If I were to tell you that obesity science has misinterpreted many of its findings due to incorrect modelling and assumptions, you would likely be dismissive. How could that be? Science and studies are so advanced that we could not be wrong. I think it is normal to dismiss such a contrary view, yet there are past examples that demonstrate it happens. We are not infallible!
We Don’t Always Get it Right
One example is stomach ulcers. The assumption that microbes could not survive in the stomach’s acidic environment resulted in the misinterpretation of research findings that directed treatment with antacids and surgery that never resolved a chronic condition. In fact, stomach ulcers are now cured with a course of common antibiotics because it was discovered that the assumption was wrong.
In nutrition, the assumption that trans-fats were not unhealthy, led to decades of recommendations to consume products made from very harmful partially hydrogenated vegetable oils. The FDA only removed their GRAS (Generally Recognized as Safe) status in 2015 when the danger was demonstrated about 1990! In hindsight, it seems obvious, and we can laugh at our past ignorance, but when you are in that moment, the dissenting voices are usually called ‘crackpots’.
I am not suggesting that crackpots are always right, or that these examples prove that we have the same situation in obesity science. I am saying that sometimes we need to go back and challenge fundamental assumptions, especially when our attempts to apply scientific knowledge in practice continue to fail.
Moving Forward Means Looking Back
For obesity science, medicine, and treatments to move forward, we should highlight inconsistencies and challenge fundamental assumptions that have not been tested or perhaps are not even recognized as assumptions. I will make the case for this, and I hope that you will approach it with an open and curious mind, like that of a juror.
What is the cost of doing this? It requires taking the time to reflect on the problem from first principles. However, if we do find that there are flawed assumptions, the payoff could be a better understanding of one of the biggest health problems of our time.
Let’s start from a common point with some facts that almost nobody should disagree with:
While some individuals have success in losing weight, even fewer can maintain long-term weight loss.
What we are currently doing and have done to address obesity on a societal level has not worked.
The indisputable cause of obesity is the accumulation of excess fat mass.
Instead of immediately jumping to hypothetical reasons to explain why facts 1 and 2 happen, the purpose here is to prompt us to explore our assumptions. Fact 3 provides us with an indisputable starting point, so what are the assumptions?
Most researchers accept that obesity is caused by positive energy imbalance using the Energy Balance Model (EBM). In other words: “When we consume more calories than our body requires, our body stores the excess energy as fat, leading to weight gain and eventually obesity.”
Exploring the Gap
I propose that we explore the gap between statements 3 and 4. If statements 3 and 4 are both true, then we should be able to connect the two using solid physics, because these statements are SOLELY within the realm of physics.
Starting with statement 3, what are the physics-based ground rules? Firstly, we are talking about the accumulation of (fat) mass resulting from net usage. The only relevant physics is the law of conservation of mass . We get heavier when we store fuel mass that is not used to make energy. The mass from fuel we use to create energy, in the majority, is breathed out as CO2 .
Unfortunately, as the survey results show below, the generally accepted view of many health professionals (perhaps facilitated by the EBM) conflates mass and energy. Weight lost is not converted into energy to disappear as energy/heat. If it did, we would all be walking nuclear bombs! In fact, it is mostly breathed out.
The Real Physics of Weight Loss
Statement 3 is only about mass and is covered by the law of conservation of mass so how do we connect mass and energy as required by statement 4? The fundamental relationship was determined by Einstein’s equation: E=mc2 .
Cutting to the chase, when we metabolize fuel for energy, the near-infinitesimal mass of the chemical bonds of fuel is converted into energy (4.56 x 10-12g per Calorie). The bulk of the weight is exhaled as waste CO2 (~85%), and the remainder (~15%) is excreted through other means. Excess fuel that we don’t use to produce energy is stored (mostly as fat), and this surplus fuel adds to our weight. You can think of it like an empty diesel tanker where the engine’s diesel tank, if overfilled, overflows into the larger storage tank, making the tanker slightly heavier. Unless the fuel from the large tank all flows back to the engine tank to be burned in the engine, over time the weight of fuel in the storage tank could become significant.
Is Flour the same as Bread?
Somewhat pedantically (but important from a system modelling perspective) calories are the output from our metabolic processes and not an input. To draw an analogy, if you bought one kilogram of flour, you could say, “I just bought two loaves of bread.”. Intuitively, we know this isn’t correct because the breadmaking process requires several other ingredients (yeast, water, and salt for taste) and processes (fermentation, kneading, proving, and baking) to turn flour into bread. Flour is an input, and bread is the output of the breadmaking process- just as food is the input and calories are the output of our metabolic processes. In fact, the flour may not become bread at all; it can fail to rise or have a different process output, such as pasta. By saying you have bought bread when you have bought flour, you have assumed both the intent and success of breadmaking.
Analogously, when if predetermine fuel is calories, we assume the intent and success of energy production. While we recognise the absurdity of saying that flour is bread, it is generally accepted that fats, carbohydrates, protein, and alcohol are calories. The packets that wrap our food even tell us so! If it were not for our inertia to accept observational scientific agreement, I think we would discard this as nonsense.
Convenience over Accuracy?
While it is convenient to use the term “calories consumed” to refer to the energy obtained from food, it is important to acknowledge that the human body is not a perfect “calorie counting” machine. The way our bodies process and utilize energy from different types of foods can vary, and factors such as nutrient composition, food processing, and individual differences in metabolism can all affect the way our bodies handle energy.
Additionally, other factors beyond energy balance, such as the quality and composition of the diet, overall dietary patterns, and lifestyle behaviours, can also play a role in the development of obesity. For example, the type and quality of macronutrients consumed (e.g., carbohydrates, fats, proteins), the presence of added sugars or processed foods in the diet, meal timing, portion sizes, and eating behaviours can all impact weight regulation and the development of obesity.
Therefore, it is important to acknowledge that the energy balance model is an oversimplified representation of the complex interplay of factors that contribute to obesity, and it may not capture the full complexity of the human body’s response to energy intake and expenditure. While further research is needed to better understand the multifactorial nature of obesity and develop more comprehensive models that consider the complexities of human physiology, metabolism, and behaviour, it’s also possible that the clues are already in the scientific literature, but they are unlikely to be found in studies that are based on a fundamental oversimplification of (and I would go further to say wrong) system modelling.
The misunderstanding of stomach ulcers and trans-fats shows that widely held views in medicine and nutrition can be incorrect.
The widely accepted view is that obesity is caused by an energy surplus as calories consumed are greater than calories expended.
It is a valid exercise to personally challenge fundamental that model assumption and may be necessary for obesity science, medicine, and treatment to solve one of the biggest health problems of our time.
Clearly, it is the accumulation of excess fuel as fat in the body leads to weight gain and obesity.
The physics ground rules for understanding obesity are the law of conservation of mass and the relationship between mass and energy (E=mc2).
From conservation of mass, most of the weight lost is through breathing out ‘waste’ CO2, while the mass of the chemical bonds of fuel converted into energy is negligible.
Calories are the output of metabolic processes, not an input, and should be seen as the output of the food-to-energy conversion process.
Summary points 4 to 7 provide a solid starting point to examine the energy balance model of obesity.
The EBM Clearly Has Some Validity
I acknowledge that studies show that when individuals consume more potential calories than they expend, they gain weight, and when they consume fewer potential calories than they expend, they lose weight, so it is reasonable to conclude that an energy imbalance has a role in the development of obesity, and while the energy balance model may have invalid assumptions, it has been useful as a principle to guide interventions for many individuals who struggle with obesity.
