## Type 2 Diabetes: Beyond Remission to a Cure

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.

## Foreword

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.

## 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.

1. 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.
2. 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.
3. 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.
4. 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’.
5. 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.
6. 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.
7. 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.
8. 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.

## Inflammatory Hysteresis

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.

## Increasing Metformin

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).

## Changes

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).

## My Pancreas at Wide Open Throttle

The gold standard test for diabetes is an Oral Glucose Tolerance Test (10). I decided to do this in month 89. You can see my preparation and the test results I took alongside the lab measurements on Twitter, which was tweeted in real-time. I ceased taking metformin for two weeks prior so that it was not a factor affecting the result. The official result confirmed that I was neither diabetic nor pre-diabetic.

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 metabolic diet and don’t try to lose weight unhealthily to reverse it like this poor fellow (13).
• Specifically, though, diabetes is most believed to be exacerbated by ectopic and visceral fat accumulation around and in the liver and pancreas (14). Liver fat may be reduced without a significant change in weight (15).
• 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:

1. 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.
2. 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?
3. 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.
4. 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.
5. 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.

## Research Reflections

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.

## CONCLUSION

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!

## References

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(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 diabetesNature 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 studyBMC Med 17, 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
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(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

## Eighteen Months of Low Carb

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.

## HbA1c Chart

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?

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.

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.

## High-Intensity Exercise

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.

## Metabolic Health

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.

Oh, that’s right. We are!

🙂

## Engineering Nutrition?

With the failure of forty years of dietary guidelines to arrest or improve the incidence of diabetes and obesity, new thinking and approaches are needed. Applying an engineering mindset to nutrition has attracted attention as some of the new thinking has emerged using root cause analysis and other engineering tools. This has resulted in new insights for the medical and nutrition communities.

This is not really new, I pay homage to doctors like Dr Bernstein who trained as an engineer first, then as a trained doctor realised how controlling diabetes was like an engineering control problem.

Recently, however, as a recovering type 2 diabetic, I plotted my HbA1c against the results of a long-term vegan ‘cure’ for diabetes study to see how it compared. I was astounded by the superior result and tweeted that it was a fifteen sigma improvement. While not really correct, it got me thinking of my recovery in terms of engineering control theory and quality management.

Putting aside whether a cure is possible (for type 2 diabetes) and considering treatment, what if we view diabetes as an engineering control problem and applied control charting to understand the quality of different management options? Note that while I have type 2 diabetes, the glycaemic control problem is common to type 1 and so much of this analysis also is relevant to them too.

## Broken Control System

You might wonder, what will happen if you don’t eat any carbohydrate? Fortunately, probably as a result of adaptation, the body is fine as it can make what you need from other sources. This happens mostly in your liver. It is called gluconeogenesis or GNG for short.

Essentially with diabetes, the control system that reduces blood glucose (BG) is broken. The homeostasis (self-regulation) of your BG is ineffective because your body’s response to insulin (which lowers BG) is diminished (called insulin resistance) and/ or your ability to produce insulin in response to carbs is insufficient to lower BG quickly enough. For type one diabetes, insulin production is at or near zero.

Consequently, glucose that your body gets from carbs (or makes in the liver through GNG) will raise your BG and it will only fall slowly because your body is unable to produce or respond to insulin properly.  So BG is easily raised but slowly and poorly lowered.

## Conventional Diabetes Management

Let’s leave the medical theories about why the system is broken alone for the moment and assume we have to do the best with what we have got.

Conventional diabetes management seeks to lower your BG towards normal but not so that it drops too low. This is done by exercise (to consume glucose), diet and medications that replace insulin, reduce glucose production or eliminate glucose from the body.

In conventional diabetes management, juggling these factors on a daily basis is hard and is the focus for someone with diabetes. Every three months you go to see your doctor to see how you are doing overall and to see if your medication should be adjusted.

Unfortunately, it is hard to achieve and maintain this great juggling job. It is hard to replace a well working system in the body once broken. The typical person with diabetes has BG that, on average, is too high. It may also drop too low with too much medication leading to coma or death. High BG is associated with all of the ill effects that people with diabetes suffer including blindness, kidney disease and amputation. For most, eventually, doctor’s visits mean an inevitable adjustment upwards in medication and higher BG. High BG results in deterioration for a person with diabetes over time, more medication, more complications. Diabetes is therefore regarded as a chronic disease with an inevitable worsening progression.

With that prognosis, it makes little sense discussing getting back to normal BG. It makes little sense to see this as a control process that can be brought under near normal control.

THAT IS (FORTUNATELY) COMPLETELY WRONG!

## HbA1c Measurement

I mentioned a three monthly visit to your doctor. Your BG changes throughout the day. In order to assess your overall BG control, a test measuring ‘haemoglobin A1c’ (HbA1c or just A1c for short) measures how ‘sticky and sugary’ (glycated) your blood is. As blood cells turn over every three months, A1c gives you about a three month average of your BG control.

I mentioned that if your systems were working properly, your BG would average about 5.6 mmol/L (or 100mg/dL). It turns out that this corresponds to an A1c of 5.1% (or 33 mmol/mol). This is an average for the healthy population or ‘population mean’. Statistically, the standard deviation from the mean is about 0.5% and it is deemed that you have prediabetes if you exceed the mean by one standard deviation or >5.6%. Similarly above about two standard deviations (>6.1%) you are diagnosed as having diabetes. The higher above one standard deviation you go, the worse becomes the health risks of diabetes.

## Control Charts

Control charts are a tool used in engineering and management science to help us understand what is happening with a process. Essentially a control chart gives you a measure of how close a controlled system is performing to expected behaviour (the mean or average target for a parameter) when considering its deviation from the desired behaviour. Control charts give you a measure as to the quality of the outcome of a process and should help decide what you may need to do to bring a process back into control.

If the aim is for a person with diabetes to approach the health of a ‘normal’ person, then we must restore the control as near as possible to the BG of a healthy person. A control chart type of methodology is used in some glucose monitoring programs to measure the quality of control of daily BG.

So when looking for long term control/ improvement, why not plot the mean of HbA1c and its standard deviations for healthy people? We can then use the control chart methodology as a yardstick to see how various treatments compare and to hopefully gain better BG control towards a cure.

## Diabetes Control Chart using HbA1c

I have reproduced the results of a study on diabetes as a control chart. That study looked at about 49 vegans and another 50 people on a conventional diabetes diet. You can read this study here.  I have added to that a plot of my history on a low carbohydrate diet. I have added in the bands of standard deviations (s, 2s, 3s, etc) in bands of colour from green to red.

1. Excellent control would see points close to 5.1% and ideally in the light green zone within one standard deviation (±s).
2. In control chart theory, any data point more than three standard deviations (±3s) is deemed ‘out of control’. Something is really wrong with the system and control process itself for this to occur.
3. Not one of the measurements is below the population mean of 5.1%

## Conventional Diabetes Diet

This diet was a low fat, calorie deficit diet designed for weight loss. This gave the worst outcome. At the end of the 74 week period, the average A1c results were nearly above where they started. No average A1c was better than 5s. By the end of the trial, only about half of the participants were adhering to the diet. This was despite cooking lessons, weekly meetings with a dietitian and other intensive assistance. This diet was high in carbs as they are 60-70% of total energy.

## Vegan Diet

The vegan diet lacked meat, eggs and dairy but was not calorie restricted. This gave a slightly better outcome. No average A1c reading was better than 4s. By the end of the trial, only 44% were still adherent and the outcome was beyond 5s. This was despite similar intensive assistance to that given on the conventional diet. Probably, as a result, some of the gains in A1c made earlier in the trial were lost and the vegans also deteriorated again. Had the trial and the upward A1c trend continued, it appears that the vegans might also have ended up worse than they started. This diet was very high in carbs being 75% of total energy.

