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G'day, I'm Dr. Paul Mason, and today I'm going to talk about nutrition. Now, most people know that doctors don't get taught much about nutrition, but the real problem is that the little we do get taught is mostly wrong.
Last year, I was giving a tutorial to some doctors who were training to become sports medicine physicians. Now, these were smart, motivated doctors. They were on a training program that was difficult to get into, and they all turned up to a four-hour tutorial. So, I gave them a short test on diabetes and nutrition to see how their medical education measured up. The average score was 9 out of 22, just shy of the score my receptionist got. And these were intelligent doctors. Their medical education had just failed them.
And this, unfortunately, means that doctors often give bad nutrition advice. And more importantly, it also means that doctors often can't recognize good advice, even when it's in front of them. And this is due to something called confirmation bias, where everything a doctor sees is filtered through the lens of their biased education.
Take this letter I received from a patient detailing his appointment with a medical specialist. This patient had commenced a high-fat, ketogenic-style diet. And by all objective markers, he was doing a lot better. He had lost weight, lowered his blood pressure, and his inflammatory markers on his blood tests had dramatically reduced. And the doctor was pleased and praised the patient on how much better he was doing. That is, until he found out these results were achieved on a diet high in fat and low in carbohydrates. At which point, he told the patient his new diet was unhealthy.
Another example of this was experienced by my 71-year-old male patient who, amongst other things, had reversed diabetes, fixed his blood pressure, stopped five medications, and put his inflammatory bowel disease into remission, all with dietary change. You'd think his diabetes doctor, an endocrinologist, would be happy. Well, his endocrinologist was able to recognize that the resolution of his diabetes was likely due to his new low-carbohydrate diet, but she couldn't get past her medical education on nutrition. She proceeded to recommend he return to his previous diet, as recommended both by guidelines and her medical education, the exact same diet the patient was diligently following when he developed all of these medical issues in the first place. And for good measure, she recommended he take a statin to lower his cholesterol, a recommendation I believe was not supported by evidence.
And this doctor is not alone. Most of her colleagues, every day, are parroting guidelines about what they get taught in medical school, to the detriment, I believe, of the health of our population. As the decades roll by, it's apparent that the population is getting sicker. But just how sick might actually surprise you.
This national survey on U.S. adults on five metabolic health markers found that only 12 percent of U.S. adults were healthy on all five metrics. 12 percent. And the problem is much worse for those over 60, with only 2 percent considered healthy. This means there are literally millions of people out there with metabolic illness, placing them at risk of diabetes, heart attacks, stroke, cancer, dementia, and more. Most who don't even know it.
And there are several simple physical signs that you could be one of them. Perhaps the most obvious sign of poor metabolic health is obesity. But did you know that skin tags can also be a marker of poor metabolic health? Because I can tell you, a lot of doctors don't. In fact, most doctors will tell you not to worry about them. This skin pigmentation, called acanthosis nigricans, and often around the neck, in the armpits, or groin, is also a sign of metabolic sickness. As is erectile dysfunction and fungal infections like tinea or thrush.
If you have prominent sock marks, that might even indicate heart failure. Basically, if the heart is not pumping properly, the pressure within the blood vessels in the legs might get too high, and that can allow the fluid from within these vessels to seep into the surrounding tissues. And when you press on this waterlogged tissue, you can displace some of this fluid, creating a depression that is left behind. If you have this, you should definitely get it checked out to be on the safe side.
So, the question is, if you're metabolically unwell, what should you do about it? Well, the first step is to consider whether you eat to the food pyramid. Because if you do, your diet might be causing you harm. This is a photo of one of my patients when she strictly followed the food pyramid diet. Overweight, in chronic pain, and taking a bunch of medications for conditions like reflux and high blood pressure. She wasn't in a good way. And don't doubt for one second that she wasn't following the advice she was given to a T. And yet, I went to dietitians, and they said to me things like, "Are you following the plan?" And I was, to the letter. So, feeling responsible for being a failure, the only way she could stop her weight from ballooning, despite exercising for more than 12 hours a week, was by literally starving herself.
"I stopped. So, I literally just thought that this is going to be me for the rest of my life. I'm going to have to be eat my salads and just be hungry." Following the advice of her doctors and dietitians had driven her literally into eating disorder territory. To put it bluntly, she'd been failed by the very people whose job it was to look after her.
But even though the food guidelines so catastrophically had failed her, it took some convincing to get her to give keto a go. "Because you told me, and I didn't believe you. I thought, no, I'm just going to pack on the weight if I eat the way that you tell me to eat." And I was only able to get through to her by appealing to science, because she was a research scientist by occupation. So, I challenged her to review the scientific literature. And fortunately, she rose to the challenge. And so began her journey with keto.
"I then started to look into all of this, and it just made sense. And then, then I secretly did it. I didn't tell a soul that I was doing it because, 'Vicki, will you be on another diet?' And try it. She did. While the sense of shame she felt from a lifetime of failed dieting led to her starting the diet in secrecy, she ended up losing 36 kilograms and coming off all her medications. In her own words, she had no idea how sick she was until she was better. And she's now kept the weight off for five years and remained off all her medications. And she's far from alone.
This is another one of my patients, aged 46 and a size 20 on the left. On the right, she's aged 48 and a size 8. And today, age 50, four years into her keto diet, she's still a size 8. And these results are not unique to my practice. In fact, when it comes to weight loss, the literature is overwhelmingly, and I mean overwhelmingly, in favor of low-carb diets.
Between 2003 and 2018, there were 62 published randomized control trials comparing weight loss on low-carb or low-fat diets. Of these 62 studies, 31 had statistically significant results, which means they had a finding unlikely to be due to random chance. Here, I've graphed the results of all these 31 studies. The green bars represent the amount of weight loss in the low-carb groups, and the adjacent red bar, the amount of weight lost in the low-fat group. If you look at each pair of results, you'll see that the low-carb arms lost more weight in all of them. All of them. Not one single study found in favor of low-fat diets.
