Concussion season is here!
It is autumn here in the States and to many Americans that means that a new football season is among us. From young children to the professionals, athletes are now participating in one of our favorite past times. To me, as a spectator, this time of year means grilling lots of meats, hanging out with friends and family, and cheering for our favorite teams. As a physician, this means that a spike in concussion rates is well on its way. I have been recommending to concussion patients that they reduce their consumption of sugar and refined carbohydrates for several years now. The belief that this was beneficial for recovery was based on a few studies that I had come across in the traumatic brain injury literature, as well as some blog posts that I had read in the ancestral health community. To consider this practice as evidence-based would not be accurate, given that I hadn’t yet fully delved into the literature myself.
Well…football season is upon us folks! Let’s dive down the rabbit hole of how diet may influence concussion recovery.
A brief word about concussions:
A concussion occurs when a physical trauma leads to a metabolic derangement in the brain . This results in a wide variety of symptoms including headaches, dizziness, visual problems, nausea/vomiting, sleep disturbances, cognitive impairments, fatigue and emotional lability among others for its victims . As you can imagine, these symptoms can significantly impact a person’s ability to function in their daily life. Fortunately, symptoms often improve within 7-10 days . Unfortunately, some patients experience a protracted recovery, taking months or even years to get back to their normal selves .
The medical community has dramatically improved its appreciation of the seriousness of a concussive brain injury as well as the importance of avoiding a second impact while a brain is still in recovery. Sports medicine personnel are also better at diagnosing concussions on the field, enabling us to quickly remove an athlete to avoid further risk. We are also improving our understanding of the potential long term consequences and the accumulative effects of multiple head traumas, however more research is on this topic is certainly needed.
Currently, concussion management is based on the avoidance of an additional injury while initiating a period of relative cognitive rest, gradual return to school/work, and eventually a gradual return to athletics . Medical treatments that enhance neurological recovery are limited, and lifestyle interventions, including diet, should be examined more closely and considered to be legitimate cost-effective strategies to help manage these challenging injuries.
Some quick broad strokes of where we are heading…
- A concussive injury to the brain disrupts its cellular metabolism which is central to its pathophysiology and symptoms .
- The food that is consumed provides the brain with its immediate metabolic fuel and brain cell metabolism is heavily influenced by what we eat [3-5].
- This concept is already used to treat other neurological conditions, particularly pediatric seizure disorders [5, 6].
- Dietary manipulation may offer an effective strategy for optimizing concussion recovery as well.
Now let’s discuss how…
In this blog post I will explore the two main dietary variables that I found to have the most weight. The first is the interplay between refined carbohydrates, fats, glucose, insulin and the ketogenic pathway. The second, which will be discussed in part II, is focused on the intake of omega-3 fatty acids.
Before you read further, a disclaimer. This turned into a pretty dense post. Lots of science and stuff. If its over your head, that’s okay! You may just want to wait for PART II where I will establish some take home points.
Also! To reiterate…the purpose of my blog posts are to facilitate thought and discussion or perhaps even motivate research to answer the remaining questions on this topic. That is all. If you think that you have a concussion, GO SEE A DOCTOR!!!
Concussion Pathophysiology 101:
Below is an over-simplified step-wise version of what happens in the brain following a concussion…
There are several mechanisms underlying the final period of impaired glucose metabolism, including…
1. Glutamate release → Calcium influx → Impaired mitochondria:
The glutamate that escaped the cells will activate receptors that cause calcium to enter the cell. The now intracellular calcium accumulates in mitochondria impairing glucose metabolism  and increasing the generation of reactive oxygen species (ROS).
2. Oxidative damage to cells depletes NAD+:
Brain trauma results in elevated levels of ROS’s which inflict oxidative damage to intracellular structures, including DNA [7, 13, 14]. This damage activates DNA repair enzymes which use and deplete the intracellular stores of nicotinamide adenine dinucleotide (NAD+). A deficit of NAD+ results, slowing glyceraldehyde-3-phosphate dehydrogenase, an important enzyme in the glycolytic processing of glucose (which needs NAD+ to do its job) [7, 12, 15-17].
3. The Pentose phosphate pathway:
Glucose is also shunted through the pentose phosphate pathway at an increased rate, further decreasing glucose availability for ATP production via the TCA cycle .
4. Neuroendocrine disruption:
Concussions can cause neuroendocrine derangements, with altered levels of growth hormone and insulin-like growth factor, both which play important roles in the body’s metabolism .
Glucose metabolism should be considered inefficient as a solitary metabolic substrate following a concussion [7, 12]. Fortunately, humans have evolved the ability to utilize multiple substrates simultaneously to generate the almighty ATP, and THIS is heavily influenced by what we eat!
One of these metabolic pathways utilizes ketone bodies, which if dialed up, can greatly improve brain cell bioenergetics during metabolically demanding situations . This important metabolic pathway is inhibited, however, by diets that induce a lot of insulin release. Let’s discuss removing the breaks before we go into adding fuel.
High fructose diets have been shown to induce insulin resistance within the brains of animal models and this is associated with poor cognitive performance [19-22]. In humans, diabetics tend to perform worse on cognitive tasks and have more brain atrophy than non-diabetics, and these differences are proportional to fasting blood glucose levels [23, 24]. In the absence of diabetes, chronically elevated blood glucose levels are still associated with worse cognition and changes seen in brain regions that are relevant to learning and memory [23, 25]. Even in the young and healthy population a diet high in refined sugar and fat (as seen in the typical modern western diet) have been shown to perform worse on cognitive tests [26, 27] and even a single high glycaemic meal has been associated with impaired memory performance in healthy adolescents [28, 29].
