Ketogenic diet safe and healthy?

ketogenic diet safe effective healthy

The ketogenic diet (in earlier iterations known as the Atkins diet and the Low Carb High Fat diet) has been vilified for decades by members of the nutrition establishment, because it is pretty much telling people to do the exact opposite of what the establishment is telling them to do. While official diet guidelines recommend cutting down on fat intake, the ketogenic diet instead recommends cutting down on carbohydrate intake. Since cutting down on one of the sources of energy virtually requires increasing intake of the other, the two diets are completely incompatible.

The reason proponents of a low fat diet are so against the ketogenic diet is because they believe that fat, and in particular saturated fat, causes heart disease. But this belief has become increasingly hard to maintain over the last couple of decades. In spite of the fact that populations around the world have been dutifully following advice from nutritionists to cut down on fat intake, they’ve actually gotten fatter and more diabetic. The prevalence of metabolic syndrome (a combination of central obesity, type 2 diabetes, and high blood pressure) has exploded since governments started recommending that people cut down on fat. And metabolic syndrome is one of the leading risk factors for heart disease.

This suggests that the nutrition establishment has got everything terribly wrong. It suggests that it’s a high intake of carbohydrates that is responsible for the current poor metabolic health of western populations, rather than a high fat/saturated fat intake. Of course, the data suggesting this is all observational, and observational data can show correlation, but they cannot prove causation.

So, let’s look at what the randomized controlled trials of the ketogenic diet have to say on the matter. A systematic review and meta-analysis was published in Nutrients in July 2020 that gathered together all the trials of a ketogenic diet. The review was funded by the South Korean government.

Fourteen trials were identified, with a total of only 700 participants. This small number shows how under-researched the ketogenic diet is, likely due to strong biases against the diet among those who fund nutrition research. However, eight of the fourteen trials were carried out in the last decade, suggesting that it is gradually becoming easier to finance this sort of research.

Eight of the trials were looking specifically at people with type 2 diabetes, while the other six were looking at non-diabetics. Of the studies not looking specifically at diabetics, all were looking at people with overweight or obesity, so all twelve were studying people who were metabolically unhealthy in one way or another at the beginning of the trials.

The study with the shortest duration lasted two hours(!) while the study with the longest duration lasted two years. Most of the trials lasted for at least a few months. The smallest individual study had 11 participants, while the largest had 146 participants.

Twelve of the trials were comparing a ketogenic diet with a low fat and/or a low calorie diet. Two compared a ketogenic diet with letting people go on eating whatever they were eating to begin with. So most of the studies were comparing two different types active diet modification, rather than comparing a ketogenic diet with just continuing on as usual. This is worth remembering as we get to the conclusions.

The reviewers determined that the overall risk of biases skewing the results was low. The size of the effect of a ketogenic on different parameters was measured using a statistical technique called Standard Mean Difference (SMD). This is a technique that is useful when different studies are measuring the same thing in different ways, because it converts all the different measurements in to one shared format, which allows for meta-analysis. An SMD of zero means that there is no difference whatsoever between groups. An SMD of 0,2 is usually considered small, while 0,5 is considered moderate, and 0,8 is considered large. The disadvantage with converting results to SMD is that they become more abstract and thereby harder to interpret in terms of real world outcomes.

Anyway, let’s get to the results.

Among type 2 diabetics, a ketogenic diet resulted in a reduction in HbA1c (a measure of average blood sugar levels over the last few months) of 0,62 SMD, an effect that was highly statistically significant (p-value 0,001), when compared with a low fat or calorie restricted diet.

Among non-diabetics, the ketogenic diet had no statistically significant effect on HbA1c. This is largely as we would expect, since non-diabetics have functioning homeostatic mechanisms that are able to maintain blood sugar within relatively strict limits regardless of what they eat.

The big effect on HbA1c in type 2 diabetics is important, and aligns with other evidence that a ketogenic diet can be used to effectively push type 2 diabetics in to remission. Back before the advent of medications to treat type 2 diabetes, the main treatment used by doctors was a low carbohydrate diet (a fact which most modern day doctors are completely unaware of). So it makes sense that a ketogenic diet would have this large effect on HbA1c.