## LCHF/Keto Diet

My diet lacked carbs. No sugar, rice, pasta, bread, sugary fruit and starchy vegetables. I also drank alcohol sparingly. Most people with diabetes are advised to eat between 200g and 300g of carbs per day spread out over the day. I aimed at first for less than 50g per day (<10% carbohydrate) and after about three months I was reliably lower than 25g (<5% carbohydrate) per day. This normally would be a ‘keto diet’ however it is hard for people with diabetes to stay in significant ketosis without extended fasting so I prefer to call it LCHF. I also did practise intermittent fasting simply because I was not as hungry as I was with a higher carbohydrate diet. Many people report this. Typically this involved not eating breakfast so that it was 16 hours after the previous night’s dinner before I ate the next meal.

There was no assistance from a dietitian or cooking lessons for me. I did read the free information on the dietdoctor.com website to get the bulk of my nutrition from real food sources (meat, eggs, fish, fruit, vegetables, nuts & dairy) that were low carb. Unlike the diets in the trial, adherence was easy for me, although I had to unlearn a lot of ‘advice’ that dietitians had previously told me on my way to developing diabetes. Unlike the study diets, I ceased three diabetes medications after three months but then began taking one-quarter of the dose of metformin again at that time.

I did no appreciable exercise like running, swimming, cycling but took an occasional walk. In the first six months I easily lost about 12KG of weight, moving from obese to overweight. My weight has been quite stable since then.

Unlike the other diets of the study and my previous diabetes history, all my readings (except baseline) were within 2s and went below s before the year on LCHF was finished. Clinically, below 2s is pre-diabetes and below s is non-diabetic so I have been very happy with that result. The downward trend was recently confirmed as still occurring with a recent estimate of A1c from my glucose meter readings.

## Engineering Analysis

Straight away we can say that the study diets are ‘out of control’. With no points less than 3s there is little prospect of either ‘process’ (diet) bringing control to equal the population mean. Further with all points 4s or higher, the mean (goal A1c of 5.1%) will never be reached. Quite simply, something is causing the A1c to be unacceptably high that the process being used cannot overcome. From an engineering standpoint, these are defective processes that cannot achieve the target. The trends were initially towards but end up moving away from the target long term. Management theory would tell you that the individual in the process (person with diabetes) will be powerless to achieve control. It is ridiculous to blame the person with diabetes for this result yet many of us blame ourselves. The theory says that to continue to expect reasonable control to the target wanted is foolish. You must use a different process or make some other significant change to the system.

That is not the case with the LCHF diet. All points are within 2s, some s, and we have a trend that may eventually result in the target being achieved although none of the measurements so far have been below the target.

## Engineering Solution

If I were presented this as a control system problem I would immediately conclude that there was an unaddressed control offset, especially in the study diets. The engineering solution would be to apply ‘Integral Control‘ to attack that offset so that the control range is eventually brought closer to the target. This means relatively slowly increasing or reducing the level of the controlling factor until control can be achieved.

Further, both diets represent a perturbation in the system that slowly corrects back to its original level. Like throwing a stone in a pond. The ripples eventually subside and things head back to what they were- in this case, a level that is too high.

We know that carbs, be they from the liver (GNG) or diet, raise BG and A1c in people with diabetes who do not have enough (or do not respond properly to) insulin. The amount of carbohydrate is the controlling parameter for BG and A1c. It is straightforward that a solution is to reduce carbs permanently- but by how much? For me, the LCHF result shows that even if we drop dietary intake to a minimum, the target would still not be reached quickly due to their production by the liver (from GNG).

So a very apt control analogy is a sink with a small inflow of water from the bottom (GNG), a drain draining away by a controllable flow (insulin action and exercise), and a tap with the ability to put in a variable inflow which by eating carbs could be continuous if spread into small meals, large and rapid if a lot of carbs (say sugar) is consumed or minimised if restricted.

Now if we want to keep the sink at a certain level (say half way) we can exercise to drop BG and eat fewer carbs to lower the level. If we leave the tap running at a rate that exceeds the draining rate or suddenly empty a large bucket of water into it, the sink fills and we will now be permanently above the level we want. This is what we see with conventional and vegan diabetes management in the study. In this situation, it is common sense to turn off the tap- carbohydrate restriction. 200 to 300g of carbohydrates per day is the problem in this control system.

## Exercise Helps but Diet Rules

Exercise is a help but consider that the average person must run about 7 km to ‘burn the carbs off’ from a 500ml serve of coca cola. Even if you do run the 7km, in the time between drinking the drink and completing your run, those carbs are giving you high unhealthy BG. Better just not to eat or drink the carbs in the first place. You cannot outrun a bad diet.

All of the diets have too many carbs for the available and effective insulin to bring down BG to normal metabolic levels and that explains why the target was never reached by any of them.

## Reaching the Target

Unlike the study diet, we should expect the LCHF diet might reach the target in the next nine months or so if the present trend continues.  The simplest course of action for the LCHF diet would be to keep going and see if the system settles to the desired target. If it does not or if a quicker result is wanted, other interventions could be tried to reduce carbohydrate including longer fasting, increasing exercise, upping metformin dosage or looking for another metabolic option. So now, as a vegan doctor (Dr Joel Kahn) commented to me upon looking at my results on Twitter, maybe slow and steady wins the race? That might well be the first of his advice I have ever taken.

## Am I a Special Case?

At this point, you may be wondering if carbohydrate restriction might help your diabetes or am I a one off? Let us explore that. My results prior to carbohydrate restriction were consistent with the conventional diet people from the study. The best HbA1c I saw was 7.3% and as you can see below, carbohydrate restriction was the difference beginning around month 31.

The value of a case study is that it shows what CAN happen. There are no guarantees, but given similar circumstances to me, yes this can happen for you. Many other people report that it happens for them. In fact, we would expect it to happen from the biochemistry and control theory I have explained. This is even though everyone with diabetes is a little different. It means your mileage may vary.

Biochem is complex. Perhaps the major appeal of LCHF to an engineering mind is that, based upon engineering theory, it makes perfect sense. Dietitians are constrained by a myriad of epidemiological studies which show increased risk of this or that from doing that or the other thing. If you accept that A1c is a measurable proxy for the underlying health issues of diabetes, clarity to focus on the job of controlling A1c occurs and carbohydrate restriction is obvious. Once that is done, focussing on optimising diet within that constraint is the task. This fits nicely with the theory of constraints as a way to tackle complex systems.

## LCHF, Vegan or Conventional Diets?

The vegan diet did perform better than the conventional diet in the study but both were a control chart fail. It is however theoretically possible that one of the 49 vegans achieved similar results to me. My result towards the end shows that my A1c was about fifteen standard deviations below the vegan mean. In other words if we assume a normal distribution and there were 100,000,000,000,000,000,000,000,000,000,000,000,000,000 vegans in the study, we could expect about one to have results as good as mine. Unfortunately, there were only 49 vegans in this study. This is a time when an n=1 (me) is statistically significant.

To be clear I am not saying that a vegan diet could not achieve the same result, but it would have to be low in carbohydrate and total energy so a vegan (or any) starvation or fasting diet would probably also work.

If common sense, the engineering theory, my simple Biochem explanation or my results do not explain why a carbohydrate restricted approach is best then read this paper. An excellent (and more complicated) comparison between the Keto (LCHF) and vegan approaches to managing diabetes is available from Marty Kendall’s website. You will also find a lot of other excellent information on nutrition there should you be concerned that restricting carbs may put you at risk of nutritional deficiency.