Additionally, approaches that focus on reducing caloric intake, increasing physical activity, and improving overall health behaviours clearly have positive effect. The energy balance model has been well-supported by observational research and is widely accepted in the scientific community but none of that makes a model correct. While the EBM appears to be based on the principle of conservation of energy, which is a fundamental law of physics of CLOSED SYSTEMS, more fundamental are the laws of conservation of mass and energy mass conversion which form a physics base that do not conflate energy with mass.
Where to From Here?
This is the end of part one and I think I have achieved the aim of demonstrating that there is a case to be answered. In further parts, I will move on to look further into the implications of these and other surfaced assumptions and incorrect systems modelling to propose different ways to consider the problem that are consistent with existing evidence and importantly, use good system modelling.
Disclaimer: This post is not medical advice. At all times you should consult with your trusted health professionals. It is a self-reported case study with discussion of type 2 diabetes pathology, much of which is unsettled.
About 500 million people have Type 2 Diabetes (T2DM), so it is likely that this case study will be useful for more than one person who is like me, and may have some use for a good many others. If you have T2DM or pre-diabetes, I hope that is you.
To the best of my knowledge, there isn’t a more detailed long-term case history with results and analysis of a cure of T2DM than in this blog. If there is, please let me know as I want to read it and learn. I’ve documented this truthfully with my lab results and tried to avoid my bias and enthusiasm for what worked for me and why.
If you are a clinician then there may be insights from my case to help the growing number of people who have achieved remission, but now wish to progress even further towards a completely normal metabolism.
Among other things, I think my success is because I took a metabolic health approach to my problem. This is a long post so I will put that detail in a separate ‘how-to/ what I did’ post, which needs to include metabolic testing and body composition. In full disclosure, convinced of the value of a metabolic approach, I now do work for Metabolic Health Solutions (MHS) after being a client.
I’d love your comments, improvement suggestions, or notification of any errors. Leave a comment here or have a discussion with me on Twitter.
My Type 2 Diabetes is Cured
It’s been about three years since my last post and my original one seeking to go beyond remission to a cure for T2DM. You might review these if you are unfamiliar with them. I have achieved my goal of curing T2DM with the proof of that coming about a year ago now, but I’ve taken my time to publish this as I wanted to get my ducks in a row.
When I say ‘cured’ what do I mean? Firstly, I have a non-(pre)-diabetic HbA1c that is now consistently less than 5%. That is better than most of the non-(pre)-diabetic population. Secondly, washed out of all medication, I passed a gold standard Oral Glucose Tolerance Test (OGTT) with a non-(pre-)diabetic result. There are no diagnostic criteria to say that I have either T2DM or pre-diabetes.
I challenge the belief that T2DM is a chronic progressive disease that has no cure, even though diabetes charities only allow you to be in remission (never cured). I challenge that T2DM is purely an unlucky genetic lottery. While genetics play their part in susceptibility, T2DM is an arbitrary diagnosis point of a condition that is actually a metabolic spectrum you are already on.
Without doubt, I have moved down that spectrum to be almost completely healthy. I don’t doubt that if I went back to the diet and lifestyle that led to it, it would come back, just as it develops in someone afresh. If I maintain a truly metabolically healthy lifestyle, I have every expectation that it will not.
T2DM as Metabolic Disease
To cure a disease, you’d better understand it’s nature. T2DM most likely starts with poor fat oxidation. If you are unable to use your body fat effectively for energy, it accumulates. Too much where it should be, then spilling to where it should not be. That includes in your liver, your adipocytes (fat cells), and in your pancreas. De Novo Lipogenesis (DNL or fat production from carbs) may be increased, exacerbating this process by depositing more fat in the liver which causes or aggravates Non-Alcoholic Fatty Liver Disease (NAFLD). One strong theory is that this fat spills over into the pancreas becoming T2DM (1). Dyslipidemia and inflammation from that are likely to be causal for cardiovascular disease (CVD). While the exact order and causation may be debated, one useful view of how all of these major conditions are linked from the same root cause is shown in Figure 1 below (2).
T2DM development is not completely understood, but in effect, because your metabolism is broken, insulin rises to high levels (hyperinsulinemia) often even without eating. Worsening insulin resistance means that more insulin is needed to hold blood glucose at desired levels. The same amount of insulin no longer produces the same lowering of glucose. As it’s governed by a control system, our pancreas obliges and puts out more insulin to try to keep blood glucose controlled. Eventually, our insulin-producing beta cells can not produce enough insulin and we get an Impaired Glucose Tolerance (IGT). When blood glucose rises past an arbitrary point, T2DM is diagnosed, however, you can see there is already a problem. Even if you’ve been to your doctor and told: “Everything is OK with your blood glucose, you don’t have (pre)-diabetes.”, you may have ‘diabetes in situ’ (3) or metabolic syndrome.
Blood glucose can be managed with lifestyle and medication but this almost certainly continues as a chronic progressive disease. It continues to rise and insulin production falls further and eventually, injected (exogenous) insulin may be needed. Unfortunately, high insulin and high blood glucose cause diabetic complications, some of which we see above. Along with CVD, you can risk blindness, kidney disease, and poor circulation with nerve damage that leads to amputation.
The T2DM Spectrum
This diagram from doctors Kushner & Johnson’s article (4) illustrates this kind of progression which occurs over many years. In my case, it was over about a decade- perhaps more.
This picture exposes that we have created a problem because we have a binary view T2DM. “You have it or you don’t.” this leads people to think “You have the bad genes or you don’t” or some other factor. While computer numbers are binary, metabolic processes rarely are. If fact, the very existence of pre-diabetes (which precedes T2DM and can also be reversed and prevented from proceeding to T2DM) shouts out to us that T2DM is not a binary condition.
Instead, we should view T2DM as a condition of extended metabolic illness where everyone is on its spectrum. Consistent with Kushner & Johnson’s view, and while not really new, I propose Figure 3 showing T2DM on a spectrum.
Accepting that spectrum is reversible, then we need to find the things that will move us left. You will note that in figure 1, I have added “poor fat oxidation and poor metabolic flexibility”. That corresponds with figure 2’s meal size, composition, timing, and low activity. If that is driving the process, it’s no surprise then that changing meal size, composition, timing, and activity to achieve better fat oxidation and metabolic flexibility would be a great place to start to move left. High insulin is a major problem, so continuing to keep that as low as possible also seems wise.
T2DM as Insulin Resistance of the Pancreas
The latest research into diabetes indicates that a problem of T2DM may be insulin resistance of the pancreas itself. This leads to the related problem that alpha cells that make glucagon (the hormone that makes your body produce glucose) make too much of that (5) because they do not react properly to high insulin, so the liver overproduces glucose.
This seemed to be my main problem. My glucose was low most of the time, but would still be high in the morning even before I’d eaten. This had improved but appeared to be why my HbA1c wouldn’t drop below my target of 5.1%. Instead it hovered around 5.6%.
Let’s summarise some important points from this discussion of T2DM.
T2DM is characterised by hyperinsulinemia, with insulin resistance affecting tissues in the body differently, including, but not limited to, muscle, kidneys, liver, and (it seems) the pancreas itself.
Both insulin and blood glucose levels are high. Both will be exacerbated by lifestyle and in particular by foods that raise blood glucose and promote insulin secretion.
While the focus is often on the problems with the insulin-producing beta cells, both the alpha and beta cells do not function normally. Especially if there is no severe damage to them, this may be reversible. Even if there is some damage, it might be possible to regain function or possibly repair them.
T2DM is actually a spectrum condition that has hyperinsulinemia and insulin resistance to varying degrees. Before pre-diabetes, we have “sub-clinical diabetes” or T2DM that has not yet passed its clinical diagnosis points. You may also hear this called ‘diabetes in situ’.
Reversal can target hyperinsulinemia by lowering insulin and improving insulin sensitivity (reducing insulin resistance) until we have moved to the left, subject to any lasting damage to tissues and organs which then may or may not heal over time.