People on a ketogenic diet lost more weight than people on low-fat/low-calorie diets, with an SMD for weight loss of 0,46. The statistical significant was pretty weak (p-value 0,03), but 7 out of 8 trials reporting data on weight change showed that the ketogenic diet performed better than the low-fat/low-calorie diet, which suggests that the effect is real. The diabetics benefited more than the non-diabetics, with an average weight loss over the course of the studies of 7,8 kilograms among the diabetics, as compared to 3,8 kilograms among the non-diabetics.

People on a ketogenic diet also did better in terms of reductions in waist circumference than people on low-fat/low-calorie diets, with four out of the five studies that measured waist circumference favoring the ketogenic diet. However, the effect was not statistically significant (p-value 0,09). This could mean that the effect isn’t real, but more likely means that there were too few participants to show a significant difference. In other words, the studies were statistically underpowered for this end point.

More importantly, however, there is no signal that a ketogenic diet results in less waist reduction than the low-fat/calorie-restricted diet. Waist reduction is particularly important, because it is the fat that accumulates in the abdomen that most strongly correlates with heart disease and diabetes. Subcutaneous fat that is more evenly spread out around the body doesn’t show anywhere near as strong a correlation.

Ok, so far we know that a ketogenic diet appears to be more effective than the conventionally recommended low-fat/low-calorie diet at both lowering blood sugar and inducing weight loss. But the main concern from establishment nutritionists about the ketogenic diet has always been that it causes heart disease, based on data that suggest it increases on LDL (“bad cholesterol”).

Before we look in to whether the ketogenic diet does in fact raise LDL, let’s think about whether this is something we need to be concerned about or not. Although LDL correlates somewhat with heart disease in observational studies, the evidence from randomized trials strongly suggests that the relationship between LDL and heart disease is not causal. A systematic review published in BMJ Evidence Based Medicine last year could not find any correlation between the amount of LDL lowering achieved with various LDL lowering drugs and the effect on either cardiovascular events or overall mortality. This suggests that we don’t need to be as concerned about LDL as many people believe.

And apart from LDL, there’s also HDL (“good cholesterol”) and there are triglycerides (the amount of fat in the blood stream). All three are considered to be risk factors for heart disease. In general, LDL and triglycerides correlate with increased risk of heart disease, so you want them to be low, and HDL correlates with decreased risk of heart disease, so you want it to be high.

Anyway, let’s see what effect a ketogenic diet has on these markers for heart diease.

Among diabetics, the ketogenic diet had no effect on LDL. It had a modest positive effect on HDL, with the SMD increasing by 0,31. The result was statistically significant. (p-value 0,005). The ketogenic diet also had a negative effect on triglycerides, with the SMD decreasing by 0,45 (p-value 0,01). In other words, in diabetics, the ketogenic diet had no impact on LDL whatsoever, and a beneficial impact on both HDL and triglycerides.

So, for type 2 diabetics, a ketogenic diet appears to protect against heart disease, at least if you go by the traditional risk factors. All the risk factors are either unaffected or affected in a way that correlates with decreased risk. Among non-diabetics, however, the picture isn’t quite so rosy. In this group LDL did increase, with a modest but statistically significant SMD of 0,35 (p-value 0,009), while HDL and triglycerides were unchanged.

So, how shall we interpret this? Does a ketogenic diet decrease your risk of heart disease if you’re diabetic, but increase it if you’re not?

It’s possible. But it seems unlikely that the same dietary intervention could have a beneficial effect on risk of heart disease in diabetics but a harmful effect on risk of heart disease in non-diabetics. Let’s move on and look at the final major risk factor for heart disease, blood pressure. The ketogenic diet did not appear to have any effect on blood pressure, either up or down, as compared to the low fat and calorie restricted diets. This was true in both diabetics and non-diabetics.

