Ten years of carbohydrate restriction: here’s why

It was almost exactly ten years ago, in March 2008, that I read Ron Rosedale’s Insulin and Its Metabolic Effects.  I now know that this is surely the one thing I’ve read that has had the most impact on my life. Rosedale’s presentation was a total revelation to me:  I had never read anything about insulin before, and his explanations of the biochemical and physiological functions and effects of insulin on the body all made perfect sense in and of themselves, but also appealed to my appreciation and reliance on complete explanations that are consistent with the facts we can observe about them.  I eliminated insulin-stimulating carbohydrates from my diet overnight.  That was that.

We were then still vegetarian at home.  Hence, the family breakfast, following Mercola’s example, became smoothies made of raw, local, pastured eggs with berries and stevia.  That lasted quite a while.  I always travelled with my hand blender and stevia, brought eggs if it was for short trip, or scouted out places to get good ones when the trip was longer.  Throughout a summer trip along the American west coast, I made our raw egg smoothies every day, in hotel rooms and campgrounds.

At one point, I discovered coconut oil and coconut milk.  The breakfast smoothies evolved to being made of eggs and coconut milk with berries, and eventually only coconut milk, berries and stevia.  This period lasted several years until we moved on to cold pressed green juice with coconut milk; it was two thirds juice and one third milk.  We also did this for several years until about two years ago when our son left for university, at which point we dropped having breakfast entirely to allow for a daily overnight fasting period of about 16 hours from after dinner to lunchtime.


Food intolerance testing in 2014 showed that all three of us were intolerant to eggs; we removed them from our diet.  My wife and I had the most and our son the least intolerances; this was not surprising given we were a lot older than him.  It also showed my wife and I were intolerant to most dairy products; we removed them from our diet.  We were also intolerant to grains: both highly intolerant to wheat, and then I, in addition, somewhat less so to barley, malt, and quinoa—we ate quinoa almost daily for years as our son was growing up.  He, although not intolerant to dairy or wheat, was intolerant to almonds, pistachios, and brazil nuts. (Here are my test results, if you’re interested.)

Imagine: vegetarian for 20 years, with a diet during these two decades from teenage hood to middle adult hood consisting primarily of wheat and grain products, beans, cheese and yogurt, eggs and nuts.  Of course, also plenty of sweet fruit, starchy vegetables, and salads, as with is true for most vegetarians.  But the bulk, both in volume and in calories, was from grain products, cheese, and eggs.  The shocker for me was that the food intolerance test painted the profile of a meat-eater:  if you remove grains, dairy, and eggs, what is left is animal flesh, vegetables and fruits.

If now, in addition, you remove fruit and starchy vegetables to avoid insulin-stimulating carbohydrates, all that is left is animal flesh and green vegetables.  That’s just how it is.  We also used to eat almonds—the richest in magnesium, and brazil nuts—the richest in selenium, almost daily.  But because our son was intolerant to both and I was intolerant to brazil nuts, we removed those from our diet as well.



These were all food intolerances; they were not allergies.  But they were nonetheless intolerances, some stronger, some weaker.  If you are concerned about health in the sense of being in the best state of health you can, then obviously you must not eat foods to which you are intolerant.  Otherwise, your immune system is triggered each time the offending molecules in those foods enter the gut and bloodstream.  This gradually but inevitably makes the intolerance greater, your system weaker, and body sicker.

Over these ten years, I’ve read quite a few books, articles, blog posts, and detailed discussions about health-related matters.  I’ve also experimented quite a bit with my own diet, and learned a great deal from that.  The other thing I’ve done a lot of, is have conversations with people about diet, nutrition, diseases, and the metabolic effects of different foods and of insulin.

My position—which has only grown stronger with time—is that the first and most fundamental pillar of optimal health is having a metabolism that runs on fat.  And this means keeping insulin levels low by restricting sugars and starches.  Not necessarily always, but most of the time, as in almost always.

