It’s long been understood that ketones, specifically beta-hydroxybutyrate (BHB), are a brain superfuel. It’s easy to explain the evolutionary reasons for this. Hunter-gatherers spent much more time in ketosis. This metabolic state tends to occur during periods of low food access. That happens in winter but also throughout the year, as hunter-gatherers tend toward a feast and fast pattern.
After a period of plenty, it might be a while until the next big kill. Some hunting expeditions could take days or weeks. They needed their brains working in top form for a successful hunt. Many hunter-gatherer tribes purposely fast on a regular basis as a demonstration of their toughness, to show that they can go long periods without food, a very important ability for hunters. Even tribal people living amongst food abundance will fast for no particular reason other than it’s part of their culture.
The Piraha, for example, can procure food easily and yet will go without, sometimes simply because they’d rather socialize around the village or are in the middle of communal dancing that can go on for days. They have better things to do than eat all the time. Besides, on a low-carb diet that is typical among hunter-gatherers, it takes little effort to fast. That is one of the benefits of ketosis, one’s appetite is naturally suppressed and so it effortlessly promotes caloric restriction.
Along with improving brain function, ketosis increases general health, probably including extending lifespan and certainly extending healthspan. Some of this could be explained by creating the conditions necessary for autophagy, although there are many other factors. An interesting example of this was shown in a mouse study.
The researchers exposed the rodents to influenza (E. L. Goldberg et al, Ketogenic diet activates protective γδ T cell responses against influenza virus infection). Most of the mice on a high-carb diet died, whereas most on the keto diet lived. In this case, it wasn’t the ketones themselves but other processes involved. Giving exogenous ketones as a supplement did not have the same effect as the body producing its own ketones. We typically think of ketosis only in terms of ketones, but obviously there is much more going on.
Still, in the case of neurocognitive functioning, the ketones themselves are key. It’s not only that they act as a superfuel but simultaneously alter epigenetic expression of specific genes related to memory. On the opposite side, research shows that feeding people sugar literally makes them dumber. Ketosis also decreases inflammation, including inflammation in the brain. Through multiple causal mechanisms, ketosis has been medically used as an effective treatment for numerous neurocognitive conditions: mood disorders, schizophrenia, autism, ADHD, Alzheimer’s, etc.
If ketosis is a biological indicator of food scarcity, why does the body expend extra energy that is limited? This seems counter-intuitive. Other species deal with food scarcity by shutting the body down and slowing metabolism, some going into full hibernation or semi-hibernation during winter. But humans do the opposite. Food scarcity increases physiological activity. In fact, ketosis is actually inefficient, as it burns more energy than is needed with the excess being put off as heat.
Benjamin Bikman, an insulin researcher, speculates this is because ketosis often happens in winter. Hibernating creatures lower their body temperature, but humans don’t have this capacity. Neither do we have thick fur. Humans need large amounts of heat to survive harsh winters. In ketosis, everything goes into overdrive: metabolism, immune system, and brain. This alters the epigenome itself that can be passed onto following generations.
They considered that increased health and so decreased inflammation could be the cause, but it’s not clear that inflammation overall has decreased. The modern industrial diet of sugar and seed oils is highly inflammatory. Inflammation has been linked to epidemic of diseases of civilization: obesity, diabetes, heart disease, arthritis, depression, schizophrenia, and much else. In some ways, inflammation is worse than it has ever been. That is why, as a society we’ve become obsessed with anti-inflammatories, from aspirin to turmeric.
The authors of the paper, however, offer other data that contradicts their preferred hypothesis: “However, a small study of healthy volunteers from Pakistan—a country with a continued high incidence of tuberculosis and other chronic infections—confirms temperatures more closely approximating the values reported by Wunderlich”. Since these were healthy volunteers, they should not have had higher inflammation from infections, parasites, etc. So, why were their body temperatures higher than is seen among modern Westerners?
It also has been suggested that there are other potential contributing factors. Ambient temperatures are highly controlled and so the body has to do less work in maintaining an even body temperature. Also, people are less physically active than they once were. The more interesting explanation is that the microbiome has been altered, specifically reduced in the number and variety of heat-producing microbes (Nita Jain, A Microbial-Based Explanation for Cooling Human Body Temperatures).
I might see a clue in the Pakistan data. That population is presumably more likely to be following their traditional diet. If so, this would mean they have been less Westernized in their eating habits, which would translate as fewer refined starchy carbs and sugar, along with fewer seed oils high in omega-6 fatty acids. Their diets might in general be more restricted: fewer calories, smaller portions, less snacking, and longer periods between meals. Plus, as this would be an Islamic population, fasting is part of their religious tradition.
This might point to more time spent in and near ketosis. It might be noted that ketosis is also anti-inflammatory. So why the higher body temperature? Well, there is the microbiome issue. A population on a traditional diet combined with less antibiotic usage would likely still be supporting a larger microbiome. By the way, ketosis is one of the factors that supports a different kind of microbiome, related to its use as treatment for epilspsy (Rachael Rettner, How the Keto Diet Helps Prevent Seizures: Gut Bacteria May Be Key). And ketosis raises the basil metabolic rate which in turn raises temperature. Even though fasting lowers body temperature in the short term, if it was part of an overall ketogenic diet it would help promote on average higher body temperatures.
This is indicated by the research on other animals: “An increased resistance to cold assessed by the rate of fall in body tem-perature in the animals as well as human beings on a high-fat diet has been reported by LEBLANC (1957) and MITCHELL et al. (1946), respectively. LEBLANC (1957) suggested that the large amount of fat accumulated in animals fed a high-fat diet could not explain, either as a source of energy reserves or as an insulator, the superiority of high-fat diet in a cold environment, postulating some changes induced by a high-fat diet in the organism that permits higher sustained rate of heat production in the cold.” (Akihiro Kuroshima, Effects of Cold Adaptation and High-Fat Diet On Cold Resistance and Metabolic REsponses To Acute Exposure In Rats).
Specifically about ketosis, in mice it increases energy expenditure and causes brown fat to produce more heat (Shireesh Srivastava, A Ketogenic Diet Increases Brown Adipose Tissue Mitochondrial Proteins and UCP1 Levels in Mice). Other studies confirm this and some show an increase of brown fat. Brown fat is what keeps us warm. Babies have a lot of it and, in the past, it was thought adults lost it, but it turns out that we maintain brown fat throughout our lives. It’s just that diets have different affects on it.
Bikman points out the relationship between insulin and ketones — when one is high the other is low. Insulin tells the body to slow down metabolism and store energy, that is to say produce fat and to shut down the activity of brown fat. Ketones do the opposite, not only activating brown fat but causing white fat to act more like brown fat. This is what causes the metabolic advantage of the keto diet, in losing excess body fat and maintaining lower weight, as it increases the burning of 200-300 calories per day (metabolizing 10 lbs of body fat a year). By the way, cold exposure and exercise also activate brown fat, which goes back to general lifestyle factors that go hand in hand with diet.
Some people attest to feeling warmer in winter while in ketosis (Ketogenic Forums, Ketosis, IF, brown fat, and being warmer in cool weather), although others claim to not handle cold well which might simply be an issue of how quickly people become fully fat-adapted. A lifetime of a high-carb diet changes the body. But other than permanently damaged biological functioning, the body should be able to eventually shift into more effective ketosis and hence thermogenesis.
In humans, there is an evolutionary explanation for this. And humans indeed are unique in being able to more easily enter and remain in ketosis. But think about when ketosis most often happened in the past and you’ll understand why it seems to be inefficient in wasting energy as heat, what is a slight metabolic advantage if you’re trying to lose weight. For most of human existence, carb restriction was forced upon the species during the coldest season when starchy plants don’t grow. That is key.
It was an advantage to not only be able to survive off of one’s own body fa but to simultaneously create extra heat, especially during enforced fasting when food supplies were low as fasting would tend to drop body temperature — an argument made by the insulin researcher Benjamin Bikman (see 9/9/17 interview with Mike Mutzel on High Intensity Health at 20:34 mark, Insulin, Brown Fat & Ketones w/ Benjamin Bikman, PhD; & see Human Adaptability and Health). Ketosis is a compensatory function for survival during the harshest time of the year, winter.
Maybe modern Westerners have lower body temperature for the same reason they are plagued with diseases of civilization, specifically those having to do with metabolic syndrome and insulin resistance. If we didn’t take so many drugs and other substances to manage inflammation, maybe our body temperature would be higher. But it’s possible the lack of ketosis by itself might be enough to significantly keep it at a reduced level. And if not ketosis, something else about the diet and metabolism likely are involved.
* * *
What is the relevance? Does it matter that average body temperature has changed? As I pointed out above, it could indicate how the entirety of physiological functioning has been altered. A major component has to do with the metabolism which relates to diet, gut health, and microbiome. About the latter, Nita Jain wrote that,
“A 2010 report observed that 36.7° C may be the ideal temperature to ward off fungal infection whilst maintaining metabolism. In other words, high body temperatures represent optimization in the tradeoff between metabolic expenditure and resistance to infectious diseases. Our reduced exposure to potentially pathogenic fungi in developed countries may therefore be another possible factor driving changes in human physiology” (A Microbial-Based Explanation for Cooling Human Body Temperatures).
That would be significant indeed. And it would be far from limited to fungal infections: “In general, a ketogenic diet is useful for treating bacterial and viral infections, because bacteria and viruses don’t have mitochondria, so a ketogenic diet starves them of their favorite fuel source, glucose” (Paleo Leap, Infections and Chronic Disorders). Ketosis, in being anti-inflammatory, has been used to treat gout and autoimmune disorders, along with mood disorders that often include brain inflammation.
The inflammatory pathway, of course, is closely linked to the immune system. Reducing inflammation is part of complex processes in the body. Opposite of the keto diet, a high-carb diet produces inflammatory markers that suppress the immune system and so compromises prevention of and healing from infections. Indeed, obese and diabetic patients are hospitalized more often and get worse symptoms of influenza infections (flu).
But it’s not merely the reduction of inflammation. As an energy source, ketones are preferred over glucose by immune cells that fight infections, although maybe some bacteria can use ketones. It’s a similar pattern with cancer, in which ketosis can help prevent some cancers from growing in the early stages, but the danger is once established particular kinds of cancers can adapt to using ketones. So, it isn’t as simple as ketosis curing everything, even if it is a overall effective preventative measure in maintaining immunological health and general health.
What interests us most here are infections. Let’s look further at the flu. One study gave mice an influenza infection (Emily L. Goldberg et al, Ketogenic diet activates protective γδ T cell responses against influenza virus infection; Abby Olena, Keto Diet Protects Mice from Flu). The mice were on different diets. All of those on standard chow died, but half survived on the keto diet. To determine causes, other mice were put on a diet high in both fat and carbs while others were given exogenous ketones, but these mice also died. It wasn’t only the fat or the ketones in the keto diet. Something about fat metabolism seems to have been key, that is to say not only fat and not only the ketones but something about how fat is turned into ketones during ketosis, although some speculate that protein restriction might have been important.
The researchers were able to pinpoint the mechanisms for fighting off the infection. Turning fat into ketones allows the gamma delta subset of T cells in the lungs to be activated in response to influenza. This was unexpected as they haven’t been a focus in previous research. These T cells increase mucus production in epithelial cells in the lungs. This creates a protective barrier that traps the virus and allows it to be coughed up. At the same time, the keto diet blocks the production of inflammasones, multiunit protein complexes activated by the immune system. This reduces the inflammation that can harm the lungs. This relates to the T cell stimulation.
From an anecdotal perspective, here is an interesting account: “I have been undergoing a metabolic reset to begin the year. I have been low carb/keto on and off for the last 4.5 years and hop in and out of ketosis for short periods of time when it benefits me or when my body is telling me I need to. Right now, I decided to spend the first 6 weeks of 2018 in ketosis. I check my numbers every morning and have consistently been between 1.2 and 2.2 mmol/L. I contracted a virus two days ago (it was not influenza but I caught something) and my ketone levels shot through the roof. Yesterday morning I was at 5.2 (first morning of being sick) and this morning I was at 5.8 (although now I am in a fasted state as I have decided to fast through this virus.)” (bluesy2, Keto Levels with Virus/Flu).