If we just try to control blood glucose without addressing high insulin, we have a chronic progressive disease. We can ‘rob Peter (increase insulin) to pay Paul (reduce glucose)’. This is, unfortunately, often the outcome of standard diabetes management.
If insulin resistance and hyperinsulinemia are the real problem, making the pancreas produce more insulin or supplementing insulin to keep it high by injecting it, is unlikely to fix the problem.
Striving for excellent metabolic health, by moving to the left in figure 3, appears to be the real goal for a cure.
Moving Towards a Cure
One interesting aspect of my case is that it was almost only a diet approach for the first years. I did little exercise and was on a fairly small dose of metformin (500mg) for most of the time. This means my case study largely isolates diet (with a small metformin dose) from other factors like exercise.
It was a low carbohydrate approach which has the advantage of also minimising the insulin my pancreas produces. This is because carbohydrates stimulate insulin the most, then protein (but also much less in the near absence of carbohydrates) and fat the least. Logically too, if I had a pancreas overworked from six years of being unable to keep up with insulin production, it makes sense to give it a holiday from that.
After 18 months (see my 18-month post), I had markedly better health. My HbA1c was consistently below 6%, but I wanted it lower than 5.1%. My weight was now about 96kg, but I wanted to be around 80kg. Both seemed to be stuck. I toyed with options like keto (higher fat), exercise (but what kind?) and further intermittent fasting as discussed in my previous 18-month post.
I did persist for about another 10 months with just diet. Strictly two meals a day (16:8 fasting). I tried more keto but my blood glucose and weight did not seem to shift. Control chart theory (and common sense) indicated that if I wanted my system to change, I needed to do something different.
Metabolic testing from MHS (the subject of my next post) showed that my metabolism was far from optimal and this provided evidence for the lifestyle interventions. With my doctor’s support, I also increased my metformin dose.
Inflammation can be caused by high blood glucose and high insulin. Neither my blood glucose nor (fasting) insulin was springing back to a level normal for the general population. Why was that and how could I shift it?
Nick Paterson who writes this blog from Finland, coined the term ‘inflammatory hysteresis’ to describe a phenomenon he saw in his own journey and people he worked with. Hysteresis is an engineering term and it made some sense to me so what does it mean?
Take a paperclip and straighten it out. Now deform the straight end slightly with a bit of pressure then let go. The clip springs back a bit like a spring. If you flex it much further, it will stay bent and if you deform it further in the same direction it will not return to the original position. It will bend further until it breaks. The inability of a system to return to normal shows that a system can hold a different persistent state. Simplistically, this is hysteresis. To straighten the clip, we need to actively deform it in the opposite direction to take it past its normal position.
The bent spring is a pretty good analogy for diabetes. You have bent your metabolism and pancreas so far that it will not snap back to normal. Hopefully, it’s not permanently damaged, but you need to ‘bend’ in the opposite direction so that it might settle back to normal again.
Diet and exercise interventions are tools, but could I somehow bend my metabolism further? Nick was doing an experiment with metformin to see if that could help. I also remembered the comment in my previous post from Dr Lance De Foa about metformin.
Most doctors would not prescribe metformin for T2DM with an HbA1c of about 5.6% if it is only to manage blood glucose. At 5.6% blood glucose is already non-diabetic and metformin will likely not lower it much further.
Clinical practice might need to be rethought for T2DM in remission. Metformin should improve insulin resistance and reduce gluconeogenesis (caused by my alpha cells) to promote further recovery ‘bending the spring’ a bit further using medication. Patients may have a goal to be medication free (I did), but metformin is not the same as insulin or sulphonylureas which may make T2DM progression worse (6) and increase the risk of cancer (7) and CVD (8). In fact, metformin is likely to improve those risks and others (9).
At about month 58 in figure 3, I began deeper fasting, resistance training, and I took my increased metformin dose. It worked almost like magic. Over the next year, my HbA1c crashed through the 5.1% barrier to 4.6%, my weight dropped 18kg to 78kg, and my fasting insulin dropped from about 12 to 6.
These were great results, but could I say I was cured? A great HbA1c on a low carbohydrate diet is often dismissed because you have just ‘hidden the problem’ by avoiding carbohydrates, however, my fasting insulin had also fallen from 26 to 6. On a low carbohydrate diet it turns out that for me HbA1c (in %), is a pretty good proxy for fasting glucose (in mmol/L) so this would indicate that my HOMA-IR (insulin resistance) had fallen from about 6.7 to 1.3. Generally, between 0.5 to 1.5 is regarded as the healthy range but this was when my pancreas was not being worked hard (during fasting).
The C-Peptide result shows that my pancreas still produces adequate insulin despite six years of quite bad T2DM. It was almost in the middle of the normal range. My HbA1c was 4.6% so it was below the population average of about 5.1%. Everything looks pretty good but the pass or fail isn’t really enough to assess where I am on the T2DM spectrum. Metabolism testing was also good (to be the subject of another post). To assess further we need a little detective work and this paper (11), particularly figure one in it, as provides us with a useful yardstick. Here is that figure reproduced with my results added to it in yellow.
Analysing my Oral Glucose Tolerance Test
Analysing the insulin, it’s a shame that I don’t have a 30-minute insulin value to compare (it was not part of the standard test that is done in Australia) but otherwise, the insulin response is fairly close to the average value for an insulin sensitive person with normal glucose tolerance.
Looking at the glucose curve, we can see that while I passed the test threshold at 2 hours, the peak is higher than would be expected for an insulin sensitive person with normal glucose tolerance. I speculate that for some reason (that may or may not be damage to my pancreas from T2DM) my first phase insulin response is still slow or low which leads to an excessive glucose peak. This might have been seen if I had an insulin measurement at 30 minutes.
What does that mean for me? Probably that it is best to still avoid food that is like 75g of glucose in one hit. Slow, complex carbs should not be as bad. Aren’t we all told to do that anyway to avoid T2DM? I’ll still generally restrict carbohydrates in my diet until I can see this improve too. It’s easy for me to repeat this test yearly myself to see how the glucose peak changes.
This may be due to a (genetic?) metabolic abnormality that I have always had or developed as I aged. If so it may be the reason I was more susceptible to developing diabetes (12). It is also possible that this is just the last thing needed to fixed before becoming completely normal. Interesting questions for me and perhaps for others.
We know from Prof. Roy Taylor’s work that first phase insulin response can improve with effective reversal or remission and this is more likely if you reverse T2DM after less than six years. It may be that six years of diabetes has left my first phase response more damaged. If that’s the case, maybe it can’t be improved or fixed, but then that’s what they’ve told us about T2DM for decades and so far ‘they’ haven’t been right for me.
There is also another possible explanation. These were the first substantial carbohydrates that I had eaten for 3.5 years. The OGTT protocol requires that you eat 150g of carbs a day for three days. I did that for four days but I cannot rule out that I might actually need longer to adapt given my very long time without them. It is fairly uncharted territory, but if anyone knows of a study that resolves this possibility or can otherwise explain this, then let me know.
“Just Losing Weight Cured You.”
I have been told this by some folks on social media. Usually, they don’t like low carb diets and/or fasting and think that a caloric deficit and weight loss are all that is needed. It’s sometimes from some who really should know better.
At 78kg down from 109kg it’s clear that I have healthier adipose tissue but there are also obese people that don’t have T2DM and thin people that do. If you consider that and now appreciate the complexity of T2DM a bit better, then you will know that saying that T2DM reversal is purely about weight loss is an oversimplification. It is as wrong as saying that weight loss has nothing to do with it. I note:
We’ve been telling people with T2DM to lose weight for decades. It hasn’t made much difference to the remission rate. Most health professionals don’t even bother to try with patients because losing weight is hard if you are unable to utilise your body fat- which is likely to be why the whole problem started. They just put them straight onto medication.
