Welp, it's just another day's work for LC bloggers collective to destroy stock nutrition lies.
Peter at hyperlipid writes the blog entries the horde of other nutrition bloggers are either too stupid or greedy to write.
You won't find pandering to the lowest common denominator of safe starches, super magical healing potato chips, or hawking other miracle cures.. You won't find a dullard regurgitating the same rehashed ideas some other guru wrote last month, while obnoxiously begging for "donations" to support their "hard work". Its kind of ironic it seems pursuit of profit and self aggrandizement predictably travels inverse their ability to fashion complex, interesting, unique ideas or perspectives. Wanting to one-up or dominate the others in society correlates with not being able to think very much differently from them, yes? The brightest march to their own beat. Tragic these same innovative thinkers usually lack the ability or drive for aggressive marketing and self promotion; their insight remains a hidden gem treasured by the few followers who discover them. Well, as a bonus: obscurity and inaccessibility keeps the quality of commenters pretty high.
Enough hyperlipid worship (but really I can NOT overstate how great this blog is and what a treasure it is). I particularly enjoyed Peter's latest entry because it specifically addresses CNS energetics in absence of glucose; the CNS specific metabolic effects of a ketogenic diet. As someone who strongly feels a ketogenic diet has controlled and helped to cure mood/emotional issues this is of relevance to woo.
CLIFFS NOTES (and woo commentary):
Symptomatic neuroglycopenia is not of consequence if one is in prolonged starvation subsisting entirely upon ketones and body fat. This means to imply glucose is not *necessarily* the primary brain energy substrate as is popularly cited; ketones in the serum can substitute glucose, as well as direct CNS level FFA is actively metabolized by astrocytes into ketone bodies. This can and will substitute brain energy almost entirely as apparently evidenced by lack of neuroglycopenia symptoms upon insulin injection to severe hypoglycemia (less than 10 mg/dl) in a very fasted individual.
Woo agrees and has many times experienced extremely low sugar 50s and 40s that is totally asymptomatic, but it seems contingent upon unimpeded access to FFA (i.e. very low insulin). IN other words symptomatic neuroglycopenia and hypoglycemic symptoms are only so in context of fat oxidation; the more your brain is using fat, the less blood sugar you need to function. This explains how many times wooo walks around blood sugar 50 and i feel fine (although usually feel more energetic if blood sugar is higher, which stands to reason as ketones/fat spare brain glucose and total brain energy is *higher* in that instance). OTOH there are times where a sugar drop from 80 to 70 produces weakness/fatigue if in a more glucose dependent condition.
Woo aside: this phenomenon is notably different from hypoglycemic unawareness which occurs to type 1 / severe type 2 diabetics with autonomic neuropathy. In hypoglycemia unawareness the person experiences an insulin injection mediated hypoglycemic event and is profoundly neuroglycopenic, but they have no ability to respond as their autonomic nervous system is damaged and does not provoke a release of glucagon or stimulation of the HPA axis/adrenal glands that normally produces hypoglycemic distress. They become a bit pallor, somnolent, lowered level of consciousness and eventually comatose, but they don't exhibit much if any anxiety, fear, trembling or sweating (which are mediated by the autonomic / sympathetic nervous system and adrenal response to glycopenia). In a fasted or ketogenic condition, blood sugar is low and your body and brain is working well without risk of coma or loss if mental faculties because the brain has an ample supply of FFA/ketones to replace glucose.
Even among individuals eating typically, glucose is still not used for energy by neurons; it is metabolised into lactate by astrocytes and the lactate is the energy supply to neurons.
FFA, like glucose, is not used by neurons for energy, however astrocytes metabolize them into ketones. Woo aside: this provides energy to neurons, but is additionally glucose/ lactate by sparing. Ironically it might be that ketogenic diets do not REPLACE glucose in the brain, but INCREASE glucose in the brain via ffa/ketones amplifying glucose delivery into lactate by astrocytes.
Peter hypothesizes it is imperative that neurons do not engage in glucose oxidation/glycolysis like other common cells. We evolved teh glucose/lactate shuttle by astrocytes to spare neurons the dirty work of glucose metabolism. They cannot become IR via superoxide, as this would potentially induce dysfunction, apoptosis and behaviorally manifest as cognitive impairment. This explains the evolutionary utility of the role of supportive astrocytes in providing lactate to the neurons which are fragile and must by design be spared the common metabolic behavior of other dispensable cells. The connections and configuration of neurons must be preserved throughout life; failure in maintaining this is equivalent to traumatic brain injury / dementia. This is supported by and offers further insight into the existence of related pathologies such as the fact astrocytes as a source of common brain cancer. We would expect this as astrocytes behave more like common cells with more frequent turn over rate; by logical deduction are therefore a target for oncogenesis capable of malignancy/tumor development. Neurons do not cause cancer because they do not have a life cycle apoptosis/replication like astrocytes do.
Basically yea, a fantastic entry.
Woo wrote a related blog entry describing that lactate is the primary controller of brain norepinephrine. KDs will cause elevations in brain lactate which is more or less the same as saying KDs provide vastly superior energy to the brain. I suspect the greater mental clarity and focus many experience on KD reflects superior brain lactate/norepinephrine , which in turn is a direct result of FFA metabolism / ketones that is glucose sparing. Total brain energy is higher.
