So people don’t get bored early on, a couple of statements I believe to be true:
“Chronic hypoketonemia is a post-agricultural aberration and permissive for most cases of Alzheimer’s, Parkinson’s, diabetes, heart disease, autism, and precocious puberty.”
“Humans maintained on standard grain-based chow stop reproducing at an earlier age and die younger than those maintained on a ketogenic, low-carbohydrate, or intermittent-starvation diet, like every other species tested thus far, including primates.”
The purpose of this piece is to encourage people to question their beliefs and their textbooks.
At one point, I asked myself, “what did our fair-skinned pre-agricultural ancestors eat that would abort ketogenesis?” I came up with: “Nothing”
Contrary to popular opinion, ketogenesis does not require ‘starvation’ or one to consume buckets of lard. A mere thirty minutes of strenuous exercise per day obviates the need for protein restriction and makes chronic ketogenesis permissive of modest amounts of carbohydrate, including fruit. If half a pound of blueberries on an empty stomach does not abort ketogenesis in a body that eats a low-carb diet and exercises every day, what grew in Ireland 15,000 years ago that did? What was in the deciduous forests of Germany that did?
Part One: Errata
The textbooks generally make statements to the effect:
“The body is capable of making and using ketones during periods of starvation for the purpose of conserving glucose”
No.
It is capable of using pure glucose during periods of gluttony in order to conserve fat.
“Glucose is the brain’s usual and preferred energy substrate but can use ketones during starvation”
NO.
The primary fuel of ketonemia is called beta-hydroxybutyrate (BHB). Relative to BHB, glucose generates less ATP/O2, increases oxygen consumption, generates more reactive oxygen species (ROS), results in lower neuronal ATP [3, 5, 6], and a decrease in the number of mitochondria per neuron [36] and per muscle cell [38]. If you don’t deny the brain the choice by aborting ketogenesis, it will use the ketones to meet between 60 to 70-something percent of its energy demand (depending which article you read).
Increased ROS likely accelerates the rate at which mitochondria accumulate mutations with age, which may be the ultimate cause of most cases of AD/PD (and aging in general). This concept remains controversial for AD [18] but gaining support from many, including our own Bradley Miller [19]. The link with is PD less controversial [20].
There is a correlation with sugar consumption and PD [16, 17] and a suggested link between sugar consumption and AD [22]. So many researchers seam to try so hard to find links between fat consumption and disease that they simply ignore sugar, the greatest modifier of the ‘bad-ness’ of fat. Furthermore, most of the calorie-restriction studies fail to measure BHB in spite of calorie-restriction being known to be ketogenic. The ketogenic diet has been tested for utility in AD with modest but positive results [4, 23]. The latter [23], but not the former [4], found an even greater benefit for Apo E4/E4 folks. (ref [4] is maybe the best article to read as a starting point for those interested in nuerodegen on account of the links). These studies employ synthetic short chain triglycerides that are even more ketogenic than coconut oil.
“The ketogenic diet clogs arteries, and is harmful to the kidneys.”
Folks who eat animal fat and little else risk clogged arteries. Exercise, vegetables, PUFAs, and antioxidants allow for dramatic improvements of lipid profiles [2, 8]. DHA (fish oil) is the most potent natural agonist of PPAR-alpha, the master ‘time to burn fat’ switch [2]. Fibrates are synthetic agonists used to treat dyslipidemia. In a normocaloric diet (consumed = burned), fat consumption is permissive for burning stored fat while carbohydrate consumption is prohibitive. I didn’t experience acetone-induced polyuria until about 80 mg/dl, exercise tolerance increased at 15 mg/dl. Like blood glucose, ketones have an optimal range. This article [1] describes people who get 63% of their calories from coconut and have a low risk of cardiovascular disease. They eat fish and little sugar or ‘fast’ carbs. The Inuit used to be ketotic their entire lives for an unknown number of generations and were healthy [15] (a fun and interesting article).
“The ketogenic diet should only be administered under close medical supervision”
Seriously? How many ‘deaths-per-prescription’?
“The liver manufactures ketones for use by brain, heart, and skeletal muscle”
Ketones are manufactured by liver, kidney, and brain astrocytes. The liver is the only organ that can not use ketones.