How do thin people with T2DM reverse it if excess body mass is wholly causative and remission is achieved just by losing 15kg? The answer is that they do this with a metabolicdiet and don’t try to lose weight unhealthily to reverse it like this poor fellow (13).
Metabolism is complex. A recent review (16) of the evidence supports that the relationship between weight loss and glycaemia (hence remission) is not as straightforward as might first be thought.
My particular case shows that weight loss is not the only thing happening in remission if therapy is sustained. For me, a very modest weight loss of about 1.5kg dropped my fasting insulin from 26 to 12. Insulin resistance was more than halved and there was no exercise to confound this! That is easily seen between months 38 and 51 in figure 3.
For the sake of people with T2DM, we need to challenge the “it’s just weight loss” paradigm, not the least because it just has not worked as a goal in itself for remission for 40 years or more. A good approach instead is a focus on overall metabolic health. That means healthy adipose tissue, healthy mitochondria, visceral fat reduction, metabolic flexibility, improved fat oxidation, increased muscle mass, total fat mass reduction and (naturally) involves weight loss.
What I Have Learned
Reflecting on my journey:
Diet is the primary intervention for T2DM, but metabolic health, which can include sleep, sunlight, exercise, and supplements (sometimes medications), is the real aim. Nonetheless, while it’s not all about diet, a low carb/ keto diet (with intermittent fasting) is a powerful metabolic tool.
Even if a dietary guidelines diet is healthy for everyone already healthy, it is an inappropriate diet for someone with T2DM wishing to be in remission or cured. It is unlikely to therapeutically address the underlying pathology, but also how could any health professional recommend an eating pattern to achieve remission that has no evidence for delivering remission?
It’s not all about weight loss. Your metabolism is complicated and T2DM puts you at the far end of a spectrum of a metabolic problem. That said, significant weight loss is a likely part of the journey if you are overweight or obese with T2DM. Losing excess fat mass improves your metabolic health, but the relationship is complex because sustained weight loss is also an outcome from an improved metabolism.
It’s much more about lowering insulin than managing glucose but we manage best what we measure. It’s easy to measure blood glucose and as it’s associated with complications so it’s the therapeutic goal, but it is not the only or best therapeutic goal. A focus on blood glucose has allowed us to mistreat T2DM with exogenous insulin, sulphonylureas, and now SGLT2’s (which are better but still not great). Evidence shows that a therapeutic diet can obviate or reduce the need for medications for many people.
Patience and persistence are important. It took me 3.5 years to reverse my metabolism to a non-(pre)-diabetic state after a decade of NAFLD and 6 years of poorly controlled T2DM. If one of the factors in reversal and cure is simply time, that’s unlikely to happen if you can’t sustain the therapeutic lifestyle needed and go back too early to a diet that may actually have caused progression. If I had tried to cure my T2DM using shakes for rapid weight loss, followed by a high carb dietary guidelines eating pattern, the result would likely have been quite suboptimal.
From here I’m going to continue my health journey. My weight hovers between 78kg and 82kg quite reliably. It’s unlikely that a decade of fatty liver and six years of poorly controlled T2DM has left me with no problems or health risks, but I’m a hell of a lot better than I would have been with a decade of T2DM.
Everyone should think about where they are on the T2DM Spectrum. I would hope if you have T2DM and are not in remission, you might now be inspired you to set that as a goal. If you are in remission, I hope it would show you there is a further path to travel, but that is also true whether you are pre-diabetic or have insulin resistance or metabolic syndrome.
For self-managing patients and clinicians, I think there are a few concepts here (and also in my next post) useful to continue to assess progress and work beyond remission.
Of course, my case can’t prove repeatability for someone else; however, it’s a more useful scientific resource than me filling in a lifestyle (food frequency) questionnaire only to have it mixed with 100,000 others, so you can look for an association with the foods to eat for a T2DM cure!
Maybe you can dismiss it as an anecdote and close your browser tab? I hope not as wisdom suggests an n=1 helps you understand a disease. Noting that I had diet as the main intervention for the first years, I think my case provides some interesting separation of the effects of those interventions for you to ponder.
I expect there are a few hypotheses in this post worth testing. 4.5 years is a long time to live without carbs and I’d like to put a few back at some point and expect I will after seeing my one hour OGTT normalise and HOMA-IR improve further. It’d be nice that if repeatable, the process heal can be sped up for others.
What is a cure for T2DM? I think it’s about getting the best metabolic health you can with a damaged pancreas (alpha & beta cells) and clearly, that is partly about restoring a healthy adipose system with reduced visceral and ectopic fat. Normoglycaemia and normoinsulinemia are surely pre-requisites for that. Diet, exercise, sleep, and medications/ supplements are the lever to get there, but time is also a factor.
You may not be able to reverse damage to your pancreas, however understanding the damage and eating (carbs) to the limitation of that can see you otherwise healthy for life and sets up the conditions that might give the best chance of pancreatic improvement. Even if you are fully reversed, you may be more susceptible to redeveloping but that does not mean you aren’t cured.
I note if you are cured of malaria, you still don’t get immunity from it and you can be more susceptible to worse disease the next time. It is my view that carbs are causal of T2DM (necessary but not sufficient) and no one has invented a vaccine against eating highly refined carbohydrates. In fact, it may be that the high carb diet many are eating is not a natural diet for humans and may be the cause of the problem.
Being cured is not the same as immunity. Setting the bar that you must be able to ‘eat carbs like everyone else again’ to be cured is subjective & clinically irrelevant unless doughnuts are clinically important. I’ll certainly not be eating them until the doughnut vaccine is developed. Good luck with that!
(1) Taylor R. Type 2 diabetes: etiology and reversibility. Diabetes Care. 2013 Apr;36(4):1047-55. doi: 10.2337/dc12-1805. PMID: 23520370; PMCID: PMC3609491.
(2) Lomanaco, R. & Cusi, N., Non-alcoholic fatty liver disease (NAFLD) in diabetes: distraction or impending disaster?, Chapter 21, Evidence-based Management of Diabetes
(3) Joseph R. Kraft, M.D., Detection of Diabetes Mellitus In Situ (Occult Diabetes), Laboratory Medicine, Volume 6, Issue 2, 1 February 1975, Pages 10–22, https://doi.org/10.1093/labmed/6.2.10
(4) Johnson, JD & Kushner, JA. Endogenous insulin: its role in the initiation, progression and management of diabetes, The Endocrinologist, ISSUE 129 AUTUMN 2018
(5) Muhmmad Omar-Hmeadi, Per-Eric Lund, Nikhil R. Gandasi, Anders Tengholm, Sebastian Barg. Paracrine control of α-cell glucagon exocytosis is compromised in human type-2 diabetes. Nature Communications, 2020; 11 (1) DOI: 10.1038/s41467-020-15717-8
(6) Genuth S. Should sulfonylureas remain an acceptable first-line add-on to metformin therapy in patients with type 2 diabetes? No, it’s time to move on!Diabetes Care. 2015 Jan;38(1):170-5. doi: 10.2337/dc14-0565. PMID: 25538314.
(7) Bowker SL, Majumdar SR, Veugelers P, Johnson JA. Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin. Diabetes Care. 2006 Feb;29(2):254-8. doi: 10.2337/diacare.29.02.06.dc05-1558. PMID: 16443869.