Ok, so those are all the results. What can we conclude?

The ketogenic diet appears to be more effective at achieving weight loss than the low fat and calorie restricted diets. Considering how much suffering is involved in the calorie restricted diet, this should be welcome news for people everywhere who want to lose weight without having to feel like they’re starving to death.

In terms of safety, the picture is a little more complex. For type 2 diabetics, the ketogenic diet appears to be more or less like a magic bullet, resulting in them becoming noticeably slimmer, while at the same time pushing their diabetes in to remission, and also decreasing their risk of heart disease. Pharmaceutical companies won’t like it if this gets out, it could put a serious dent in their profits!

For non-diabetics, however, there is one concerning fact, and that is that LDL goes up. Why it does this in non-diabetics but not in diabetics, I have no idea. Could it be a statistical artifact, i.e. not real? Yes, it could. The result is based on just four studies, with a total of 235 people. But all four studies show a similar increase, suggesting that the effect is real. As mentioned, however, LDL only correlates with heart disease in observational studies, and not at all in randomized clinical trials of LDL lowering drugs, so it is somewhat questionable how important it actually is to consider as a risk factor. And people over the age of 60 tend to live longer if they have a high LDL rather than a low LDL, so for elderly people an increased LDL might actually be a good thing.

In other words, the overall evidence to suggest that a ketogenic diet isn’t safe is very weak. It is based entirely on one surrogate marker, LDL, and not on any hard outcome data. Until someone does a longitudinal study that follows people on a ketogenic diet over an extended period of time to see what happens, and compares them with a matched cohort, we won’t know for certain.

Things can often seem to be one way when we look at surrogate markers, and then when we do a proper study, looking at hard outcomes, things turn out to be very different. A good example of this is the Women’s Health Initiative study, a massive randomized trial with 49,000 women that was meant to show that a low fat diet decreases risk of heart disease, but which failed to find any benefit whatsoever. And if a low fat diet doesn’t decrease risk of heart disease, then it’s quite reasonable to think that a high fat diet probably doesn’t increase risk of heart disease.

One last thing worth repeating is that the systematic review discussed here was mostly comparing a ketogenic diet with a low-fat/low-calorie diet. Other studies have, for example, found that the ketogenic diet is effective at lowering blood pressure when compared with a standard western diet. The reason no effect was found here was likely because it was being compared to the low-fat/low-calorie diet, which is also effective at lowering blood pressure. Any diet that causes you to lose weight will cause your blood pressure to drop.

So, to sum up: the ketogenic diet is highly effective as a treatment for type 2 diabetes and as a weight loss strategy. The fact that it modestly raises LDL in non-diabetics is somewhat concerning, but it is questionable whether this actually means anything in terms of real world outcomes.

Please provide your e-mail address below and you will get all future articles delivered straight to your inbox the moment they are released.

Join 23.6K other subscribers

53 thoughts on “Ketogenic diet safe and healthy?”

  1. Medical students are taught that ‘LDL is bad, HDL is good, and triglycerides go along for the ride’. Similarly, no attention is paid to ketogenic diets in the medical curriculum. Will this ever change? I’m not holding my breath.

    1. This is a reply to Peter Hill, PhD, but the website doesn’t let me fit it in there:
      Ever since Malcolm Kendrick, Gary Taubes, and others, showed that there is zero evidence to support the cholesterol hypothesis, its defenders have kept on coming up with what Karl Popper would call ‘ad-hoc hypotheses’, which are devices that scientists use to explain away apparent contradictions to much-loved hypotheses. e.g. the idea that “LDL-cholesterol per se is not the issue. It appears that its the sub-class pattern that determines risk.”
      To quote Kendrick:
      “Ad-hoc hypotheses work along the following lines. You find a population with a low saturated-fat intake (and few other classical risk factors for heart disease) – yet, annoyingly, they still have a very high rate of heart disease. One such population would be Emigrant Asian Indians in the UK. The ad-hoc hypothesis used to explain away their very high rate of heart disease is, as follows. Emigrant Asian Indians are genetically predisposed to develop diabetes, which then leads to heart disease. Alakazoom! The paradox disappears. On the other hand, if you find a population with a high saturated-fat intake, and a low rate of heart disease, e.g. the Inuit, you can always find something they do that explains why they are protected. In their case it was the high consumption of Omega 3 fatty acids from fish.”