The Vegan propaganda machine is fond of saying that restricting carbs (the keto diet) masks the problem by addressing the symptoms whereas only the vegan diet ‘cures the disease’. Based upon the study we looked at, it appears to be an untrue claim. I don’t care whether you eat live chickens or just grass to avoid animal harm, the first thing that someone with diabetes should do is minimise their carbohydrate intake. If you must eat some, then not too many and make sure they are ‘complex’ and unrefined.

## Dietitian Says ‘No’

So what if you see a dietitian and they try and dissuade you from a carbohydrate restricted approach. They may have the following objections to which I give you some answers:

1. You need carbs and your diet will lack fibre and vital nutrients from foods you will exclude like whole grains.
Answer: Some fats and proteins are essential but carbs are not. Even if you could have zero carbs in your diet, your body makes them (via GNG). If fibre is of concern then eat more low carb vegetables. Vital nutrients? See Marty Kendall’s website. If a dietitian can’t give you a healthy carb restricted eating plan, time to walk!
2. It helps some people but people can’t stick to it in the long-term. We also don’t know how safe it is in the long term.
Answer: Well what if a person it can help is me? Shouldn’t I try it? Looking at the conventional and vegan diets in the study, adherence was also less than 50%. Adherence is a matter for any way of eating and it is up to you. You don’t have to be a statistic. Finally, what does the long-term look like if your A1c stays at ~6, 7 or 8% and above? The risks of a high A1c are very well known. If LCHF is a devil, it is the devil you want to know.
3. Keto? Low Carb? Control charts? [Insert other doubt raised here]? Do they have any evidence of success from a study in a peer reviewed journal? My clients have excellent success on [insert a diet/ program here] instead.
Answer:  Please give me evidence of a study showing [insert their diet/ program] can achieve an A1c approaching 5.1%. Please give me evidence of the success rate of your clients achieving a sub 5.6% A1c.
4. On LCHF/ keto you are limited. Studies show that eating [insert food of concern] or not eating [insert dietitian ‘superfood’] will make you die sooner.
Answer: Have you ever seen someone on dialysis or with a diabetic foot? It is your job to give me a diet for normal blood glucose, then we can optimise it for other concerns. Do your friggin’ job and shelve your dogma.

The system is failing all of us. More of us are getting obese and diabetic following the standard way of doing things. I developed diabetes on a near exemplary low-fat diet. I can only encourage you to be a robust health consumer. You should not assume that in the face of the diabetes epidemic that has grown under national eating guidelines and dietetic advice, that the experts have it right. Diabetes takes no prisoners and you shouldn’t compromise your outcome just to be nice to a health professional.

Dietitian’s organisations lampoon ‘Dr Google’ just like clothing retailers said people would never buy clothing online. Honestly though, if you are seeing a dietitian who is not on board with carb restriction for diabetes, you are wasting your precious time and health.

If you can’t get proper help from a local professional then there are sites like dietdoctor.com, forums like the ketogenic forums and facebook groups like type 2 diabetes straight talk or type one grit. If you are in the US, Virta’s service could be a good choice. Any of these would be preferable to a low carb inexperienced dietitian!

If you DIY then be conscious that some medications that you may be on (notably sulphonylureas and insulin) can be very dangerous to take if you suddenly reduce your dietary carbohydrate. If trying this, you should consult your doctor to clear or adjust your medications appropriately.

## Low Carb Yoghurt: Tips & Tricks

For a change of pace after a lot of heavy posts,  I thought I would share some money saving tips about yoghurt- inspired by Joseph Finau who is helping people do low carb on a budget.

Some people don’t eat dairy at all on a low carb diet, and many following a paleo lifestyle also do not regard it as paleo. Coconut yoghurt may be an option, but that is a different beast to the milk based yoghurts that I will discuss and it often has gelatine or other thickeners. Unlike dairy milk, coconut milk is also already low carb and sugar is sometimes added to ferment it.

This post is about getting the sugar (lactose) and cost out of dairy yoghurt. Some people are lactose intolerant but can tolerate yoghurt which has reduced lactose. Many others have a high regard for fermented foods like yoghurt in their diet. Yoghurt (and especially Greek yoghurt) can be very expensive. If you do eat dairy, but are put off by its carbs or price, then this post is for you.

Many commercial yoghurts are high in added sugar and carbs. They may have additives like gelatine or other thickeners. Most of all they are expensive. A one-kilo tub of premium yoghurt can cost $7 to$8. Making your own can make it more carb friendly, even lower in lactose and a lot cheaper.  Would you believe $1 a litre or maybe less? It is pretty easy once you get the hang of it. We never buy made yoghurt, and you will probably not do that either once you learn some tricks. So how do we do it? ## Do You Need Yoghurt Maker? You can make yoghurt in a warm place in a bowl, but a yoghurt maker takes the guesswork out of it. A 1-litre electric yoghurt maker can be picked up on eBay for around$12. I recommend getting a bigger one (1.5 to 2 litre in capacity) if possible.

If you don’t use a yoghurt maker, then an insulating the container like a wide mouthed vacuum flask or wrapping the bowl in a tea towel might be useful. Having somewhere warm to keep it while it ferments (like a warmed oven) is useful. Using a light bulb for heating (as it a chicken incubator) may also be an option. Whatever you do, it is important to keep it below 45C or 113F or the culture may be killed.  If the temperature is lower than 40C or 103F then it may take much longer to ferment.