So, to all those naysayers out there who say low-carb and high-fat ketogenic diets are just too hard, don't even bother trying. Just ask yourself, what are the consequences of not doing it? I have hundreds of patients who are doing it, doing it well, and doing it for years, myself included. So, please, stop being blinded by your biases. Open your eyes to what is possible.
So, you might be wondering, what is a low-carbohydrate or ketogenic diet actually? Well, they're diets that reduce the amount of carbohydrate you eat. And the difference between them is not based on the specific amount of carbohydrates, but rather how your body responds to it. While both diets lower the amount of carbohydrate you eat, on a ketogenic diet, you reduce the amount of carbohydrates sufficiently to allow your body to burn enough fat to produce ketones. And these ketones can be detected in the blood. And when the ketones are detected, this is called nutritional ketosis, and it indicates you're on a ketogenic diet. Basically, the only difference between a low-carb and a ketogenic diet is that the carbs tend to be lower on a ketogenic diet.
And I believe that most of the benefits of these diets specifically arise from restricting these two substances, the combination of which, I believe, is extremely toxic to your health. And these are sugar and seed oils. And both low-carbohydrate and ketogenic diets tend to restrict both sugar and seed oils. Processed foods, which are common in Western diets, have sugar and seed oils in spades. Take these four-star-rated Beasley bars on the left, or the organic almond milk on the right. Both contain seed oils and sugars.
So, the question is, why is this combination such a problem? And the answer is, they both cause insulin resistance. And as you're about to see, insulin resistance is the root cause of metabolic sickness. Insulin is a hormone which normally circulates around our body in the bloodstream, and it's actually essential to life. But sometimes, the insulin we have circulating doesn't work as well as it should. In which case, we are said to be insulin resistant. So, to compensate for this resistance, our body will try to make more insulin. Which is why, for many people, insulin resistance predictably leads to high levels of circulating insulin. And this is why high levels of insulin on blood tests are a bad sign. It means your insulin is not working properly.
And the high insulin levels, which occur with insulin resistance, are an important cause of obesity. This is a picture of a 34-year-old female who had a tumor producing insulin. In this picture, she weighed 107 kilograms, and she was only 152 centimeters tall. She then had surgery to remove the tumor, which led to a big drop in the level of circulating insulin. And over the next 50 days, she lost 18 kilograms. And this was without any conscious changes in her diet or exercise.
And any diabetic who's ever had to inject insulin understands full well, the insulin promotes fat gain. Weight will rise quite rapidly with increasing insulin doses. Many diabetics will also note this localized fat accumulation at the site of insulin injections, called lipo-hypertrophy. In fact, about a quarter of patients with type 1 diabetes who habitually inject into the same site will develop this.
And high insulin levels in the blood is a strong predictor of future weight gain. This study followed some initially lean subjects for eight years to see who developed obesity. Those with the lowest insulin levels over the eight-year period had a 2 percent chance of becoming obese. While those with the highest insulin levels had more than a 70 percent chance of becoming obese. Not just overweight, but obese.
But the real problem of insulin resistance is not obesity on its own. Rather, it's a myriad of other health consequences that result from high blood glucose levels, of which insulin resistance is a direct cause. One of the most important roles of insulin is to remove sugar from our circulation and allow it to be taken up by our muscles and liver. And by doing this, the glucose level in our blood is controlled. It's prevented from getting too high. But with insulin resistance, insulin resistance isn't able to do its job properly. So, the muscle and liver are not able to take our blood glucose out of the circulation. This means our blood glucose begins to rise, eventually to the point where we can be diagnosed with diabetes.
And this high blood sugar damages multiple organs as it circulates around your body. For example, diabetes is the single biggest cause of kidney failure in the developed world. It's also the biggest cause of blindness, as well as nerve damage leading to amputations. Also, erectile dysfunction. And get this, research shows the risk of having a heart attack is higher in someone with diabetes than even in someone who has already had a heart attack without diabetes. It also doubles your chance of having a stroke.
And in case you thought I was exaggerating about the consequences of high blood glucose, which is caused directly by insulin resistance, this paper from 2001 looked at 208 individuals and divided them into three groups based on their level of insulin resistance. You can see that over six years, the group with the highest level of insulin resistance developed a number of cases of diabetes, high blood pressure, cancer, heart disease, and stroke. While the group with the lowest level of insulin resistance didn't develop any of these problems at all. The message is clear: looking after your metabolic health could save your life, or at least make it more pleasant to live. And the best way to do this is with a diet that is low in seed oil and low in sugar, also known as a low-carbohydrate or a ketogenic diet.
A question I often get asked is, what is worse for you, seed oils or sugar? And though a difficult question to answer, this recent paper from the British Medical Journal is informative. An analysis of over 195,000 participants concluded that seed oils increased mortality when compared to sugar, when the intake exceeded about six or seven percent of energy intake. And understand that most individuals exceed this 6% threshold. In fact, the average Australian gets more than 13% of their energy from seed oils, which gives you an idea of the extent of this problem. Indeed, when it comes to the average Western-style diet, it would seem that seed oils are perhaps a bigger issue than even sugar. And that will be news to a lot of people.
But don't think that knowledge of the problems of seed oils is new. This study was from 1967, and it looked at the death rate from heart disease in more than one million Indian railway workers over a five-year period. And because it was a national study, the influence of different dietary habits between regions could be assessed. And most of the fat in the diet of northern Indians was derived from saturated animal fats, while those in the south got their fats mainly from seed oils. And the striking finding was that the risk of ischemic heart disease was seven times greater in the seed oil consuming south, and this is also in the context of them consuming 19 times less fat in total.
Now, while this is only an epidemiological study, which cannot demonstrate causation, the relative risk of seven times is hugely significant. And more importantly, randomized control trials soon followed, which confirmed the harms of seed oils. For example, the Sydney Diet Heart Study was a randomized control trial examining the effects of replacing saturated fat with polyunsaturated fat in men who'd had a heart attack. And it found, though the findings were not published for 40 years, that increasing the content of polyunsaturated fats from seed oils actually increased the death rate by 62 percent. A finding that would have been almost impossible to ignore, had it not been hidden for 40 years.
