Another blog on ketogenic diets
The ketogenic diet, originally developed for the treatment of epilepsy in non-responder children, is spreading to be used in the treatment of many diseases of the brain, including Alzheimer’s disease. The main activity of the ketogenic diet has been related to improved mitochondrial function and decreased oxidative stress. Relative to its size, the adult human brain requires a disproportionately large amount of energy that is provided principally by glucose. During times where glucose supply is lacking, the brain relies heavily on ketone bodies for energy. In conditions like AD, brain glucose uptake is defective, evidenced in certain regions of the brain such as the parietal, posterior congulate and temporal cortex (S. C. Cunnane et al., 2016). Interestingly, the risk of neurodegeneration is elevated years before the clinical onset of the disease, and this is thought to be due to hypometabolism of glucose in regional areas of the brain. “Examples of conditions in which regional brain glucose hypometabolism is present pre-symptomatically include carriers of the Pre-senilin-1 mutation, carriers of apolipoprotein E4, maternal family history of AD, cognitively healthy aging, and insulin resistance in both young and older persons” (S. C. Cunnane et al., 2016). The brain’s need for energy during prolonged starvation can be met by the high ketogenic capacity of the liver which can produce up to 150 g ketones/day. During prolonged starvation, skeletal muscles can use free fatty acids more efficiently, so ketones become increasing available for the brain which has no other energy substrate to replace glucose when levels are low. Interestingly, when ketones and glucose are both available, the brain glucose uptake decreases, which supports the notion that ketones are the brain’s preferred fuel source. However, it is rare to have both present at the same time, since most people are either eating a high carbohydrate or low carbohydrate diet, making glucose the dominant fuel source for the brain, but not the preferred fuel source.
There are ways to enhance nutritional ketosis by using ketogenic substrates. One method is to use medium chain fatty acids (MCFA’s), which is mostly absorbed from the gut directly into the portal vein. MCFA’s have a more rapid route to the liver than longer chain fatty acids. “which are absorbed as chylomicrons via the lymphatic system and pass into the peripheral circulation before reaching the liver” (S. Cunnane et al., 2011). In addition, MCFA’s do not require carnitine for beta-oxidation like the long chain fatty acids require. MCT’s are a rapid energy source in which the cognitive effects of MCT supplementation has been seen to last several months in AD studies. Other substrates include salts of B-hydroxybutyrate (exogenous ketones), which has also been demonstrated to improve some aspects of cognitive function in advanced cases early onset of AD. MCT’s and exogenous ketones are available over the counter, and below I will reference a company I use myself and recommend for clients. MCT’s are also found in coconut and palm kernel oils. “The ratio of caprylic and capric acids and their proportion of the total can vary widely from one MCT product to another designs to assess their metabolism, there is a signiﬁcant positive correlation between the oral dose of MCT taken and the maximal plasma β-HBA level achieved” (S. C. Cunnane et al., 2016). As a result of the discrepancy, I prefer to use the products produced by supplier that specializes in ketogenic diet support.
Clinical trials with ketogenic interventions in AD, mild cognitive impairment (MCI) or insulin-induced hypoglycemia start to improve some cognitive outcomes within hours to days. It is also argued that the ketogenic approach can also reduce the amyloid burden seen in AD, but it’s a secondary effect. In essence, dealing with brain energy deficits may help the brain metabolize abnormalities such as beta-amyloids as it normally should. In regards to aging, it should be pointed out that immunosenescence can favor a pro-inflammatory state. A heighted immune system consumes a lot of energy, which can compete with the brain or energy intake. This is further exacerbated by infection, inflammation or other chronic responses of the immune system, which favors an energy intake that supports the immune response and takes it away from the brain (S. C. Cunnane et al., 2016). Pro-inflammatory cytokines can also impair ketone production. Hence, brain energy deﬁcits, neuropathology, neuroinﬂammation and cognitive decline all feed oﬀ each other in a vicious cycle that can lead to rapid progression of neurodegeneration (S. C. Cunnane et al., 2016).
“Several diﬀerent ketogenic interventions including prolonged fasting, a very high fat ketogenic diet containing no MCT, or a regular diet to which MCT or ketone esters all have a broadly similar neurological/cognitive beneﬁt”(S. C. Cunnane et al., 2016). I prefer my clients to follow a modified lower carbohydrate diet, to prevent restricting important indigestible fibers, with ketogenic substrates. Small clinical observations have seemed to have really helped some of my clients that have pretty severe hypoglycemia. “The cognitive beneﬁt of ketones is observed under diﬀerent conditions including in the presence of chronically impaired brain glucose availability or utilization due to disease (i.e., MCI or AD), or when the brain glucose deﬁcit is acute, i.e., severe hypoglycemia experimentally induced by insulin infusion and starvation” (S. C. Cunnane et al., 2016). At present, a keto-neurotherapeutic approach is a safe and scientiﬁcally well-supported strategy to bypass deteriorating brain energy metabolism, and something to consider for future brain-based clients.
Here are the exogenous ketones I use. I like to mix the MCT with the ketones, and I put in my bulletproof coffee for a brain fueling breakfast! —>>http://bit.ly/2QgTBm5
The bundle I recommend is the MCT, keto and collagen protein powder. Collagen will help tighten the junctions in a leaky gut.
Cunnane, S., Nugent, S., Roy, M., Courchesne-Loyer, A., Croteau, E., Tremblay, S., . . . Rapoport, S. I. (2011). Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 27(1), 3-20. doi:10.1016/j.nut.2010.07.021
Cunnane, S. C., Courchesne-Loyer, A., Vandenberghe, C., St-Pierre, V., Fortier, M., Hennebelle, M., . . . Castellano, C. A. (2016). Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer’s Disease. Front Mol Neurosci, 9, 53. doi:10.3389/fnmol.2016.00053