. This anaerobic metabolism slows the energy availability, which reduces seizures. The anticonvulsant propriety of a decrease in glucose metabolism has been shown in experimental models in which the administration of 2-Deoxy-D-glucose elevates the seizure threshold (Garriga-Canut et al., 2006). The anticonvulsant effect of the KD can be quickly reversed after glucose infusion (Huttenlocher, 1976). Based on these data, we can postulate the influences not only of the KB, as discussed above, but also the reduction in glucose levels as a mechanism of action of the KD.
So what, exactly, does “ketogenic” mean? The name refers to a specific type of energy-carrying molecule, called a ketone. “Most people are always in a state of glucosis, meaning they’re burning glucose from carbohydrates for energy,” Westman says. “But you determine what your body burns for fuel based on what you feed it.” By severely restricting carbs and increasing your fat intake, your body can shift into a state of “ketosis,” which means it’s burning fat instead of glucose. “Ketosis used to be considered abnormal, but it can actually be very healthy,” Westman says.
Once the body is adapted to ketosis, constipation and/or diarrhea are the most commonly reported side effects along with increased urination. Continuing to keep your mineral intake high and ensuring adequate water and fiber intake will help to counter these effects. People in ketosis may also notice a sweet or fruity odor on their breath, which is the result of increased production of the ketone acetone, which is a very volatile compound that is eliminated mainly through respiration in the lungs. 50
The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains, and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter. Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.
That plan didn’t allow much variety or leeway. Eggs, two small green salads a day, gelatin for dessert, cheese (up to 4 ounces daily), bone broth, no-calorie liquids, and lots of meat: That was pretty much it for the first week. After level one, you added vegetables like broccoli. Yes, you would be in ketosis doing the original Atkins diet, but for most people, that spartan plan would get boring quickly.
The understanding of the mechanisms of action of KD is incomplete; however, some theories have been advanced about how it modifies the neuronal metabolism and excitability in order to reduce the seizure frequency. Possibly, the real mechanism of reduction of cortical hyperexcitability involves multiple factors. Some of the systems involved in seizure reduction are related to metabolic changes in the blood and cerebrospinal fluid (CSF), including a decrease in glucose levels and an increase in KB. The mitochondria function and energy reserve may also play a role in the KD mechanisms, resulting in synapse stabilization and excitatory decrease.
For many years, LDL-C tests have been used as the primary method of measuring LDL in the blood. It is cheaper and easier to measure. Recent research has called into questioning how effective LDL-C is compared to LDL-P in precisely assessing cardiovascular risk. After reviewing cross-sectional data, a recent peer-reviewed paper from the world-renowned Framingham Heart Study stated that
Unfortunately, there’s no long-term data on ketogenic diets versus other diets. In a 2015 Italian study, those on a ketosis diet lost 26 pounds in three months. About half of the participants stayed on the diet for a year but lost little additional weight in the next nine months. People in a 2014 Spanish study who followed a very-low-calorie ketogenic diet lost an average of 44 pounds in a year—but a third of them dropped out, possibly because it was too hard to maintain.
So rather than giving one-size-fits-all dietary advice or weaponizing the word “balanced” it might be better if the medical community suggested that there are Individual differences that need to be considered. This might also help those lay folk who have had success with one dietary lifestyle or another also realize that what’s valid for them may not be good advice for others.
This week we’re introducing a slight fast. We’re going to get full on fats in the morning and fast all the way until dinner time. Not only are there a myriad of health benefits to this, it’s also easier on our eating schedule (and cooking schedule). I suggest eating (rather, drinking) your breakfast at 7am and then eating dinner at 7pm. Keeping 12 hours between your 2 meals. This will help put your body into a fasted state.
High-protein ketogenic diet (HPKD): This version of the keto diet is often followed by folks who want to preserve their muscle mass like bodybuilders and older people. Rather than protein making up 20 percent of the diet, here it’s 30 percent. Meanwhile, fat goes down to 65 percent of the diet and carbs stay at 5 percent. (Caution: folks with kidney issues shouldn’t up their protein too much.)