And the reason seed oils are so harmful is because they are very prone to forming oxidation products, which we can absorb into our tissues and which directly lead to damage. It's not, as many people think, simply because seed oils contain a lot of omega-6 fats. It just so happens that they usually are. But the damage comes from oxidation. If you have a look at the structure of polyunsaturated fats, which are found in seed oils, you'll see that these unsaturated double bonds, these unsaturated double bonds are chemically reactive and readily oxidized. In comparison, saturated fats don't have any of these double bonds, which means they're much more chemically stable.
Take, for example, this paper which looked at the tendency of fats to produce toxic compounds. And you can see that the saturated lard on the left was much better than the polyunsaturated sunflower oil on the right. And you'll also note that olive oil is also more oxidation-prone than the saturated lard and butter. This is because it contains a single unsaturated bond, which too is prone to oxidation. And while olive oil is often touted as some kind of magical elixir, study findings are far from conclusive. While there is evidence that olive oil is better than carbohydrates, there is not clear evidence that it is in any way superior to saturated fat.
And don't think that avoiding cooking with seed oils will avoid the problem of oxidation. This study looked at polyunsaturated walnut oil and found high rates of oxidation occurred within a matter of days when stored. And that oil in your cupboard is likely to have been around for months, if not longer. And after we ingest oxidized seed oil, the oxidation products are absorbed into our body. Compare the absorption of these products between a low-oxidized oil and a highly-oxidized oil, like much of the seed oils commonly consumed. And after being absorbed by our intestines, these oxidation products enter our circulation, whereupon they can inflame and damage multiple organs. One of these being the liver. And it's damage to the liver that can cause insulin resistance.
Here is an electron microscope picture showing the accumulation of oxidized fats in a liver after consumption. And this slide demonstrates liver inflammation and fibrosis associated with this oxidative stress. And the result of this damage to the liver is insulin resistance. Our insulin doesn't work as well as it should, and the process of metabolic disease begins.
And please don't think that fish oil is somehow different to any other oil. Omega-3 is every bit of polyunsaturated fat and as such is prone to oxidation. In fact, multiple studies have shown that oxidation of fish oil occurs rapidly upon storage. In 2017, independent researchers purchased fish oil supplements from major pharmacies in Sydney, choosing wherever possible samples with long expiries to ensure freshness. And 38 percent of the samples selected failed a voluntary standard for primary oxidation products, a standard, in my opinion, which was quite lax. And it's likely that the fish oil oxidation is one of the main reasons why most studies looking at fish oil do not find any benefit. In fact, 16 of the 18 studies in the review listed here did not find any advantage to fish oil supplementation.
I'd like to come back to the common misunderstanding that seed oils are toxic because they contain a high amount of omega-6 fats. That is not true. In and of itself, omega-6 fats are both essential and healthy. In fact, arachidonic acid levels, a product of omega-6 consumption, actually increases on low-carb diets due to reduced inflammation. You see, while arachidonic acid can be converted into the inflammatory products you see down the bottom, it only does so if there is an inflammatory stimulus. Low-carb diets tend to be anti-inflammatory, and so there is actually less conversion of arachidonic acid into these inflammatory products. Despite consuming less omega-6 fats, low-carb diets can actually see arachidonic acid levels rise. And this was clearly shown in this paper, where low-carb subjects ended up with higher arachidonic acid levels than their high-carb counterparts.
So, the advice I would give on polyunsaturated fats, both omega-3s and 6s, is yes, they're both essential to good health, but you don't want them oxidized. And that means you don't want to get them from an oil, which will be invariably oxidized. Instead, get them from fresh food. Take pasture-raised beef, for example. It contains both omega-3 and 6, and if it's fresh, as in it's not rancid, by definition, the fats it contains are not oxidized. This really is one situation where fresh is best.
And for the final word on seed oils, here is a study from 1965, which looked at coronary heart disease risk in three groups. Double-blinded, randomized controlled trial with vegetable and olive oil intervention groups, and a control group consuming mainly saturated fats. And the study went for two years. And the overall results were that five patients in the vegetable oil group died from heart disease, three in the olive oil group, and only one in the control group. And the researchers appropriately concluded that the use of corn vegetable oil should not be recommended.
Of course, this finding landed on deaf ears with the wider medical establishment. But I thought there were also some other very interesting findings contained within the text of this paper as well. For example, it was noted that many subjects in the vegetable oil group complained of nausea, diarrhea, and other gastrointestinal complaints, common symptoms I still see in patients consuming oils in their diet, but an effect that is not widely known within the medical profession. It was also documented that the oil exacerbated one of the subjects who was placed in the vegetable oil group in terms of his diabetes. It was noted that he started urinating large amounts of sugar soon after the study commenced. This then resolved when the oil was ceased, and then commenced again when the oil was once more resumed. As clear a case of seed oils contributing to diabetes as I have not ever seen in a paper. And given these clear findings were published 55 years ago, it's quite amazing we persisted with the misguided notion that seed oils could ever be healthy.
Let's now move on to carbohydrates in general. Carbohydrates are made of one of these molecules: glucose, which is what starchy complex carbs like bread and pasta are made of, and fructose. Fructose, which makes up 50 percent of sucrose, or table sugar. Let's start by exploring the effect of starchy carbohydrates, which contain only glucose. First, complex carbs are quite literally made of glucose molecules, and after digestion, this glucose will find its way into your blood. If you're trying to lose weight, or are pre-diabetic, or even worse, this type of carbohydrate can really pose problems. You see, when insulin is working normally, we can remove most of the glucose that enters our circulation by placing it in tissues like muscle and liver, and this keeps the glucose level in our blood low. The problem is, in people who are pre-diabetic, they're almost certainly insulin resistant. This means that the insulin doesn't effectively remove glucose from the blood. This results in high levels of glucose in the circulation. And dare I say, I don't need to remind you of the potential consequences of high blood sugar again.