“Ketosis reduces exercise tolerance”
At first, yes, after a period of adaptation, it increases exercise tolerance [3, 15]. Try it. Rats ran longer and had lower lactate [39]. The diet has been stated to “result in glycogen depletion.” If muscle were allowed to grab all the blood glucose it wanted, strenuous exercise would cause hypoglycemia; this is presumably the reason cells store glycogen granules. The diet has been suggested (not proven) to decrease anaerobic capacity secondary to decreased glycogen, but this is not in agreement with studies showing protective effects of ketones in experimental ischemia in both heart and brain. This is likely because ketones generate more ATP per O2 and generate less reactive oxygen. Ketones were protective in those studies even though glycogen was not limiting, oxygen was. It would be at least equally accurate to state “hypoketonenia necessitates increased compensatory glycogen storage.” Unlike glycogen, ketones don’t deplete. Muscle cells also contain lipid 'granules' in a number and distribution comparable to glycogen granules. Almost all authors fail to acknowledge the fact they even exist. I’m doing the same number of repetitions I’ve always done. If any weight lifters actually try the diet, tell me what you think.
There are ketones in your blood right now. One of the biggest problems in the field is that the definition of ketosis seems to have been defined by the nitroprusside reaction (urine test strips you can buy at CVS). If they’re negative, everyone ignores BHB levels. Research will move forward when this stops, as in [4, 11, 14, 23]. I suspect that exercise blurs the borders between the classic ketogenic, calorie restricted, and intermittent starvation diets. They all unambiguously elevate ketones. Studies tucked away in nutrition journals show that modest exercise roughly doubles BHB in regular people on regular diets [25]. A 50-mile walk increases it 20 fold from 0.036mM to the ‘ketotic’ level of 0.6mM [45] (which is close to where I am all the time). BHB has been measured in adults on a ‘regular’ diet and, while low, was found to be decreased by sugar consumption with concomitant decrements in cognitive performance [11]. There are ‘ketogenic diets’ and diets that are ketogenic. Every diet allows for some concentration of BHB.
Part Two: Conjecture
Sugar
Why do young children have an exaggerated euphoric response to refined sugar?
Decreased ATP combined with increased ROS is capable of resulting in increased dopamine release [42], [43] (see picture). Ketone levels in 1-week-olds ranges from 0.4 – 0.9 mM, in 1-6 month-olds they are about 0.2 mM [40], mine are about 0.5 mM, yours are about 0.05 - 0.1 mM [11], and sweet-toothed kids between 6-8 years old are about 0.24 mM [40]. I think the reason adults on a ketogenic diet don’t have the same euphoric response that kids do in spite of elevated BHB is because kids’ brain glucose utilization is very much higher [24] (my brain glucose utilization should be much lower than an adult on ‘standard’ diet). Aborting the significant ketogenesis by eating sugar in a brain with such a high metabolic demand would be expected to lower neuronal ATP and increase ROS production far more than in your brain or my brain. It would be interesting to see if kids can differentiate between pure glucose and fructose as the latter results in a much lesser insulin response but is even more effective than glucose at terminating ketogenesis. By the way, this is the mechanism by which organic solvent abuse causes dopamine release. Both sugar and organic solvents have been correlated with Parkinson’s disease.
I don’t think we know what ‘normal aging’ is, at either end of the spectrum.
