Ketosis

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Introduction to ketosis

The body’s primary source of energy is glucose. When the body does not have enough glucose for energy, it burns stored fats instead; this results in a build-up of acids called ketones within the body. This state of using ketones is called ketosis. Some people encourage ketosis by following a ketogenic diet or, more simply, a low-carb diet.

When a person is in ketosis, they are able to switch the “gas tank” from glucose to fat. If a person is a glucose burner this “metabolic flexibility” only comes after they’ve adapted first. This process, called keto adaptation, or "fat adaptation" is necessary because the fat “gas tank” can be likened to as deep storage and not easily accessed. During the keto adaptation process, some experience “keto flu” where the body goes through withdrawal from sugar and carby foods. This keto flu can last anywhere from one day to a few weeks.

Ketogenesis is the biochemical process by which the body uses ketone bodies through the breakdown of fatty acids and ketogenic amino acids. This supplies energy to certain organs, particularly the brain.

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies. The three main causes of ketoacidosis are alcoholism, starvation, and Type 1 diabetes. Exclusive of those conditions, it is not a potential side effect of following a low carb diet.

Exogenous ketones are ketone bodies that are ingested through a nutritional supplement. Consuming exogenous ketones alone will not result in ketosis.

The ketogenic diet was developed in the 1920s as a therapeutic treatment of pediatric epilepsy. It was widely used until the introduction of anticonvulsant drugs.

Ketosis and the brain

Proportionately, the brain consumes a great amount of energy, about 20-30% of the body’s total energy needs. Most of the brain’s energy consumption goes toward sustaining neurons. The brain typically gets it’s energy from glucose (blood sugar) but ketone bodies (ketones) are the brain’s main reserve fuel when glucose supply is compromised.<1>

There is a significant link between Alzheimer’s disease (AD) and impaired fuel metabolism in the brain, specifically disturbed cerebral glucose metabolism.<2> In Alzheimer’s, the uptake and metabolism of glucose in the brain deteriorates. This reduced glucose metabolism is likely both: (1) contributing to AD development (hypothesized, not yet scientifically proven), and (2) a consequence of AD (known fact)<3> In other words, there’s a vicious cycle: the slowed brain glucose uptake (hypometabolism) leads to chronic brain energy deprivation, that in turn deteriorates the neuronal function, which further diminishes the demand for glucose thereby furthering cognitive decline. This hypometabolism may begin 30 or more years before the onset of AD especially in individuals with ApoE4 genotype or maternal family history of AD. Brain metabolic deregulation in AD was found to be specific to glucose metabolism, while ketone metabolism is unaltered. <4> <5>

Since introducing ketone bodies to AD patients has resulted in improvements to cognitive ability, a ketogenic diet is one of the lifestyle strategies recommended in the “Bredesen Protocol” for reversal or treatment of cognitive decline. Bredesen Protocol <6>

A ketogenic diet is also followed among some ApoE4s who have not yet experienced cognitive decline, but given that it can take 30 years or more of hypometabolism before symptoms manifest, a ketogenic diet is adopted as a preemptive measure.

References:

<1>Stephen C Cunnane, et al., 2016 “Can ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer’s disease” Annals of the New York Academy of Sciences, Issue: Nutrition in Prevention and Management of Dementia, PMID: 26766547, DOI: 10.1111/nyas.12999, www.ncbi.nlm.nih.gov/pubmed/26766547

<2>Berger AL. “Insulin resistance and reduced brain glucose metabolism in the aetiology of Alzheimer’s disease” Journal of Insulin Resistance. 2016;1(1), a15. http://dx.doi. org/10.4102/jir.v1i1.15</ref> <ref>Chen Z, Zhong C. “Decoding Alzheimer’s disease from perturbed cerebral glucose metabolism: Implications for diagnostic and therapeutic strategies” Prog Neurobiol. 2013;108:21–43. http://dx.doi.org/10.1016/j.pneurobio.2013.06.004

<3>Stephen C Cunnane, et al., 2016 “Can ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer’s disease” Annals of the New York Academy of Sciences, Issue: Nutrition in Prevention and Management of Dementia, PMID: 26766547, DOI: 10.1111/nyas.12999, www.ncbi.nlm.nih.gov/pubmed/26766547

<4> Rand T. Akasheh, PhD candidate, Aug 18, 2016, “Alzheimer’s Disease: Pathophysiology and Nutritional Implications” -Presented at the Ancestral Health Symposium 2016, https://www.youtube.com/watch?v=OKH3AE1dOb4 18:33

<5>Richard S. Isaacson, MD; Stephen C. Cunnane, PhD; Russell H. Swerdlow, MD, “Brain Glucose Hypometabolism, Ketosis, and Alzheimer Disease From Controversy to Consensus, www.medscape.org/viewarticle/809725_transcript

<6>Dale E. Bredesen, MD, September 2014, “Reversal of Cognitive Decline, A Novel Therapeutic Program”, Aging Vol 6 N9, Table 1, PMID: 25324467, PMCID: PMC4221920, DOI: 10.18632/aging.100690, www.ncbi.nlm.nih.gov/pubmed/25324467