Carbohydrates are also a major factor in obesity. When we ingest carbohydrates, our pancreas will release a lot of insulin, much more, in fact, than an equivalent amount of fat. And this insulin is very effective at growing our fat stores. You see, in the blood that reaches our fat cells, we have both circulating fats in the form of triglycerides and glucose. And insulin is able to stuff both of these into our fat cells in their complete form. Triglycerides can't enter fat cells, and this is where insulin comes in. Insulin stimulates this enzyme, lipoprotein lipase, which then clears this larger molecule into glycerol and three fatty acids. These fatty acids can then diffuse into the fat cell. Insulin also activates the GLUT4 transporter, which is a gate that allows glucose to enter the fat cell. Once inside, the glucose is converted into glycerol, and then the glycerol and the fatty acid combine to form triglyceride. And this is how fat is stored. Without insulin, it couldn't happen.
But if you want to lose weight, then the triglyceride must be sliced up again to allow them to exit the fat cell for metabolism. And this requires an enzyme called hormone-sensitive lipase. This separates the glycerol from the fatty acids, allowing them to leave the fat cell. Insulin, however, blocks this enzyme, putting the brakes on. And without this step, fat can't be metabolized. Insulin blocks fat burning.
So, putting it all together, we can see that insulin both pushes fatty acids and glucose into fat cells, and for extra insult, it prevents them from leaving. And this is why a high insulin level means you burn less energy. The body is literally blocked from metabolizing energy stored as fat when insulin is high. So, when you go on a low-carbohydrate diet, which lowers insulin, you burn more energy, even at rest. You can see in this study that participants on low-carb diets, shown in blue, expended far more energy than those on high-carb diets, shown in red. And the difference between the two groups was significant, about 278 kilocalories a day. This is the equivalent of exercising at moderate intensity for an hour. This difference could lead to a 10-kilogram weight loss over three years. And this is why low-carb diets are superior for weight loss when compared to low-fat diets.
And while glucose-containing carbs can be a huge problem if you're already insulin resistant, fructose-containing sugar is even worse. The main reason fructose is worse is that it is preferentially processed by the liver. Unlike glucose, which can be stored and used by several other tissues in the body, this means it's far more potent at causing fatty liver and therefore more potent at causing insulin resistance.
Let's explore the metabolic difference between glucose and fructose in the liver. In this study, subjects were fed more glucose-containing carbohydrates than they could burn. These blue bars show how much of the glucose was burnt each day, and these yellow bars, how much glucose was able to be stored in muscle and liver as something called glycogen. You can see that after a few days, these stores were full. And when the overall intake of glucose exceeded the combined capacity of burning it (in blue) and storing it (in yellow), the excess was converted into fat, which, as you can see, increased as the available storage capacity for glucose (shown in yellow) was progressively exhausted. And what this elegantly demonstrates is the protective effect of storing glucose. It was only when the capacity to store excess glucose was full that fat production really took off.
And the problem is, unlike glucose, fructose does not have this storage capacity to act as a safety buffer before it gets turned into fat by the liver. This means that proportionally more fructose consumed gets turned into fat by the liver, and this contributes to insulin resistance. And we have clear evidence that it is fructose specifically that causes more harm than glucose.
This study was performed on 41 children with a habitual high sugar intake. Fructose-containing sugar was replaced with complex carbohydrates, so that fructose was reduced from 12 percent to 4 percent of total energy, with total energy intake kept constant. In effect, the only change was replacing some fructose with glucose. And after just nine days of consuming less fructose, there were big reductions in liver fat. In fact, the median liver fat decreased from 7.2 percent to 3.8 percent. And not surprisingly, this was also accompanied by big improvements in insulin resistance, with fasting insulin secretion reduced by almost 25 percent. And all of this after just nine days.
And this finding has been replicated. 40 children with fatty livers were randomly assigned to one of two groups in this study: an intervention group where sugar was reduced, and a control group who remained on their usual diets. And to be clear, the intervention wasn't a particularly low-carb diet, nor was it terribly restrictive. The children still consumed fruit and starches like pasta. They could eat as much as they wanted. The goal was to only restrict their sugar, and therefore their fructose intake. And again, simply reducing their fructose intake reduced the mean liver fat from 25 to 17 percent.
When it comes to causing metabolic damage, fructose-containing sugar is clearly far more toxic than glucose-containing complex carbs. It can sometimes be hard to avoid the added sugar, though, because it can wear many different disguises. Food manufacturers have mastered the art of deception. Foods proudly proclaiming their credentials on sugar don't come up smelling of roses when you take a close look at their ingredients. It really is a situation of "buyer beware."
Now, you might also be wondering about high-fructose corn syrup. After all, "high-fructose" is within the name. Well, in general, table sugar can generally be considered to be as bad as high-fructose corn syrup, which in most cases contains either 42 or 55 percent fructose. They're both bad for your health. And even if you're not consuming sugar, you still might have fructose problems. You see, insulin resistance can mean that your body converts some of the glucose you eat into fructose. This is known as the polyol pathway. And when we've got normal levels of glucose in our blood, this conversion is minimal. But if we have even a small rise in our blood sugar level, this conversion can increase by 10 times. Yet another reason why only the perfectly metabolically healthy should be comfortable consuming carbs.
I'd like to now shift our attention to diabetes, specifically, and how we really should be focusing on insulin for an early diagnosis. The standard testing for diabetes only looks at glucose levels. The problem with this is that while your insulin levels may be progressively increasing over many years, glucose levels often remain near normal for some time. This graph shows the fasting blood glucose level of a typical diabetic in the years leading up to their diagnosis. And you can see that the glucose takes about 10 years before it starts to rise. During this period of time, however, we would have been able to detect a problem if we were looking at insulin levels. Here, we see the progressive increase in insulin levels occurring to compensate for insulin resistance. And finally, as the pancreas begins to fail, the insulin levels fall away.