For example, a pretty large number of animal studies have shown that a ketogenic diet can reduce tumor growth and improve survival rates. There was one 22-day study in mice that looked at the differences between the ketogenic diet and other diets. That study found that a ketogenic diet reduced tumor growth by up to 65% and nearly doubled survival time in some cases.
As these battles waged in the early 1990s, I had long left Dr. Good’s group, having returned to New York and private practice. Nonetheless, this story had a personal ring to it, as had the interferon story, since Dr. Good had completed the first bone marrow transplant in history, in 1969, and long hoped this technology would be, yes, an answer to cancer.
However, in most cases, avoiding all foods that contain cholesterol (like eggs or cheese) isn’t necessary to support heart health, especially since some sources of cholesterol can be nutrient-dense foods. What’s important is practicing moderation and finding balance in your diet, as well as eating a combination of natural foods that fight inflammation.
2. I agree, progression of the score is now all that matters. Any concern with the NMR/other biomarker results, or am I a classic Lean Mass Hyperresponder, hyperabsorber? The literature is FILLED with studies showing raised TC/LDL on a fasting/ketogenic protocol. So is this simply physiological "view" and not an underlying fundamentally artherogenic profile?
Additionally, research suggests that during menopause, women may experience an increased thickening of the carotid intima and media layers of the arteries, a marker of subclinical atherosclerosis. In a study of 249 middle-aged women, those who were postmenopausal or in the late stages of perimenopause were much more likely to show progression of carotid intima-media thickness (CIMT) than those in early perimenopause (11).
In another parallel experiment the mice used did not have cancer at the start, but were bred to have a genetic predisposition toward breast cancer. Almost half of these mice, when fed on the Western diet, showed cancer within the first year (the average life span of these mice is two years). Only one of the mice in this group reached its normal life expectancy, and 70% ultimately died of cancer. Of the group on the ketogenic diet, only 30% ever developed cancer, and over half reached their normal life expectancy or exceeded it.
A ketogenic diet typically leads to a broad range of improvements in blood lipids as well as other cardiovascular risk factors such as blood pressure and inflammation. However, the changes we see in total and LDL cholesterol levels are much less predictable than the changes in other blood lipids such as triglycerides and HDL cholesterol. For some people, calculated LDL cholesterol goes down, and for others it goes up, sometimes quite a bit. This tendency for some people to see an increase in their LDL cholesterol has been a focus of research over the last decade because the question remains – “What, if anything, does this tell us when assessing one’s risk of heart disease?”
Is the keto diet safe for someone with high cholesterol? Because keto is rich in fats, including saturated fat and cholesterol found naturally in animal-derived foods like eggs and meat, many people will experience an increase in cholesterol after beginning the keto diet. However, studies suggest the connection between the keto diet and cholesterol is actually positive.
In addition to neuroblastoma, various researchers have investigated the efficacy of KDs as an adjuvant therapy for other types of cancer. The strongest evidence (> 3 studies) for a tumor-suppressing effect has been reported for glioblastoma, whereas little or no benefit was found for two other brain tumors (astrocytoma and medulloblastoma). Good evidence (2 - 3 studies) is available for prostate, colon, pancreatic and lung cancer ; neuroblastoma also falls into this category (Figure 1). Some of those studies report a tumor-suppressing effect of KD alone and/or in combination with classic therapy and/or caloric restriction. One study on prostate cancer applied the KD in a preventive, instead of a therapeutic, study setting. Only limited evidence (1 study) supports the anti-tumor effect of an unrestricted KD on breast, stomach, and liver cancer.
You can change that genetics. I can’t change the genetic tendency, it’s going to be there. By golly, I’m going to pay attention to everything that I put in my mouth for that sake alone. Anyone with that kind of history, I don’t think it’s reason to freak out. I don’t think it’s a reason to think it’s an inevitability for you. It’s just one of those things that you have to pay attention to all of your numbers, anal retentively. That’s why I pay attention to my HSCRP so closely, that’s why I run my numbers so often. I know I have that tendency. I probably, had I not lost the 180 pounds in 2004, I would be in an early grave just like my brother.