Within the context of brain trauma, high sucrose diets given to rats resulted in worse cognition and less expression of brain derived neurotrophic factor (BDNF) in the brain following traumatic injury [12, 30]. BDNF is important for neuroplasticity. It is also well established that hyperglycemia after severe traumatic brain injuries is associated with significantly worse outcomes in humans [31, 32].
Tapping into the ketogenic pathway. It’s so easy, a caveman could do it. What about modern man?
How do we remove the breaks on this alternative metabolic pathway? Insulin levels need to drop, and the first step to accomplish this is by manipulating macronutrients. With less insulin release, the ketogenic pathway is ‘disinhibited’ allowing ketone body synthesis to occur (via fatty acid metabolism in the liver) . A ketogenic diet has been used to treat drug-resistant pediatric epilepsy since the 1920’s  and uses a fat to combined protein and carbohydrate ratio of about 4:1 [6, 34]. This is considered the classical ketogenic diet and achieves high levels of serum ketones.
Eating a diet that can facilitate this metabolic pathway (to some degree) has a lot of therapeutic potential for concussion recovery…
1.) Ketone bodies enter the TCA cycle more efficiently than glucose and greatly improve ATP yield [7, 35]. Greater ATP yield will likely allow the brain to perform all of its healing processes at an optimal level, and obviously provide more energy for when the brain is working hard (i.e. in school, in work, or in highly stimulating environments), a situation that usually triggers symptoms.
2.) Ketosis is associated with reduced generation of reactive oxygen species after brain trauma  resulting in less repair-enzyme activity and therefore less depletion of NAD+. Greater NAD+ availability likely improves glucose metabolism by improving glyceraldehyde-3-phosphate dehydrogenase function [7, 12]. In this way, ketones can simultaneously help glucose metabolism be more efficient too (double whammy!?).
3.) Lactate is also known to accumulate in the brain after a traumatic injury, which is another potential energy source. If ketones can help mitochondria recover their ability to work, this third substrate may be better utilized to supply the ATP demands . (triple whammy!?)
I like the mechanism, but come on man, what’s the evidence???
Traumatic Brain Injury + Ketosis in Animal Models
Animal models of TBI have demonstrated smaller contusions, better cognitive performance, reduced reactive oxygen species, less edema, reduced apoptosis, and LESS impairment of glucose metabolism [36-40]. These benefits appear to be more pronounced in younger rats  indicating that the ability to utilize ketones maybe somewhat age dependent .
Caloric restriction is another way to induce ketosis and it too has been shown to have beneficial effects in rat-models of TBI, including increased expression of BDNF, again an important protein for neuroplasticity [42, 43].
I could only find one study in humans. It compared standard tube feeds to a low carbohydrate high fat regimen in patients with severe TBI . Patients receiving a low carbohydrate, high fat regimen had lower blood lactate levels, higher ketone levels, improved urinary nitrogen balance and increased euglycemia .
Concussions vs. TBI?
Concussion pathophysiology overlaps a lot with TBI, though there are certainly some differences. A rat model of concussion (with absence of any physical damage to tissues or bleeding) was also demonstrated to have significantly disrupted glucose metabolism  . When a ketogenic diet was introduced, cognitive performances improved following a repeat concussive injury .
What about human studies looking directly at ketosis and concussions???
A Quick Word on Medium Chain Triglycerides:
A full blown ketogenic diet is incredibly challenging for most people, though there may be a slight work-around. Fat can come from long-chain triglycerides (LCT’s, C13-C21) and medium-chain triglycerides (MCT’s, C6-C12)  and MCT’s are much better at generating ketones when metabolized. A variation of the ketogenic diet is used for pediatric epilepsy called the medium chain triglyceride diet (MCTD) [5, 6] which uses large amounts of MCT oil. This allows for more liberal carbohydrate consumption, a greater number of food options, and better palatability for patients while still achieving high ketone levels [5, 6].
A recent case study even describes a patient with greatly improved seizure control after MCT oil was added to a regular diet . Mild ketosis has been demonstrated with MCT supplementation on a regular diet in healthy adults , and serum ketones increased 7.7-fold when older adults with memory deficits were provided exogenous ketones (on top of a regular diet again) and this was associated with cognitive benefits .
Is ketogenesis more like a light switch, or more like a faucet? It’s likely a bit of a combination with at least some ability to achieve lower levels with less stringent dietary changes [48, 50]. And plasma levels therapeutic for a concussion maybe lower than what is required for increasing seizure threshold. In fact, the brain significantly increases its expression ketone transporters (monocarboxylate transporters) after a TBI , indicating an improved ability to utilize ketones in the blood. Perhaps lower serum levels pack more punch in the traumatized brain. The ability to boost ketogenesis with MCT’s and more moderate carbohydrate reduction may provide a useful intermediary here. It would certainly be an interesting variable to research!
I find his discussion of glycolytic (high intensity) exercise and its relationship to cerebral metabolism very interesting as well. Concussion patients certainly do tend to experience increased symptoms during higher levels of physical exertion.
Conclusion to Part 1:
Am I suggesting that we should be putting all concussion patients on a full blown ketogenic or MCT diet?
Not so fast! Pump those breaks! We will get there I promise.
In PART TWO of this blog post, I will attempt to wrap this epically long blog post into a nice little bow and establish some practical takeaways.
Before the takeaways, however, I will delve into how omega-3 fatty acids may, or may not, provide benefits for concussion recovery.
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