You need milk and some starter, and that is all.  You can use some store bought yoghurt (if it has live cultures) as a starter or you can purchase the culture from a cheese supply store some of these stores sell online and ship the live culture in a cool pack. Here is a google search that you can add your country’s name onto to find a possible online source.  Although more expensive (about $13), once you are a committed yoghurt maker I recommend purchasing the starter because: • It gives consistent results. Most cultures are a mix of two or more bacteria. Re-using yoghurt batch after batch may deteriorate the ratio. • It is small and stores in the freezer • Commercial strains may be chosen for sweetness. You want a high acid/ low lactose variety • I only use a tiny amount (about 1/8 teaspoon) • You can search for a more acid tolerant starter culture which should give you lower carbs. • My last small jar of culture went for more about eight years of yoghurt making! So divide the cost by 300 to 400! Which starter? There is some technical info here. You can always email the vendor and ask for their most acid tolerant starter or ask for one leaving the lowest lactose. ## Instructions 1. Heat the milk until it is nearly boiling. 2. While hot, pour into the container you will make the yoghurt. 3. Allow it to cool to be lukewarm. Use about 1/8 a teaspoon of yoghurt culture or a tablespoon of yoghurt from a commercial yoghurt. If the milk is too hot (>45C / 113F), you will kill the culture and the milk will not ferment. 4. Allow the milk to ferment for 12 hours (or longer) in a warm place (40 to 45C/ 103 to 113F ). That is what your yoghurt maker does. 5. If there is a clear liquid on top, don’t worry, that is normal. It is whey. 6. For Greek yoghurt, allow it to strain through a sieve until it is the right consistency. 7. Store in a container in the fridge adding in low carb sweetener when you use it. ## Making Lower Carb Yoghurt As the lactose is fermented by the bacteria in the culture, it is converted to lactic acid which makes it sour. Commercial yoghurts may shorten the fermentation time to save money or to make a sweeter product. Only 20 to 25% of the sugars are converted. Once they are chilled, further fermentation is very slow. By making your own and fermenting it for longer, you can make sure it is much a lower carb yoghurt. It is suggested to ferment it until the whey (clear liquid) separates which can be as long as 20 hours. The fermentation slows as the acidity rises stopping at about 4 to 5 grams of carbs. This is where a high acid culture can help to reduce carbs further. Now you have basic yoghurt. If you paid$1 a litre for your milk, you now have a litre of low carb yoghurt for $1. The next trick to go even lower carb is straining. ## Straining Greek yoghurt is yoghurt with some of the whey strained out usually for about 4 to 8 hours. Labneh is a yoghurt cheese that has substantially all of the whey removed, often using a weight or pressure. It may have salt, sweetener or herbs and spices added. By straining yoghurt for longer (1 to 2 days), you get labneh. You can buy a commercial greek yoghurt strainer, but a colander with filter paper or muslin cloth over a bowl or the sink does an excellent job. If you use a bowl, you can use the whey in other cooking. It is possible to just use a very fine sieve (metal or plastic) if you very carefully spoon the set yoghurt into it using a large spoon and taking care not to disturb the ‘curd’. I prefer this as I don’t like buying filter paper to throw away or washing muslin cloth. If your yoghurt runs through your sieve then your sieve is too big, you didn’t ladle it carefully, or it wasn’t fermented for long enough. ## Advantages and Disadvantages of Straining The benefits of straining are: • You lose more of the lactose and other sugars that were not digested by the bacteria as they are soluble and in the whey, so it becomes lower carb even still. • You lose the whey which is a protein that some people with diabetes regard as being insulinogenic (stimulates insulin to rise). • The yoghurt becomes thicker naturally without adding anything, and this makes it more versatile for use as a dip or cream cheese. • The acids are also soluble and disappear with the whey so the yoghurt can be less tart. The disadvantages of straining are: • You lose about a third of the volume of the yoghurt (hence why I recommend a large yoghurt maker). • The lower acid may mean it will keep for less time. On the shorter shelf life, it usually isn’t a problem as you are making it at home you don’t need to factor in time for it to sit in the supermarket waiting to be purchased. Salt is often added to labneh, and this probably extends its shelf life a little. You and your family may find it so yummy that it may also be irrelevant. ## What is the Carb Count? Here are a few commercial yoghurt carb facts. Standard unsweetened commercial yoghurt may have 8g of carbs however this can halve to about 4g when more fully fermented which is where commercial greek yoghurts and labneh also sit. You should do even better than that. I expect that my home-made Greek yoghurt and labneh approaches 2g. This article has a good overview. ## Squeezing Out the Cents Having squeezed out the carbs, let’s squeeze out the cents. I often make yoghurt with the milk that the supermarket is selling cheap because it is close to the ‘use by’ date. It is fine for that because you pasteurise it and the yoghurt bacteria do an excellent job of acidifying and creating other antibacterial agents that stop other mould and fungi anyway. Making yoghurt is a biological ‘reboot’. If you don’t want to invest approximately$40 capital in your yoghurt factory, by now you can see that you could get your yoghurt factory to pay for itself.  Make your first few batches without a yoghurt maker and using some leftover yoghurt.  Make it with reduced price milk from the supermarket to save even more. By putting your savings into a piggy bank, a few batches of that pays for your yoghurt maker.  The next few batches pay for some starter which you can even share with a friend if you wish to get going sooner.

After that, you are miles ahead.  It isn’t difficult or time-consuming to make, but you do need to plan ahead.  I often make it overnight, and it is nice to think of billions of bacteria working for you for free while you sleep. It is kind of therapeutic like counting sheep.

## Time to Rethink Yoghurt?

If you are like me, you may have dropped yoghurt when you stopped eating horse food (aka cereal). It could be a chance to rethink this naturally fermented food. Make your own to keep it low carb and real. As for uses, there are plenty of yoghurt recipes that you might have been avoiding due to the carbs. How about for dressings, sauces or as a (frozen) dessert? How about a refreshing lassi made with your own low carb yoghurt- great on a hot day. It sure beats coca cola or franken-soft drinks full of chemicals.

## Our Shame

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.

## Ketogenic Lifestyle

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!

## The Numbers

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.

## The Implications

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!

## Can We Trust Dietitians?

Not to re-invent the wheel as Foodmed.net did an in-depth series of articles on the Dietitians Association of Australia (DAA). These reports questioned in particular whether food industry sponsorship skewed their advice, whether their spokespeople were in touch and not influenced by industry, how there was likely to be dubious media information from such involvement and how there was apparent suppression of opposing views. The author, Marika Sboros, was not the first investigative journalist to report on the issue of possible industry influence in the DAA. She did not pull punches in suggesting that they engaged in fake news and disclosed that significant amounts of their revenue came from industry sponsorship. The DAA’s only response (that I am aware of) was this statement on their website.

What is the reality?  Can we trust the DAA and its dietitians in general for their advice? It is an important question for health consumers and not just Australian ones.  DAA is part of an international organisation, and they all appear to sing from the same dietary hymn sheet (standards).

In our analysis of the paper behind the DAA press release we discovered that the women with PCOS were part of a self-help charity and were probably following a lower carb approach out of the ‘wisdom of the crowds’. That said it did not appear to be a very low carbohydrate diet being on average 42% carbs by energy. The DAA seemed to recommend increased carbohydrate consumption when we found that there was no evidence for that from the cited study.

In fact, from reviewing the literature and interpreting the evidence, the advice should be that PCOS sufferers would benefit by reducing carbohydrates starting with sugar.

## Press Release Review

Now considering the press release analysis, I note that among other things the DAA:

• Did not make it clear to a largely uninformed public that this was not an intervention study. In other words, there was no experiment to put equally sick subjects a low carbohydrate diet and evaluate their health improvement.  At best it is a small epidemiological study.
• Did not clearly disclose that the reason for the reduced carbohydrates was likely to be due to self-help information. This made it appear to the health consumer that the lower carbohydrate intake could be causing their problems.  This type of study cannot be used that way, but this would not be known to a health consumer.
• Recommended the consumption of whole grains which was an untested outcome. Again, for the health consumer who did not read and interpret the full paper, this would be misleading. The study made no reference to whole grains whatsoever.
• Did not disclose that the reduction in carbohydrates was significantly from a reduction in sugar. Sugar reduction is in line with WHO and Australian Dietary Guidelines, and the PCOS cohort was statistically closer to the WHO target.
• Did not disclose that neither the PCOS nor healthy women were complying with dietary guidelines or physical exercise recommendations.
• Made no comment on the relative good health of the PCOS women.

Now the DAA might say that some of this were the author’s responsibility. However, I also note that they managed the peer review and accepted the quality of this paper for publication in their journal, so they also bear that responsibility.

I cannot find a sound evidence-based reason why the DAA would produce such a press release from that paper.

## Industry Influence?

In the DAA example, I cannot say that this paper was influenced by the desire to ‘market’ whole grains for the food industry as Marika Sboros’ articles might suggest, but that is one possible reason. Many dietitians work in food manufacturing, and the commercial pressure to maximise profits for shareholders look to be at odds with the consultant dietitian’s advice that consumers need. How does one organisation properly reconcile these very different aims?

I note that one of the corporate partners of the DAA is the Australian Breakfast Cereal Manufacturer’s Forum. They would have something to gain if more women eat wholegrain cereal for breakfast because they are fearful for their fertility.  It would be scandalous if that were the aim of the DAA in producing this press release.

## Other Explanations?

Another possible explanation is that they are incompetent to interpret research and apply an evidence-based approach. If that is the case, it makes it hard to recommend seeing their members (APD dietitians) carte blanche as the DAA is responsible for monitoring their ongoing training and providing information.

Another possible explanation is that they have dogma and dietary beliefs rather than science and have simply used this research to push pre-conceived dietary information on the public. That would also be quite scandalous if it were true.

It could just be an advertisement to drive concerned women, trying to conceive, to see their APD members. The need to see their members indeed featured as a media message.