(8) O’Brien MJ, Karam SL, Wallia A, et al. Association of Second-line Antidiabetic Medications With Cardiovascular Events Among Insured Adults With Type 2 Diabetes. JAMA Netw Open. 2018;1(8):e186125. doi:10.1001/jamanetworkopen.2018.6125
(9) Campbell JM, Bellman SM, Stephenson MD, Lisy K. Metformin reduces all-cause mortality and diseases of ageing independent of its effect on diabetes control: A systematic review and meta-analysis. Ageing Res Rev. 2017 Nov;40:31-44. doi: 10.1016/j.arr.2017.08.003. Epub 2017 Aug 10. PMID: 28802803.
(10) Phillips, PJ,. Oral glucose tolerance testing, Emergency Care, Volume 41, No.6, June 2012 Pages 391-393
(11) Wang, Q., Jokelainen, J., Auvinen, J. et al.Insulin resistance and systemic metabolic changes in oral glucose tolerance test in 5340 individuals: an interventional study. BMC Med17, 217 (2019). https://doi.org/10.1186/s12916-019-1440-4
(12) Gerich JE. Is reduced first-phase insulin release the earliest detectable abnormality in individuals destined to develop type 2 diabetes? Diabetes. 2002 Feb;51 Suppl 1:S117-21. doi: 10.2337/diabetes.51.2007.s117. PMID: 11815469.
(13) Odhaib S A, Mansour A A (June 03, 2019) A Patient Loses 18 kg and Type 2 Diabetes Mellitus: The Challenge of Complete Remission. Cureus 11(6): e4817. doi:10.7759/cureus.4817
(14) Sattar N, Gill JM. Type 2 diabetes as a disease of ectopic fat?BMC Med. 2014 Aug 26;12:123. doi: 10.1186/s12916-014-0123-4. PMID: 25159817; PMCID: PMC4143560.
(15) A. Mardinoglu, H. Wu, E. Bjornson, C. Zhang, A. Hakkarainen, S.M. Rasanen, S. Lee, R.M. Mancina, M. Bergentall, K.H. Pietilainen, S. Soderlund, N. Matikainen, M. Stahlman, P.O. Bergh, M. Adiels, B.D. Piening, M. Graner, N. Lundbom, K.J. Williams, S. Romeo, J. Nielsen, M. Snyder, M. Uhlen, G. Bergstrom, R. Perkins, H.U. Marschall, F. Backhed, M.R. Taskinen, J. Boren An integrated understanding of the rapid metabolic benefits of a carbohydrate-restricted diet on hepatic steatosis in humans, Cell Metabolism., 27 (3) (2018), pp. 559-571
(16) Fridman M, Lucas ME, Paprocki Y, Dang-Tan T, Iyer NN. Impact of Weight Change in Adults with Type 2 Diabetes Mellitus: A Literature Review and Critical Analysis. Clinicoecon Outcomes Res. 2020;12:555-566. Published 2020 Sep 29. doi:10.2147/CEOR.S266873
Dietitian’s organisations frequently criticise low carbohydrate diets for not being proven safe in the long term. Poorly controlled diabetes (where blood glucose is higher than for people without diabetes) on the other hand, has been proven extremely unsafe in the medium to long-term. For people with diabetes, a restricted-carbohydrate diet is almost certain to lower blood glucose and remove or eliminate medications. This one ‘radical’ diet change can hardly fail to alleviate most of the ill effects of diabetes, medicinal side effects and both of their risks. Clearly, the ‘unknown risk’ of the low carbohydrate diet in the long term can be weighed against the near certain risks of diabetes. Otherwise, blindness, amputation, cardiovascular disease, dialysis from kidney failure and a shortened lifespan will nearly always be the end result.
I have now passed eighteen months on a low carbohydrate diet. That means I have exceeded the 74 weeks of the ‘best’ vegan diet study by Barnard. I thought it was time to wrap up the comparison and reflect on my health progress to see where my health journey could now go. That is the focus of this post.
Let’s get straight into that with an update to my HbA1c chart.
At the end of August, I was a little disappointed. The downward trend ceased and my result was actually 0.1% higher than in May. This was mitigated by the fact that the result is only accurate to one decimal place anyway and the later result in December came in again at 5.6%. All these results are still in the non-diabetic range. I still take 500mg of metformin as this remains beneficial to further recovery despite having non-diabetic blood glucose. That can be compared with 2000mg of metformin, Januvia and Diamicron before low carb.
Unlike the conventional and vegan diets in the trial, my blood glucose has stabilised and not led to an increasing HbA1c after three to six months that sustains and increases medications. Compared to HbA1c population statistics, it is about four standard deviations lower than the vegan diet and that is maintained on a minimum amount of metformin- unlike the more heavily medicated study participants.
Finally, my ending HbA1C is about ten standard deviations less than the vegan study statistics. Statistically, it is practically impossible for any of the 49 vegan (or 50 conventional diabetes diet) participants to have achieved a similar result.
Long-Term HbA1c & Glucose Control
In the context of my long-term results, the last eighteen months of a low carbohydrate diet since month 31 on this chart, have been an unqualified success. I have had non-diabetic blood glucose for fifteen months, and even non-pre-diabetic blood glucose for at least 6 months.
It is important to realise that HbA1c is really only an average. Large fluctuations up and down can still give a good average but have the considerable risk of complications due to glycaemic variability. My blood glucose measurements have a standard deviation of an excellent 0.8 mmol/l and the tight glucose control that a low carbohydrate diet gives can be seen below. I have a normal non-diabetic HbA1c with low glycaemic variability. My blood glucose measurements were 98% within target showing tightly controlled blood glucose. Such is the efficacy of carbohydrate restriction for diabetes.
You can also see the effect of one inadvertent meal which included carbohydrates at my daughter’s graduation function. Refined carbohydrates are insidiously a part of our food supply and no one is perfect!
My Overall Health
Unfortunately, with very high blood glucose, I had just about every bad effect from diabetes that researchers have shown. So how is my health after eighteen months on a ‘fad’ diet of unprocessed foods low in refined carbohydrates and no ‘healthy’ whole grains?
My total and LDL (‘bad’) cholesterol is about the same despite having increased my saturated fat intake greatly
My HDL (good) cholesterol is up by about 40% and triglycerides are down by about 33% meaning that my ratio of triglycerides to HDL more than halved! The ratio of triglycerides to HDL is an important predictor of coronary disease.
My blood pressure is an excellent 117/74 despite adding ample salt to my food.
I don’t have irritable bowel symptoms anymore. Among other discomforts, I was prone to unexplained and fairly frequent bouts of diarrhoea. My energy levels are good and I rarely feel bloated and my ‘gas’ production is negligible.
My weight loss is 16 Kg and importantly my neckline and waist have shrunk. I have moved from obese to just overweight.
But not everything is the same. I do have one negative. I am more prone to constipation which I almost never suffered from before. This is almost always a problem if I do not hydrate properly. Looking at the list above, I sure can live with that!
It is undeniable that my health is vastly improved. My doctor is extremely pleased, I am extremely pleased and my family is extremely pleased.
Social Effects & Adherence
Quite bizarrely, the Dietitian’s Association of Australia cited (without evidence) that the low carb diet should not be used for diabetes because the health of other family members could be impacted. Would they make that comment for a coeliac? Nonetheless, I can report that when we have meals, the family generally eats the potatoes or carbohydrates and I have a different vegetable. If only I could get my children to avoid processed foods, skip the fries and stop asking for sugary drinks completely like I do! It seems that is even beyond my powers as a role model. However, because of my eating requirements and awareness, we have less refined carbohydrates and processed foods and my children have reduced their sugar intake. Maybe they meant that they didn’t want anyone’s health to improve?
When I go out to eat, I rarely have a problem finding something. If there are carbohydrates, I usually can get another vegetable substituted.
This is otherwise an unremarkable non-issue.
Measuring My Metabolism
In late September, I had my metabolism measured by Metabolic Health Solutions (MHS). In full disclosure, this was done for me at no cost. I had not understood before how metabolism, weight loss and diabetes tied together. Now I think I do!