The first question that people ask when they find out is why: Why do you not eat bread? Bread has forever been essential to humans.  I simply couldn’t live without bread.  Or, why don’t you eat potatoes, or rice, or pasta?  They’re so good!  I simply couldn’t live without potatoes and pasta.  And, you don’t even eat fruit? But isn’t fruit full of vitamins and minerals?

The way I have answered has depended on a lot of things: the setting, the atmosphere, the company, the time available, but most importantly on the person.  Some people are actually interested to find out, and maybe even learn something.  Most, however, are not.  Consequently, I have made the answer shorter and shorter over the years.  Now, I even sometimes say: well, just because, and smile.

Maybe you have wondered, or even still wonder why.  Maybe although you’ve read so many times in my writings that I think everyone seeking to improve their health should restrict insulin-stimulating carbohydrates, you still wonder what the main reason is, what the most fundamental reason for which I don’t eat sugars and starches.  Here’s why:


It’s not primarily because carbs and insulin make us fat by promoting storage and preventing the release of energy from the ever larger reserves of fat in our body: I am lean and always have been.

It’s not primarily because carbs and insulin lead to insulin resistance, metabolic syndrome, and diabetes; inflammation, dyslipidemia, water retention, and high blood pressure; kidney dysfunction, pancreatic dysfunction, and liver dysfunction: my fasting glucose, insulin, and triglycerides have been around 85 mg, 3 mili units, and 40 mg per dl for years; my blood pressure is 110/70 mg Hg, glomerular filtration rate is high, and all pancreatic and liver markers are optimal.

It’s not primarily because carbs and insulin promote cancer growth since cancer cells fuel their activity and rapid reproduction by developing some 10 times the number of insulin receptors as normal cells to capture all the glucose they can, fermenting it without oxygen to produce a little energy and tons of lactic acid, further acidifying the anaerobic environment in which they thrive.  My insulin levels are always low, and my metabolism has been running on fat in a highly oxygenated alkaline environment for a decade.

It’s not primarily because carbs and insulin promote atherosclerosis, heart disease and stroke by triggering hundreds of inflammatory pathways that compound into chronic inflammation and damage to the blood vessels, which then leads to plaque formation and accumulation, restriction of blood flow, and eventually to heart attack and stroke: my sedimentation rate, interleukin-6, C-reactive protein, and Apolipoprotein-A are all very low.

It’s not primarily because carbs and insulin promote the deterioration of the brain, dementia, and Alzheimer’s, both through the damage to blood vessels around and in the brain itself, and insulin resistance of brain cells, which together lead to restricted blood flow, energy and nutrient deficiency, and accumulation of damaging reactive oxygen species and toxins in the cells, and, unsurprisingly, eventually to dysfunction that just grows in time: because my metabolism runs on fat, this means that my brain runs on ketones, and is therefore free of excessive insulin or glucose exposure.

It isn’t primarily for any of these reasons, which, I believe, are each sufficient to motivate avoiding sugars and starches in order to keep tissue exposure to glucose and insulin as low as possible.


My main reason is that, at the cellular level, in its action on the nucleus and on gene expression, insulin is the primary regulator of the rate of ageing.

Insulin is essential for life: without insulin, cells starve and die. It is essential for growth: without insulin cells don’t reproduce, and there can be no growth.  This is why at that most fundamental level, insulin regulate growth in immature individuals.  But in mature individuals, once we have stopped growing, insulin is the primary regulator of the rate of ageing, both in terms of its effect in suppressing the production of antioxidants and cleansing and repair mechanisms within the cell, but also in stimulating cellular reproduction. And the more reproduction cycles, the greater accumulation of DNA transcription defects, the faster the shortening of telomeres, and the faster the ageing.

This is a fundamental fact that appears to be true for all living organisms.  It is as true for yeasts and worms, as it is for mice and rats, as it is for dogs and humans.  And the rate of ageing is the rate of degeneration, of growing dysfunction, of more damage and less repair, of lower metabolic efficiency and less energy, of increased cell death and senescence.  I personally wish to be as healthy, energetic, strong, and sharp as possible for as long as possible.  This is why I avoid sugars and starches.  This is why I restrict insulin-stimulating carbohydrates.