  2. LDL-cholesterol per se is not the issue. It appears that its the sub-class pattern that determines risk.
    “The LDL subclass pattern characterized by a preponderance of small, dense LDL particles was significantly associated with a threefold increased risk of myocardial infarction, independent of age, sex, and relative weight.” JAMA 1988;260:1917-1921

    A relatively easy and cost effective way of determining which LDL-particle size is most prevalent in a given sample is to divide the triglyceride value by the HDL-cholesterol value. Aim for a ratio of 1:1 or less.

  3. Thanks for this review. Personal experience makes me a great believer in the ketogenic diet for weight control and as a “cure” for dysmetabolic syndrome. All my cholesterol related numbers significantly improved, including LDL (albeit it remained minimally elevated) and blood glucose normalized (as did Hgb A1c).
    The question is whether elevated cholesterol is an isolated issue or part of a larger issue. Excluding hereditary hypercholesterolemia is it part of the “dysmetabolic syndrome”. (Diabetes type 2/hyperglycemia, dyslipidemia (including triglycerides) with or without obesity. Dysmetabolic syndrome is at a epidemic, or better, pandemic level.

    The fact that DM can be seen in both the obese and non-obese is a significant clue. This leads to 4 phenotypes (fat on the outside/fat on the inside; fat on the outside/thin on the inside; thin on the outside/fat on the inside; thin on the outside/thin on the inside).

    Fat on the outside/thin on the inside is the Sumo wrestler phenotype is a mystery if the “standard diet theory” is used.
    Fat on the outside/fat on the inside is the standard dysmetabolic phenotype.
    Fat on the outside/thin on the inside is a mystery if the “standard diet theory” paradigm is used.

    The rise in dysmetabolic syndrome/obesity parallels the introduction of heavily sugared/high fructose corn syrup in the food supply.

    This is an association and becomes meaningful if known biological mechanisms exist.
    The resolution of a paradox (thin on the inside/fat on the outside) is the clue necessary to resolve the paradox.

    From a genetic metabolic point of view, the population gain be divided into 90% +(a “normal lipogenic genetic predisposition and <10% with a pro-lipogenic genetic disposition/pleomorphism in one genes, such as leptin, adiponectin, P-1 enzyme).
    High carbohydrate diets cause weight gain in both groups.
    What is the difference?
    The sumo phenotype (fat on the outside/thin on the inside) is found with high carbo-hydrate diets rich in starches and poor in sugars.
    In terms of dysmetabolic syndrome, the high carbohydrate diet is high in sugar.
    This leads to a more subtle distinction: High carbohydrates makes one fat but only high sugar diets induce dysmetabolic syndrome.
    If one gets fat from eating excessive starchy carbohydrates without sugar, one gains weight but does not enter into dysmetabolic syndrome. (Sumo phenotype; fat on the outside; thin on the inside).
    If one gets fat from eating excessive sugar, then one develops dysmetabolic syndrome.
    What is the difference: Starches are essentially glucose; sugar is essentially 50/50 glucose and fructose.
    This leads to the conclusion that the difference is fructose. The body can only handle minimal amounts of fructose.
    What is the difference between fructose and glucose from a metabolic point of view? Fructose is handled like an alcohol and is predominantly metabolized in the liver resulting in hyperglycemia and insulin resistance. As an extra-detriment, excess fructose is dumped into the colon and alters the microbiome., resulting in right sided polyp formation (aka, "sessile serrated adenoma"), increasing inflammatory bowel disease/irritable bowel syndrome, and increased colo-rectal cancer at an ever younger age).