It could be just due to very poor management of this organisation or even just one dumb mistake.

The circumstances around this paper and press release, coupled with questions that Marika Sboros has raised about the DAA, also call into question the very peer review process of this paper and subsequent use of it as a consumer health message. I am not a nutrition scientist, but to me, it raises questions about the integrity of the DAA’s journal to be free of industry influence. It is one thing for the authors to declare conflicts of interest (and I do not suggest that the authors of this study have any undeclared conflicts); but what about the journal owner (the DAA) itself?

It is speculation because we do not have all the facts, and I don’t think there is much point in speculating further. My comment section is, of course, open to the DAA, its staff, its dietitians or the public to comment. If you are a whistleblower or do not want your comment published, I will also respect that. If we can definitively answer this, I would be happy to update in this or a future post for the many health consumers out there that would be bewildered, like me, about this issue.

## Ripple Effects

Whatever the reasons and motivation, unfortunately, among the media to pick this up were the Huffington Post and News. You can see that if you read those articles, you would not find an alternate view. You might take the advice as those news outlets appear to have done no critical analysis of the DAA press release.  Their many female readers may have taken this message to heart.

It also appeared to generate social media activity and some women ‘tagged’ their friends to read this article. Did those friends have extra grainy bread or cereal after reading it?

As a health consumer, I find this unsatisfactory. It does demonstrate how the media ends up reporting health advice that misleads the public. We can partially blame the media for this.  They should have sought alternate views rather than taking a press release and just reporting it and only speaking to the DAA.  However, the journalists apparently relied on the science in a press release from the DAA to be fair, evidence-based and accurate.

## The Outcome for PCOS Women

The net effect of the press release is to give the exact opposite advice that they should have. If anything, the message should have been to reduce carbohydrates starting with sugar. The effect could be child-denying for a woman with PCOS trying to conceive and potentially life-threatening. It is horrific to me, and I am appalled that the DAA has not yet corrected this of their own volition.

I call for this press release to be retracted and for better advice to be given. The DAA should also make efforts to contact every woman who may have read this press release. In fact, in my opinion, it is appropriate for any woman with PCOS who read this to be offered free dietetic sessions with the corrected advice lest it spawns a future class action.

I note though that they tried to diminish Marika Sboros’ work by calling them blog posts and calling her a blogger when she has had a distinguished journalistic career spanning decades.  They also make the point that she is not Australian based with the implication that it diminishes her journalism.  That approach indicates both arrogance and a tendency to run on spin rather than facts. That behaviour is akin to the arrogance of Donald Trump’s handling of Whitehouse reporters. DAA, health consumers, deserve answers, not dietetic spin; but why would you listen to an Australian consumer health blogger like me?

DAA management, if you feel you don’t owe health consumers a public explanation, how about coming clean to your dietitian members? After all, they pay most of your salary. Your training, advice and alleged intimidation of those with new ideas may be exposing them to lawsuits and liability. We can vote by not engaging your members’ services, and they can vote to sack you if your answer to them is unsatisfactory.

## Media Manipulation or Setting Journalism Standards?

I note that the DAA gives out a cash and in-kind award for what it regards as good nutrition journalism. The award can be majority decided by the CEO, who presumably approved that PCOS press release, and their media manager who wrote it. Should the award be meaningful when its own press release standards appear to be so poor or if it has an agenda to push particular nutrition dogma rather than evidence-based science? If the journalists who won the award, wrote favourably of nutrition advice that marries with DAA sponsors or favours the DAA’s views, it could be seen as a cash incentive for having promoted its sponsors interests or dietary dogma. While it has sponsors of any kind, it seems a very ethically-sensitive undertaking for the DAA to be doing this.

## Lessons from this Case Study

I think you need to make up your own mind about all of this. The bottom line is that, as health consumers, we need to be mindful that organisations can be influenced by many factors. Those factors can be other than for our health. My suggestion is that as health consumers we should boycott not-for-profit organisations that have industry sponsorship or donations. Otherwise, at least have very low regard for their advice.

While the DAA looks to be quite poor about communicating evidence-based nutrition science, it would be unfair to say that all their members or dietitians are useless to give low-carb dietary advice. These are highly trained nutrition specialists. They know more about metabolism than we are likely to. If well trained and of an open mind, they should also be able to learn and grasp new concepts. They should interpret them rather than being mired in their organisation’s dogma or other interests.

There is something we can learn from this if we are looking for help. There was some public outrage at the press release. Some people posted negative Facebook comments. Many of these people appeared to share an alternative view towards low carb. As an idea, perhaps you could try communicating with them to ‘health network’ for a solution.

In my next post, we will look further at how we could perhaps find helpful dietitians and other advice.

## Where Can we Get Advice?

If you have read my previous posts, you may have decided to trial a Very Low Carb Ketogenic Diet. In my last post, I thought I would start to give you some practical advice to achieve that.

Before we start looking at that, I would like to state the Macro Four principles of chronic disease management.

The experts do not care about N=1 but you do!

And now I introduce the third and probably the most important one.

Find people who have walked a mile in your shoes.

Why do I say this? Well, suppose that there is a cure out there and that people have discovered it.  Let us say that cure is effective and people have been quietly taking benefit from it for a while. Let us say that cure has not been given the official anointment in your country or local area but has been widely practised in another- officially or unofficially.

The official channels of your health system may not offer you that cure for decades. However, there would exist a pocket of people quietly benefitting from that cure but because they are probably ‘unofficial’ you may not hear of it.  You could perhaps find a group of fellow sufferers and talk to them. Alternatively, lets say you have decided to try a ketogenic diet, find a large group and ask- Has anyone found this has helped condition X? You have little to lose from this approach. It is just talking to people.

## Health Networking

Health networking is your surest way to find that is to find a group of fellow sufferers and talk to them.

Before we talk about where you may find those people to get some advice, let us talk about the common places that you won’t find those people. After all, your time without relief is time suffering.  You want to spot the time wasters.

You are unlikely to find someone with a advice for a better solution at a self-help group educated by your local, not for profit organisation for your chronic condition.  That is because those ‘experts are dead’ and they will offer you conventional therapies that mean that you will remain chronically sick. Their advice may be complementary to a path you choose to take, or they may even discourage you from an alternate solution.

Why would they do that? The reasons are many and varied.

1. They follow the standard treatment.
2. You probably won’t find ‘cured’ people there.
3.  Their mission statement probably perpetuates the ‘learned helplessness‘ that you want to leave behind.
4. That standard treatment might be as preferred by outside interests like the pharmaceutical or food industries.

If that seems strange to you it isn’t. Let me state that I do not believe in ‘conspiracy theories’. On the other hand, there is almost always an explanation for human behaviour however, nonsensical or odd. Most of the time it can be understood by looking at the flow of money.

Earlier, I focussed on PCOS because I expect that by the time many of you read this blog, the example of type 2 diabetes will seem so obvious in retrospect. Then again, maybe not!

## Following the Standard Treatment

Nonetheless, here is my experience as someone with type 2 diabetes.  I was diagnosed with type 2 diabetes about five years ago. I duly followed what Diabetes Australia recommended. Without repeating some of my earlier blogs, it was a disaster. My health deteriorated.

After some three months on a VLCKD and with greatly normalised blood glucose, I rang up their help line to see what advice they would give.  Sure enough, the CREDENTIALED DIABETES EDUCATOR told me to eat more carbohydrates. That would have been a disaster.

## You Won’t Find ‘Cured’ People

Me ringing up was an oddity.  I am just the kind of contrarian individual who would do that. I have toyed with the idea of going to one of the self-help groups to spread the word but who wants an ugly scene with the group expert? So once someone has found a solution, they won’t frequent those social circles.  You need to find the people who have the ‘cure’ and talk with them!