My testing showed that my Resting Metabolic Rate (RMR) was 2145 kcal which is towards the top end for my age and body. That is good. It explains that I have the metabolism to potentially lose weight without vigorous exercise. My efficiency (FEO2) was 17.3% confirming that I am no athlete as it would be optimal if less than 15!
Very surprisingly, the test showed that my fuel mix was 24.7% from fat and 75.3% from carbohydrate. This surprised me as I thought that, being on a low carb diet, I would automatically be a good fat burner! Ideally, this should be almost opposite with 80% fat burning and 20% carb burning.
It seems my metabolism is more than happy burning carbohydrates from protein. It does explain why I generally have had trouble losing weight and still have trouble. Clearly, if one is a good fat burner and does not eat a lot of fat then one will burn body fat. Being a carb burner fully explains why, when I went on a slightly higher fat moderate protein diet, I stalled. Even though it was low carb, my body was still getting most of its energy by making glucose from protein.
Solutions for me include some longer fasts, a more ketogenic diet to encourage fat metabolism, and exercise.
Since that testing (and to be transparent as my blog is non-commercial) I have begun working with MHS because I am impressed with how this information can inform your weight loss and metabolic health strategy. The world has a lot of metabolically sick people.
Where to From Here?
It is still my aim to achieve an HbA1c of 5.1% or below. As I indicated in my last post, control theory would indicate that I am unlikely to achieve that on the current trajectory. The steady progression downwards has arrested and I am about one standard deviation from the target. I do want to lose further (fat) weight. I must change my approach or it seems I will always be above the setpoint or take a very long time to reach it. My sleep patterns are pretty good and my diet is working well. I am still doing only a little exercise. Here are some options.
A Ketogenic Diet
Presently my diet has quite a bit of protein in it. This does not raise my blood glucose as carbohydrates do but it keeps me out of ketosis a lot of the time. By operating more deeply in ketosis, my blood glucose would fall markedly more and I would likely achieve my 5.1% HbA1c. That means a higher fat diet. If I limit my protein I will also have reduced capacity to burn carbs (presuming I can spare muscle) and this may help me become a better fat burner.
I enjoy the higher protein low carbohydrate diet. I do not see a ketogenic diet as a long-term option for me since it more difficult to get sufficient nutrient density on a high-fat diet- but this might be something I do for a while if it helps me to become a better fat burner.
Some Longer Fasting
Most days I fast 16:8 by skipping breakfast. By extending this I can cause my metabolism to use my own body fat since while fasting it will not have carbohydrates, fat or protein from diet and should prefer to use my own body fat. As a 75% glucose burner, I need to be careful that my body does not decide to obtain glucose by catabolising muscle until I can change that.
I do not exercise much and have exercised little over the 18 months. Among other things, I wanted to see how far I could go with diet and did not want to confound diet and exercise. By building more muscle and doing high-intensity exercise I should be able to deplete my glycogen more easily and frequently, leading to a reduction in average blood glucose, as well as increasing my insulin sensitivity. High-intensity exercise will also be helpful, combined with fasting or a keto diet to reduce muscle loss, and help me to become a better fat burner.
To be honest, I have never been a marathon runner and likely never will be, so part of my challenge is to find the exercise that I will enjoy.
Having some real numbers from metabolic health testing has allowed me to focus on what I can do to improve my metabolic health. I am now more motivated to exercise and then be re-tested to see how I have improved.
A Note for Vegans
Sorry, but in my case, it was no contest. A vegan diet can (without question) improve your health if you are obese and have diabetes mainly by its calorie restriction, but Barnard’s study compared with my journey shows that it is neither as sustainable nor as optimal for me as carbohydrate restriction when compared against the study people. I went the distance of 78 weeks versus the study’s 74 weeks and it is “Game Over”.
Final Word to Dietetic Associations
Shouldn’t I be dead by now from the ‘fad’ diet? In fact, if I had listened to you I might have been well on my way to dialysis or amputation. I think you need to get over your prejudice against low carbohydrate and higher fat diets. After all, despite some health-washing to make the much-lauded Mediterranean Diet appear as a low-fat diet- it is actually also a high-fat diet.
It is without question for me or my doctor that a low carbohydrate approach has led me to vastly improved health and a reversal of diabetes. If you have any real semblance of taking an evidence-based approach, that should also be obvious to you. You say that your members deliver services that are not ‘one size fits all’ but in practice if you have dietary guidelines uniformly applied to everyone (sick and healthy) it really is lip service!
More importantly, when you get medically and metabolically tested, it is well apparent that your dietary, exercise and eating must be individualised to optimise your metabolic health and that it is likely to change over time. It is reprehensible that dietitians are not systematically identifying the people for whom a low carbohydrate diet is beneficial and helping them with an individualised journey.
It is a shame that you (dietetic associations) keep your members in the Dark Ages of dietetic practice. I suggest that if you don’t change then consumers should figure it out for themselves and vote with their feet.
The official statistics I have quoted on indigenous health related to diabesity are appalling. Anecdotally too, there are horrific case examples.
We looked at the nonsensical state of innovation in diabetes and diet. In a situation analogous to the slowness to accept the cure for scurvy, we have seen forces that appear to be holding back effective dietary solutions for indigenous health. Those solutions, based on a traditional diet, were demonstrated back in the 1980s.
The situation looks bleak, but the low-carbohydrate movement has always focussed on grassroots solutions. That is a good strategy. You see the stakeholders who have the most to gain are people whose health is improved. The problem with low carb is that almost everyone else has something to lose. That is particularly the case for the food and pharmaceutical industries who benefit from the status quo. If you are in government and reading this, I have a message. It is incredibly short-sighted not to openly understand whether there are the disempowered stakeholders you should put first. This is an ancient problem for bureaucracy. You need to be counter-intuitive and anthropological. But we are getting deep. The efficient management of innovation by the government is a topic for another post.
Be Like Daphnis
The good news is that change is happening at the grassroots. I came across this Internet meme about Daphnis. It is one of the smaller moons of Saturn and the small ripples it makes in the rings of its much larger neighbour, and it seems appropriate to represent the change we can individually make. I think it is also very apt for this post.
I want to focus on the efforts of one individual in New Zealand who is making a difference. Joseph Finau commented on one of my posts, and I think it is worth considering his recent journey.
Joseph is a single dad from Auckland, New Zealand who has a remarkable story of battling diabesity and weathering personal tragedy. Losing 100KG (220 lb) is something entirely amazing but moving beyond that I want to celebrate his success in innovating within his community.
According to the 2013 NZ census, about 60,000 people of Tongan descent live in New Zealand. Most live in the North Island in and around Auckland. Like many Pacific peoples, and in common with the Aboriginal and Torres Strait Islanders, Tongans have suffered from diabesity in the transition from a hunter-gatherer diet and lifestyle to a Western diet and lifestyle. For their diet, diabesity is commonly blamed on the eating of turkey tails, lamb flaps and corned beef. Joseph has a different point of view- one born from the perspective of his success.
I believe that going back to the way our ancestors ate is the only way to cure ourselves from this western disease (Diabetes). for the last 3 years I’ve been eating Island foods mixed in with Western foods. example: Taro leaves & coconut cream & corned beef. Tongans loves corned beef but told it’s no good. the thing is? CORNBEEF has NO CARBOHYDRATES or SUGAR which means it’s low carb.
Joseph has adapted the Western foods Tongan’s love with some traditional food (less the starchy staples) to make Tongan and Pacific island dishes the low-carb way. That is also what the Nigerians have done and it is also what Western low-carbers have done. Corned beef cooked with cabbage in coconut cream and raw fish (AKA ceviche or kokoda) are but two dishes. Joseph has addressed one of the complaints, that low carb is too expensive, by also thinking about the economics for large families who need to be fed on a budget.