Maybe that is a normal response for someone in ketosis. The mouse study suggests there is something about the process itself in producing ketones that is involved in the T cell stimulation. The ketones also might have a benefit for other reasons, but the process of fat oxidation or something related to it might be the actual trigger. In this case, the ketone levels are an indicator of what is going on, that the immune system is fully engaged. The important point, though, is this only happens in a ketogenic state and it has much to do with basil metabolic rate and body temperature regulation.
Nearly 150 years ago, a German physician analyzed a million temperatures from 25,000 patients and concluded that normal human-body temperature is 98.6 degrees Fahrenheit.
That standard has been published in numerous medical texts and helped generations of parents judge the gravity of a child’s illness.
But at least two dozen modern studies have concluded the number is too high.
The findings have prompted speculation that the pioneering analysis published in 1869 by Carl Reinhold August Wunderlich was flawed.
Or was it?
In a new study, researchers from Stanford University argue that Wunderlich’s number was correct at the time but is no longer accurate because the human body has changed.
Today, they say, the average normal human-body temperature is closer to 97.5 degrees Fahrenheit.
“That would be a huge drop for a population,” said Philip Mackowiak, emeritus professor of medicine at the University of Maryland School of Medicine and editor of the book “Fever: Basic Mechanisms and Management.”
Body temperature is a crude proxy for metabolic rate, and if it has fallen, it could offer a clue about other physiological changes that have occurred over time.
“People are taller, fatter and live longer, and we don’t really understand why all those things have happened,” said Julie Parsonnet, who specializes in infectious diseases at Stanford and is senior author of the paper. “Temperature is linked to all those things. The question is which is driving the others.” […]
Overall, temperatures of the Civil War veterans were higher than measurements taken in the 1970s, and, in turn, those measurements were higher than those collected in the 2000s.
“Two things impressed me,” Dr. Parsonnet said. “The magnitude of the change and that temperature has continued to decline at the same rate.” […]
“Wunderlich did a brilliant job,” Dr. Parsonnet said, “but people who walked into his office had tuberculosis, they had dysentery, they had bone infections that had festered their entire lives, they were exposed to infectious diseases we’ve never seen.”
For his study, he did try to measure the temperatures of healthy people, she said, but even so, life expectancy at the time was 38 years, and chronic infections such as gum disease and syphilis afflicted large portions of the population. Dr. Parsonnet suspects inflammation caused by those and other persistent maladies explains the temperature documented by Wunderlich and that a population-level change in inflammation is the most plausible explanation for a decrease in temperature.
This substantive and continuing shift in body temperature—a marker for metabolic rate—provides a framework for understanding changes in human health and longevity over 157 years.
Very interesting paper. Well done. However, a hypothesis still remains to be tested. The decline of the infectious burden well corresponds to the decrease of the body temperatures between the XIXth and XXth century cohorts (UAVCW vs NHANES), but it does not explain the further and much more important reduction between the XXth and XXIth century studies (NHANES vs STRIDE); see Figure 1 (distributions gap) and Figure 1 / Supp 1 (curve gap), where the impact seems to be twice as large between 1971 and 2007 than between 1860 and 1971.
Besides regulating the ambient room temperature (through winter heating in the early XXth century and summer air conditioning in the late XXth and early XXIth century), another hypothesis was not discussed here ie the significant decline in daily physical activity, one of the primary drivers of physiological heat production.
Regular physical activity alters core temperature even hours after exercising; 5h of moderate intensity exercise (60% VO2max) also increase the resting heart rate and metabolic rate during the following hours and night with a sympathetic nervous system activated until the next morning (Mischler, 2003) and higher body temperatures measured among the most active individuals (Aoyagi, 2018).
As in most developed countries, the North American people – who worked hard in agriculture or industry during the XIXth century – lost their active daily habits. We are now spending hours, motionless in front of our screens, and most of our adolescents follow this unsettling trend (Twenge, 2019); such an effect on temperature and energy regulation should also be considered as it may have an important impact on the potential progresses of their life expectancy and life duration.
Jean-François Toussaint Université de Paris, Head IRMES
Mischler I, et al. Prolonged Daytime Exercise Repeated Over 4 Days Increases Sleeping Heart Rate and Metabolic Rate. Can J Appl Physiol. Aug 2003; 28 (4): 616-29 DOI: 10.1139/h03-047
Aoyagi Y, et al. Objectively measured habitual physical activity and sleep-related phenomena in 1645 people aged 1–91 years: The Nakanojo Community Study. Prev Med Rep. 2018; 11: 180-6 DOI: 10.1016/j.pmedr.2018.06.013
Twenge JM, et al. Trends in U.S. Adolescents’ media use, 1976–2016: The rise of digital media, the decline of TV, and the (near) demise of print. Psychol Pop Media Cult, 2019; 8(4): 329-45. DOI: 10.1037/ppm0000203
Nita Jain (edited Feb 15) Feb 14
Although there are many factors that influence resting metabolic rate, change in the population-level of inflammation seems the most plausible explanation for the observed decrease in temperature over time.
Reduced body temperature measurements may also be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, the authors mention that a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.
Rosenberg et al. reported that heat provision is an under-appreciated contribution of microbiota to hosts. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.
Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus.
Although heat production by symbiotic microbes appears to be a general phenomenon observed in both plants and animals, its significance in humans has hardly been studied. Nonetheless, the concomitant loss of diversity and heat contribution of the gut microbiota may have far-reaching implications for host metabolic health.
I would like to propose that our reduced body temperature measurements may be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.
Heat provision is an under-appreciated contribution of microbiota to hosts. Microbes produce heat as a byproduct when breaking down dietary substrates and creating cell materials. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.
Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus. The relationship also appears to be bi-directional, as host tolerance to cold has been shown to drive changes in the gut microbiomes of blue tilapia.
Heat production in goats was found to decrease by about 50% after emptying the rumen to values similar to what would be expected during a fasting state. These observations suggest that during fasting, microbial fermentation is responsible for half of the animal’s heat production while host metabolism accounts for the other half. The warming effect of microbes has also been reported in plants. Yeast populations residing in floral nectar release heat when breaking down sugar, increasing nectar temperature and modifying the internal flower microenvironment.
Silas Weir Mitchell was a famous doctor that first learned about neurological disease during his service in the American Civil War. He is most well known for his views on hysteria and neurasthenia, but he was considered an expert on other neurological conditions as well. One area he was respected in was the treatment of epilepsy, for which he preferred to use drugs. “Despite the prevalent views on lifestyle modification as a treatment for epilepsy during this time period, as well as Mitchell’s own development of the “rest cure” for certain disease states, he was not a proponent of these types of interventions for epilepsy” (David B. Burkholder & Christopher J. Boes, Silas Weir Mitchell on Epilepsy Therapy in the Late 19th to Early 20th Centuries).
From his writings on neurasthenia, he had articulated a common view of this disease in terms of nerves and energy, libido and sexuality. And he applied a similar understanding to epilepsy: “Still, in Mitchell’s first discussion of amyl nitrite as an abortive therapy, he clearly agreed with a common thought of the day by attributing the patient’s epilepsy to sexual vices, stating he had partaken in “…great excess, and that the punishment was distinctly born of the offence” (Burkholder & Boes). But in 1912, he questioned his prior causal explanations, having had written that, “It is conceivable that in nerve centres normal or abnormal substances may accumulate until they result in irritative symptoms and discharges of neural energy. But how then could this sequence be arrested by a mere sensory stimulation, like a ligature on an arm, or by abruptly dilating the cerebral vessels with amyl? The explosions would only be put off for the minute; the activating poison would remain.” These doubts were expressed when in his early 80s, after a long career in medicine.
Still, he never suspected any role to be played by diet or lifestyle. This is strange, considering his professional expertise in his having used diet and lifestyle for those suffering from neurasthenia, a neurological disorder like epilepsy. Even in his theorizing, the factors he considered for both overlapped to some degree in specific details and through general framework. Yet for epilepsy, he couldn’t somehow make a connection in the same way between physical health and mental health. Meanwhile, others were attempting to make such connections. There was much experimentation going on with epilepsy, including dietary protocols.
William Spratling, in Epilepsy and Its Treatment (1904), partly shared Mitchell’s assessment in writing that, “have been unable to determine that different foods have any specific effect on epilepsy itself beyond that which they have on the organism in general.” That didn’t stop him from having suggested a mixed/balanced diet that, though not having excluded carbohydrates, did tell epileptics to eat moderately and slowly while avoiding pastries, alcohol and over-sweetened drinks. In certain extreme cases, he went even further by asserting that, “Foods should be in liquid form and highly nutritious from the start. Various preparations of milk, eggs, and beef extracts may be given; but plain peptonized milk is by far the best food of all. It should be given often and in small amounts.”
Spratling’s professional advice for treatment in some cases potentially could have been ketogenic, if not in a systematic manner. The same might’ve also been true of Sir J. Russell Reynolds’ even earlier 1862 epileptic protocol of avoiding “Salted meats, pastry, preserved vegetables, and cheese” (Epilepsy: Its Symptoms, Treatment, and Relation to Other Chronic Convulsive Diseases). Besides openly advocated low-carb diets like that of William Banting, many scientific experts, medical practitioners, public intellectuals and popular writers during that era flirted around the edges of restricting starches and sugar for various reason, though not to treat epilepsy. That is significant, since the average diet was already far lower in carbohydrates than what was seen in the following generations. Some patients would have found relief from seizures through ketosis without realizing what had helped them. The seeming randomness of who did and who did not experience improvements had to have been frustrating to doctors of the time.
In 1914, two years after having fallen into self-questioning, Mitchell would die without having learned of an effective treatment. Only a few years later in 1921, there was the discovery of dietary ketosis (Rollin Woodyatt) and the discovery of the medical use of a ketogenic diet for epileptic seizures (Russel Wilder), although ketosis was used for this purpose through fasting as far back as 500 BC. Despite this failure, like so many others, he approached the territory of a ketogenic diet while entirely missing it, such as in his recommendations of meat and dairy for neurasthenics which potentially could’ve put a patient into a state of ketosis. He came so close, though. After graduating from medical college in 1851, he moved to Paris and spent a year studying under Claude Bernard. About a decade later, the British Dr. William Harvey heard Bernard speak about the relationship between diet and diabetes, and this information he used to formulate a low-carb diet for his patient William Banting to lose weight. Banting then popularized this diet, but at that point it had already been in use by others going back to the 1790s.
During Mitchell’s lifetime, most Americans would have still followed a diet where carbohydrates were a small portion of meals and a small percentage of calories. It’s probable that the majority of the population during the 19th century was regularly in a state of ketosis, as the common diet back then consisted of mostly animal foods — what Nina Teicholz describes as the “meat-and-butter-gorging eighteenth and nineteenth centuries” (The Big Fat Surprise; see context of quote in Malnourished Americans). Mitchell himself might have experienced ketosis at different points in his life without realizing it. This wouldn’t have been an unusual thing for most of human existence, if not from a low-carb diet then from caloric restriction, intermittent eating, and fasting — ketosis isn’t exactly hard to achieve in a traditional setting. For example, it used to be standard for Americans to eat only one meal a day (Abigail Carroll, Three Squares) and that was in the context of a labor-intensive rural lifestyle. Sugary cereals, Pop-Tarts, etc were not available for breakfast. And snacking all day on crackers, chips, and cookies simply was not an option.
It’s interesting to note that meat-and-butter or rather meat-and-milk was what Mitchell, working as a doctor in the 19th century, told his neurasthenic patients to eat. But for unexplained reasons, he didn’t advise the same or a similar eating pattern to his epileptic patients. Low-carb and animal-based dieting was popular in his lifetime and was used by many doctors for various conditions, often for obesity but far from limited to that. It’s odd that no one made the connection of the ancient practice of fasting for epileptic seizures with the 19th century practice of potentially ketogenic diets. No one managed to figure this out until the 1920s and not for a lack of experimentation with diverse alimentary regimens. Then when it was finally discovered, after a short period of research, it was mostly forgotten about again for another three-quarters of a century. Yet even now drugs remain the primary treatment for epilepsy, despite ketosis being the most effective, not to mention safest, treatment; and, if ketosis is the normal state of physiological functioning, we might call it a cure for many people.