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Living healthy to 160 – insulin and the genetics of longevity

Of the most remarkable discoveries of the last 15 years, discoveries that might well turn out to be the most remarkable of the 21st century, are those of the telomere—a little tail at the end of our DNA whose length tells us how long we have left to live, and of the enzyme telomerase—the specialised protein whose job it is to try to repair the telomeres so that the cells (and we) can live longer and, from an evolutionary perspective, increase the probability that we’ll have more babies. This and other research into the biology of ageing and the details relating to the transcription of DNA, and the expression or suppression of genes is truly amazingly fascinating. I will turn to this in time, but think it would be jumping the gun to do so now.

What is definitely one of the most remarkable discoveries of the 20th century pertains to the hormone insulin. I am not, however, here referring to the fact that its discovery revolutionised medicine by allowing the saving of countless diabetics from highly premature and painful deaths, usually preceded by torturous amputations of their feet or legs and all the of the horror and misery brought on by these seemingly barbaric and radically extreme measures. (And don’t for one second imagine that such amputations are a thing of the past: I know for a fact—heard directly from the mouth of a practicing orthopaedic surgeon—that amputations are the reality of his everyday, performing sometimes two in a single day.) I’m not either, at least this time, talking about insulin as the master metabolic hormone that regulates the storage into cells of nutrients circulating in the bloodstream. What I am referring to as one of the 20th century’s greatest discoveries in regards to insulin is that of its role in regulating the rate of ageing.

Something that is almost as remarkable is that we hardly ever hear or read about this. For me, that’s really strange. But whatever, I’m not going to hypothesise and speculate to come up with an explanation for why this is. Insulin as regulator of the rate of ageing is what we’ll look at in this article.

Why do mice live two years but bats fifty? Why do rats live three years, but squirrels fifteen. Why do some tortoises live hundreds of year? Why do the smallest dogs, like Chihuahuas, live about twenty years, while the largest, like Great Danes, live five to seven years only? And why do we, humans, live around 80 years, rarely making it to 90, and very rarely to 100 years of age? It is this line of questioning that triggered in the late 80’s and early 90’s a geneticist working in evolutionary biology to hypothesise, for the first time, that ageing could be genetically regulated, at least to a certain extent.

It was the discovery and subsequent realisation in evolutionary biology at that time, that a large number of fundamental cellular processes and mechanisms regulated by a variety of genetic expressions were common to widely different organisms. The realisation was that because all animal life must necessarily share a common ancestor, it is not only logical that the most fundamental functions of cells and especially of how genes express themselves under the influence of hormones essential for life could be the same, but that it should be, to a great extent, expected to be that way. And even though these considerations may seem obvious in retrospect, the fact is that there was only one person with this knowledge, asking these questions, and having the means to do something about seeking an answer to some. Cynthia Kenyon, Professor at UCSF, was this person.

The subject was quick to choose: the tine worm that Kenyon had already been studying for years, C. elegans, was perfect because it is simple but nonetheless a complex animal, and because it has a short natural lifespan of about 30 days. The first step was clearly defined: find at least one long-lived individual. What seems very surprising from our current vantage point it that she couldn’t readily find one: she couldn’t convince anyone to join with her in this endeavour. Everyone was at that time convinced that ageing was something that just happened: things just wore out and deteriorated with use and with time; nothing to do with genes. But how could this be if different species—some very physically similar—are witnessed to have such widely different lifespans? It just had to be genetic at some level, Kenyon thought. Eventually, after a few years of asking around and searching, she found a young PhD student that was up to it, and set out to find a long-lived mutant.

A number of months down the road a long-lived mutant was found and immediately identified as a ‘DAF-2 mutant’. This mutation made the DAF-2 gene—a gene responsible for the function of two kinds of hormone receptors on a cell’s membrane—less active. The next step was to artificially create a population of DAF-2 mutants and see how long they live, statistically speaking, compared to normal C. elegans. It was found that the genetically ‘damaged’ worms, the ones for which they had turned down the expression of the DAF-2 gene, lived twice as long: starting with exactly the same number of worms, it took 70 days for the last one of the mutants to die compared to 30 days in the normal population.