Parents don’t get angry when you suggest they’re raising their children improperly; they get angry when they’re afraid they’ve raised their children improperly:
Autism:
A number of diseases are purported to be on the rise: depression, ADHD, diabetes, autism, Alzheimer’s. I think some are due to overdiagnosis and some because baby boomers are aging. Diabetes and autism [35], however, do appear to truly be on the rise. What’s interesting about autism is that most kids go through a period of normal development then experience a ‘regression’ that sometimes coincides with a metabolic drain, such as fever [28]. This also is during the time when kids’ brains’ glucose utilization is very high [24]…probably because their brains are struggling to meet demand with a barely-sufficient fuel while on a carbohydrate rich, ketone-aborting diet. In one study (says it’s the largest to date), 96% of autistic kids have biochemical evidence of mitochondrial dysfunction [30]. Half a pound of blueberries will not abort ketogenesis in my body but 10 grams of table sugar will. Scaled down to kiddie size, that’s 2-3 grams of sugar. The transient and modest neuronal ATP depletion + ROS generation I suspect occurs might make a healthy kid act funny for an hour but might be catastrophic for a kid with a mild defect in ATP production. I’m sure studies have tried to link sugar with autism. They probably tried to correlate amount of sugar with disease incidence and came up nil. I doubt any studies tried to compare kids who consume no ketogenesis-aborting food with those who consume any because there aren’t enough kids in the former group. How many parents let their kids eat 2-3 grams of sugar per day? How many prior to weaning from the otherwise ketogenic mother’s milk? Standard Similac has lactose and coconut oil. Coconut oil is the most highly ketogenic lipid occurring naturally is annoyingly expensive. Lactose is the only common sugar that doesn’t abort ketogenesis (try it) and is pricier than glucose. Mom’s body probably goes through the trouble to manufacture lactose rather than simply secrete glucose into breast milk for this reason. Obviously, the people who came up with the formula had ketogenesis in mind. Blood sugar is probably supposed to be a little lower in infants because they are unambiguously on a ketogenic diet if drinking breast milk. I was surprised to see that there are formulae available that have enormous amounts of glucose or ‘corn syrup solids’. Have those formulae become more popular? Because they’re cheaper? What does continually prohibiting ketogenesis in an infant from day one do? Is that why bottle fed kids have lower IQ than breast fed kids? [46 meta analysis]. Has anyone compared IQ in the lactose-only formula to the corn-syrup solids formula? Some authors ague that the proximate cause of autism is a defect in developmental pruning (too little). Maternal valproate use causes a syndrome including autistic behavior. It’s a messy drug and syndrome, but in addition to being an HDAC inhibitor, it kills microglia and interferes with mitochondrial ATP production to an extent that it’s known to be toxic to patients with known mito mutations. Microglia are known to play an active role in at least some developmental pruning. Perhaps microglia are targeted by postnatal hypoketonemia in those kids with mild defects in ATP production.
Precocious puberty
Girls used to reach menarche at the much more reasonable age 15-16 just a couple of hundred years ago [34], and age 18-19 on ‘subsistence’ diets. The average is now age 12.5 in the U.S. People used to say kids reached sexual maturity so early due to ‘good nutrition,’ now they’re saying because kids are fat. Mothers who reached puberty early tend to have obese kids [37] and early menarche is associated with mortality from heart disease and stroke. Interesting that metformin can delay menarche [32], reduce blood sugar, elevate BHB in rats [33], and lazy ketone-runners have used it to induce ketosis with speed and ease. Whatever Germans used to feed their kids in the 1800s allowed for menarche at 16.5 [34]. Maybe we should call it ‘The German Paradox.’ I couldn’t find BHB levels measured in young teens but by extrapolation, it’s probably between mine and yours. If a child were raised on my diet, what might be his/her body mass index? Age of puberty? While it may be less to do with ketones and more to do with body fat, the two are inseparable. If you need a reference to believe that there’s something wrong with pubic hair on 11-years-olds and impregnable at 13-14, then there’s something wrong with you. I call it the Grass Fad Diet; it is not “good nutrition.” Wheat, barley, corn, rice, sugar cane are all grasses. Missing from the list are potatoes, of course. If you showed a metaphorical Darwin the food pyramid, he would point to the base and say, “what’s that?”
Dopamine
Read article [50]. These authors attempted to induce lifelong dopaminergic miswiring in rodents by feeding them a high fat diet but instead corrected the defect induced by 'standard' corn chow. They didn't describe 'high fat diet.' What ratio of omega-6 to omega-3? Nevertheless, they succeeded in producing mice with more dopaminergic innervation and dopamine in the nucleus accumbens (reward button of the brain) that persisted for the entire life of the animal. The mice weaned on a high fat diet exhibited a reduced locomotor sensitization response to amphetamine. Enhanced initial response and sensitization to amphetamine is widely accepted as evidence of dopaminergic dysregulation. The very references they cite to support their work refute it: [51] describes decreased dopaminergic innervation of the NAc in rodents exposed perinatally to ethanol. [52] describes enhanced response to amphetamine in rodents artificially reared in a deprived environment. Considering that we've succeeded in reducing the age puberty by 4-5 years in almost every human on the planet by changing what we eat and that the downward trend in menarche is continuing to follow increasing percentage of carbohydrate consumption (see pic 2, it links to original source), I believe that there is a possibility of ever increasing paucity of dopaminergic innervation.
Experiments that I believe are worth spending tax dollars on include:
1) repeating [50] with a better defined 'high-fat' diet and maintaining them on it, followed by a battery of behavioral tests to assay for learning, memory, depression, anxiety, propensity for aggression, drug-liking, and age at which they stop reproducing.