Humans are born into ketosis and will remain in ketosis while breastfeeding, whether or not the mother is in ketosis. For hunter-gatherers, breastfeeding commonly lasts for the first couple of years, the most important time for growth and development, especially the brain. So, evolution has created ketosis as a protected state for infancy. But it goes far beyond that.
Unlike other carnivores, evidence indicates humans remain in ketosis even while eating higher amounts of protein. We are capable of gluconeogenesis, a necessary function turning protein into glucose, but we don’t so heavily rely upon it. Under normal evolutionary conditions, humans would spend much, probably most, of their time in ketosis. No other species so easily goes into and remains in ketosis. The human brain, in fact, preferentially uses ketones. And it is probably because of our large, energy-hungry brains that we are so ketosis-prone in the first place. That is likely why babies are born so fat, so that they can have a ready supply of ketones.
It was a trade-off of the human brain growing larger as the gut grew smaller, as it requires a lot of energy to digest plant matter and that energy was needed for the evolutionary development of a larger brain. So, humans turned to eating fat from animals, to replace a digestive system needed to break down fibrous plants to produce fat. Herbivores are forced to spend all day eating vast amounts of plant matter and it is energy intensive work. Ketosis freed humans from this activity and simultaneously freed up immense energy to be used for other purposes, specifically greater neurocognitive functioning and higher thought.
The benefits and advantages of ketosis are amazingly numerous. It protects against or improves epilepsy, along with other neurocognitive disorders and mental illnesses, from bipolar disorder to ADHD, not to mention much more serious diseases such as Alzheimer’s. It also shows benefit for autoimmune disorders, cancer, and trauma. There is no health condition I can think of, besides type 1 diabetes, that would be worsened by ketosis. And if one were on a ketogenic diet in the first place, one would be unlikely to develop type 1 diabetes and so that is moot.
One would be forgiven for thinking that ketosis might be the natural state of the human species. Still, whatever one thinks of evolutionary arguments, no one can deny that ketosis is a far healthier state to be in, or at least there is no evidence to the contrary. That said, one doesn’t have to be in constant ketosis to see many of these benefits. Even in epilepsy, after a period of healing, some patients can stop a ketogenic diet and stay free of seizures. There are many mechanisms for this healing power of ketosis, such as the related autophagy, but the general anti-inflammatory effect might be more important considering inflammation is found in so many diseases.
I’d love to see this question approached systematically, but the survey does at least suggest that protein levels above our minimum needs based on positive nitrogen balance still support ketosis. […]
Obligate carnivores are always on very low carb diets, so you might think they are always in ketosis, but that’s not at all the case. In fact they are specialised at gluconeogenesis, that is, getting all their energy needs met by converting protein into glucose. Protein needs tend to be high.
Cats have much higher protein needs than omnivores and surprisingly, they don’t adapt well to reduced protein or fasting [Cen2002]. They don’t seem to have good mechanisms to compensate for the various amino acid and vitamin deficiencies that develop, so they suffer from ammonia toxicity, methylation problems, and oxidative stress. They do produce ketones fasted, but they don’t seem to use them in a productive way. and they actually accumulate fatty acids in the liver when fasted; the opposite of what humans do, Because they are still producing glucose, they become like human type two diabetics.
Dolphins are particularly interesting because they have really large brains, and they eat a diet that would be expected to be ketogenic if fed to humans. However, they don’t seem to even generate ketone at all, not even when fasting. Instead, they ramp up gluconeogenesis [Rid2013].
They keep their bodies and their brains going by increased glucose.
When faced with this observation that humans use ketosis even when they don’t have to for glucose production, one obviously wonders how this happens from a mechanistic standpoint. I have never seen the question raised in the literature, let alone answered. If I were to take a guess, I’d say it probably happens somewhere in this process.
CPT1A is a kind of gatekeeper, transporting fatty acids into the mitochondria for oxidation. This is normally a necessary step in the creation of ketone bodies. The coenzyme malonyl-CoA inhibits CPT1A [Fos2004]. The functional reason it does that is because malonyl-CoA is a direct result of glucose oxidation and is on the path to de novo lipogenesis. It could be inefficient to be both generating fat and oxidizing it. So this is a convenient signal to slow entry of fat into the mitochondria.
However, its action is not stictly linear. It uses hysteresis. Hysteresis is a way of preventing thrashing back and forth between two states at the threshold of their switch. For example, if you set your thermostat to 20°C, you would not want the heater to be turned on when the temperature drops to 19.999 and turned off again at 20. This would result in constant switching. Instead, a thermostat waits until the temperature drops a little lower before activating the heater, and heats it a little more than required before deactivating it.
Hysteresis is implemented in CPT1A by its becoming insensitive to malonyl-CoA when levels of it are low [Ont1980], [Bre1981], [Gra1988], [Gre2009], [Akk2009]. That means that once CPT1A becomes very active in transporting fatty acids, it takes time before the presence of malonyl-CoA will inhibit CPT1A at full strength again. That means that fluxuations in glucose oxidation, or small, transient increases in glucose oxidation don’t disturb the burning of fatty acids or the production of ketones.
It could be the case that humans develop more insensitivity to malonyl-CoA under ketosis than other species do, allowing them to metabolise more protein without disturbing ketosis. Among humans, this is case in populations such as some Inuit with the Artic variant of CPT1A. That mutation slows down CPT1A activity immensely. This was permitted by their diet which was very high in polyunsaturated fats from sea mammals. Polyunsaturated fats upregulate fatty acid oxidation by a large proportion compared to saturated fats [Cun2002], [Fra2003], [Fue2004], so this mutation would not necessarily have been disruptive of ketosis in that population when eating their natural diet [Lem2012]. But a second effect of the same gene further decreases the sensitivity of CPT1A to inhibition by malonyl-CoA. That means they are less likely to be knocked out of ketosis by high protein intake. […]
But it’s not just epilepsy that ketosis is good for. Epilepsy is just the condition with the most research, and the widest acknowledgment.
Other conditions for which at least some evidence supports improvement via a ketogenic diet include neurological disabilities in cognition and motor control [Sta2012]; the benefit here may have to do with the proper maintenance of brain structures such as myelination (Recall phases: tear down damage, rebuild)
Survival after brain damage, the hypoxia of stroke or blows to the head is improved in animal models [Sta2012]. There is even animal evidence that brain damage due to nerve gas is largely mitigated by being in a state of ketosis during the insult [Lan2011]. Again, this suggests a structural support and resilience provided by a ketogenic metabolism. Resilience comes in part from not being as susceptible to damage in the first place, and that could be from reduced oxidative stress when using ketones for fuel.
Ketogenic diets as a treatment for cancer are controversial, but some of the best evidence in support of it comes from glioblastomas. See e.g. [Zuc2010], [Sch2012]. This could be due mostly to the hypoglycemia stalling the rate of tumour development.
And to venture into an area less well studied, but of critical importance given the epidemic that would be more apparent were it less taboo, there is preliminary evidence in the form of case studies that ketogenic diets may be promising treatments for many psychiatric illnesses too, for example, [Kra2009], [Phe2012]. Given that anticonvulsants are also used to treat bipolar, and the solid results of ketogenic diets on epilepsy, this may not be surprising. Additionally, the enhanced availability of AA and DHA may play a crucial role Because these fatty acids are critical for the brain, and dysregulation in their flux has been associated with bipolar disorder and schizophrenia. See e.g. [McN2008] and [Pee1996].
I would almost like to call a ketogenic diet a brain-growth mimicking diet.
The question of how and why humans are so ketosis prone may lead to interesting new insights about us as a species. We seem to avoid giving up ketosis as long as possible. only halting it when we take in so much glucose exogenously that we have to store it.
It seems likely that it facilitated the evolution of our brains, that organ that makes us so different from other animals that we sometimes forget we are animals.
A common viewpoint among both conventional and alternative health practitioners is that fiber is good for you. Not only good but necessary. Millie Barnes, as an example, identifies her expertise as a chef and nutrition coach. She apparently comes from a functional medicine approach, common among those advocating traditional foods diet that is plant-based and fiber-heavy (another example is Dr. Terry Wahls).
Barnes wrote a post about fiber and short-chain fatty acids (SCFAs), Why Short-Chain Fatty Acids Are Key To Gut & Overall Health, Plus How To Get More — her position is typical: “SCFAs are produced when bacteria—the good kind—ferment fiber in the gut, thereby providing your body with energy, keeping your metabolism humming, and even thwarting a wide range of digestive disorders.” There is nothing necessarily wrong about this position, although the scientific evidence is severely limited and highly contested. The problem is in treating the science as settled.
I’m not against fiber. I eat some high-fiber vegetables, especially fermented, along with other cultured foods. I used to eat even more fiber and vegetables, back when I was doing a paleo diet. And there was benefits to it, at least in comparison to my prior high-carb diet of processed foods. But I’ve also tried the carnivore diet and felt freaking awesome! I never realized how hard to digest are most plant foods (Like water fasts, meat fasts are good for health.).
I’m much more cautious about the plants and hence plant substances, including toxins and anti-nutrients, I allow into my body. Still, I have nothing against plants on general principle and I’m persuaded by Siim Land’s argument for hormesis and antifragility, that is to say beneficial stress (in case you’re interested, there is an intriguing scientific paper to check out: Hagen, Roulette & Sullivan, Explaining Human Recreational Use of ‘pesticides’). I now think of plants as more medicine than food, but nonetheless quite useful as medicine.
SCFAs are a complex topic, as is the microbiome of which we know little. As aside note, while some SCFAs (acetate and butyrate) are ketogenic, others (propionate) is glycogenic. They play an important role in health. That much we can agree on. What is less understood or at least less acknowledged is that SCFAs can come from other sources besides fiber. Butyrate, for example, is found in dairy fat. The cow eats the fiber and makes the butyrate for us.
So butyrate deficiency shouldn’t be a problem for anyone on a reasonably healthy diet, plant-based or animal-based. That is assuming they are getting plenty of high-fat dairy, pasture-raised all the better, and most Westerners tend to consume tons of dairy. As for myself, I get plenty of ghee (clarified butter) which means I’m probably fine on butyrate levels. By the way, my preferred mode of ghee delivery is through coffee and tea, what has been made famous as Dave Asprey’s Bulletproof Coffee, but he got the idea from a Tibetan woman who served him tea with yak butter. This maybe is not such a foreign practice. My mother recalls her Kentuckiana grandmother regularly pouring coffee over butter, although she also mixed in saltine crackers — that latter part probably less traditional and certainly not low-carb.
To get back to our discussion of SCFAs, I’m not as familiar with acetate, but apparently you can get it from apple cider vinegar (ACV), something I also take on a daily basis. I assume that the microbes in the ACV produced the acetate and so bypasses the need of the microbes in your own gut to do the work. No fiber is required, at least not in the diet. Furthermore, one can get acetate from ketosis as well and ketosis is my preferred state. Acetate/acetoacetate sometimes is what is measured for ketone levels. Some amino acids such as leucine and lysine can be converted into acetoacetate through fatty acid synthesis. Acetoacetate then is reduced to beta-hydroxybutyrate and the latter gets turned into acetone and acetate.
Now on to propionate, even more fascinating. It is a food additive that the modern person is getting overdosed on and appears to be a causal factor behind such conditions as autism (The Agricultural Mind). Those on the autistic level tend to have high levels of the bacteria that produce propionate and tend to crave foods that are high in it. Rodents injected with propionate express autistic-like behaviors. And those on the autistic spectrum show decreased behavioral problems when propionate is removed from their diet or when an antibiotic kills off some of their microbiome. SCFAs are a key part of a health diet, but they are powerful substances not to be taken lightly. They potentially can do harm as well.