## They Mean Well but Teach Learned Helplessness

Chronic disease charities do say they want to end their illness.  In the end, they accept donations for a mission and are a corporation in their own right. They probably honestly want to give you help and advice. Take it. Check it. Then discard any notion that is the end of it. Avoid any learned helplessness that may come from depending upon them and seek to do better.

## The Influence of Industry

Now we get onto the thorny question of the influence of industry on not-for-profit entities. There are no conspiracy theories on this blog. It is normal corporate behaviour to protect and maximise a revenue stream for shareholders by spending budget to create profits. That is just business. When was the last time you heard a CEO say: “We think there is a better solution than our product.  Please use that solution.”?  Primarily for the health and pharmaceutical industries, the expenditure to protect a revenue stream comes under the ‘marketing budget’ and the ‘Research and Development’ budget.

Not-for-profit’s too are still corporations. They do not have to look after your health although they may state that they do.  It would be rare for a government to legislate that. If a not-for-profit says that they are there to look after your health, it is (in most countries I know of) pure self-regulation. They are more likely to take care of their member’s interests, but they are not even obliged to do that!

You might bump into someone at your local chemist who has a solution but will they talk to you to tell you? So here is a story. I had just gone to the chemist to buy some glucose testing strips after I had ceased my diabetes medication due to going low carb.  There was a lady about 70 years old. She was filling her prescription for the diabetes drugs that I had just ceased. I almost spoke to her to tell her that there was another way but then realised that she would probably think I was crazy.  I was not her doctor or dietitian.  Now I am no shrinking violet, so your chances are not good for that to happen. On the other hand, if you are that person who is told this by some ‘crazy’, maybe you should give it some consideration?

## Pharmaceutical Marketing

But there is another reason your chemist may not provide advice. I give you a ‘wonderful’ website to manage your diabetes if you are Australian. Now you have to look hard to the copyright message at the bottom to see that this site is owned by Sanofi- a pharmaceutical company. It is a standard commercial behaviour to protect revenue streams so, while their advice is probably valid to help you manage your diabetes through their medicines, don’t expect to find any therapies to get you off them on this website. Want proof? Have a look for any mention that, with diabetes, you should avoid sugar or reduce carbohydrates.

Also, do not expect to get such advice at the chemists that they point you to. They tell you that they have educated these pharmacists. Education is usually part the marketing budget. So if you want advice on how to manage a lifetime of medications, then those chemists and their pharmaceutical company education will suit you well. Alternatively, if your desire is to eliminate or reduce your dependency on medicines, I would now be asking my pharmacist if they have any pharmaceutical company training in my medication and be aware that may cause bias. I do not know what else the pharmacist receives in this arrangement (if anything), but maybe one of them or Sanofi could tell us in the comments below. Still, that website could be useful to tell you which chemists to avoid.

Does this shock you?  Maybe mildly?  Well, get used to it health consumers with some dollars to spend. This is normal commercial behaviour. In this blog, we will examine many other examples as we find out how we might find that elusive cure for our chronic disease.

Next, we will consider whether you may get a solution from Dietitians.

## Reconciling Strange Advice from Dietitians

If you are reading these posts, you will remember that we started this journey because we saw a media release that seemed odd. The Dietitian’s Association of Australia (DAA) recommended that ladies with Poly Cystic Ovarian Syndrome should eat more ‘grainy bread’. We found that advice not to be supported by the evidence and discovered that a Very Low Carbohydrate Ketogenic Diet (VLCKD) might be a solution. If you have come straight to this post, I recommend you read the previous three posts first.

So if the weight of evidence supports lowering our carbohydrate intake, is this going to harm our health and particularly, will it be harmful to undertake a VLCKD?

## Revisiting the Evidence from the Studies

Our starting point is the very study that the DAA cited to suggest that ladies with PCOS (who reduced their carbohydrates) were harming their health and chances of fertility.

We note that these ladies only cut their carbohydrates by 5% and this appears to be cut by reducing sugar mostly.  Did that harm their health?

Well, we need to remember that PCOS is a serious disease that can often progress to diabetes.  Sufferers may have worse cardiovascular health.  The case-control study cited by the DAA shows us something kind of interesting.

Despite the PCOS ladies all being sick, there was no significant difference in their health markers except for some of those indicating PCOS!

All of the following were not significantly different from the healthy ladies: Fasting glucose, Fasting insulin, HOMA2-β, HOMA2-IS, HOMA2-IR, All Cardiovascular risk factors, SHBG, DHEA-S and FSH.

By that information, dropping carbohydrates by 5% and increasing saturated fat appears to have done these ladies little harm when compared to the control group.  That is especially the case for cardiovascular risk. We need to be mindful however that a VLCKD cuts carbohydrates much more aggressively.

We have the other studies cited by us that showed insulin resistance markers improved, cardiovascular markers remained insignificantly different or improved, and the ladies lost weight. It does not appear that any of these studies support that lowering carbohydrates has worsened the health of study participants. This was so even when they were following a VLCKD.

## Evidence of Danger of a VLCKD

If you google “dangers of a ketogenic diet” you may see some issues raised.

1. You may have low blood sugars
2. You may have flu-like symptoms for a few days
3. Concern over a life-threatening condition called “Diabetic Ketoacidosis” or DKA
4. Acidosis (a more acidic body chemistry)
5. Kidney Stones
6. Thyroid problems
7. Nutrient Deficiency
8. Constipation

Should you consider these? Yes, of course, you should. Will all of these apply to you? Almost certainly not. For example, DKA is almost exclusively a concern for type 1 diabetics.  Even then, you are reducing your blood sugar, and this is a condition of high blood sugar.

Should you be concerned that you may have low blood sugar for example? Of course you are as one of the effects you are seeking is precisely this. The health effects of too high blood sugar are well documented.   However, if you are on blood glucose-lowering medicine this may be of concern as some types of medicine (although not metformin which you are likely to be on for PCOS) could cause hypoglycemia (dangerously low blood sugar).

If you are on any medications, obviously you need to discuss this with your doctor and be mindful that this is a therapeutic diet and your medication may need adjustment. For example, if you were on a diet to reduce your blood pressure and it was effective, you would need to adjust medication you were using to lower blood pressure.

## Other Information on Risks and Safety

The Diet Doctor website has an extensive array of information about low carb and keto diets and particularly some of the concerns that there may be. I won’t cover those here on my blog because I don’t want to reinvent the wheel.

Now if I were to recommend to you to start cycling for your health and give you public advice to do so, I would need to run through all the things that you should consider.  You should respect other traffic, wear a helmet, pump up your tyres to the right pressure, ring your bell to warn pedestrians, wear bright clothing, eye protection from dust and glare, adequate footwear, etc.  Does that mean you should not try cycling for your health? I think you probably get the idea.

## Long Term Considerations

I have seen “authorities” (including the DAA) warn that a VLCKD is dangerous because it has not been tested in the long-term. The implication is that you should not try it in the short term for this reason. I find that logic a little strange. It is important to realise that we are not committing to this diet long-term.  A VLCKD is something that we are potentially going to to try for three to six months- about the length of those studies. We could expect that our results may not be too different from the study participants; but if they are, then like all trials we can re-assess from what we have learned.

So to be clear the approach is to do the N=1 trial on ourselves.  If a medical professional monitors us, we will have N=1 results from relevant tests. Assuming that our health improves, we can continue. If there are adverse changes, then we can reassess and look for other reasons why our outcome differed from that expected.