But an additional observation was made: the curve that traced the fraction of worms remaining was stretched by a factor of two from about the start of adulthood for the mutants. They had the same relatively short childhood but then for the remainder of their lives, for every day in the life of the normal worms, the mutants would live two days. The most impressive was that they were really half their chronologically equally aged cousins in all respects: external appearance, level of activity and reproduction.

To make your appreciate this point as much as you should, this observation with respect to not just the lifespan but notably the healthspan of C. elegans would translate in human terms in someone being 80 years old but looking and acting like a 40 year old in the sense that nobody could tell that they were not 40, let alone 80 years old. Just like Aragon in the The Lord of the Rings. This person would be like a 40 year old at 80, like a 60 year old at 120, and like an 80 year old person coming to the end of their life by the time they were 160! Can you even imagine that? Hard isn’t it. But this is exactly what Kenyon and her team were looking at in these experiments with these little worms.

Now they wanted to understand the effect of the DAF-2 gene, or rather, understand the effect of suppressing its expression in the DNA of each cell’s nucleus at different developmental stages. If it was turned off completely, the worms would die: clearly, DAF-2 expression, at least in C. elegans, is essential for life. If it was suppressed immediately after birth (hatching), the little worms would enter the Dauer state in which they don’t eat, don’t grow, don’t reproduce, and basically don’t move either: they just sit and wait. Wait for what? For better times!

This Dauer state is a remarkable evolutionary adaptation seem in some species that allows the individual to survive during periods of severe environmental stress such as lack of food or water, but also high UV radiation or chemical exposure, for example, for long periods of time with respect to their normal lifespan in a very efficient kind of metabolic, physiological and reproductive hibernation. What’s really cool is that inducing worms out of the Dauer state, no matter how long they’ve been in it, they begin to live normally again, moving and eating, but also reproducing. So, in the Dauer state C. elegans literally stops ageing altogether and waits, suspending metabolic activities and physiological functions until conditions for reproduction and life become adequate once again.


Taken from Worms live longer when they stop eating  (http://www.bbc.co.uk/nature/2790633)

If DAF-2 expression was turned back up to normal, then they moved out of Dauer and resumed their development stages equivalent to childhood, teenage-hood, and then adulthood, but didn’t live any longer as adults. Finally, suppressing DAF-2 expression at the onset of adulthood resulted in the extended lifespan as originally observed. The conclusion was therefore clear: DAF-2 expression is essential for life and necessary for normal and healthy growth and development in immature individuals from birth until they reach maturity, and suppressing DAF-2 expression was only effective at extending both lifespan and healthspan in mature individuals.Going further, they now wanted to understand how DAF-2 suppression actually worked to extent healthspan: what were the actual mechanisms that made the worms live longer when DAF-2 expression was turned down. For this, Kenyon’s team needed to look at all of C. elegans’s 20000 genes and figure out how they affect each other. (Note that this is also more or less how many genes we have, but C. elegans has only 3 chromosomes and is also hermaphrodite.) The sequencing of the worm’s genome was done in 1998, and what was found after analysis was very interesting:

The DAF-2 gene activate a phosphorylation chain that attaches phosphate groups onto the DAF-16 transcription factor. In normal individuals the DAF-2 gene is expressed normally, the phosphorylation chain works unimpeded, and the DAF-16 transcription factor is inactivated. In the mutants, the DAF-2 gene expression is suppressed, and as a consequence, the DAF-16 transcription factor is not inactivated and instead accumulates in the nucleus. There, DAF-16 encodes what Kenyon’s team showed to be the genetic key to health and longevity they were looking for from the start of this now decade long pursuit: the FOXO gene.

What does FOXO do? It promotes the expression of other genes, at least four other genes: one responsible for manufacturing antioxidants to neutralise free radicals the largest amount of which are produced by the mitochondria as they make energy for the cell, a second responsible for manufacturing ‘chaperons’ whose role as specialised proteins is to transport other proteins and in particular to bring damaged ones to the cell’s garbage collector and recycling facility to promote the replacement of those damaged proteins by new and well-functioning ones; a third responsible for manufacturing antimicrobial molecules that increase the cell’s resistance to bacterial and viral invaders; and the fourth that improves metabolic functions and in particular fat transport (reduce) and utilisation (increase).