  4. As a healthy person who has been on the ketogenic diet for over 7 yrs now, I can say that my LDL has crept up over the years; however, as I’ve kept track of my numbers, it’s ratio to HDL remains exactly the same. My HDL was recently so high that it wasn’t accepted by the Framingham risk calculator as a legitimate value (110 mg/dL). Yet, I no longer put much if any stock in cholesterol values because I now understand the primary root causes of heart disease, and I address those to the best of my ability in my diet and lifestyle–the value of my LDL is certainly not one of them!

  5. Sebastian, talking about ketogenic nutrition we need to mention the state of ketosis, measurement of ketones, glucose and ketogenic enzymatic long term adaptation stages accounting for fatty acid oxidation effectiveness from 10 to 120 g/hr, there are four stages – from one week up to several years of adaptation. They can be measured in relation of the gradient of change of AcAc and BHOB levels related to the particular stable low blood glucose level. If the studies used these aspects they would be even more trustworthy.

  6. The fact that ketogenic diets lead to elevated LDL is based on measuring LDL density. LDL particle size and particle number matters bigly.

  7. I read most of the posts on this blog. The conclusion seems to be that neither exercise, a ketogenic diet nor a low fat diet result in evident weight loss. What should I do if I want to achieve weight loss?

    1. Hmm, I don’t think you read this article right. The ketogenic diet is probably the most effective dietary method to lose weight. Note that the reductions seen here were during the study periods, which were for the most part months, not years, and the reductions seen are in relation to a low fat/low calorie diet, which also results in weight loss, just not as much. If you compare a ketogenic diet with a standard western diet rather than a low fat/low calorie diet, and follow it for years rather than months, then you will usually see large amount of weight loss.

      1. Ok, thanks for clarifying! I will re-read the article in the light of this information.

        As a sidenote:

        Keep up the good work with the blog! I am trying to adapt my lifestyle (at least slightly) according to your findings.

        Will you write about anti depression pills? I think it’s an important topic to write about. I can imagine it’s not super easy to find good studies as the outcome is a bit subjective.

    2. Roland, I saw your question about anti-depressants. I have a friend who has really struggled with the side effects from her medication. This book had a lot of helpful information

  8. What I would really like to see are some studies comparing the Keto diet to a whole foods plant based diet. Sebastian, there is a book called the China Study about plant based diets I think you might find it very interesting and I’d love to hear your opinion on it.

    1. I do have an opinion on the China study. It was a small, low quality, observational study, with a few thousand people, carried out in China in the 1970’s, long before the existence of and other innovations to ensure the integrity of research. I don’t think it was ever even published in a peer-reviewed journal. Basically, the China study is worthless.

  9. Thank you, Dr Rushworth, for another interesting article. Your review of the meta study is – as usual – good, but I am amazed that you can write an article about the keto diet without mentioning insulin at all. My understanding from the past decades of research is that metabolic syndrome is not ‘a combination of central obesity, type 2 diabetes, and high blood pressure’, but that these are symptoms of what is called, by some, MIRS – Metabolic Insulin Resistant Syndrome.

      1. Dr Rushworth

        Is insulin resistance a proper label? Wouldn’t it be better to call this condition ”glucose saturation” in the cells? When this happens insulin can not put more glucose into the cell. There is not necessarily anything wrong with the insulin response, it’s just full.

      2. I don’t believe at all in this “glucose saturation” thing. There’s basically endless capacity for energy storage in the fat tissue, and indeed, that’s where the excess glucose eventually goes, unless you have a bad diabetes and pee it out. Isn’t the problem rather, that the liver continues to manufacture glucose, even though blood glucose is high, i.e. it doesn’t get the message of insulin? Or is the origin of the problem in the alpha cells of the pancreas, which produce too much glucagon?

  10. Dr. Rushworth
    Very thoughtful article as ever.
    part 1
    Pathcoin above made some nice points. Thin in – thin out and you are safe. Thin in -fat out most likely safe, if you can still add to outside. If not, insulin resistant…
    Also, it is always good to separate with starch (pure glucose) and added sugars or fruits (glucose + fructose). The fructose part needs some context, but it is always consumed with glucose, so most likely the liver glycogen storage gets full and the problem with remaining fructose prevails.