Now if someone wishes to make headlines of the fact that I am advocating “self-experimentation” they obviously haven’t walked a mile in the shoes of someone with a chronic condition. The alternative is the following process.  We could wait to have:

1. Experts do all the experiments on hundreds or thousands of people.
2. The experts write it up.
3. It accepted by a reputable journal.
4. That study peer reviewed.
5. The paper accepted by peers and published.
6. It further accepted by the research community.  Acceptance may take a very long time- particularly if it is against orthodoxy.
7. The study converted into treatment protocols.
8. Bureaucrats anoint the treatment protocol as effective and safe.
9. Clinicians accept the treatment protocol as effective and safe.
10. Your doctor now advise you to make the change to stop eating some foods.

You are looking at a process that takes multiple years or decades.  We will probably come back to this in a later post. Now if that is a new drug with potentially toxic side effects I would, in almost all circumstances, want that process to be robust.

## Wait or try now?

1. If you are trying to conceive, your biological clock is running down.
2. You are probably suffering from side effects and symptoms that are unpleasant.
3. An unresolved condition like PCOS is likely to progress to more serious health concerns.
4. We are talking about reducing, avoiding or eliminating certain foods from our diet.  We aren’t looking to take an experimental cancer drug!

What is a significant and risky change for the ‘system’ to recommend to the general population for N=millions is a different decision for N=1.  Is it safe to for millions of people to try a VLCKD? If it were cycling and I recommended it, some people would die as a result of that recommendation. Is it safe for you and is the risk worth the potential benefit?  I think we can both agree that you are capable of making that decision.

It is your decision. Do you take it?

Assuming that you do, then next we will look at some of the practicalities of doing your trial.

## The Case for a Low Carbohydrate Diet for PCOS

We are moving through some questions to determine if we should try a Very Low Carbohydrate Ketogenic Diet (VLCKD) to help with PCOS.  If you have not read them, then you should read the previous posts before this one.

In previous posts, we examined the Dietitian’s Association of Australia’s (DAA) press release recommending that ladies with PCOS increase their carbohydrate intake with ‘grainy bread’.  We concluded that the evidence cited by the DAA did not support that recommendation.

The next question we will look at is:

## Is there Other Evidence that Supports Lowering Carbohydrate Intake?

Here, with appropriate cautions, we can leverage the work of an expert.  I point you to this post by Franziska Spritzler a dietitian who favours a low-carb approach for PCOS.

To be clear, we should be as sceptical of Franziska as we are of the DAA and need to be of all experts when ‘the experts are dead’.

In summary, she says:

1. Her opinion is that standard carbohydrate amount, and timing advice for people with diabetes and PCOS is unhelpful.
2. Women with PCOS are likely to have metabolic problems, type 2 diabetes and cardiovascular disease.
3. She mentions the VLCKD pilot study that interested us.
4. She focuses on hyperinsulinemia and insulin resistance (IR) as core problems for PCOS. The previous study and DAA the press release that we examined also noted that.
5. She puts forward that the usually recommended carbohydrate diets are not helpful for those conditions whereas a low carbohydrate approach is.
6. A study looking at the best dietary approach (examining six) was inconclusive; however, none of those was a VLCKD.
7. She is in favour of a very low carb diet to address PCOS.

I don’t feel that it’s enough to simply encourage weight loss without providing guidance on how to do so in a sustainable way that  has been shown to improve IR and insulinemia — i.e., limiting carbs to 50 net grams per day or less.

## What is the Common Ground?

But now I recall that the DAA referred paper put forward that saturated fat caused insulin resistance.

So it seems that most dietitians would agree that a diet that addresses hyperinsulinemia and insulin resistance is best for PCOS; however, they differ over whether those conditions cause (or remediate by the removal of) saturated fat or carbohydrates. Also diets for weight loss are recommended.  Now we are getting somewhere!

The DAA referred paper cites this study to support that saturated fat (expressed here as fat quality) is the villain.  That study concludes:

Most studies (twelve of fifteen) found no effect relating to fat quality on insulin sensitivity. However, multiple study design flaws limit the validity of this conclusion. In contrast, one of the better designed studies found that consumption of a high-saturated-fat diet decreased insulin sensitivity in comparison to a high-monounsaturated-fat diet. We conclude that the role of dietary fat quality on insulin sensitivity in human subjects should be further studied …

It is inconclusive to me from this study that saturated fat causes insulin resistance.  Further, we find this study which found that in laboratory testing, saturated fat did not cause insulin resistance.  It said about that conclusion:

We acknowledge that this does not agree many epidemiological reports supporting the notion that diets high in saturated fats are associated with insulin resistance and an increased prevalence of type 2 diabetes [1].

It appears that saturated fat causing insulin resistance is far from proven.

## More Evidence to Lower Carbohydrates for PCOS?

So back to carbohydrate restriction for PCOS and there is this study.

An 8-week low-starch/low-dairy diet resulted in weight loss, improved insulin sensitivity and reduced testosterone in women with PCOS.

I note that this was a low carb diet, but not necessarily low enough to be ketogenic.  It was also not a randomised control trial as there was no control group. Most participants would have been on less than 130 grams of carbohydrates per day. At 79g of fat (19.5g saturated), this is a high fat, high saturated fat diet.

Nonetheless, the results showed improvements in weight, testosterone and insulin sensitivity (insulin resistance) and an improvement in vitamin D levels, blood lipids (triglycerides, VLDL) with no adverse effects to ‘cholesterol’ overall.

Finally, a third study is this study, which might be missed by many because the 15 PCOS participants were in the cohort of sixty people.

Patients with polycystic ovary syndrome lost 14.3%+/-20.3% of TBW (P=.008) … at 24 and 52 weeks, respectively, without adverse effects on serum lipids.

The diet in this study was a ketogenic diet. The results were similar to the last study. They lost weight, reduced fasting insulin and had no adverse effects on their ‘cholesterol’.

I think it is significant enough to comment that anecdotally, women have a hard time losing weight with PCOS yet the experts are unanimous that overweight women with PCOS should lose weight.  These studies all demonstrated weight loss by carbohydrate reduction for women with PCOS was significant and effective.

## Decision Time

But at about this time I come back to the point.  Do I cut my carbs or not or do I I wait for the boffins to settle their argument?

Well this is where I invoke another macrofour principle:

The experts do not care about N=1 but you do!

In case you are not familiar “N=1” is the retort from an expert to refute an anecdote that someone was cured by doing something. You see they need a lot more evidence than one person before they will agree with or recommend it.  You don’t because you care about your N=1. So at this point, it is simple. You are not getting advice because scientists haven’t solved their arguments in time to advise you now.  You can make this decision for yourself- or it may be years for them to settle their argument.

Personally, I am uninterested in scientist’s careers, egos and the various other distractions that could come into it like pharmaceutical profits or that someone wants to sell me a box of cereal.  I just want to get well.

If you have followed a low-fat (and particularly a low saturated fat diet) and your PCOS has not improved enough, then you have already tried the low saturated fat advice.  Did it work for you? If not then your N=1 says to favour the low-carb diet.  Alternatively, if you have been on a low-carb diet for a while and have PCOS, then try cutting saturated fat.

Finally, if you have followed a high carbohydrate and high saturated fat diet you are either going to have to choose or cut both.  Before we move on to the safety of carb reduction, let us see whether we should lean one way or the other.

## Low Carb or Cut Saturated Fat?

I think that the reader can conclude that the weight of evidence presented leans towards reducing carbohydrates, not saturated fat as having a positive effect on PCOS. We couldn’t find anything to suggest that increasing carbohydrates would help.

So despite dietitians being discordant, the weight of evidence leans towards carbohydrate restriction for PCOS.