In summary, astrocytes supply energy to the brain, and glucose is by no means what so ever required. They can use FFA such as palmitic acid and create ketones just as well.
This segues nicely into explaining why monitoring serum ketones is limited at best and useless at worst; as one becomes progressively more keto adapted, one will not see a huge rise in serum ketones on a very LC diet as the body becomes more adept at using FFA for energy directly w/o spilling ketones everywhere to replace glucose. OTOH, the cognitive and mental clarity benefits at the site of CNS are preserved, because the astrocytes metabolize palmitic acid into ketones via cpt1. In other words, your serum ketones might only be moderate, but your brain might be subsisting almost entirely on fat and ketones because you are using FFA for energy after years of carbohydrate restriction. It's safe to say if you are consuming a 70% fat diet for any length of time this is likely the situation. You can't create something from nothing, and you can't create enough glucose for your brain when you're eating almost entirely of dietary fats.
As supporting evidence moderate to mild ketogenic diets convey similar CNS benefits to full fledged starvation ketosis there is evidence even regular high protein atkins helps control seizures and conveys neurological benefits; the intensely ketogenic 80-90% diets are really not necessary even for the notoriously vulnerable group of epilepsy patients. This is likely because even regular atkins will induce ketosis and increase brain energy from fat; it just is not necessary and increasingly more complication prone (and compliance prone) the more limited and ketotic one makes their diet. Here is one of many case reports; this used a very liberal 30% protein, 60% fat, 10% carb typical atkins ratio and the patients almost invariably all responded with a reduction in seizures. I want to repeat: it is a myth that the only ketogenic diets that work for neurologic problems are the intensely ketogenic diets. Any diet you consume >60% fat can be considered "more ketogenic", but 60% is sufficient for epilepsy control for most patients.
When it comes to those neurological conditions which are particularly benefitting from the lactate/enhanced brain energy profile of a ketogenic diet such as epilepsy and likely many mood disorders, it seems pretty clear that the medical super strict ketogenic diet is not NECESSARY. It might be "more" therapeutic, but it is not necessary for a therapeutic effect in general.
OTOH, for other disease such as cancers, a more strict protein restriction may be the mechanism of action (ablating IGF1) and a moderate ketogenic diet would fail in this instance. It is important to tease out the mechanism of action from which one benefits from a KD. In epilepsy / mood disorders it is likely enhanced brain lactate, enhanced brain energetics, superior control of glutamate and inhibitory tone of brain. For cancers, suppression of GH/IGF1 dynamics by low protein intake may be more important than ketosis and a high protein is very counterintuitive.
ANYWAYZ, for brain energy enhancement / glutamate & GABA processing (benefitting: epilepsy, BPAD/SCZ, autism, OCD, et cetera) it seems pretty clear that even regular pedestrian atkins works pretty well. Perhaps this explains why so many of these disorders feature feeding problems and ritualistic self starvation? Autistic children often demonstrate feeding problems. OCD / glutamatergic excess is pretty common in anorexia. Mental illnesses feature failure to eat as a self care deficit and may improve patients well being. Of course practitioners dismiss all of this as symptom level only, no one really cares to think about the deeper implications (such as , perhaps, that autistic child might feel BETTER not eating, they just can't tell you that as they are limited verbal abilities; there are huge overlaps between autism, obsessional behaviors, and anorexia ; these pathologies often exist in the same patient).
While on this subject I would like to rant about the *pathetic* state of medicine in typical woo fashion. The ketogenic diet for epilepsy and related neurological disorders has been needlessly depicted as an impossibly restrictive and even long term dangerous regimen resulting in growth stunting and severe nutrient deficiencies. In reality, there are plenty of case reports describing epilepsy pts obtaining control on very healthy, very sustainable, mildly ketogenic atkins diets... but for reasons which can really only be summed up as PRACTITIONER GREED, patients are willfully misinformed. Your epilepsy patient is only presented with this extreme diet that is a last resort when toxic dangerous drugs fail. No one is telling patients "hey, regular atkins works too and is actually much much healthier than a SAD diet". If I was a neurologist and my goal was to help my patients, the first thing I would tell a new epileptic is to go on atkins and then we will try medicine after we see whats left. There is literally zero risk of advising your epileptic patients go on a reasonable mildly ketogenic diet. The worst thing that could possibly happen is any metabolic syndrome improves and excess weight is lost. The best thing that happens is they never need to see you again and stop having seizures.
Then again, I'm not a neurologist with a summer home and a new gold walking stick habit to finance. If I was, I would likely behave more like common neurologists who will first try a drug merry go round and the diet is this horribly restrictive last resort that will obliterate your physical health unless you are diligent with supplements (and sometimes even then).
Rant aside, it's clear the more energy one consumes of dietary fat, the greater brain energetics, the lower the need for CNS glucose to support minimum brain function. Fat - whether as FFA or ketones - is a substrate in the brain which is glucose/lactate sparing. If one follows a lower fat diet, one better be increasingly starving themselves regularly in fasts or chronically in calorie restriction. If not, hopefully you have some pretty good genetics. I suppose it is fortunate that the advice to eat low fat is always coupled with regular / chronic starvation behaviors (nom nom thigh palmitate), but why not skip the self flagellation and just eat eggs and bacon? Your brainz will thank yew.