As a last comment, no studies have been done on the microbiome of those on a carnivore diet or near-carnivore diet such as the Inuit. Heck, there has been no research even on a more general healthy omnivore diet including meat — the studies on the Standard American Diet (SAD) don’t count. But from what we do know about biology in general, it appears humans have multiple pathways of producing or obtaining SCFAs. The microbiome, in particular, is probably extremely adaptable to a wide variety of diets that were necessary during evolution (e.g., the microbiome of some hunter-gathers completely alters from season to season). Dr. Paul Saladino has talked a lot about this kind of thing — take what he had to say in an interview with Geoffrey Woo (Nose-to-Tail Carnivore Diet: Organ Meat, TMAO Implications, & Reaching Ketosis ft. Dr. Paul Saladino; & video):
“There are many bacteria which can metabolize fat, protein and animal-based collagen. That’s the thing I think that most people are missing. That our gut microbiome can shift. There’s a study where they put people on what I would consider to be a very poor version of a carnivorous diet and they compare it a plant-based diet. What they see is a divergence in the gut flora within a week. The animal-based eater, again, it’s not an ideal diet. The animal-based eaters had more bile acid tolerant organisms and more organisms to ferment fat and protein. They made isobutyrate and they made acetate and they made propionate as short chain fatty acids.
“The plant-based eaters made butyrate as a short chain fatty acid and had different colonic and small intestinal microflora. The investigators in that study jumped to the conclusion. Look, we know what’s going on with the gut because they have this organism. What’s worthy of biophilia or they don’t have this organism. They clearly have an unhealthy gut microbiome and I think that is an extrapolation. We do not know that. Clinically, nobody is assaying anything clinically in that study. They didn’t do inflammatory markers. They didn’t follow those people moving forward. It was almost like a setup. They were just trying to prove that these bile acid tolerant organisms would show up when they gave people a bunch of foods, which promote the formation of bile.”
Dr. Paul Saladino was on the paleo diet before trying carnivore, but Dr. Will Cole went from vegetarian to a more paleo-style diet. Dr. Cole wrote a book, Ketotarian, about how to do a plant-based keto and so he is right in line with the likes of Millie Barnes. That didn’t stop him, in an interview with Vanessa Spina, from pointing to evidence that a high-fiber diet may not be necessary, even going so far as to mention the carnivore diet:
“Because we have an epidemic of gut problems in the United States and around the world and Europe as well that this is going take time. Sometimes some people can have it right out of the gate. Some people can’t. It’s important to know what’s right for your body and what’s not right for your body. But as you heal, what you used to not be able to have the goal is to be able to reintroduce these things as your body heals.
“So the carnivore diet, for example, it’s the ultimate elimination die because it’s removing a lot of these fibers. But the goal isn’t to be carnivorous forever and ever, even though maybe some people would prefer that. But the goal is to use something like that to drive down this inflammatory cascade to bring things back in, as long as it’s nutrient-dense. And there are studies to show like the Hadza tribe in Tanzania they have good bacterial diversity during those months where they are eating less vegetables. But they’re eating more raw meat or getting like drinking blood and doing things that most people that are on the carnivore diet in the West are not doing today.
“So there are other there are other ways to get back to our diversity beyond fiber. I would just say it is the most common, most well researched way to get back to our diversity.”
Vanessa Spina, in that interview, then added an important point, not all prebiotics are fiber or necessarily come from plants at all: “I found this list of prebiotic foods that were non-carbohydrate that included cellulose, cartilage, collagen, fructooligosaccharides, glucosamine, rabbit bone, hair, skin, glucose. There’s a bunch of things that are all — there’s also casein. But these tend to be some of the foods that actually have some of the highest prebiotic content. So it’s interesting, I think, if someone has less tolerance for fiber, they can also explore some of these other product prebiotics.” That is something I never hear anyone talk about.
This might explain why so many people do so well on a carnivore diet. They are still getting prebiotics. And we know those on entirely or mostly meat diets retain functioning microbiomes. But there has been so few scientists looking into this.
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3/2/20 – The first video below is a quick overview by Dr. Paul Saladino. And for more detail, see the second video (time mark 77:00-84:00) where he talks with Dr. Joseph Mercola. But to get his full argument, you’ll have to read his book that just came out, The Carnivore Code.
An interesting side discussion formed over the issue of fasting, ketosis, and autophagy. I must admit that my understanding was always a big hazy about the relationship between the latter two, both of which can be results of fasting. Despite common factors involved in both processes, I didn’t think there was a causal link.
My number one reason for drinking black coffee in the morning is to not interfere with IF, which cream does.
Rob W. James
The benefits of IF are overstated in my opinion. Most of the benefits come from calorie restriction, which a splash of milk isn’t going to make much difference too
The main benefit is clearing out damaged cells. It’s an anti-aging hack. You lose that benefit by breaking fast.
Coffee is still a xenobiotic, you are breaking a fast by drinking coffee and you are breaking a fast by drinking 2 tbsp cream. Regardless, autophagy is stimulated via ketogenesis, neither coffee nor cream Inhibit ketogenesis. https://www.ncbi.nlm.nih.gov/m/pubmed/26303508/
Autophagy doesn’t really hit significant levels until 48hrs though. So benefits are mininal if any during IF
This is not to say autphagy isn’t present until 48hrs, rather it hits full scale around 48hrs.
And if autophagy is why you “fast” an extended fast.. past a normal IF, is necessary to achieve what you’re after.
Autophagy happens downstream via BHB regardless, when you are on a ketogenic diet you have these elevated BHB levels at that point for long periods, where fasting takes 48 hours to get you where a Keto diet keeps you
So if you are IF and eating plenty of carbs I totally agree. It takes longer to get to the higher BHB levels because BHB and carbohydrate are inversely proportional
This is such an important point I don’t see anyone talking about.
That’s why I was talking about fasting a few weeks ago.
No one is talking about needing to be in ketosis to be fasted. So most of these guys doing IF are basically just TRE.. Which is a good enough reason to IF
The contents creators aren’t talking about this though and selling false promises of autophagy and fountain of youth.
I read an article about IF that showed signs of arteriole smoothing with a 16:8 diet. If this is true then autophagy at 48 hours isn’t necessary for sole benefit and daily fasting does have vasculature anti-aging properties.
There are benefits for every hour you fast according to Salk institute researchers . What we will need to see is calorie matched studies between TRE/ IF and CR. But to say there is zero additional benefit if you are healthy is wrong. The amount of benefit is arguable
Beta hydroxy butyrate is an HDAC inhibitor and downstream via that action increases autophagy. Cream doesn’t matter. The longer you fast for the higher the bhb. Or a ketogenic diet can increase the bhb. Ketogenic diet mimics fasting and vice Versa.
They are not synonymous. Of course, however elevated BHB levels are a common thread and a little cream in your coffee is not going to matter at all in that regard.
Myriads research over the last two years and mixing more underway showing the mechanisms by which you still see these benefits from BHB weather or not you fast. I am compiling all the links and will sends them over when done if you would like
Why do we hear so little about the ketogenic diet? At this point, there has probably been thousands of studies done on it going back a century. In the 1920s, it was first demonstrated effective as a medical treatment for epileptic seizures. And since then, it has been studied with numerous other health conditions, especially for weight loss in obesity.
The results are often dramatic. Dr. Terry Wahls, in using a ketogenic diet in a clinical study, was the first to prove that multiple sclerosis could be put into remission. Dr. Dale Bredesen, also through a ketogenic diet in a clinical study, was able to reverse Alzheimer’s which has never before been accomplished, in spite of all the massive funding that has gone into pharmaceuticals.
This connection is also seen in how depressives have higher rates of diabetes and diabetics have higher rates of depression, and to emphasize this point those with both conditions tend to have more severe depression. Unsurprisingly, the keto diet has been useful for treating depression.
It likewise has been used to treat other neurocongnitive conditions, including major psychiatric disorders like bipolar disorder and schizophrenia, arguably the same. Lessening of symptoms has been seen with schizophrenics on a keto diet (Chris Palmer, Chronic Schizophrenia Put Into Remission Without Medication). And in one case, 53 years of schizophrenia went entirely into remission and remained in remission for years following. That patient, after doing a keto diet under the care of Dr. Eric Westman in order to lose weight, found she was able to stop taking all psychiatric medications and became independent in no longer needing assistance to do daily tasks.
Now Dr. Stephen Phinney has done the same thing with diabetes, although less surprising as ketogenic research on diabetes goes back several generations. What has been the response from government health officials, non-profit health organizations, and mainstream doctors? A combination of silence and fear-mongering. A revolution in medicine is happening and few seem to be paying attention. But think how many lives could have been saved and improved, if the promising research on the keto diet hadn’t been shut down earlier last century.
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Ketones are fascinating. They are far more than an alternative or, if you prefer, primary fuel in the body. The energy produced is different as well, in being more efficient and cleaner. Furthermore, they don’t merely shift metabolism and can promote effortless fat-loss. Ketones act like master hormones and alter gene expression. This is why they are so powerful in reversing and curing serious diseases. But it isn’t miraculous, as it is entirely natural. This is how the body is supposed to function.
After Inkinen’s pre-diabetes diagnosis in 2012, he spent the next few years researching the disease and treatments and ultimately teaming up with Stephen Phinney, MD, Ph.D in 2014 to form Virta Health, a research and virtual medical clinic whose mission is to reverse type 2 diabetes.
The results are impressive. At the end of two years, the keto group saw incredible improvements: 55% were able to reverse their diabetes and stop all medications except Metformin, and 18.5% were able to achieve remission. That is, they were both officially out of the diabetic range and off of all diabetes medications. Plus they maintained that state for at least one year.
The keto dieters were also able to lose weight (an average of 12% of body weight), reduce their dependence on insulin — dosages dropped 81% — and reduce triglycerides, inflammation and other markers for metabolic syndrome.
By contrast, just 10.5% of the participants in the control group were able to reverse their diabetes, and none was able to achieve full remission.
The control group also gained an average of 5% of their body weight, had a 13% increase in insulin dosages, and saw only modest improvements in triglycerides, inflammation and metabolic syndrome markers.
It’s also worth noting that this research is entirely self-funded — Virta receives its funding from venture capital investors.
Last week, we saw the news that the world’s largest diabetes organizations, including the International Diabetes Federation, the American Diabetes Association, the Chinese Diabetes Society, and Diabetes India, are embracing bariatric surgery as a radical new approach to treating type-2 diabetes. According to these experts, surgery should be the standard protocol for many patients.
At the same time, these experts are becoming increasingly dismissive of diet and lifestyle approaches to reversing type-2 diabetes. The crux of the problem is that “the experts” recommend a low-fat, higher-carbohydrate approach, which simply doesn’t cut the mustard when compared to low-carb, higher-fat approaches.
In the information era, however, the truth always comes out.
Today, The Times is reporting on what they are referring to as “an online revolt by patients.” Diabetes.co.uk, a health organization that opposes the official dietary guidelines for diabetes treatment, launched a study, which included over 120,000 participants, the majority of whom suffer from weight related type-2 diabetes.
These people ate low-carb diets for 10 weeks, in defiance of the UK government’s Eatwell Guidelines, which mimic official US guidelines.
Over 70% of participants lost weight and improved their blood glucose levels.
“The results from the low-carb plan have been impressive and this is a solution that is clearly working for people with type 2 diabetes,” said Arjun Panesar, chief executive officer of diabetes.org.uk
Aging in man is accompanied by deterioration of a number of systems. Most notable are a gradual increase in blood sugar and blood lipids, increased narrowing of blood vessels, an increase in the incidence of malignancies, the deterioration and loss of elasticity in skin, loss of muscular strength and physiological exercise performance, deterioration of memory and cognitive performance, and in males decreases in erectile function. Many aging‐induced changes, such as the incidence of malignancies in mice 82, the increases in blood glucose and insulin caused by insulin resistance 39, 78, and the muscular weakness have been shown to be decreased by the metabolism of ketone bodies 18, 83, a normal metabolite produced from fatty acids by liver during periods of prolonged fasting or caloric restriction 12.