Further, by looking behind the press release, we found that in particular, some women were reducing sugar.  So, to finish off, here is a recent post from Dr Jason Fung about sugar and insulin resistance.  Dr Fung is a Canadian kidney disease specialist. He advocates low-carb and fasting to help fix insulin resistance and to stop you losing your kidneys to diabetes.

While you read, please consider whether the wisdom of the crowds was present when the PCOS ladies in the DAA referred study chose to cut their sugar. I will prime you with the fact that sugar is the same as sucrose and each sucrose molecule breaks down into a molecule each of glucose and fructose.

Next, we will look at the safety of a VLCKD.

## A Cure for PCOS?

In our previous post, it seemed there might be a dietary treatment for ‘our’ chronic condition of PCOS. The treatment was a Very Low Carbohydrate Ketogenic Diet (VLCKD). That advice lowers carbohydrate intake against the opinion of the ‘expert’ dietitians (DAA). Before we do that, it is prudent to ask a few questions to see if we could use that to aid our condition,  These are:

1. What is the evidence for raising carbohydrate intake?
2. Is there other evidence that supports lowering carbohydrate intake?
3. Is a VLCKD going to be safe?
4. On balance, is this worth trying (or should I eat more wholegrain bread)?

Let’s tackle these questions over this and the next few posts.

## What is the evidence for raising carbohydrate intake?

The Dietitian’s Association of Australia (DAA) cites one study to justify that women should increase (wholegrain) carbohydrate intake.  We can read an abstract of that study at the link below. This DAA published the study in it’s journal ‘Nutrition & Dietetics’ which the DAA says is: “Australia’s leading peer-reviewed journal in its field …”.

Suboptimal dietary intake is associated with cardiometabolic risk factors in women with polycystic ovary syndrome

Let’s take a closer look, but before we start, I will uncouple comments about saturated fat. The focus here is on carbohydrate recommendations.  The reason for that is not to avoid the issue.  Saturated fat is a topic on its own, and you can have a VLCKD that is high in protein or fat. Also, any fat in a VLCKD need not be mostly saturated.

The paper concludes that:

The present study has identified suboptimal dietary patterns in women with PCOS, and highlighted dietary factors associated with cardiometabolic risk factors that warrant monitoring in both lean and obese women with PCOS.

In plain English, the authors found: Ladies with PCOS are not eating to the dietary guidelines. Dietitians should look closely at the diets of women with PCOS regardless of their weight.

## How was the Study Conducted?

The study came to that conclusion by comparing the diets of 38 women who had PCOS to 30 women who did not have PCOS (control).  This type of study is a matched case-control study.  The women were matched to be roughly similar in body mass index (how overweight or obese they were). The participants recorded what they ate in a seven-day food diary, and then that was analysed and compared between the two groups.

This is not a randomised control trial (RCT) nor is it a crossover study. It is not designed to test a hypothesis about a low carb diet. It does look at the different diet and health of an average ‘healthy’ group with a sick group.

The DAA appears to have taken this study and indicated an association between the level of carbohydrate in the sick group compared to the control group. The reader might conclude that the healthy group is more healthy because they eat more carbohydrates. The reader might also conclude that the sick group became sick because they eat fewer carbohydrates.  Those would both be wrong conclusions. A problem with using this study in that way is that while there may be an association, the reason for that connection may not be apparent or even investigated. In fact, there may be no reason for the connection at all.

Food diaries are regarded as being better than food questionnaires, but still may not be accurate- especially if the seven day period does not reflect long-term eating patterns.  Some of the problems with associational studies and food diaries are discussed in more detail here.

## Key Results

However imperfect food diaries and associational studies may be, though, the paper (not the abstract) is detailed about what the researchers did and what the outcomes were.  The PCOS group had 42% of calories from carbohydrates vs. 47% for the ‘healthy’ subjects. The PCOS women ate significantly less sugar (88 grams per day) than the ‘healthy’ women (114 grams per day). That is about six teaspoons per day. As sugar is a carbohydrate, that difference accounts for almost all (about 95%) of the reduction in carbohydrates!

## Analysis of Sugar is Omitted

We can conclude from the study that the PCOS women were eating fewer carbs (according to their diaries), and it appeared that the reduction was mostly by reducing sugar.  Anything outside the seven days of a diary is extrapolation.  It tells us nothing about whether, if the two groups and control increased or decreased carbohydrates (sugar consumption), they got better or worse. It says nothing about the diet that women were on when they developed the condition.

The World Health Organisation recommends that a maximum of 10% of daily energy come from free sugars with a target of 5% being desirable. I note that the ‘healthy’ group were getting about 23% of their energy from total sugars compared with about 18% for the PCOS group. The study did not break down the free sugars. However free sugars are a significant proportion of most people’s total sugars. For some reason, the study made no comment whatsoever about the lower total sugar and neither did the DAA.

## In the Paper, not in the DAA Press Release

There are some other things that we cannot learn from the DAA press release or abstract that are significant.  We need to read the paper to find out that:

1. Neither of the two groups was compliant with dietary and physical activity recommendations for health!
2. Two-thirds of the PCOS sufferers were of healthy weight.
3. When we compare the ‘sick’ (PCOS) group with the ‘healthy’ group, the PCOS group do exhibit health markers indicating PCOS (as expected). In other health markers (such as cholesterol) they are not significantly different to the ‘healthy’ group. Given the sad progression of PCOS to affect cardiovascular risk, this is an interesting finding.
4. The PCOS participants came from a PCOS self-help charity, and it was possible that many had lowered their carb (sugar) intake after diagnosis (joining). While the charity does not advocate a low carbohydrate diet, there were articles on their website that discussed low carb diets. This provides the most likely reason for the lower sugar intake in the diet of the PCOS sufferers.

This last point may also actually indicate that some patients have discovered that a low carbohydrate approach works. However, if more moderate carb approach after diagnosis had effectively improved or worsened their condition, then this study was simply not set up to evaluate that.

## In the DAA Press Release, not in the Paper

Finally, I note that the DAA mentions the following foods that are suggested as good to eat:  (whole)grain, apples, (grainy) bread, legumes and oats and tells you to avoid: butter, coconut (oil), (fatty) meat, biscuits, cakes and pastries.  None of these was specifically mentioned in the paper, and as far as can be told from reading the paper, it is just as likely that both groups ate or avoided them all.

I think the researchers did perhaps owe us a mention of the sugar differences in their results. However, the extraordinary thing is that the DAA seems to have taken this research and used it to suggest women with PCOS should be eating more carbohydrate by promoting the eating of grains, legumes and bread in particular.

It is my understanding that there is no specific diet guideline for PCOS although dietary plans for weight loss are recommended. I would have thought that the DAA would have highlighted the reduction of sugar that the women practised before advocating people eat more carbohydrate. If the aim was weight loss, then a message about sugar reduction should also help. The WHO targets are probably being exceeded, and dietary guidelines are to limit free sugar. At best, sugar is empty calories.

## No Evidence to Increase Carbohydrates

There is no clear evidence that I can find from this study that women with PCOS should be increasing their carbs. There is nothing in this study that showed increasing carbohydrates would improve PCOS symptoms.

Alternatively, this study does indicates there is likely to be a trend or practice for some women with PCOS to lower their carbs.  That seems mostly due to them lowering their sugar intake.

Although it was a little frustrating to have to go beyond the press release, I am glad that we looked into the detail and did not discount lowering our carbohydrate just yet. If anything, it is of curious interest that some women with PCOS are reducing their carbs and sugar intake while the DAA does not appear to think this is a good strategy.  Is this the wisdom of crowds?

In my next blog, we will examine the next question on our list.

Is there other evidence that supports lowering carbohydrate intake for PCOS?