Let's now look at glucose and insulin levels together. At this point, both glucose and insulin are normal. The first sign of metabolic sickness is seen with the rise of insulin. You'll note, however, that the glucose levels are still essentially normal. So, if this is all you or your doctor are looking at, this is a blind spot. Eventually, despite an increase, insulin is not able to fully control the blood glucose level, and pre-diabetes might be diagnosed, often a decade or more after insulin resistance has begun to occur. Then, as the cells in the pancreas begin to die off and can no longer secrete insulin, glucose will precipitously rise. You now have your diagnosis of type 2 diabetes, possibly two decades after it all started, and having missed the chance to intervene early because your doctor didn't look at your insulin levels.
Fortunately, this process in most people is reversible on low-carb and low-seed oil diets. These are the insulin results of one of my patients over two hours after ingesting 75 grams of glucose. And the same patient, six months after commencing a low-carbohydrate diet. You can see big reductions in insulin levels, and unsurprisingly, this was associated with a 17-kilogram weight loss. And I've seen this type of response countless times. And for diabetics, blood glucose levels can improve literally overnight. Understand that diabetes is a condition of elevated blood glucose level, and that glucose has to come from somewhere. So, if you simply stop putting it into your body, your blood glucose has to come down.
This graph here is from a 71-year-old diabetic who was graphing his morning fasting glucose levels after starting a low-carb diet. From day one, he recorded a big drop in his morning glucose level, and quite literally halved it in two weeks. And this was at the same time that he stopped two diabetic medications.
And this large-scale study confirms reversal of diabetes is possible on low-carb diets. The grey line shows average blood sugar levels over a two-year period in patients receiving standard diabetes care. And the light blue line shows the average sugar levels of diabetic patients on low-carb diets, clearly lower than those receiving the standard care. In fact, at two years, 53 percent of those in the low-carb group met the criteria for diabetes reversal. Is it any wonder the CEO of the American Diabetes Association herself follows a low-carbohydrate diet, which, not incidentally, has allowed her to stop injecting insulin?
Let's now consider two key points I've made so far today: one, that seed oils can cause insulin resistance, and two, that sugar can cause insulin resistance. The question is, what happens if you combine both oxidized seed oils and unstable blood glucose levels from sugar consumption? Well, this combination is uniquely toxic, because unstable blood glucose levels, like you see on this trace here, have also been shown to contribute to oxidative stress. And the effect is multiplied.
And this was shown by this study, which compared oxidation load in subjects with good and bad blood sugar control. In subjects with good blood glucose control, oxidation load from a meal was quite moderate. While for the very same meal, in poorly controlled diabetics, there was a much bigger load of oxidation, and the adverse effects were prolonged. While the healthy subjects were able to clear the oxidation products from their circulation within eight hours, the oxidation products persisted in the diabetics for three days. And this is why I encourage all of my patients to strive for stable blood glucose levels, as seen in this trace on the bottom.
I'd like to now look at the role of seed oils and sugar in causing a condition that invokes more fear than even cancer, and that's dementia. Despite decades of research costing billions of dollars, we're no closer to a cure for dementia than we were when Alzheimer's disease was first described more than 100 years ago. The frustrating thing is that had only a tiny amount of this money been directed at nutritional research, I believe we would be in a much, much better place today. And that's because, for the most part, dementia can be considered a metabolic disease of the brain. And the vulnerability of the brain to metabolic disease is obvious. While it constitutes only two percent of the body's volume, it consumes over 20 percent of its energy. In fact, dementia is now commonly referred to as type 3 diabetes.
And the same health impacts associated with type 2 diabetes are also associated with dementia. Take obesity, for example. This study looked at abdominal obesity in over six and a half thousand subjects, and over 30 years, they found that obesity was significantly correlated with the risk of developing Alzheimer's disease, three times the risk, in fact, when comparing the leanest and the most overweight individuals. And several studies have now convincingly demonstrated that obesity is associated with reduced brain volume. Obesity quite literally shrinks your brain.
And insulin resistance, common in metabolic disease, is apparent in the brains of those with Alzheimer's disease. This scan here is called a PET scan, where glucose uptake by brain cells is indicated on a heat map. You can see that a normal brain is able to take in large amounts of glucose, much of it through the action of insulin, which permits its entry into brain cells. Contrast this to the Alzheimer's brain on the right, where insulin is not working properly, and you can see that despite having elevated levels of glucose in the bloodstream, the glucose is impaired in entering brain cells. The brain is effectively being starved of energy, and this is one of the reasons for the cognitive impairment we see in Alzheimer's disease.
Let's now compare how a brain affected by insulin resistance and Alzheimer's disease can utilize ketones, which can be produced on a ketogenic diet as a result of fat metabolism. Here, on the left, you can see that an Alzheimer's disease-affected brain is unable to utilize significant amounts of glucose for energy. But when the same brain is supplied with ketones, it just sucks them up. Providing ketones to the energy-starved demented brain bypasses the block caused by insulin resistance and improves neuronal function.
And have no doubt about the ability of low-carbohydrate ketogenic diets to provide ketones to fuel the brain. Here, you can see negligible uptake of ketones in a brain in someone on a high-carb diet, and the very same brain on a low-carb ketogenic diet, massive uptake. It's therefore logical that ketogenic diets would improve the energy supply to insulin-resistant brain neurons, improving brain function. And that's exactly what the research shows. This recent study demonstrated a significant enhancement of brain activity in elderly adults after commencing a ketogenic diet. And make no mistake, these benefits are not seen on low-fat diets. The same study also included a high-carbohydrate arm following a diet recommended by the American Heart Association, with a resounding lack of benefit.
So, it's very clear ketones can be absolutely beneficial in improving cognitive function in those suffering from dementia. But I'm going to take it a step further. I also believe that a healthy diet low in sugar and seed oils can help prevent Alzheimer's disease in the first place.
If we look at a brain affected by Alzheimer's disease under a microscope, we'll see these clumps of protein known as beta-amyloid plaques. And these are thought to be toxic to our brain neurons and lead to much of the damage in Alzheimer's disease. And we've now got imaging techniques where we can visualize these toxic plaques. Compare this healthy brain with relatively little beta-amyloid deposited to the brain of an Alzheimer's disease patient. The interesting thing is that the formation of these beta-amyloid plaques can be strongly influenced by our diet.