2) comparing dopaminergic innervation, receptor densities, and dopamine levels in in-bred, 'standard' chow fed mice to those caught in Yellowstone. Results would only be suggestive, but it's a pretty low-cost experiment.
3) comparing dopaminergic innervation and receptor densities in age-matched human archival tissues from 50 years ago versus today. This might require a large sample size and be inconclusive. If material could be acquired from the folks living on the Polynesian atoll in [1] who get more than 50% of their calories from fat (and are healthy) any difference would more likely be apparent with a smaller sample size.
4) comparing dopaminergic innervation and receptor densities from autopsy material in human children reared on breast milk versus lactose-only formula versus glucose-containing formula.
5) comparing dopaminergic innervation and receptor densities from school shooters versus suicide victims (assuming the NAc is still intact.) I'm kidding. I'm half kidding. When I read that article the term 'wallpuncher' came to mind.
Most ridiculous thing you’ve ever heard:
In spite of the 96% incidence of biochemical evidence of mitochondrial dysfunction in autistics found in [30], mutations were not identified in most; complex I defect was found in 64% but they still couldn’t pin down a mutation, maybe due to very low heteroplasmy (ratio of good to crappy mitos). The Miller-style single-cell laser capture of neurons from post-mortem brain might be able to. Enough mutations accumulate in neuronal mitochondria in 70 years to detect and to interfere with function. Oocytes have very, very low metabolic rates. It could take thousands of years for them to become detectable with current techniques if they can’t find them in most of those autistic kids. If a woman eats a ketogenesis-aborting, ROS-generating, mitochondrial-mutation-rate-enhancing diet her whole life, is there an increased chance her child will have a tiny degree of heteroplasmy? If the child is a girl, and she eats a ketogenesis-aborting, ROS-generating, mitochondrial-mutation-rate-enhancing diet her whole life, is there an increased chance her child will have a slightly higher degree of heteroplasmy? They haven’t found it yet. One of the most common, most mild, most late-onset symptoms resulting from the most common known mitochondrial mutations at low heteroplasmy is: diabetes. Again, studies very rarely find mutations in ‘regular’ diabetics, but I’m not convinced they’re up to the task yet and they’re always looking in blood. Glucose compared to BHB is known to increase mitochondrial ROS, mitochondrial ROS is known to induce mutations over time. Each mito has 4-10 copies of DNA and each oocyte has about 100,000 mitos; maybe in another 200 hundred years the mutation burden will be great enough to be detectable. Authors have suggested that increases in maternal age account for increases in mito-related diseases. I don’t doubt it. But I can’t think of a reason that cross-generational oocytic heteroplasmy should not be increasing from very low to low. Excepting certain deletions, mutated mitos do not have a reproductive disadvantage within a given cell. The only way they get ‘cleaned up’ is when the burden is high enough to confer a disadvantage between proliferating cells, as surely occurs during embryogenesis and has been observed in white blood cells (but not muscle or brain) of people with known mito mutations. What I’m suggesting is that chronic hypoketonemia may be having a cross-generational effect akin to increasing background radiation levels but that the DNA damage is mito-specific. Such a hypothetical radiation would not result in kids with 2 heads, cancer, or people dropping dead; most people would still be mostly healthy most of the time. Imagine there were such a radiation, which diseases do you think would become more prevalent?
‘Slow’ Neuroscientists
The things that elevate ketones in my body:
Exercise, coffee, green tea, smoking.
The first two (three?) have been negatively correlated with AD
All have been negatively correlated with PD. Smoking has the strongest inverse relationship (with corroboration in animal models) and turns my strips the deepest shade of purple. All of these things increase lipolysis probably via a quite simple adrenergic mechanism +/- modest uncoupling (uncoupling decreases ROS and is a good thing even with modest decrease in ATP.) Most NSAIDs are very weak uncouplers. NSAID potential to prevent AD is probably due to altered a-beta cleavage, bla-bla, but worth checking BHB levels anyway (ibuprofen may actually decrease BHB due to PPAR-gamma agonism).