Is Low Carb Too Expensive?
The economics of low carb are an interesting topic perhaps for a future post. Let us just say here that the current criticism that low carb is expensive has some validity. It is also true that economies of scale have not yet kicked into the food supply. For sure there will be winners and losers. We only need to look at what has happened to the cost of solar power as economies of scale kicked in. A technology that was always a great idea but was uneconomic is now economic.
However, for the moment Joseph does have solutions that work for him and his community on a budget. As he shows, it doesn’t have to be about grass fed steak, tinned corned beef (which Tongans already eat) is fine.
LOW CARBZ 4 STARTERS & BIG FAMILIES. (Food is medicine)
Joseph has a Facebook group to reach out to people in his community and around the world. He runs cooking workshops, and his group has a procession of recipes from the one thousand or so members.
Now one thousand members may be small compared to the 340,000 now in the Ketogenic Lifestyle (Nigerian) group, but with 190,000,000 Nigerians and only 170,000 Tongans and Kiwi Tongans, it is actually quite significant.
What are the lessons for Australia?
Many people have long regarded Tongan diabesity as an intractable problem. Joseph is proving them wrong.
It seems that low-carb can be adapted to almost any cuisine and budget. By analysis of the Nyungar diet and by looking at the work of Prof. O’Dea and (most importantly) consulting with the communities, we should be able to adapt Western food to be closer to the macronutrients that Aboriginal and Torres Strait Islanders became metabolically used to for 30,000 to 50,000 years. It should be possible to make it affordable, available, and it should be more culturally appropriate than the food choices available today.
I am not saying it would be easy. I hesitate to suggest solutions for a people who have had plenty of ‘advice’ from my kind in the past. Social issues are always complex. Any solution must come from their grassroots. We need some champions like Joseph to lead the way to say eating needs to be different. Staple ‘modern’ bush tucker needs to be redefined and delineated from a preference for McDonalds or KFC. Awareness needs to be built about traditional diet and the reasons that fats and sugars are sought after, but need not be consumed in excess. That needs to be internalised. If it is hard for urban dwellers to avoid fast food, then the other side of the coin is poor access to healthy food in remote communities.
In the end, it will be a personal choice. However, if people and communities don’t have knowledge of this option, how can they choose a traditionally oriented diet for optimum health?
‘Blind Freddy’ can see that the existing approach is not working. It doesn’t work for the indigenous people of the world, and it isn’t working for us. We need different thinking.
Is a ‘Sugar Tax’ a Solution?
A sugar tax might provide revenue for some change while food supply economics normalise. If we are to have a sugar tax, why not apply it to tax the majority of unhealthy eating Australians to subsidise the food supply of those who may struggle to afford healthy food because of their socioeconomic or geographic disadvantage? Focus the funds on innovation to change ingrained food habits. This would be likely to normalise when the economics of the food supply and demand and supply settle down anyway.
No-one is arguing any more against sugar being unhealthy (apart from the food lobby). Before taxing other ‘unhealthy’ foods, the science needs to be settled.
It is in the nature of researchers to always call for more research funding. Frankly, when you see misguided research that appears to be being undertaken into diabesity, there are much better uses for the money. I am neither anti-research nor anti-academic, but funding should be judicious and focussed on settling the science for starters.
What are the lessons for NZ?
My Anzac cousins, you chose not to federate with us, and I get that. The last thing you need is some Aussie blogger telling you what to do! Joseph is doing fine, and you have other fantastic people in the low-carb community, but I have to question:
Why on Earth do your bureaucrats and food policy people follow Australia when we think that our dietary guidelines and institutions are dumb and broken?
It perhaps says a lot about the power of trans-Tasman economics over trans-Tasman rivalry, and there is probably a PhD thesis somewhere in that.
I think it is time to assert some of that famous independent Kiwi thinking. Otherwise, pretty soon the change will be over in Australia, and we will claim that Prof. Grant (Schofield) was really an Aussie researcher- just like Split Enz was an Aussie rock band.
Keep Going Joseph
My message to Joseph is simple. You may not have 340,000 group members on facebook but you are like Daphnis, and you are making waves at the grass-roots and leading by example.
You are not half the man you used to be, but twice the man most of us will ever be.
“Kai mate”, my Kiwi Tongan friend, and may that eating be low carb for a long and healthy life.
In Australia, our fat-cat bureaucrats, egghead scientists, over-lobbied politicians, salivating not-for-profit CEOs, conflicted dietitians organisations, greedy pharmaceutical companies and over sweetened food industry CEOs are debating obesity strategy and sugar or health taxes. The government has already dispensed a National Diabetes Strategy that this motley crew put together that wouldn’t even make it onto the fiction best seller’s list, let alone solve the problem, as it fails to contemplate changing dietary recommendations as solutions. Taxing us to tackle obesity? Unfortunately, they take themselves too seriously.
As a health consumer, what do you think? Before you answer, I’ll tell you that you should simply not give a damn (or insert your favourite four letter word here). Sorry for the language but when you realise that other than your statistic, it is not about you. Not one of these is truly advocating for you with your chronic obesity or diabetes. It is all to do with their interests like funding for their members and organisations, research buckets of money or profits. They have forgotten you and the experts are dead. After all, if they actually fix your chronic diabetes or obesity, what would they do with themselves?
Meanwhile, In Nigeria…
A quiet revolution is underway. Let us look at something that really should matter to you much more than the business plans and career advancement of all those types above.
Nigeria’s population is pushing 190 million. The traditional diet is quite high in carbohydrates with palm oil and other fats, and it used to be a sign of affluence to be chubby- but not anymore. It has upwards of five percent of those people with diabetes, many more pre-diabetic and far too many are obese. The obesity rate climbed eight times from 1.3% in 1974 to 10.3% in 2014. Fertility is impacted by PCOS. Yessiree, Nigeria has an insulin resistance problem.
Is Nigeria Lacking Dietetic Advice?
How can this be? Surely most people are not so affluent as to be obese? Nigerians probably have a good deal of plant-based diet as meat is more expensive. They have national dietary guidelines that are just as good as ours. Those guidelines recommend that Nigerians have a rich carbohydrate diet, limit fat and avoid saturated fat. Those guidelines say they should have lots of fruits and vegetables and not eat too much red meat. They have a dietitians association that gives them the same advice as everyone else in the world gets. Perhaps Nigerian Dietitians have the same problem as the DAA in that they have the same fantastic dietary guidelines, but no one follows them. Strangely this is an epic fail in every country, but we keep on doing the same thing and hearing the same excuses.
Perhaps it is all the new sedentary jobs in Nigeria that have caused these health problems? The Internet penetration is at about 52%- approximately 97 million people and about 16 million of those are on Facebook. Of course, to think of Nigeria as a poor, backwards country is not only insulting, it is untrue. There is one key technology statistic they lead in. I noticed that they even beat the United States.
If you search for the term ‘ketogenic’ on Google Trends, you see that Nigeria beats all other places in the world. “It must be some mistake,” you say? It is not. While our societies are nauseatingly debating sugar taxes, how to prevent obesity, coming up with ineffective national diabetes strategies and suppressing low carb for greed under a thin veneer of philanthropy, the ladies of Nigeria are transforming their health and the health of their country.
Now the low-carb deniers are probably going to suggest some tin-foil hat conspiracy. Maybe Prof. Tim Noakes has been commuting North every week spreading his vile message? No. It is a grassroots revolution.
In Nigeria, the low-carb diet is best known under the term ‘ketogenic’ diet, and so it has slipped under the radar compared to terms like Paleo, LCHF and Banting.