It is these four genetically regulated cellular protection and repair mechanisms, the cumulative combined effects of all these increased expressions of antioxidants, chaperons, antimicrobials and metabolic efficiency—all of them at the cellular level—that allow the lucky DAF-2 suppressed mutants to live twice as long twice as healthy. Remarkable!

Now that all the cards about how the long-lived mutants actually live twice as long as expected under normal conditions are laid on the table, and that there is only one detail I left out of the story up to this point, tell me: can you guess what are the two sister hormones to which the cell’s sensitivity through the activity of its receptors for them are controlled by the DAF-2 gene? It’s a trick question because I told you half the answer in the introduction: The DAF-2 gene encodes the hormone receptors for both insulin and the primary form of insuline-like growth factor IGF-1. Surprised? It isn’t surprising, really. In fact, it all makes perfect sense:

Insulin and IGF-1 promote growth; nutrient absorption and cellular growth and reproduction are essential for life and thus common to all living organisms, including the more primitive of them like yeasts; growth in immature individuals is fundamental for health and for ensuring they reach maturity; but growth in adults, in mature individuals, just means ageing, and the more insulin and IGF-1 there is, the faster the rate of cellular damage and deterioration, the more genetic mutations from errors in transcription, the more pronounced the deterioration of the brain and the heart, of the arteries and the veins, of the muscles, the bones and the joints, and obviously, the faster the rate of ageing. Because what is ageing if it is not the word we use to describe the sum total, the multiple negative consequences, the end result of all of these deteriorations in these vital organs and systems but also everywhere else throughout the organism, all of it starting at the cellular level, in the nucleus of every cell.

About the necessity of insulin for normal growth, you should definitely not think that these observations impliy we should stimulate insulin secretion in the young in order to ensure proper growth. Totally not! The body knows exactly when and how much insulin is needed at any given time. In fact, any additional stimulation of insulin promoted by eating simple and starchy carbs actually deregulates the proper balance of hormones that the body is trying to maintain. This deregulation from a sugar laden diet in children is the very reason for many wide spread health problems in our youth most important of which is childhood obesity and the metabolic and physiological stresses this brings on. So, leave it to mother nature to know how to regulate the concentration of insulin in the bloodstream. Do not disrupt the delicate biochemical balance by ingesting refined carbohydrates: it’s the last thing anyone needs for good health and long life.

The first results were so interesting that several other groups joined in this research into the genetics of ageing. Not as much as one would think, but at least a handful of other groups began to apply and expand the techniques to other species. Unsurprisingly, the same effects, although with different magnitudes, were seen in these very different species, from an evolutionary standpoint: fruit flies and mice. In addition, the connection was made with lifespan-extending experiments using calorie-restriction, which have also been carried out on mice and other animals (we’ll look into this another time). And beyond the work around DAF-2, DAF-16 and FOXO, Kenyon’s group investigated other ways to influence lifespan and found two more.

The first was by disabling some of the little worm’s sensory neurones of which there are very few, making it easy to test and determine the influence they have separately and in combinations. They tested smell and taste neurones, found that disabling some would extend lifespan while disabling others didn’t. They also found that disabling different combinations of smell and taste neurones could have nulling effects. The second was playing with the TOR gene expression. For now, however, we will leave it at that.

As the fact that it is rare and relatively hard to come by this work without actually looking for it, there is something else I find very hard to comprehend. In Kenyon’s various lectures on this work, there is usually a mention of the biotech company she founded called Elixir Pharmaceuticals and how they aim to find one or more drugs that can suppress DAF-2 expression in humans without causing negative side-effects in order to extend lifespan and healthspan as was done in C. elegans with genetic manipulation. That’s fine, and does make sense to a certain extent, especially if we can find not chemical drugs but natural plant-derived compounds that have this effect on us.