    Now, I do not know anybody, who knows what causes T2D. However, en route and once there, there is massive imbalance with everything: glucose, free fatty acids FFA, VLDL carrying triglycerides (let’s leave lactose and keto for simplicity); hormones insulin, glucagon. Imbalance means abundance and thus overly reactions. I would call this “energy poisoning”. And insulin resistance, the main job of which is to prevent FFA into blood. (see below)

    This total fasting or keto thing, the only therapeutic measures 100 years ago, what do they do? Cut the glucose from entering the blood directly, and since carbs arouse insulin, there’s less need of it. Insulin was anyhow for lesser benefit, FFA were leaking into blood anyways. With proper reaction, the hunger, i.e. a need to tank more energy, becomes less with more alternative energy in blood. Extra fat oxidation, extra FFA conversion to keto… Cutting carbs is like a two-edged sword, thus very effective. I would presume adding extra proteins and less fat would result in the same but more slowly; amino acids have 56% of insulin reaction compared to carbs. But any reduction i.e. dose dependency seems to be fine!

  11. part 2
    I have pointed out to Virta Health (keto) and DiRECT (low calories 800 kCal/d) before. They intend to heal people from T2D, and both have success. DiRECT emphasizes “weight loss first”, which results in remission. They apparently did not realize, that their 55% of carbs in the soup meant 130g which is low carb. Virta wants low carb which is verified thru keto in the blood. Both have run for 2 years and still running; let’s hope these are the long-term evidence the “dinosaurs” are screaming for. They are especially fond of DiRECT, because it proves their point of “weight gain causes, weight loss heals”, and without sacrifying the “essential” percentage of carbs.

    There is one more point for keto or moderated carb intake. The incretin effect means effectively, that there is no hormone to guard the upside of blood glucose. There are three major plus a few minor hormones to ensure the minimum level of blood glucose. Incretin hormones from the upper gut (GIP, GLP after swallowed food) and background FFA seems to be the driving force for insulin secretion; should you emulate the blood glucose of OralGTT by IV glucose infusion, you would get an insulin response of 1/8 of the oral load. This was for a healthy person, T2D is emphasized for the worse. So, try to avoid “oral stimulation of insulin” if you please, your blood glucose concentration per se does not stimulate like anything. It will harm you, though.

    Since GIP reaction to bread is far less than to bread and butter, consequently less insulin is being secreted. This might explain why in history the fat-free (fish only) diets have also cured “energy poisoning”. Less energy and less insulin is always a good recipe.
    ps. I guess my post was too long as one comment…sorry

  12. Ketogenic diet might be effective in lowering blood presssure due to less retained water in the body.

  13. Because I am insulin resistant because of PCOS, I tried to stick to a strict Keto diet. However, I found it was too hard to give up all carbs, especially fruits and a little bread. Now I avoid refined sugars, flour, all processed foods and fast food. That part was not hard at all because I dislike fast food and nearly all of the ready-to-eat junk from the supermarket. I do eat meat, fish, butter, and dairy. I never did buy into the sugar is good, fat is bad story.

  14. I’ve been reading ‘The Hybrid Diet’ by Jerome Burne & Patrick Holford. Burne comes from a keto perspective, Holford from a low glycemic load perspective (plus intermittent fasting in some of his books). They reconcile their approaches with the idea of switching between the two. They make a reasonable case, although the ratio they come up with seems arbitrary.

    I find it impossible to stick to other people’s meal plans, so I’m going to use a device that measures when I’m in ketosis, experimenting with diet to see what gets me there. I’ve never been overweight, but for whatever hormonal reason have always been prone to “diabetes of the skin”. Fat emerges in pimples on the face, not round the waist. If this is an early warning system for insulin resistance, I already have an idea of which foods in which quantities are dangerous, and I know fasting and ‘training low’ i.e. long duration, low intensity exercise on low levels of carbohydrate to be beneficial. It’ll be interesting to see how these compare with a high fat approach for ketone production and skin health. Not really relishing the thought of digesting loads of fat though.