I couldn’t find that anyone had measured BHB in coffee drinkers or smokers. When someone does, it will be elevated and the author will propose that it’s part (not all) of the neuroprotective mechanism with a list of supporting references, thereby ‘discovering’ what hundreds of ketone-runners have known for years. Studies tucked away in nutrition journals show that exercise roughly doubles BHB in regular people on regular diets [25] and marathon walking increases it 20-fold to the classic ‘ketotic’ level of 0.6mM [45]. The study that found modest improvement in AD with ketones achieved a level about half that [4]. That’s probably partly why exercise is preventive/therapeutic for neurodegenerative diseases.
Someone should measure BHB in ADHD kids upon Ritalin treatment (it will be elevated by drug).
B.T.W. exercise also increases phenylethylamine which can increase BHB independent of exercise. Everyone knows the former increases dopaminergic transmission probably via a postsynaptic mechanism.
Ketones may possess therapeutic potential for congestive heart failure. Maybe someone is working on that already, I didn’t look.
Presumably, liver makes ketones for every organ except itself. It has been suggested that brain ketone use is limited by blood-brain-barrier transport of ketones, but I’m not sure that’s 100% logical. The situation may be more like: astrocytic glycogen:blood glucose::astrocytic ketogenesis:ketone transport. Meaning that astrocytic ketogenesis may be an emergency backup just like astrocytic glycogen is. Someone needs to fit infants with microdialysis probes that can measure ketones, ATP, ROS, and dopamine and see what’s really going on when ketogenesis is aborted at various stages of life. I did at least find a study that employed a hot ketone tracer for PET (maybe easier to get that protocol approved, huh?)
I’ve searched extensively (for a total of about four hours), but could not find that anyone had definitively demonstrated that BHB is or is not an HDAC inhibitor and increases hTERT transcription (like n-butyrate does in non-cancer cells). Why did I spend so long searching for this one piece of information? Because I could not believe that no one had performed the most obvious, summer-rotation-student simple experiment. Check it out:
“Interestingly, we observed that the modification of histone/protein acetylation status by two well-known class I and II HDAC inhibitors, TSA and n-butyrate [14, 15], induced strong, diverse responses in the expression levels of seven SIRT mRNAs. SIRT2, SIRT4 and SIRT7 were upregulated, whereas SIRT1, SIRT5 and SIRT6 were downregulated.” [49]
So, the effects of BHB are basically indistinguishable from those of SIRT2 (not SIRT1). BHB and Sirt2 activity are known to be increased by calorie restriction. Did I miss something?? I found an article about butyrate being metabolized to BHB….in sheep gut. I couldn’t find anything about in vivo metabolic fate of n-butyrate outside of colon. What gives? Am I returdid? Bad search terms? This is only, like, the key to health and longevity ‘nshit. Based on the fact that ketones show up in my pee 5 minutes post adrenergic stimulation, I’d put money on BHB being Step One in that key. This study [53] acknowledged that there is a small amount of endogenous butyrate in human serum, that the half-life is 6 minutes, that metabolites don't account for much of the infused dose and state, "these observations suggest that butyrate is readily metabolized." In spite of this, these researches continue to believe that butyrate is a drug rather than a metabolic fuel. Perhaps they forgot how the 'drug' got its name (butter).
Why so slow?
I believe there are two reasons
One:
I feel there has been a disturbing trend in the biological sciences over the last couple of hundred years away from learning the unknown and toward producing a ‘product.’ Gone are the days of Ramón y Cajal. No one writes a grant anymore without ‘disease relevance’ because the NIH won’t fund it. Instead of textbooks being revised to reflect the established accuracy of my Part One and it becoming common knowledge, we have “AC1202: patentable synthetic ketogenic agent for the treatment of Alzheimer’s” which I don’t think will ever offer more than modest benefit because the preventable damage has been done. What I’m saying can perhaps be best demonstrated by performing a pubmed search with the term ‘beta hydroxybutyrate’ You’ll get more hits for n-butyrate (as cancer drug, not naturally in your gut) and GHB (chemically related street drug) than the compound as central to normal human physiology as blood glucose.