Beta-amyloid plaques are aggregates of these single beta-amyloid peptides, but these peptides don't just clump together out of the box. We have to damage them first. First, we add sugar, which then covalently binds to these beta-amyloid peptides, producing something called an early glycation product. This then makes the beta-amyloid peptides vulnerable to clumping. These early glycation products can then progress to advanced glycation end products, which are essentially the beta-amyloid plaques. And understand that this final step is strongly driven by oxidative stress, the same stress we experience when we consume oxidized seed oils or have unstable, fluctuating blood glucose levels. And again, remember, the combination of both poor sugar control and oxidized oil consumption multiplies it. It's especially toxic.
This is the amount of oxidation products absorbed in study subjects with good blood sugar controls. And this was what was absorbed in subjects with poor blood sugar levels. If you ever needed a reason to avoid processed foods containing both sugar and seed oils, avoiding dementia would have to be it.
We also have a natural mechanism in our body to remove beta-amyloid plaques. And not only can poor metabolic health increase the deposition of these plaques in the first place, it can also interfere with their removal. HDL cholesterol particles in our brain, through this ApoE protein embedded in their membrane, are able to remove some beta-amyloid deposits. The problem is, these ApoE proteins themselves can be damaged, preventing effective removal of the plaques. We also have genetic factors that can increase the chance that our HDL particles get damaged. You see, we have slight variations in the genes that code for these ApoE proteins, and some are much more susceptible to damage from sugar and oxidation than others.
The two most common variations are ApoE3 and ApoE4. And this is the one that is especially vulnerable because of its specific molecular structure. This paper here shows the amount of sugar and oxidation damage to ApoE3 compared to ApoE4. For the same exposure, the E4 variant had three times the damage. And this damage will prevent HDL from effectively removing beta-amyloid plaques, increasing the risk of Alzheimer's disease. And this is why that people with two of these ApoE4 genes are probably about five times more likely to develop Alzheimer's disease.
But I would argue that understanding this mechanism also gives us hope. For even if you happen to carry two of these E4 genes, we know the problem is related to glycation damage, which can be effectively managed by controlling the amount of sugar and seed oil in our diet. For proof of this, let's look at this clever study. Now, the investigators of this study had recognized that while those with the ApoE4 gene did have an increased risk of Alzheimer's disease, not everyone with the gene developed Alzheimer's. So, they set about investigating the impact of environment.
Study subjects were recruited from an African population in a single city in Nigeria, and African Americans from Indianapolis in the United States. The two study populations, as a result of the slave trade, were ethnically similar, both with very high carrier rates of the ApoE4 gene. And the findings were that the rate of Alzheimer's disease in the Nigerian population was two and a half times less than their genetically identical U.S. counterparts. In my mind, a likely result of the high rate of metabolic disease in the U.S. and strong evidence that environmental factors play at least a significant role as genetics when it comes to Alzheimer's disease.
And for the final word on diet and dementia, we have this recent paper which provided evidence that low-carbohydrate diets may not only prevent brain deterioration, they can even reverse existing damage. And evidence for this was found in just the space of one week. In this arm of the study, subjects were fed a standard diet for a period of one week, after which they had a brain scan to assess for network instability, which is a reliable marker for brain aging or deterioration. The same subjects were also given a ketogenic diet for one week, with the same brain scan following. The result being that there was significantly less damage to neural pathways. Essentially, damage to neural pathways accelerated whenever the brain was reliant on glucose for energy, and reduced when ketones were metabolized. Yet more evidence of the benefit of ketogenic diets for brain health.
I'd like to now talk about bone health. And this is another area of medicine where conventional wisdom has gotten it wrong. In medical school, I was taught that bone density peaks in early adulthood, and from there, it is a relentless and progressive decline. After we've reached this supposed peak bone mass, we're unable to ever improve our bone health, just perhaps slow its decline. Well, conventional wisdom is wrong. Would you be surprised if I told you that you could actually improve your bone mineral density as you age, even if you happen to be a postmenopausal female, and all without drugs? Well, you can, and there's randomized control trial evidence to prove it.
Perhaps the most damaging myth regarding bone health is that protein is bad for your bones, because the exact opposite is true. This myth likely arose from this 100-year-old piece of research, where it was found that by adding extra protein into the diet, we could actually increase the amount of calcium detected in the urine. Back then, this was interpreted as an indication that protein was degrading bones, given that they contain calcium. What was not known back then, however, is that this extra calcium in the urine didn't represent a loss of calcium from bones; rather, it only occurred because more calcium was being absorbed in the first place. We now fully understand that increasing our protein intake leads to increased calcium absorption, with a net gain of calcium by the body. So, the net effect of protein consumption on bone is actually positive.
And this makes a lot of sense when you consider that protein makes up 40 percent of the dry weight of bone. Here you can see the underlying protein scaffolding of bone, distributed between these protein fibrils and minerals. So, bone can really be thought of as mineralized protein. Without either protein or minerals, you can't make bone. And this explains why calcium supplementation alone cannot restore bone mass, but it can slow the decline, because bone acts as a store for calcium within the body, and when calcium is needed elsewhere in the body for something else, bone can release some. Understand, however, given that the calcium-containing minerals are embedded within the protein, the whole structure of bone needs to be degraded to release the calcium. So, by providing extra calcium, we can slow down the degradation of bone. But what calcium cannot do on its own is to build bone back up. To do this, it needs, amongst other things, available protein. Just think, you're trying to bake a cake, and the only ingredient you have are eggs. You can't bake the cake.
This study took into account the importance of protein. It was a randomized controlled trial comparing calcium and vitamin D supplementation to placebo on bone mineral density. There were 342 subjects, all over the age of 65. First of all, they predictably found that supplementing with calcium and vitamin D could slow down bone loss. But the striking finding of this study was when they stratified the results based on protein intake. The group in the lowest tertile of protein intake demonstrated a small reduction in bone mineral density over three years. The median protein intake saw a slight improvement, while those with the highest protein intake saw a striking improvement in their bone mineral density. And remember, this was in an elderly population. Clearly, it's not only calcium that is important to bone health.