The thing that doesn’t make sense and that is hard to understand from the naive perspective of the honest scientist looking for the simplest possible solution to a problem of inferring something we don’t know from information that relates to what we want to know: in this case this mean the simplest way to make the best use of this information and apply what we have learnt from these two and half decades of research in a way that we know would be beneficial in promoting a longer and healthier lifespan in humans without risks through the introduction of foreign substances in our body. Because they haven’t, here I offer my attempt to do this.

We have, thanks to Kenyon and others, understood in great detail how lifespan in complex organisms can be, to a great extent, genetically regulated, and which genes, transcription factors and mechanisms are involved in the process of regulating the rate of ageing in conjunction with the propensity for developing age-related degenerative diseases. In the final analysis, the main players are the DAF-2 gene that tunes up or down the sensitivity of insulin and IGF-1 receptors, the DAF-16 transcription factor that encodes the FOXO gene but is made inactive by the expression of DAF-2, and the star FOXO longevity gene that promotes the expression other genes responsible for stimulating the cell’s most powerful protection and repair mechanisms.

We have, from many decades of research on calorie-restriction and fasting in animals including humans (and which we’ll explore elsewhere), understood that this is an extremely effective way to extent both lifespan and healthspan and basically eliminate the occurrence of age-related degenerative diseases by greatly increase resistance to health disorders of all kinds. Some key observations on calorie-restricted animals include their very low blood levels of sugar, insulin and IGF-1, high metabolic efficiency and ability to utilise fat demonstrated by low blood levels of triglycerides, and their remarkably younger appearance with increased energy and activity levels.

And finally, we have, from more than a century of observations and research, concluded that diabetics, whose condition is characterised by very high levels of blood glucose, insulin and triglycerides, are plagued by a several-fold increase in rates of cancer, stroke, heart disease, kidney disease, arthritis, Alzheimer’s and dementia, basically all the age-related degenerative diseases known to us, and in addition, also a several fold increase in their rate of ageing based on the spectrum of blood markers used for this purpose, their appearance, but also on the length of their telomeres.

Is it not, therefore, obvious from these observations that high blood sugar, high insulin and high triglycerides are hallmarks of accelerated ageing and a propensity for degenerative diseases, while low blood sugar, low insulin and low triglycerides are instead necessarily related to extended lifespan, extended healthspan and increased resistance to all disease conditions including those categorised as degenerative, and this, independently of the actual mechanisms involved?

Is it not, therefore, plausible from these observations that the genetic mechanisms relating to the function of the DAF-2 gene, DAF-16 transcription factor and FOXO gene in conferring to the DAF-2 mutants twice as long a life can, in fact, be activated and enhanced epigenetically by creating an environment in the organism that is conducive to it: simply by keeping blood sugar, insulin and triglycerides as low as possible? In other words, isn’t it plausible from these observations that by manipulating the biochemistry to ensure that blood sugar, insulin and triglycerides are throughout the day and night as low as possible depending on the organisms requirements, that this will actually translate into the activation of the FOXO gene to enhance protection and repair at the cellular level and thus extend lifespan and healthspan?

And what is, not only the easiest and simplest, but also the most effective way to do this? It is to eliminate insulin-stimulating carbohydrates—sugars and starches—from the diet completely. This, within 24-48 hours, will allow sugar levels to drop to a functional minimum. The low blood sugar will allow the pancreas to reduce production and insulin levels to drop bit by bit. Lowered insulin will eventually allow the cells to start using the fat circulating in the blood, and in time, increase in efficiency, thereby dropping triglyceride levels lower and lower.

Why is it you think that Kenyon never mentions this anywhere? Do you think that this has simply not occurred to her? I honestly don’t know. But if there is a single thing to remember it is this: insulin is necessary for life; in the immature individual, insulin regulates growth; in the mature individual, insulin regulates the rate of ageing and the propensity for degenerative diseases. Hence, if you are a mature individual, and by this I mean full grown, and if you want to live long and healthy, the very first thing you need to do is to keep the concentration of insulin circulating in your blood as low as possible. Everything else that we can do to extend healthspan and lifespan is secondary to this.

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