God forbid you want to learn about phenylethylamine (increased by exercise, increases dopaminergic transmission, elevates BHB and has been casually suggested to play a role in whatever that feeling is that we get when we fall in love)….your pubmed search will be flooded nearly to exclusion by the hundreds of millions of tax dollars we’ve spent to prove that swallowing 10-40 tablets of the chemically-related ecstasy is bad for you. Yes, 10-40 tablets [47]. The next time you’re at a neuroscience conference, take a stroll down the ‘crystal-meth’ isles (plural). Most of those studies employ doses that would induce immediate florid psychosis. Imagine if all that money were spent studying endogenous phenylethylamine which I’m sure has more relevance to P.D. than crystal meth does. The best phenylethylamine studies I found were from the 50’s. The level of ketones in infants and children? A Swedish study from 1966 [40] and an Italian study from 1982 [14]. This is why I log on to those forums to hear what the psycho hard-core, muscle-head bodybuilders have to say about ketogenesis, a fraction of whom are very well informed and know that cycling between keto and carb-loading results in exaggerated glycogen storage. I read it from the muscle-heads first then found the rodent study.
The majority of studies on the effects of a high fat diet are carefully stacked to produce a preconceived notion. Researchers are careful to avoid feeding ratios of omega-6:omega-3 that existed ubiquitously prior to agriculture, to include too much DHA, or a running wheel because they are perfectly aware that it will 'spoil' their results. Very high concentrations of omega-6 and long-chain saturated fats? Where do they come from? More things that Darwin never heard of. The Red Man's grass-fed bison had a ratio of about 4:1 which is thought to be optimal (grain-fed bison are about 20:1).
I consider my need to write this blog a failure of the biological sciences, specifically, the government funding practices that guide them and the researchers who review and score grant proposals.
Two
Psych 666
There was a time when people rolled their eyes at the suggested dangers of leaded gasoline, “we’ve been using it for years and we’re fine” People are just now coming around to bisphenol-A and yet to come around to phthalate esters. “I wouldn’t let my baby drink from those poison plastic bottles.” “Of course I did my nails when I was pregnant, my boy is fine.” “We’ve been aborting ketogenesis in ourselves and our kids for hundreds of years and we’re f” pubic hair on 11-year olds…accelerated telomere shortening…DNA hypoacetylation.
I feel the problem stems from a childishly oversimplified conceptualization of the role of various nutrients in the human body that is more akin to an emotion-based Jungian collective subconscious than a comprehension of fact. What do you feel when you read the following terms?
Bagel
Fat
Carb-loading
Ketosis
Cat
Dog
Rattlesnake
Dogs kill more people per year than snakes. Yes, there are more dogs than snakes, but most dog victims are children. Moreover, the snake only strikes when it feels threatened. If not startled, it will slither away, try to warn you by rattling, and will never, ever chase you down. I’d bet most of the dogs who bite take at least one pace toward their victim who is trying to get away. Ever watch a cat catch a mouse? It will let it go just to slowly torture it to death in a playful game. A logical mind would call the cat or dog evil and the snake neutral. But dog/cat = good, snake = bad.
Then somehow snake = ugly, disgusting, evil.
“fat” ….it piles up on people’s bellies and arteries. It’s gross, slimy, food for gross, dumb people. It’s food for the marble-eyed slow-walkers who clog the isles of Walmart. Nevermind that carbohydrate is what proactively prohibits the body from burning the more efficient and cleaner fuel.
“Carb-loading” ….what healthy weight-lifters and runners do. Carbs are the food of motivated, educated people with an understanding of nutrition and physiology. Never mind the less ATP/O2, increased ROS, decreased mitos per cell, and hypoketonemia-induced reliance on storage granules.
“Ketosis” …it has a disease suffix. I intend for the terms hypoketonemia and euketonemia to be taken seriously and believe minds and textbooks will remain closed to the topic until they become adopted. It blows my mind that a lot of pediatricians don’t even know infants are supposed to be ‘ketotic,’ Trained professionals with a degree higher than my own charged with ensuring the health of our children don’t know basic physiology. Even the few articles that acknowledge that infants have elevated ketones suggest the purpose is to “conserve glucose for the brain” ?!? These people get grants funded? They treat your baby? I accept no excuse for this level of ignorance in MDs.
I’m not challenging your beliefs; I’m challenging you to challenge your own as I have done. I spent most of my life being wrong and it took until a few months ago to question what I was taught, which came about by pure chance.
Most people who go on the diet feel shitty for a few to several days, then…I’m not going to tell you because you need to hear it from your own body.
If after 2 months on the diet you think something in Part One is bullshit, then it is bullshit.
An hypothesis is an evidence-conceived notion, as inseparable from the ego as any we have chosen to bear, to embrace. At some point, we must endeavor to prove ourselves not correct, but incorrect, to throw our ‘child’ into the deep end and make careful notes poolside on any thrashing or gasping.
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