The unique ability of ketone bodies to supply energy to brain during periods of impairment of glucose metabolism make ketosis an effective treatment for a number of neurological conditions which are currently without effective therapies. Impairment of cognitive function has also been shown to be improved by the metabolism of ketone bodies 84. Additionally, Alzheimer’s disease, the major cause of which is aging 20 can be improved clinically by the induction of mild ketosis in a mouse model of the disease 85 and in humans 86. Ketosis also improves function in Parkinson’s disease 87 which is thought to be largely caused by mitochondrial free radical damage 19, 88. Ketone bodies are also useful in ameliorating the symptoms of amyotrophic lateral sclerosis 89. It is also recognized that ketosis could have important therapeutic applications in a wide variety of other diseases 90 including Glut 1 deficiency, type I diabetes 91, obesity 78, 92, and insulin resistance 20, 39, 93, and diseases of diverse etiology 90.
In addition to ameliorating a number of diseases associated with aging, the general deterioration of cellular systems independent of specific disease seems related to ROS toxicity and the inability to combat it. In contrast increases in life span occur across a number of species with a reduction in function of the IIS pathway and/or an activation of the FOXO transcription factors, inducing expression of the enzymes required for free radical detoxification (Figs. 1 and 2). In C. elegans, these results have been accomplished using RNA interference or mutant animals. Similar changes should be able to be achieved in higher animals, including humans, by the administration of d‐βHB itself or its esters.
In summary, decreased signaling through the insulin/IGF‐1 receptor pathway increases life span. Decreased insulin/IGF‐1 receptor activation leads to a decrease in PIP3, a decrease in the phosphorylation and activity of phosphoinositide‐dependent protein kinase (PDPK1), a decrease in the phosphorylation and activity of AKT, and a subsequent decrease in the phosphorylation of FOXO transcription factors, allowing them to continue to reside in the nucleus and to increase the transcription of the enzymes of the antioxidant pathway.
In mammals, many of these changes can be brought about by the metabolism of ketone bodies. The metabolism of ketones lowers the blood glucose and insulin thus decreasing the activity of the IIS and its attendant changes in the pathway described above. However, in addition ketone bodies act as a natural inhibitor of class I HDACs, inducing FOXO gene expression stimulating the synthesis of antioxidant and metabolic enzymes. An added important factor is that the metabolism of ketone bodies in mammals increases the reducing power of the NADP system providing the thermodynamic drive to destroy oxygen free radicals which are a major cause of the aging process.
What causes health? It’s such a simple question, but it’s complex. The causes are many and the direction of causality not always clear. There has been a particular challenge to dietary ideology that shifts our way of thinking. It has to do with energy and motivation.
The calorie-in/calorie-out (CICO) theory is obviously false (Caloric Confusion; & Fung, The Evidence for Caloric Restriction). Dr. Jason Fung calls it the CRaP theory (Caloric Reduction as Primary). Studies show there is a metabolic advantage to low-carb diets (Cara B. Ebbeling, Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial), especially ketogenic diets. It alters your entire metabolism and endocrine system. Remember that insulin is a hormone that has much to do with hunger signaling. Many other hormones are involved as well. This also alters how calories are processed and used in the body. More exercise won’t necessarily do any good as long nothing else is changed. The standard American diet is fattening and the standard American lifestyle makes it hard to lose that fat. Even starving yourself won’t help. The body seeks to limit energy use and maintain energy stores, especially when it is under stress (NYU Langone, Researchers Identify Mechanism that May Drive Obesity Epidemic). All that caloric restriction does is to slow down metabolism, the opposite of what happens on carbohydrate restriction.
We associate obesity with disease and rightly so, but that isn’t to say that obesity is the primary cause. It too is a symptom or, in some cases, even a protective measure (Coping Mechanisms of Health). The body isn’t stupid. Everything the body does serves a purpose, even if that purpose is making the best out of a bad situation. Consider depression. One theory proposes that when there is something wrong we seek seclusion in order to avoid further risks and stressors and to figure out the cause of distress — hence the isolation and rumination of depression. It’s similar to why we lay in bed when sick, to let the body heal. And it should be noted that depression is a symptom of numerous health conditions and often indicates inflammation in the brain (an immune response). Insulin resistance related to obesity also can involve inflammation. When the cause of the problem is permanent, the symptoms (depression, obesity, etc) become permanent. The symptoms then become problems in their own right.
This is personal for me. I spent decades in severe depression. And during that time my health was worsening, despite struggling to do what was right. I went to therapists and took antidepressants. I tried to improve my diet and exercised. But it always felt like I was fighting against myself. I was gaining weight over time and my food cravings were persistent. Something was missing. All that changed once I got into ketosis. It’s not merely that I lost weight. More amazingly, my depression and food addictions went away, along with my tendencies toward brooding and compulsive thought (The Agricultural Mind). Also, everything felt easier and more natural. I didn’t have to force myself to exercise for it now felt good to exercise. Physical activity then was an expression of my greater health, in the way a child runs around simply for the joy of it, for no other reason than he has the energy to do so. Something fundamentally changed within my body and mind. Everything felt easier.
This touches on a central theory argued by some low-carb advocates. It’s not how many calories come in versus how many go out, at least not in a simple sense. The question is what is causing calories to be consumed and burned. One thing about ketosis is that it forces the body to burn its own energy (i.e., body fat) while reducing hunger, but it does this without any need of willpower, restraint, or moral superiority. It happens naturally. The body simply starts producing more energy and, even if someone eats a high-calorie diet, the extra energy creates the conditions where, unless some other health condition interferes, increased physical activity naturally follows.
It’s not merely that being in ketosis leads to changed activity that burns more energy. Rather, the increased energy comes first. And that is because ketosis allows better access to all that energy your body already has stored up. Most people feel too tired and drained to exercise, too addicted to food that trying to control it further stresses them. That is the typical experience on a high-carb diet, mood and energy levels go up and down with the inevitable crashes becoming worse over time. But in ketosis, mood and energy is more balanced and constant. Simply put, one feels better. And when one feels better, one is more likely to do other activities that are healthy. Ketosis creates a leverage point where health improvements can be made with far less effort.
In the public mind, diet is associated with struggle and failure. But in its original meaning, the word ‘diet’ referred to lifestyle. Diet shouldn’t be something you do so much as something that changes your way of being in and relating to the world. If you find making health changes hard, it might be because you’re doing it wrong. Obesity and tiredness is not a moral failing or character flaw. You aren’t a sinner to be punished and reformed. Your body doesn’t need to be denied and controlled. There is a natural state of health that we can learn to listen to. When your body hungers and craves, it is trying to tell you something. Feed it with the nutrition it needs. Eat to satiety those foods that contribute to health. Lose excess weight first and only later worry about exercise. Once you begin to feel better, you might find your habits improving of their own accord.
This is a challenge not only to dietary belief systems but an even more radical challenge to society itself. Take prisons as an example. Instead of using prisons to store away the victims of poverty and inequality, we could eliminate the causes and consequences of poverty and inequality. We used to treat the mentally ill in hospitals, but now we put them into prisons. This is seen in concrete ways, such that prisoners have higher rates of lead toxicity. As a society, it would be cheaper, more humane, and less sociopathic to reduce the heavy metal poisoning. Similarly, studies have shown the prison population tends to be extremely malnourished. Prisons that improve the diet of prisoners result in a drastic reduction in aggressive, violent, anti-social, and other problematic behaviors. A similar observation has been made in studies with low-carb diets and children, as behavior improves. That indicates that, if we had increased public health, many and maybe most of these people wouldn’t have ended up in prison in the first place (Physical Health, Mental Health).
We’ve had a half century of unscientific dietary advice. Most Americans have been doing what they’ve been told. Saturated fat, red meat, and salt consumption went down over the past century. In place of those, fruits and vegetables, fish and lean chicken became a larger part of the diet. What has been the results? An ever worsening epidemic of obesity, diabetes, heart disease, autoimmune disorders, mood disorders, and on and on. In fact, these kinds of health problems were seen quite early on, following the fear toward meat that followed Upton Sinclair’s 1906 muckraking journalism on the meatpacking industry in The Jungle. Saturated fat intake had been decreasing and seed oil intake had been increasing in the early 1900s, in the decades leading up to the health epidemic that began most clearly around the 1940s and 1950s. The other thing that had increased over that time period were grains, sugar, and carbs in general. Then the victims who followed this bad advice were blamed by the experts for being gluttonous and slothful, as if diet were a Christian morality play. We collectively took the hard path. And the more we failed, the more the experts doubled down in demanding more of the same.
Do we want better lives for ourselves and others? Or do we simply want to scapegoat individuals for our collective failures? If you think we can’t afford to do the right thing, then we really won’t be able to afford the consequences of trying to avoid responsibility. The increasing costs of sickness, far from being limited to healthcare, will eventually bankrupt our society or else cause so much dysfunction that civil society will break down. Why choose such a dark path when an easier choice is before us? Why is the government and major health institutions still pushing a high-carb diet? We have scientifically proven the health benefits of low-carb diets. The simplest first act would be to change our dietary guidelines and all else would follow from that, from the food system to medical practice. What are we waiting for? We can make life hard, if we choose. But why not make it easy?
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I’ve long wondered why we humans make life unnecessarily hard. We artificially construct struggle and suffering out of fear of what would happen if people were genuinely free from threat, punishment, and social control. We think humans are inherently bad and must be controlled. This seeps into every aspect of life, far from being limited to demented dietary ideology.
We are even willing to punish others at great costs to ourselves, even to the point of being highly destructive to all of society. We’d rather harm, imprison, kill, etc millions of innocents in order to ensure one guilty person gets what we think they deserve. And we constantly need an endless parade of scapegoats to quench our vengeful natures. Innocence becomes irrelevant, as it ultimately is about control and not justice.
All of it is driven by fear. The authoritarians, social dominators, and reactionaries — they prey upon our fear. And in fear, people do horrific things or else submit to others doing them. Most importantly, it shuts down our ability to imagine and envision. We go to great effort to make our lives difficult. Struggle leads to ever more struggle. Suffering cascades onto suffering. Worse upon worse, ad infinitum. As such, dietary ideology or whatever else pushed by the ruling elite isn’t about public good. It’s social control, pure and simple.
But let all of that go. Let the fear go. We know from science itself that it doesn’t have to be this hard. There are proven ways to do things that are far simpler and far easier and with far better results. We aren’t bad people who need to be punished into doing the right thing. Our bodies aren’t fallen forms that will lead us into sin. What if, instead, we looked to the better angels of our nature, to what is inherently good within us?
About imagining alternatives, I’ve been reading Edward Bellamy’s Looking Backward. It’s a utopian novel, but in many ways it isn’t all that extreme. The future portrayed basically is a Nordic-style social democracy taken to the next level. That basic model of governance has already proven itself one of the best in the world, not only for public good but also wealth and innovation.
In reading about this fictionalized world, one thing stood out to me. The protagonist, Julian West, was put into trance to aid his sleep. He was in a sealed room underground and apparently the house burned down, leaving behind an empty lot. As a leap of imagination for both author and reader, this trance state put him into hibernation for more than a century. His underground bedchamber is discovered by the Leete family who, in the future world, lives on his old property although there house was built on a different location.
The father is Doctor Leete who takes particular interest in Julian. They have many conversations about the differences between the late 19th and early 21st centuries. Julian struggles to understand the enormous changes that have taken place. The world he fell asleep in is no longer recognizable by the world he woke up in. When he questions something that seems remarkable to him, Doctor Leete often responds that it’s more simple than it seems to Julian. The contrast shows how unnecessarily difficult, wasteful, and cruel was that earlier society.
The basic notion is that simple changes in social conditions can result in drastic changes in public good. The costs are miniscule in comparison to the gains. That is to say that this alternative future humanity chose the easy path, instead of continually enforcing costly punishment and social control. It’s quite amazing that the argument I make now was being made all the way back in 1888 when Bellamy began writing it. From the novel, one example of this other way of thinking is the description of the future education system in how it relates to health:
I shall not describe in detail what I saw in the schools that day. Having taken but slight interest in educational matters in my former life, I could offer few comparisons of interest. Next to the fact of the universality of the higher as well as the lower education, I was much struck with the prominence given to physical culture, and the fact that proficiency in athletic feats and games as well as in scholarship had a place in the rating of the youth.