    1. Just curious, what foods and in what quantities seem to cause insulin resistance in you?

      1. Unless I’ve been fasting and physically active all day, anything but the tiniest quantity of refined sugar or dried fruit – raisins and figs being the worst. With fresh fruit, the sweetness level is generally a fair guide – pineapple and sweeter varieties of grapes are the worst. A small apple or pear is usually okay. 100 grams or so of berries or plum is okay. With grains, three tablespoons or so of millet, buckwheat or quinoa are okay, rice, oats and wheat not so good, although spelt not as bad as most wheat. The worst possible combination is sugar plus a digestive upset as I struggle to get rehydrated. Ameliorating foods – egg, avacado, raw red onion, chicory (especially red) small quantities of raw red cabbage or beetroot. Is there something about that purpley red colour?

  15. For a far better explanation of LDL please read these reports:

    From The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong? by James J DiNicolantonio


    Saturated fat is not the major issue by Malhotra A. BMJ 2013;347:f6340.

    Then eat meat and more meat, but make sure it’s grass-fed, wild-caught seafood, or Omega-3 meat.

  16. How have humans have lived in the Arctic for tens of thousands of years eating only meat and fat without peer reviewed studies?

    1. Thanks for this. I suppose everyone’s diet should be tweaked depending on their genetic heritage, but the fact is that we have evolved over time via eating a certain amount of animal protein (ergo saturated fat) coupled with plant matter (complex carbs.) In contrast, processed foods have been around for just four generations – and the damage is there for all to see.

      If you eat a modicum of healthy (i.e. responsibly produced) saturated fats it will crowd out the craving for sugar (which is even more addictive than cocaine) and tamp down the craving for the simpler carbs (i.e. bread, pasta, etc.) Throw in, of course, regular exercise, sunshine, intermittent fasting, and a positive attitude and the chances are good you will end up with insulin sensitivity, the metabolic key to weight control.

      “Why We Get Fat” by Gary Taubes is a good book. “Deep Nutrition” by Kate Shanahan is good too.

      1. Do we know how much difference genetic heritage makes? It’s a fascinating question because although, as you point out, processed food is quite recent, there are a wide range of traditional diets. Are people with tropical origins better adapted to consuming sweet tropical fruit?

      2. That is an interesting question. My guess would be that people whose ancestors have been farming for 10,000 years are better adapted to a high carbohydrate grain based diet than people whose ancestors were hunter-gatherers until a few generations ago.

      3. Interest ask, how quickly does the human genome follow a change in its diet?
        In the case of cereals, this happened quite quickly (10000 yars). And in the case of dairy products, it requires a longer period. Such conclusions can be drawn from the prevalence of individual intolerance to gluten and lactose.

      4. I don’t know that humans have adapted to a high carb grain based diet. There are several problems people develop with such diets. Leaky gut, insulin resistance, metabolic dysfunction to name but three. Humans developed to eat fat for energy, and it was easier to get energy from consuming what predators had left from large herbivores, and later to take down the animals directly.

    2. Very good point. This debunks the whole red meat, saturated fat, cholesterol canard.

      (I think it was Amudsen’s crew about a century ago which found itself in the Arctic for a time and forced to subsist on the Eskimo diet. At first they found it repellent. After a few weeks they became habituated to it and resisted giving it up once they had the option of returning to a more modern diet.)

      1. Roland,
        Fruit is very seasonal. Even in southern FL fruit is not a year-round event. Also, in the past 10,000 years farmers learned how to select for sweeter fruit. So the fruit available today is much sweeter and BIGGER than 10,000 years ago and before. The chemistry of animal bodies hasn’t changed much in the past four million years. The foundation food still remains the green leaf which is why grass-fed meats and wild-caught seafood is so good for you. We all need to keep the green leaf at the bottom of our food chains.