But there are also other minerals that are very important. In addition to calcium, bone contains several other inorganic salts, including magnesium, sodium, potassium, phosphate, and chloride. And each one of these is necessary for healthy bone. Bone is very specifically made of each one in a precise ratio, and the absence of any one of these will affect the ability to form healthy bone. For example, this graph here shows the tight relationship in bone between sodium and calcium. One cannot increase one without increasing the other. Likewise, decreasing one must necessarily decrease the other. Think of it like a recipe for a cake which requires two eggs, and you've only got one. You can't make up for it simply by adding more flour. You can really only make less cake.
Let's now take a look at a study which demonstrates the importance of some of these other elements to bone health. I love this 1975 study, not only for its elegance but also for the fact that we'll
Probably never see a study quite like it again, mainly because it wouldn't pass muster with an ethics review board. In it, 11 subjects were completely fed directly into a vein. By doing this, the investigators had complete control of every nutrient going in. The nutrient mixture being provided included all of the substances we've previously mentioned, plus protein and glucose. Then, the investigators step by step removed some of these nutrients in isolation from the feed, and the impact on the capacity to form bone, muscle, and fat tissue was measured.
The results were striking. When protein, sodium, or phosphate was withdrawn, bone and muscle tissue stopped being formed. All of the excess energy went into fat, proving two points: the current focus on calcium as the only nutrient needed for good bone health is short-sighted, to say the least, and two, deficient diets with respect to particular nutrients might even make you fat. In fact, in the words of the study investigators, "the only requirement to increase fat mass was an abundant supply of glucose."
Sleep is also commonly overlooked when it comes to improving one's metabolic health. Chronic sleep disturbance is causally associated with metabolic disease. In fact, this four-year prospective study of 738 nurses found those working night shift had a cumulative incident of metabolic syndrome of nine percent, which was five times greater than those working day shifts. The reason for this is that the hormonal changes caused by sleep deprivation ultimately exacerbate insulin resistance.
Take this study, which compared the morning blood sugar levels of diabetics with good and poor sleep quality. Those with poor sleep quality were more than four times as likely to suffer elevated fasting blood sugar levels, something known as the dawn phenomenon, caused by insulin resistance. The weight gain associated with sleep disturbance can further impair sleep quality in a vicious cycle. The tongue, which actually takes up most of the space in the mouth, gets fat as we do, and this is the main factor causing sleep apnea, which is where the airway repeatedly blocks off when you sleep, leading to low levels of oxygenation in the brain.
Fortunately, losing weight in general will also lead to reduced fat in the tongue, literally shrinking it. You can see on this MRI-generated image of the tongue that losing weight can lead to a significant shrinkage, and this study conclusively demonstrated that this shrinkage of the tongue improved sleep apnea. In the time of coronavirus, we shouldn't overlook the benefits of improved sleep on immune function. In fact, sleep apnea increased the chance of ending up in ICU with the flu by about five times.
This study assessed the ability of subjects to fight off the common cold after it was squirted up their noses. Subjects who were sleeping for fewer than seven hours a night were three times more likely to catch the cold than those who were sleeping for more than eight hours.
But when it comes to the immune system, it is again hard to go past the influence of insulin resistance. This study, published in Nature last year, elegantly demonstrates how the immune system is impaired with insulin resistance. When we get infected with a virus, a key factor in the immune response is the release of various small proteins called growth factors and cytokines, which communicate between different cells and basically rally the troops. This study looked at many of these growth factors and cytokines in response to viral infections, and certain of these are particularly important in coordinating the defense against viral infection.
Here are five of these. You can see in the metabolically healthy population, infection with a virus led to a robust and appropriate immune response in all of these areas. Now, compare this to the amplitude of response in subjects who were insulin resistant. It's no wonder the authors of this study concluded that insulin resistance leads to an overall impairment of immune system function, not exactly something you want in a global pandemic.
I'd like to now dispel another long-standing, well-accepted, and completely false nutrition myth: that of salt being harmful. The key thing to understand is that while sodium, which is in salt, is often thought to be the major cause of high blood pressure, it is in fact caused by insulin. High insulin levels. This myth first arose because sodium can attract and hold on to fluid inside our blood vessels, which increases blood volume and then the pressure. The thing is, in most people, it is actually high insulin that influences how much sodium we'd retain in our body, even more so than the total amount of sodium in our diet.
This is because insulin activates four specific transporters in our kidneys which retain sodium in the body. That is, insulin directly increases the amount of sodium in our body. As you can see from this four-year-long study, those with the highest levels of insulin were more than twice as likely to suffer from high blood pressure. Indeed, the evidence is that low levels of sodium might even increase your risk of dying.
This paper from 2014 looked at the urinary sodium excretion of more than 100,000 subjects and it found that as the level of sodium excretion, which reflects somewhat how much sodium is being ingested, fell below four to six grams a day, the risk of dying increased sharply. Remember, sodium represents only 40% of salt, so six grams of sodium equates to a daily salt intake of 15 grams, and 10 grams of table salt is a lot. Here, I'm grinding one gram of salt, or 0.4 grams of sodium.
When you remove processed foods from the diet, the amount of salt that most people consume drops dramatically. Attention then needs to be paid to ensuring sufficient sodium intake, lest you suffer what used to be called the Atkins flu. This often led to dizziness and lightheadedness, in large part due to the combination of reduced sodium in the diet combined with lowering of insulin levels, which reduce the capacity of the body to hold onto the sodium.
As a footnote, it may surprise you to learn that the Australian Dietary Guidelines no longer specify a recommended upper limit for the intake of sodium in adults. Indeed, in their own words, "the previously recommended limit on sodium intake was based on early interpretations of very limited data." While the recommended limit was removed three years ago, there's been remarkably little, if any, promotion of this fact to the public. It makes me wonder whether someone might have a little bit of egg on their face.