“The faculty of education,” Dr. Leete explained, “is held to the same responsibility for the bodies as for the minds of its charges. The highest possible physical, as well as mental, development of everyone is the double object of a curriculum which lasts from the age of six to that of twenty- one.”
The magnificent health of the young people in the schools impressed me strongly. My previous observations, not only of the notable personal endowments of the family of my host, but of the people I had seen in my walks abroad, had already suggested the idea that there must have been something like a general improvement in the physical standard of the race since my day ; and now, as I compared these stalwart young men and fresh, vigorous maidens, with the young people I had seen in the schools of the nineteenth century, I was moved to impart my thought to Dr. Leete. He listened with great interest to what I said.
“Your testimony on this point,” he declared, “is invaluable. We believe that there has been such an improvement as you speak of, but of course it could only be a matter of theory with us. It is an incident of your unique position that you alone in the world of to-day can speak with authority on this point. Your opinion, when you state it publicly, will, I assure you, make a profound sensation. For the rest it would be strange, certainly, if the race did not show an improvement. In your day, riches debauched one class with idleness of mind and body, while poverty sapped the vitality of the masses by overwork, bad food, and pestilent homes. The labour required of children, and the burdens laid on women, enfeebled the very springs of life. Instead of the these maleficent circumstances, all now enjoy the most favourable conditions of physical life ; the young are care fully nurtured and studiously cared for ; the labour which is required.of all is limited to the period of greatest bodily vigour, and is never excessive ; care for one’s self and one’s family, anxiety as to livelihood, the strain of a ceaseless battle of life, all these influences, which once did so much to wreck the minds and bodies of men and women, are known no more. Certainly, an improvement of the species ought to follow such a change, In certain specific respects we know, indeed, that the improvement has taken place. Insanity, for instance, which in the nineteenth century was so terribly common a product of your insane mode of life, has almost dis appeared, with its alternative, suicide.”
I’m throwing this in for a number of reasons. It is showing how low-carb views are basically the same as dietary advice from earlier last century. Heck, one can find advice like that going back to the 1800s and even 1700s. Low-carb diets were well known and mainstream until the changes at the AHA and FDA over the past 50 years or so.
The return of low-carb popularity is what inspires such articles from the corporate media. Reader’s Digest would’t likely have published something like that 10, 20, or 30 years ago. Attitudes are changing, even if institutions are resistant. Profits are also changing as low-carb products become big biz. Corporate media, if nothing else, will follow the profits.
Here is what really stood out to me. In the article, two major dietary experts are quoted: Dr. Jason Fung and Dr. Robert Lustig. Both of them are leading advocates of low-carb diets with Dr. Lustig being the most influential critic of sugar. But neither of them is presented as such. They are simply used as authorities on the topic, which they are. That means that low-carb has become so acceptable as, in some cases, to go without saying. They aren’t labeled as low-carb gurus, much less dismissed as food faddists. No qualifications or warnings are given about low-carb. The article simply quotes these experts about what the science shows.
This is a major advance in news reporting. It’s a positive sign of changes being embraced. Maybe we are finally turning off the hard path and trying out the easier path instead. Some early signs are indicating this. The growing incidence of diabetes might be finally leveling out and even reversing for the first time in generations.
“Can my kids do keto too? Yes, kids can do keto. In fact, ketogenic diets were first tested on children that had epilepsy, and it was found to be safe and effective.”
How come no one ever asks if sugary breakfast cereal, grape juice, and white bread with margarine is “safe for kids?” We have entered bizarro world when we’re asking if it’s safe for kids to not eat sugar or carb-load like they’re about to run a marathon. As I explain here, there is nothing — no vitamin, mineral, or other essential nutrient — that you can get from high-carb foods that you cannot get from LOW-carb foods.
He feels people don’t understand that carbohydrates are not a food. Carbohydrates are a highly neuroactive drug that we’ve now placed in our food system and we’ve told our population that this highly neuroactive drug is healthy for them. People don’t have a relaxation methodology. Babies are weaned onto carbohydrate rich foods so they’re getting this wonderfully neuroactive euphoria that is satisfying even before they know they’re human. And so they develop this euphoric relationship with a drug called carbohydrates. They seek it in their diet and society gives it to them. Society condones it.
from LowCarbUSA, Keto For Kids, Autism and ADHD
Soon after birth, human babies are in ketosis, and remain so while breastfeeding . They use ketones and fats for energy and for brain growth.
When this has been studied, in the first couple of hours after birth, babies aren’t immediately in ketosis. There is a short delay . During that brief period before ketogenesis starts, lactate (confusingly not to do with lactation) becomes an important fuel to suppport the brain . Some researchers speculate that this delay in ketogenesis could be because of a limited supply of carnitine, which is supplied by milk, but they also note that glycogenolysis and gluconeogenesis (the process by which glucose is made out of protein) are not active immediately . Therefore, it could simply be the case that ketogenesis takes time to get started. In other words, it may just be keto-adaptation.
Note, though, that the mothers of these babies were unlikely to have been ketogenic. As it happens, if the mother is in ketosis (as has been studied through fasting), ketone bodies will pass through the placenta and be used by the fetus , . At the same time, gluconeogenesis is induced in the liver of the fetus, likely as a result of the insulin-to-glucagon ratio , . Therefore, it is possible that the fetus of a ketogenic mother would already be independently ketogenic at birth.
As far as nutrition on the ketogenic diet, there are some specific ways ketogenic foods are beneficial for kids:
Infants, toddlers, and growing children need a good amount of iron [*] and fat [*] in their diet for proper growth. Healthy ketogenic foods provide plenty of both. These are important for brain development and growth as well as absorbing and using fat soluble vitamins and building nerve tissue [*].
With refined, high-carbohydrate foods widely available and affordable, it’s unfortunately no surprise that one in six U.S. kids and teens are obese and type 2 diabetes is now seen so commonly in children. The connection between the intake of these foods and high blood glucose and insulin resistance is reason enough for parents to show concern about the high-carb foods their children are consuming.
If you look at these foods’ labels, you’ll see they’re fortified with vitamin and minerals for this exact reason—on their own, they’re very nutritionally poor.
We can see that glucose is not the primary fuel because babies are born in ketosis(1) and mother’s milk is low carbs high fat (LCHF), which keeps the newborn in ketosis all through nursing. Milk gets more glucose as it matures, and at full maturation, its nutritional content per cup (8 oz) is 10.77 gr fat, 2.53 gr protein, 16.95 gr carbohydrates (in the form of lactose) and total energy of 172 kcal; it also contains 87.5 gr water. Subtracting the water and looking at the macronutrient ratios only, this glass of mature nursing milk is 55.5% fat, 5.57% protein, and 38.71% carbohydrates (in lactose so not free sugar). In terms of fatty acid composition: 4.942 gr saturated fat, 4.079 gr monounsaturated fat, and 1.223 gr polyunsaturated fat, which in percentages: 48.24% saturated fat, 39.82% monounsaturated fat, and 11.94% polyunsaturated fat(2). One must agree that babies are not fed poison by their mothers and that Nature didn’t provide nursing milk such that it is toxic. In fact, we can see that babies grow very rapidly by nursing milk and we know from studies that babies who are nursed, have a better chance for survival, grow healthier, faster, and their brain develops better.
As babies grow, they retain metabolic flexibility, meaning they stay in ketosis for periods time, which changes by age and how often they are fed, and they may temporarily enter the carbohydrate metabolic process when they eat (1,3,4). […] Note that babies are born with 0.5 mmol/L or higher level of BHB and remain in ketosis until they are fed. In the case of infants, the needs for energy arises very quickly, as shown in Figure 1, and in approximately 20 minutes after feeding the baby is back in ketosis.
Thus ketosis, in one scenario, is a state into which our metabolism reverts to when food is not immediately available on demand — this is labeled “starvation”. However, studies on the fetus in utero show that the fetus, which is never under nutritional duress, is also in ketosis time to time(5,6) and there are ketones in the placenta(7). Therefore, it is very difficult to suggest that ketones are a backup fuel of any kind if even the fetus is in ketosis time to time in the womb. Clearly, being in ketosis provides some benefits that are not possible to achieve using the glucose metabolic process. The ketogenic and the glucogenic metabolic processes have distinct functions, each specialized to benefit us in some way.
And here is the important part. The human body is a smart one. It had millions of years in which to figure out the order via evolution. It picks based on an order of urgency, and priority will be given to the most dangerous of fuels, which have negative consequences if they remain in the body for long. The body will use the dangerous fuel first over fuel that can be stored without negative consequences.
So what will the order of preference be in burning the 3 fuels?
Alcohol, glucose, and then fat (aka ketones).
And this is in order of urgency and not based on which is primary.[…]
In the original article, you will find discussion on Cahill’s landmark article (1), which you may or may not be familiar with. His work is focused mostly on ketosis during starvation. By starvation, understand “fasting” in modern terms. Babies, for example are in ketosis all through their early teenage years–as per Cahill–even 20 minutes between feeding initiates starvation responses in babies. But there are articles showing that the fetus is also in ketosis in the womb, where there is no starvation, and babies remain in ketosis even after eating–clearly no starvation there. So there is more to ketosis than meets the careless eye. […]
With all due respect, I disagree with glucose as the primary human fuel. Glucose is not primary or secondary or any-ary. It is a fuel that is urgent to be used up as fast as possible and so it gets used first (after alcohol) but not because it is primary but because we need to get rid of it faster than fat.
I have had the opportunity to evaluate the 5-hour blood test results of children of all ages—I think the youngest was 5 years old and the oldest 16, so far. I have yet to see a blood ketone test of a child anywhere in this age group that is not showing ketosis both before and after a meal—even if the meal has fruits and dairy in it.
I suppose ignorance is bliss. Few doctors or researchers have the same opportunity I have in being able to measure the blood ketones of various ages of children for five hours postprandial plus fasting and premeal measures, therefore, most don’t realize just how much our kids are in ketosis.
Thus, while today in most countries around the world any type of food is just a short walk/drive away 24/7, and we need not experience hunger and starvation, our children are still in ketosis 24/7. Shouldn’t that tell us something about the importance of ketosis?
As well as needing fat for fuel, a baby’s brain requires specific fat for normal cognitive development and intellectual skills. Without that specific fat, there is the serious risk of developing brain dysfunction.
There are two fats that are essential for optimal brain function in the developing foetus and the newborn baby: the omega-3 fatty acid DHA (docosahexaenoic acid) and the omega-6 fatty acid ARA (arachidonic acid).
Both these fats form part of each cell membrane, and control what passes in and out of each nerve cell. They help develop the central nervous system. They are involved in communication between nerve cells, the firing of neurons, the regulation of neurotransmitters and the development of cognitive skills. […]
What happens without enough of these two fatty acids?
Only two mammalian species have disproportionately large brains and advanced cognition — humans and bottlenose dolphins. Both depend on DHA for that cognition.
Children who lack DHA are more likely to have increased rates of neurological disorders, in particular attention deficit hyperactivity disorder (ADHD), and autism.
“It is our contention that the movement in the 19th to 21st centuries away from traditional use of sea foods and increased emphasis on land based food supply is a likely cause in the rise in brain disorders including mental ill-health, stress, and other psychiatric disorders.”(Crawford et al 2014).
Today, ADHD is the most frequently diagnosed neuro-behavioural disorder of childhood, and it is becoming increasingly prevalent. In 2014, the Centers for Disease Control and Prevention confirmed that there had been a 42% increase in the number of children diagnosed with the condition since 2006. In America today, 11% of children aged 4 to 17 live with ADHD.
There is a growing body of evidence to suggest that ADHD may be preceded by low DHA in the womb.
The link between dietary fat and autism is also strong, and low levels of both DHA and ARA have been found in children on the autistic spectrum. In a study published in 2015 in International Journal of Molecular Sciences, the fatty acid profile of 121 autistic children, aged 3–7, was analysed and compared with children without the condition. The autistic children were found to have levels of ARA and DHA that were “particularly decreased”, compared to the non-autistic controls.