  17. Paul, eating less might work if there is no food available, as giving in and eating when your hunger signal turns on the other thing to do is to eat saturated fats for energy and not so much carbohydrates . Robert Lustig on calories.

  18. Dave, the primary exercise in weight loss is to eat nutritious food. That way your system stops demanding when it is nourished.

  19. « Ketogenic diet safe and healthy? »

    Of course it is. Otherwise you wouldn’t bother to lose your time, your words and your brain cells with this subject.
    Wish you good health and wealth.

  20. Something that is hardly ever spoken about when it comes to diet is how does the diet make the person feel. From personal experience having been overweight most of my adult life and tried just about every diet and exercise regime. A low calorie or low fat diet just drains me of energy, spending a life of waiting for the next mealtime and just trying to get through the day. I stumbled across Low Carb and found that the less carbs I eat, the more energy I had. Even better was that as I wasnt spiking my insulin (bodies reaction to carbs) I wasnt hungry either. Nowadays I am more of a keto-vore, pretty much meat based and normally just one meal per day (perhaps two on a weekend). my energy levels are through the roof, I feel 20 years younger. Exercise is something I incorporate into daily life, why take the car to the shops when I can walk etc. wouldnt even think about joining a gym but rely on walking and lifting of weights at home. As for the weight loss side of it, I have lost 140 lbs (60kgs) Which I am sure has to be of benefit to my long term health. One final thought to the low fat promoters is just how are fat soluble vitamins supposed to get absorbed on a low fat diet ?

    1. Why humans are not designed to be vegan, and even meat eating is not top of the list. It is fat (animal fat) that gives humans the advantage, and ability to run their comparatively large brains. It’s 40mins from Jess Thompson

    2. In my humble opinion, there is a certain limit beyond which further reductions in dietary fat impair the absorption of fat-soluble vitamins. However, this limit is low enough to cause concern.

  21. I have immense respect for Dr. Seyfried and his ketogenic brain cancer therapy, but I find it crazy to take ketogenic therapy as a regular diet. Why?
    First, the long-term effects of the ketogenic diet are not well understood; most of the studies were of a short-term nature.
    Second, while for clinical professionals (as Dr. Seyfried), keto is a low-calorie diet (1,800 calories per day), for the majority of the uninitiated public, keto is simply a highfat diet.
    Last, my own study of the association of diets and breast cancer incidence around the world led me to the conclusion “more fat – more cancer.”
    Incidence declined non-linearly with decreasing calorie intake.
    The fat/risk curve had the same relationship.
    However, the ratio of fat to carbohydrates in total calories was found to be critical.
    The animal-to-plant fat ratio was also statistically significant between the group of countries with the highest risk and the group of countries with the lowest risk.
    The Big Pharma may really not like the fact that a dietary change could rob them of their profits. However, it seems to me that a fatty diet is a poor alternative to other diets. At least this is the case for breast cancer.

  22. Nice article. I was very interested to read how hba1c as a marker can be measured over two time points and if dietary change doesn’t much adjust the value then all is working normally. This is good to know.

    If you’ve only got the number to go on and see no reduction over a period of three months even though switching to lower carbs, it seems as if the low carb approach doesn’t work, but actually what you are saying is that there is nothing wrong and your hba1c level was and is fine. And you don’t have prediabetic issues.

  23. Maybe this meta-analysis of ketogenic diets was not guilty of it, but a lot of “low carb” and “keto” studies do not reduce carbs enough, or the time period of the study is too short; it takes someone’s metabolism a few weeks to acclimatize to ketosis.

    Another thing to pay attention to when reading this kind of study is the kind of fat included in the diet. It’s starting to look like polyunsaturated fats have a huge adverse metabolic impact, unlike more evolutionarily-appropriate saturated fats.

    If it’s a rodent study you have to drill down and investigate the actual chow components. Hyperlipid is really good at pointing stuff like this out.

  24. Has anyone looked at the role of inflammation? My Keto diet has coincided with a lot less inflammation.

Leave a Reply

Your email address will not be published. Required fields are marked *