A lot of people ask me how medicine could have gotten things so wrong. Why, if I find the evidence so compelling that saturated fat is indeed not harmful, why do so many other doctors disagree? Indeed, this is a question I ask myself. Many educated people hold beliefs that really don't bear scientific scrutiny. So, let's look at a couple of the big elephants in the room: saturated fat, cholesterol, and statins, and see if we can perhaps understand why there is still so much disagreement about this.
This prospective study looked at more than 135,000 participants and followed them for more than seven years, looking at saturated fat consumption and mortality rates. It found that those habitually obtaining about 10% of the energy from saturated fat (not much) had a death rate of about 7 people for every 1,000 person-years. But in those who were consuming more than three times as much saturated fat, the equivalent death rate was only 4. There was no upper level of saturated fat intake which appeared problematic. As energy from saturated fat increased, so too did the apparent benefits.
Before you start getting too worried about saturated fat increasing LDL levels, look at this systematic review, which examined 19 cohort studies with over 68,000 participants. 16 of these studies found an inverse relationship between LDL cholesterol and all-cause mortality. That is, the higher your LDL level, the lower your chance of dying.
The data on whether statins, a medication designed to lower LDL cholesterol, will make you live longer might surprise you too. Most people take statins to prevent dying, but that's not the right way to think about it, because everybody is still going to die. Rather, a better question is: how long will taking a statin extend your lifespan by? This review set out to answer that question. It included data from 11 studies involving over 90,000 participants and followed them for about four and a half years. It assessed data based on whether or not subjects had either a previous history of cardiovascular disease or no previous history of cardiovascular disease.
It found that if you did have a history of cardiovascular disease, you might anticipate, on average, an increase in lifespan of about five days. If you didn't have this cardiovascular history, you were looking at three days. Now, understand that this review was performed on available data. What I mean by that is that not all the data relating to the many statin trials is available for independent review. Why not, you might ask? Well, let's put it down to commercial reasons.
To this very day, independent scrutiny of much of the research performed over the years has been blocked. If you were making claims about a drug, wouldn't you welcome the chance to show your data to prove your point? It's not exactly as if drug companies have unblemished records either. It took Bayer four years to remove this statin from the market after multiple deaths, and Merck took five years to recall Vioxx after it was prescribed to more than 20 million people. Do you think they might have noticed some problems a little bit sooner?
Another example of potential pharmaceutical industry misconduct is the story of Roche and Tamiflu. By misrepresenting clinical studies and making unsupported claims about their effectiveness, Roche saw governments around the world purchase around $8 billion worth of their product. In effect, Roche hid eight of ten clinical trial reports on Tamiflu to encourage sales, and they broke no laws in doing so. Should we not be concerned that data from many clinical trials on drugs, including statins, are shrouded in secrecy? When we're told that commercial reasons prevent access to statin trial data, do we implicitly accept it and trust that the pharmaceutical companies will do the right thing? When we have review data that indicates that statins might increase your survival by only three days, do we wonder whether this effect would still hold out if we had access to all the data?
Misrepresentation or obscuration of trial findings is not limited to drug studies; we see it in nutritional studies as well. Let's take a look at three influential nutrition studies where the results to the public were misrepresented. The Sydney Diet Heart Study was a randomized controlled trial examining the effect of replacing saturated fat with polyunsaturated fat in men who'd had a heart attack. Despite being finished in 1973, the results regarding whether this actually reduced death rates was not published, well, not until 2013, some 40 years later, and only after an intrepid researcher located the original study data in a basement. Those findings: reducing saturated fat in the diet by increasing the intake of polyunsaturated fats increased the death rate by 62%. Remember, this finding was destined to never be published by the original authors.
A very similar story exists for this study, which also finished in 1973. This was a double-blinded, randomized control trial on more than 9,000 men and women comparing a high saturated fat diet with a high unsaturated fat diet. Again, there was a delay in publishing the results, and even after 16 years, when some results were finally published, the results on death rates were missing. When the now-deceased lead author was asked about this delay of publication, he explained it was because some of the findings were disappointing.
Again, the same intrepid researcher uncovered the original study data from magnetic tapes and punch cards and finally published the full results in 2016. What did they show? Well, increasing polyunsaturated fats and reducing saturated fats increased the risk of dying. This was the disappointing result that was knowingly hidden for decades.
This kind of behavior is not just an aberration of last century. We also have the Women's Health Initiative study, published in 2006. A massive study of over 48,000 females who were randomized to either a low-fat or a controlled diet, costing $700 million US dollars in total. The only difference was that the study authors of this study were more subtle about how they hid their unpalatable findings. They didn't totally neglect to publish them; they just didn't put it in the conclusion or the results table or ever discuss it publicly. Instead, you have to go to page 661 of the journal publication and interpret a single sentence of obscure text. The finding being that those on a low-fat diet, so if you went on a low-fat diet with a history of heart disease, had a 26% higher chance of having complications like repeat heart attacks. Hardly a compelling case to reduce saturated fat in the diet.
Finally, now in 2020, the record is finally beginning to be straightened out. In fact, the American College of Cardiology, which has a long history of promoting the US dietary guidelines, has finally begun, now in 2020, to correct the record. This recent review acknowledging that the weight of evidence does not support restriction of saturated fats in the diet, instead explicitly recommending that dairy, meat, and eggs should be freely consumed. Still, it's going to take a long time for the rest of the medical profession to catch on.
I think I've said enough for now, but before I go, I should confess that every single one of the nutrition myths that I've discussed today, I, at one point of time or another, used to believe. It's often stated that 50% of what we learn in medical school is wrong, and that we just don't know which 50%. Well, while once I didn't truly believe this saying, I sure do now. This is a time of changing knowledge, and I hope we can get a lot more people coming along for the ride.
In the meantime, I'm going to leave the final word with Vicki. "Please, if you're a doctor or dietitian out there listening to this, think that what's best for your patients. Give them a fighting chance in their weight loss. You know, give them some hope that there's something out there that could possibly work for them. I know it's worked for heaps of people, but to just dismiss something like this is just, it's just cruel."