* * *
This reminds me of the case, in South Africa, brought against Tim Noakes. He recommended a low-carb diet to a pregnant woman. Public officials considered it to be a crime against humanity that must be harshly punished. After the first attack on him failed, he was forced to endure a second trial. The government spent millions of dollars persecuting him and he not only proved his innocence but proved that the low-carb diet was scientifically valid. It was the greatest boost for the low-carb diet since Ancel Keys led his crusade against it.
Lore of Nutrition by Tim Noakes & Marika Sboros pp. 32-34, Introduction by Marika Sboros (see more at: The Creed of Ancel Keys)
This is the story of a remarkable scientific journey. Just as remarkable is the genesis of that journey: a single, innocuous tweet.
In February 2014 , a Twitter user asked a distinguished and world-renowned scientist a simple question: ‘Is LCHF eating ok for breastfeeding mums? Worried about all the dairy + cauliflower = wind for babies??’
Always willing to engage with an inquiring mind, Professor Tim Noakes tweeted back: ‘Baby doesn’t eat the dairy and cauliflower. Just very healthy high fat breast milk. Key is to ween [ si c ] baby onto LCHF.’
With those few words, Noakes set off a chain of events that would eventually see him charged with unprofessional conduct, caught up in a case that would drag on for more than three years and cost many millions of rands. More difficult, if not impossible, to quantify is the devastating emotional toll that the whole ordeal has taken on him and his family, as critics attacked his character and scientific reputation at every turn.
At the time, it was open season on Tim Noakes. Doctors, dietitians and assorted academics from South Africa’s top universities had been hard at work for years trying to discredit him. They did not like his scientific views on low-carbohydrate, high-fat foods, which he had been promoting since 2011 . His opinions contrasted sharply with conventional, orthodox dietary ‘wisdom’, and the tweet provided the perfect pretext to amp up their attacks and hopefully silence him once and for all.
Within 24 hours of his tweet, a dietitian had reported him to the Health Professions Council of South Africa for giving what she considered ‘incorrect’, ‘dangerous’ and ‘potentially life-threatening’ advice. To Noakes’s surprise, the HPCSA took her complaint seriously.
Noakes is one of the few scientists in the world with an A 1 rating from the South African National Research Foundation (NRF) for both sports science and nutrition. In his home country, he has no equal in terms of expertise in and research into LCHF. Few can match his large academic footprint – quantified by an H-index of over 70 . The H- or Hirsch index is a measure of the impact of a scientist’s work. Noakes’s impact is significant. He has published more than 500 scientific papers, many of them in peer-reviewed journals, and over 40 of which deal exclusively with nutrition. He has been cited more than 17 000 times in the scientific literature.
Yet, remarkably, the HPCSA chose to back the opinion of a dietitian in private practice over an internationally renowned nutrition research scientist. They charged him with ‘unprofessional conduct’ for providing ‘unconventional advice on breastfeeding babies on social networks’ and hauled him through the humiliating process of a disciplinary hearing.
The public quickly dubbed it ‘the Nutrition Trial of the 21 st Century’. I’ve called it Kafkaesque. The HPCSA insisted that it was a hearing, not a trial, but the statutory body’s own conduct belied the claim.
At the time of Noakes’s tweet, I wanted to give up journalism. After more than 30 years of researching and writing about medicine and nutrition science, I was frustrated and bored. People were growing fatter and sicker, and the medical and dietetic specialists I wrote about weren’t making much difference to patients’ lives. Neither was my reporting.
Then I started investigating and writing about the HPCSA’s case against Noakes. The more questions I asked, the more walls of silence came up around me, and from the most unexpected sources. There’s an old saying that silence isn’t empty, it is full of answers. I found that the silence was loudest from those with the most to hide. I could not have foreseen the labyrinthine extent of vested inter ests ranged against Noakes, or the role played by shadowy proxy organisations for multinational sugar and soft-drink companies in suppressing and discrediting nutrition evidence.
It took a US investigative journalist to join many of the dots I had identified. Russ Greene’s research led to the International Life Sciences Institute (ILSI), a Coca-Cola front organisation. In an explosive exposé in January 2017 , Greene showed how the ILSI has worked to support the nutrition status quo in South Africa, as well as the health professionals and food and drug industries that benefit from it. It has opened a branch in South Africa and has funded nutrition congresses throughout the country. It has also paid for dietitians and academics opposed to Noakes and LCHF to address conferences abroad . *
Of course, it might be coincidence that so many doctors, dietitians and academics with links to the ILSI became involved, directly and indirectly, in the HPCSA’s prosecution of Noakes. Then again, maybe not.
The HPCSA’s conduct throughout the hearing and since its conclusion has been revelatory. To a large extent, it confirms the premise of this book: that those in positions of power and influence in medicine and academia were using the case to pursue a vendetta against Noakes. The trial highlighted the inherent perils facing those brave enough to go against orthodoxy.
Tim Noakes: The Quiet Maverick
by Daryl Ilbury
Into this turgid culture of food and identity stepped Tim Noakes on 5 February 2014, when he replied to a question posted two days earlier on Twitter, addressed to him and Sally-Ann Creed, a nutritional therapist (and co-author with Noakes of The Real Meal Revolution ). It was from a breastfeeding mother, Pippa Leenstra: ‘Is LCHF eating ok for breastfeeding mums? Worried about all the dairy + cauliflower = wind for babies??’ Noakes’s reply was the following: ‘Baby doesn’t eat the dairy and cauliflower. Just very healthy high fat breast milk. Key is to ween [ sic ] baby onto LCHF.’
It’s neither an offensive tweet by any stretch of the imagination, nor does it fall foul of any media law – it’s not libellous and there’s no encouragement of harm to others. People could disagree with him and had a voice to do so; that’s the point of social media: it is a platform for public discussion. And people did disagree, quite vocally, and there were others who supported his advice, equally vocally. Importantly, the question demanded a public, not private, response, which the person asking the question was free to accept or reject. And, as a medical doctor, Noakes didn’t cross any ethical boundaries in replying on a public platform. He didn’t publish any confidential patient information or dispense a diagnosis for a specific patient without seeing that patient; he simply provided generalised nutritional advice based on scientific evidence. Breast milk is high in fat, and there is scientific evidence to support the benefits of an LCHF diet. There is also evidence to the contrary, but, as we’ve realised, that’s science for you. The secret in making sense of science is context, and this is where it clashes with social media.
The character limitation of Twitter is one of its selling points; it demands concise expression, a sub-editor’s dream. It also means that tweets can be short on context, unless accompanied by click-through links to supporting evidence. Therefore tweets can be open to interpretation. However, this misses the main point of the brevity of Twitter messages: they are designed to encourage debate. Whether Noakes should have said ‘Key is to wean a baby …’ as opposed to ‘Key is to wean baby …’ is a matter for retrospective semantic debate. The fact is he provided a broad opinion on a public platform as a scientist and researcher of human nutrition.
Importantly, in her original tweet, to which Noakes replied, Pippa Leenstra never referred to herself or her baby. She spoke of ‘breastfeeding mums’. She was doing the media equivalent of asking a question in a town hall where the discussion was around LCHF. At that moment, Leenstra was a media consumer of medical or health information.
Not everyone saw it that way. One of those was Claire Julsing-Strydom, who at that time was president of the Association for Dietetics in South Africa (ADSA), the professional organisation for the country’s registered dietitians. Julsing-Strydom’s reaction was to register a complaint with the Health Professions Council of South Africa. It was a decision that would effectively threaten to destroy Noakes’s career, and make Julsing-Strydom the focus of a social media witch-hunt.
According to its website, the HPCSA provides the public with the right to request an investigation of any registered health practitioner whom they believe has acted unethically or caused harm. The site includes a downloadable form and an email address for Legal Med, the department within the HPCSA that handles complaints. To make sure that no health professional is a victim of a truculent member of the public with a hefty doctor’s bill in one hand and an axe to grind in the other, there is a due process of investigation and assessment before any measure of disciplinary action is followed. Only the most serious cases demand a professional-conduct committee hearing, which is what Tim Noakes would be called before.
As I said at the beginning of this book, I am not going to go into the trial in detail; instead, I will focus on the following: the complaint, the charge that resulted, two key components in the case against Noakes, and the unexpected outcome of the hearing. The main focus will be on how this was all covered in the media.
By now you know that whereas content is king, context is King Kong, and in this case the context behind the complaint makes for interesting reading, for two reasons: firstly, it shows that Noakes’s tweet was judged in isolation, and, secondly, it suggests that the complaint may not have been thought through.
What most people may not know is that directly after Noakes’s reply on Twitter to Pippa Leenstra, someone else entered the discussion: Marlene Ellmer, a paediatric dietitian and someone well known to Julsing-Strydom. Ellmer tweeted the following: ‘Pippa, as a paeds dietician I strongly advise against LCHF for breastfeeding mothers.’ Leenstra replied by posing the following question to both Noakes and Ellmer: ‘Okay, but what I eat comes through into my milk. Is that not problematic for baby and their winds at newborn stage?’ Ellmer responded by tweeting another message with her email address, encouraging Leenstra to contact her directly. Noakes didn’t do this, which is important to note, as we shall soon see. Leenstra tweeted to Ellmer that she would contact her, and after the discussion played out further with various people providing input, Leenstra tweeted: ‘Thanks, but I will go with the dietician’s recommendation.’ This she did, rejecting Noakes’s LCHF suggestion.
Let’s summarise: at that point Leenstra had posted a question on a public forum, received different opinions, including from two health professionals – one of them a registered dietitian – and been provided with the contact details of one of those professionals with an invite to get hold of her. Leenstra was free to choose which one to follow up with, and she agreed, publicly, to contact the registered dietitian. Theoretically, things could have stopped there.
However, the day after Ellmer’s invite for Leenstra to contact her, Julsing-Strydom entered the discussion and reacted with a tweet directed to Noakes, written thus: ‘I AM HORRIFIED!! HOW CAN YOU GIVE ADVICE LIKE THIS??’ For those unfamiliar with the idiosyncrasies of social media, the use of uppercase letters is normally reserved to express a strong feeling of annoyance, displeasure or hostility. On its own, Julsing-Strydom’s use of uppercase in a tweet is perfectly acceptable; it shows how she must have felt reading Noakes’s tweet, and there are possible reasons for that. Firstly, she had a four-month-old daughter she was breastfeeding, so she had a personal as well as a professional interest in the topic under discussion. Secondly, as she would later testify, she had had a strongly worded engagement the previous month with Noakes over what she saw as his dispensing nutritional advice to breastfeeding mothers during a talk. It’s easy to imagine that for Julsing-Strydom the tweet was the last straw, and so she submitted her complaint, including screenshots of Noakes’s tweet, to Legal Med. The accompanying email read:
‘To whom it may concern. I would like to file a report against Prof Tim Noakes. He is giving incorrect medical [nutrition therapy] on Twitter that is not evidence based. I have attached the Tweet where Prof Noakes advises a breastfeeding mother to wean her baby on to a low carbohydrate high fat diet. I urge the HPCSA to please take urgent action against this type of misconduct as Prof Noakes is a celebrity in South Africa and the public does not have the knowledge to understand that the information he is advocating is not evidence based. It is specifically dangerous to give this advice for infants and can potentially be life-threatening. I await your response. Claire Julsing-Strydom.’
The wording is a little breathless, and the reason for that would emerge in the hearing.
The complaint contains many factors that Legal Med would have considered, but five pertain to focus points covered so far in this book: the limits to the public’s understanding of science, in this case that of human nutrition; the complexity and unreliability of academic research behind that science; the media profile of Tim Noakes, and the idea that he is a ‘celebrity’; that the complaint related to something said within a disrupted media environment; and the suggestion that nutritional advice is a clear-cut case of right or wrong.
What the legal department would have known when they received the complaint was that the complainant was another health professional; this wasn’t just someone with a beef about their proctologist having cold hands. This meant that the complainant would have understood the potential outcomes of submitting her complaint, especially one claiming that an act by a fellow health professional was ‘life-threatening’. The fact of the matter is that Legal Med saw sufficient seriousness in the complaint to investigate.