The Google trend search also shows that adoption has been extremely rapid. From a near standing start, it accelerated in about August of last year. It had the usual January bump that we see in diet trends. What is driving this? No surprises folks. It is because it works and the ladies know it.
One of the largest groups on Facebook is called “Ketogenic Lifestyle”. It started posting its ketogenic information in August of last year when the surge happened. It has about 316,000 members and has grown very fast. What may surprise you is that this group caters to provide support for Nigerian low-carbers. Almost all of the members are Nigerian, and the majority are women. How the three admins manage a Facebook group with over 300,000 people is probably worthy of a separate post (and a gold medal)!
This group was started by Joy Aghogho whom some of the members refer to as “Aunty Joy”. Joy is exactly what they feel every time a sister, infertile in the past from PCOS, announces their pregnancy. The posts are a procession of advice and information and then beautiful ladies. Beautiful and large before, beautiful and healthier after keto. They know the keto diet is a therapeutic diet that can counter the health scourges of their country (diabesity) as well as PCOS and epilepsy. There is not a dietitian in sight. These are ketogenically educated ladies, and they seem to know it better than most Australian APDs!
Let us just run some numbers for the bureaucrats and CEOs who may happen to come across this health consumer’s blog. 316,000 Nigerian Facebook users can actually be doubled when you consider that their partners are probably eating keto too. That is four percent of the Facebook user population. Given that societies like Nigeria have very dynamic and active personal networks radiating from each user, that figure may well be a good proxy for the penetration of the ketogenic diet into Nigeria itself. This figure is significant as the official rate of diabetes in Nigeria is 5%, and the ketogenic diet normalises and reverses type 2 diabetes and offers type 1s normal blood glucose. There is likely to be a great crossover between the obese and diabetic population (10.3% and 5%) and the ketogenic diet population.
So here are some questions and implications for various people from the ketogenic health explosion in Nigeria.
For Government Health Ministers and Health Bureaucrats:
Will Nigeria beat diabesity before your country even considers the right move? It looks like you need to get away from the noisy lobbyists and interest groups and investigate what is happening for health in our own Facebook communities.
For Pharma CEOs:
Nigeria is probably not even a blip on your sales figures, but you now have a duty to your shareholders to inform them of the risk from other country populations adopting low carb- particularly at the rate of growth seen in Nigeria.
For Pharma Shareholders:
Along with the Credit Suisse report, time to reassess your long-term investment unless your CEO has communicated a clear strategy to manage dietary change to low carb.
For Diabetes Not-for-profits:
Are you really committed to innovation to improve the lives of people with diabetes? If not then find another job.
For Food and Drink Industry CEOs:
Time to stop resisting with marketing that will damage your future brand. Consider what your products will be in a low carb future and like pharma executives- consider your projections carefully.
For Food and Drink Company Shareholders:
Along with the Credit Suisse report, time to reassess your long-term investment unless your CEO has communicated a clear strategy.
For Dietitians and their Not-for-profits:
Even if you STILL think this is a diet fad, shame on you to force health consumers to fix themselves via Facebook. Ignoring this health revolution is making you irrelevant.
For the higher carb chronic disease sufferer:
Time to try what these smart Nigerian ladies know.
For the researcher:
Plenty of epidemiological data here about the mass-effect of ketogenic diets on weight loss, POCS, Diabetes and health. Time to pull out your head and head to Abuja or talk nicely to Joy.
For the existing low-carber:
See what the low carb community can do.
Keep calm and keto on with our Nigerian sisters!
So the experts have told you that you have a chronic or incurable condition? Maybe you have diabetes, metabolic syndrome or obesity or just cannot lose weight? Possibly you are someone who wants to understand medical innovation? Perhaps you were caught by the title and wanted to know how the experts died, who killed them and why?
Let us start to make some sense of an ‘unsatisfactory predicament’.
What is a chronic disease? It is a medical problem that doesn’t go away on its own or with finite treatment for complete cure. It may have a symptom or multiple symptoms. Those symptoms may get better or worse in severity over time. You may be taking medicine to manage the condition. It usually isn’t communicable to others and usually isn’t ‘believed’ to be caused by yeast, parasite, virus or bacteria. I say ‘believed’ because it may be that it is and yet the experts do not acknowledge it. It could also be that some organism is opportunistic and remains present or recurs because of low immunity and there is an underlying reason (the root cause).
Our Medical Systems
What happens with chronic disease in our medical system? You see the doctor, and the doctor diagnoses you or refers you to s a specialist who diagnoses you. You take your medicine- which helps- but it doesn’t get better. It is a managed condition. Eventually, you accept this. The condition is chronic or terminal, and you learn to ‘live’ with it. The problems continue because you have not addressed the ‘root cause’.
Alternatively, you hop from doctor to doctor hoping for a later opinion to give you a cure. (However, there is a problem with this which we will understand better later). Maybe then after a while, you accept it and learn to ‘live’ with it. You may manage the condition for the rest of your life.
Alternatively, you get secondary effects, the condition worsens, and you have unwanted complications like blindness, amputation and kidney failure. You may have more radical treatment like surgery or and eventually, it is terminal. That would be typical for diabetes for example. If it were cancer, say prostate or breast cancer, it could be more aggressive, but the outcome is still the same- a continued decline.
Adding complication, you may have multiple symptoms. You may get depression (or this may, in fact, be your primary problem), hypertension, high cholesterol or any number of other problems. Pretty soon you can be on a cocktail of medicines- polypharmacy- and you need them long term. In a further complication, your livelihood, work, family, and social life may be adversely affected.
Example of Obesity
If you want a simple example that fits many of us, then I give you- obesity. Well, I don’t literally give it to you because many of us already have this chronic condition. Is it a disease, symptom, condition, malady or just a fact of life? Obesity could be any of the above. It can make us depressed or at least unhappy, and it often gets progressively worse. We diet and lose weight yet it most often comes back. We follow the experts to ‘move more and eat less’ but despite weight loss industry being worth billions of dollars no one seems to know the root cause. The best they can say is:”It is complicated. It is multi-factorial.”. Obesity is a chronic condition, and the experts are dead.
Whether your problem is obesity, diabetes or something more immediately serious, I would hope for you is that there is an alternative. There is a solution out there to your medical problem. Someone has beaten the incurable problem. Someone is treating the problem successfully and perhaps unconventionally. There is perhaps new research that you could try or a study in which you could be involved. How would you find that?
Type 2 Diabetes and Obesity Solved!
Well if your problem is obesity or type 2 diabetes, then there almost certainly is such a solution. If you have type 1 diabetes, there is also the chance for marked improvement. If you remember I said that you could learn by imitation? You certainly can for those (and related) conditions because the solution I have followed should also work for you.
At this point, medical people would be telling you that I am “peddling false hope”. You see they ‘know’. They are the experts and what is happening to you is what happens to all of their patients. If the best expertise, which they embody, cannot cure you- then everything else is just pseudoscience. I am understanding of that logic, and you also need to be. I would not want to get your hopes up. What I did may not work for you. The solution to your problem may not surface in your lifetime, or indeed it may be lost in time.
I can tell you that in my case it was true that I went through years of managing a chronic condition, that if I had the correct advice from the start, would never have progressed. In fact, as it occurs, my problem has reversed by addressing the root cause. I could have saved much heartache and damaged health. In my case, it would have mattered little if I went from expert to expert. The only solution that would have helped me was to understand that, for my problem, the experts were dead. When you accept that metaphor, you can open up the possibility that there is a better solution out there and find it for yourself.
That is not to say that the conventional wisdom is all wrong. What we need to do, while getting the best possible outcome from the conventional wisdom, is to explore the alternatives.
Take a Journey
If that prospect is something you would like to evaluate through my experience, or if you are a medical professional wanting to understand how to lift your innovation game, then this blog is for you.