However, inconsistencies in Julsing-Strydom’s complaint soon came to light. She supposedly submitted it on behalf of ADSA, and yet didn’t make that clear in the complaint. When questioned in the HPCSA hearing that her complaint triggered, she replied that it was the first time she had registered a complaint, saying, ‘I was not aware that this email would actually be, you know, used at this level.’
Now, after 30 years of interviewing people for the media, if there’s something I’ve learnt it’s that the most honest comments are usually unconsidered – made as an aside, when thoughts are wandering, or if a little flustered. Perhaps, I thought, Julsing-Strydom hadn’t really thought through what was going to happen once she submitted the complaint.
Furthermore, a forensic analysis of Twitter timelines and the submission date and time of the complaint shows that Julsing-Strydom publicly expressed her horror on Twitter on 6 February 2014 at 07:48, and sent her email to Legal Med less than an hour later, at 08:47. It’s fair to say that Julsing-Strydom was upset when she wrote that email.
Based on the findings of a preliminary committee of inquiry, the legal department of the HPCSA sent a letter to Noakes on 28 January 2015, saying that he was to be summoned before the Professional Conduct Committee of the Medical and Dental Professions Board. The charge against him was attached to the letter, and it makes for puzzling reading: ‘That you are guilty of unprofessional conduct, or conduct which, when regard is had to your profession is unprofessional, in that during February 2014, you acted in a manner that is not in accordance with the norms and standards of your profession in that you provided unconventional advice on breastfeeding babies on social networks (tweet).’
It is so badly written that it would send any sub-editor reaching for a stiff shot of whisky, so it was invariably presented in the media thus: ‘charged with providing unconventional advice on social media to breastfeeding mothers’.
When I first read the charge, that part about ‘social networks’ intrigued me the most. Providing advice on a public social media platform is an ethical catch-22 for any clinician: if they provide generalised information, they can be accused of not taking into consideration the specifics of the patient; yet if they ask for specifics, they risk encouraging the sharing of confidential information on a public platform. There’s also the ethical conundrum that if they open a consultative dialogue with someone other than a patient, they can be charged with supersession, essentially ‘stealing’ a patient; and for the HPCSA, that is grounds for discipline. How is that for irony?
I sensed confusion in the poorly worded charge. On a hunch I contacted the HPCSA and asked for a copy of their guidelines for how registered health practitioners should engage with the public on social media – if the HPCSA were charging Noakes because of his use of social media, they’d obviously have the necessary guidelines in place. I received the following reply: ‘Kindly note that the HPCSA doesn’t have guidelines around how registered health practitioners should engage with the public on social media.’ The HPCSA was clearly in unfamiliar territory. I thought it didn’t bode well for a speedy, clear-cut course for the hearing; and I was right.
What started on 4 June 2015, and was supposed to be wrapped up in little over a week, would drag on for almost two years, and if its aim was to deliver a swift, unsparing and public reprimand of a dissident scientist, it failed.
Here is some information about ketones, ketosis, and ketogenic diets. The focus is on treating Alzheimer’s, although the topic applies to many other conditions as well. Let me begin by explaining the basics.
Ketosis is the primary burning of fat, dietary fat or body fat, to produce ketones that the body uses. A ketogenic diet is sometimes called nutritional ketosis, as opposed to ketosis through other means such as fasting. When ketone levels are high enough, it is called ketosis — the term being used more strictly for medical purposes. The body has two main options for fuel, glucose and ketones. With Alzheimer’s as type 3 diabetes, insulin resistance in the brain decreases the ability to use glucose and so the brain slowly starves. Ketones can mostly replace glucose, especially for brain cells. Some argue they’re the preferred source of energy, since for most of human evolution there were limited amounts of carbohydrates in the diet. This is shown in how, when both glucose and ketones are available, the brain prioritizes the latter. Ketones are a more efficient and steady source of energy because few people have to worry about running out of dietary or body fat to make ketones.
Ketones are a superfuel that allows the brain function at a higher level. In ketosis, not only does metabolism change but so does brain functioning. This is why ketogenic diets have been medically used to treat diverse neurocognitive conditions: epileptic seizures, autism, ADHD, depression, multiple sclerosis, Alzheimer’s, etc. Part of this has to do with inflammation, as ketosis is anti-inflammatory. This is important because inflammation is often involved in problems with brain health and many other problems as well (arthritis, autoimmune disorders, etc). I can vouch for this in my own experience when my depression disappeared after going low-carb. Partly that is because my glucose, insulin and serotonin levels would have stabilized, but cutting back my carbs further to go into ketosis definitely made a difference. I generally feel better.
Immediately below is a chart comparing ketogenic strategies and the resultant increase in ketones. If multiple strategies are combined, ketone levels can be higher still. Ketoacidosis is thrown in the chart below for comparison, but it only happens to diabetics and it is harmful — it’s an entirely separate condition from ketosis, although both involve ketones. People sometimes confuse ketoacidosis with ketosis, but what causes each is separate. As you can see below, ketoacidosis raises ketone levels to a degree that nothing else does. Unless one is diabetic, that isn’t a concern.
Ketogenic Strategy —> Ketone Levels (mmol/L)
Caffeine —> 0.2 to 0.3
Coconut Oil —> 0.3 to 0.5
Vigorous Exercise —> 0.3 to 0.5
Overnight Fast —> 0.3 to 0.5
MCT Oil —> 0.3 to 1.0
Branched Chain Amino Acids —> 0.3 to 1.0
Ketone Mineral Salts —> 0.5 to 1.0
Classic Ketogenic Diet —> 2 to 6
Starvation/Long-Term Fasting —> 2 to 7
Ketone Esters (Oral or IV) —> 2 to 7 or higher
Diabetic Ketoacidosis —> 10 to 25
This chart and most of the other info I share here comes from Mary T. Newport’s book, The Complete Book of Ketones. There is also good info available in Dale E. Bredesen’s The End of Alzheimer’s, Amy Berger’s The Alzheimer’s Antidote, and Bruce Fife’s Stop Alzheimer’s Now. All I’m discussing below is the most basic info. For a more in-depth approach, I’d recommend checking out Dr. Bredesen, the author mentioned above, who is an Alzheimer’s researcher and clinician at UCLA. He has a complex protocol, going beyond ketosis, that requires working with a doctor trained in it. The clinical trial he did is the only confirmed reversal of Alzheimer’s. But back to increasing ketones and suppressing mental loss.
How to get into ketosis:
The most dependable method of entering into ketosis and maintaining it is through diet. Put in the simplest terms, there needs to be strict limits on starchy carbs and sugar (bread, crackers, noodles beans, potatoes, fruit, fruit juice, pop, candy, most processed foods, etc) combined with moderate amounts of protein and lots of fat/oil. Specific details can be found below. It is not necessarily easy, since those are some of the foods we enjoy most. Even so, it still allows a fair amount of diversity. Many foods are low in carbs: non-starchy vegetables, fruits like olives and avocados, most nuts and seeds, etc. The difficult part is that many convenience foods aren’t allowable other than as occasional foods eaten in limited amounts.
Of course, there are simpler methods of increasing ketones. Here are three:
(1) Exogenous ketones can be taken directly and will give a quick mental boost that doesn’t last long, but it is easy for the body to use since it is already in the needed form. A single dose peaks out in 30-60 minutes with the body fully eliminating them in a few hours. Exogenous ketones would need to be regularly taken in smaller amounts throughout the day to maintain higher ketone levels. One thing to keep in mind is that as ketone levels go up blood sugar and insulin levels drop. This can be an issue for people with diabetes or pre-diabetes. There are two options of exogenous ketones: ketone esters and ketone salts. The former are more easily used by the body, but the latter are more available on the market. I haven’t found ketone esters in any local store. They can be obtained online, though. I’d probably stick to the ketone salts, as there is much more research done showing their safety. Exogenous ketones are of more limited use since most people can’t safely handle more than one or two servings a day.
(2) Or one can use MCTs (medium chain triglycerides) which turn into ketones without much effort. MCT oils and powders can be added throughout the day and the body uses them fairly quickly. There are also MCTs in coconut oil and Mary T. Newport found that, in treating her husband’s Alzheimer’s, that coconut oil had a longer lasting effect. She used a combination of all three: exogenous ketones, MCT oil, and coconut oil. This gave a more steady level of ketones throughout the day. Her husband showed improvement despite her not doing anything else initially, not otherwise changing his diet. As a side note, Newport says to use cold-pressed coconut oil for reasons of general health. The main advantage is that greater amounts of MCTs and coconut oil allow the body to produce ketones even when carbs aren’t as restricted, not that one can eat carbs unlimited.
(3) An even simpler way is fasting, although easier still if one is already in ketosis (trying to go from a high-carb diet to fasting can be a challenge). A person is guaranteed to go into ketosis by not eating. Even a full night of sleep is enough to begin increasing ketone levels. Skip a meal or an entire day of eating and ketone levels will keep going up to a much more noticeable degree. If you break your fast with a ketogenic meal of low-carb and high-fat, that will extend ketosis into the rest of the day. Starting your day with fat in your coffee can be even better, as caffeine will also boost ketones (I add ghee and MCT oil to my coffee and mix it up with a battery-powered frother). In fasting for ketogenic purposes, one can do a fat fast by eating only fat, such as drinking fat-filled coffee all day. Without starches and sugar, the body is forced to burn fat and produce ketones. There isn’t anything easier than a fat fast nor as satiating.
The only potential downside is not everyone digests and metabolizes fat equally well. MCT oils, in particular, can require some adaptation. Too much can cause diarrhea for those sensitive to it. It’s best to start off with small amounts (1/2 to 1 tsp or less at a time, once or twice a day) and build up a tolerance (upwards of 1 to 2 tbsp or possibly higher, two to four times a day). If sensitive, take MCT oils with other foods, such as mixing it into cottage cheese or Greek yogurt. Coconut oil is easier for the body to handle, as it is a mix of other fats such as lauric acid that has some of the traits of MCTs. There is evidence that lauric acid works as a ketogenic fat directly in the brain. Coconut oil also helps with the thyroid and Alzheimer’s patients often develop thyroid problems.
By the way, here is what Mary T. Newport writes: “When Steve [her husband with Alzheimer’s took just coconut oil in the morning, his ketone levels peaked at about three hours but had returned to nearly normal after eight to nine hours, just before dinner time. With just MCT oil, Steve’s ketone levels went higher, peaked at about ninety minutes, but were gone within three hours.” So, she used both in a 4:3 ratio (MCT to coconut oil) to maintain stable ketone levels throughout the day. Newport suggests gradually increasing coconut oil (and MCT) intake up to 4-6 tablespoons a day or even as high 8 tablespoons, but gradually is the key part.
If one wants to ensure ketosis, there are ways to measure ketone levels. I’ve never done this, but I keep my carbs so low that there is no way for me to avoid ketosis. Without a ketogenic diet, it will be more difficult keeping ketone levels elevated and stable. Still, any greater amount of ketones is better than nothing when it comes to how the brain is starving for fuel in Alzheimer’s or in relation to many other conditions. If you want to try a ketogenic diet, here are some variations explained in detail and with good visuals about what the macronutrient (carb, protein, & fat) ratios should look like as a plate of food: Diet Plans – Charlie Foundation. Also, keep in mind protein levels, which can be an issue for with diabetes, pre-diabetes, etc: Too Much Protein?
Eating in such a way that ketosis is frequent is not always easy, although it can be the easiest diet in the world. It is not easy for many people because such diets reduce the foods they ‘love’ (sugar and carbs), reduce the foods they know how to prepare, and reduce the food options found in most restaurants. Further, these diets run contrary to the traditional food pyramid that we have been trained on for years. They seem downright unhealthy, when in fact, current research is showing they have been healthier all along. It requires changing how one thinks about food. In short, one must be very intentional. One cannot coast along and provide optimal brain nutrition. The first step for most people is breaking their food addiction, but it’s worth the effort.
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