Doctor in the House – Watch Diabetes Not Being Reversed Using Low Carb on BBC, While LCHF'ers Freak Out.

This post is about Doctor in the House – Watch Diabetes Reversed Using Low Carb on BBC, While Old-School Dietitians Freak Out.

The YouTube videos may be gone, but the image lives on!
Available to view in the UK on iPlayer 'till 19.12.15 at https://www.bbc.co.uk/iplayer/episode/b06q6y95/doctor-in-the-house-episode-1

In Dr. Eenfeldt's blog post, he makes some schoolboy errors.

1. T2DM (type 2 diabetes mellitus) Reversed with LCHF (low-carb, high-fat) diet. Uh, nope!
a) Sandeep's HbA1c fell from 9.0 to 7.0, which is an improvement but by no means a reversal, as Dr. Chatterjee agrees in https://twitter.com/drchatterjeeuk/status/669875378568171520.
b) Sandeep has T2DM, not T1DM. See When the only tool in the box is a hammer...
Sandeep's BG (blood glucose) went down on LCHF, but what about his dyseverything elseaemia? *sound of crickets chirping*

2. Old-school dietitians freak out. Uh, nope!
In BDA alarmed by controversial and potentially dangerous advice in BBC’s ‘Doctor in the House’, Dr. Duane Mellor sounds pretty cool, calm & collected (though I expect that he sustained injuries from all of the eyeball rolling, as he had to refute for the umpteenth time yet another load of LCHF bullshit).

3. He plays the Shill Gambit card.

Oh, the comments! In typical echo-chamber fashion, LCHF commenters praise Eenfeldt's flawed points. I wonder how long my comment will stay up for?

My comments on the programme (c/p'ed from Facebook):-
"6 minutes in. I think that Priti is deficient in Magnesium (Mg), from her stress levels, anxiety, headaches and difficulty in getting to sleep. Blood tests are useless, as they don't correlate with Mg stores. Need CSF (cerebrospinal fluid) test (lumbar puncture - very painful).

12 minutes in. Priti's blood test results normal. Sandeep has hypovitaminosis D, which is a cause of IR (insulin resistance, it's what caused mine). This important fact is not mentioned. unsure emoticon See http://www.ajcn.org/content/79/5/820.full.pdf

16 minutes in. Talked about sugar in foods & drinks but ignored the large amount of cheese that Sandeep ate earlier. Cheese is *very* energy-dense. Sandeep has been in positive Energy Balance for *way* too long.

24 minutes in. Priti's getting sugar cravings in the morning. Lack of Magnesium also causes IR & poor BG regulation. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549665/

29 minutes in. HIIT (high-intensity interval training) for Sandeep is good for increasing his IS, but little use for reducing his VAT (visceral adipose tissue). You can't out-run your fork.

33 minutes in. Walking for Priti to lose weight? You can't out-walk your fork. If 1,000 steps takes 10 minutes and burns an extra 40kcals, then 10,000 steps takes 100 minutes and burns an extra 400kcals = one chocolate bar.

33:47 minutes in. Sareena has had a full-time job working indoors for the last year. Less sun exposure = falling Vitamin D3 level = deteriorating immune system, deteriorating mood & deteriorating IS. See https://nigeepoo.blogspot.co.uk/2008/12/vitamin-d.html

I don't think that I can watch much more of this programme!"

followed by:-
"In conclusion:-
1. Anyone who suffers from chronic anxiety is probably deficient in Mg.

2. Anyone who lives in the UK (United Kingdom :-D) and has coloured skin and/or works indoors is probably deficient in Vitamin D3.

3. ~85% of people who have T2DM have excessive VAT. Asians who were skinny in early adulthood have limited SAT (sub-cutaneous adipose tissue) hyperplasia, resulting in small skin-folds but large bellies. A LCHF diet is not suitable for over-fat people with T2DM. It should be a LCLF diet i.e. a low-calorie diet, to deplete over-full cells. Calories count.

4. You can't out-walk/run your fork.

5. Dr Chatterjee has a strong bias. This is not a good trait for someone who's supposed to be practising Evidence Based Medicine."

It's interesting that Priti is fatter than Sandeep, yet Priti doesn't have T2DM and Sandeep does. Priti was most likely fatter than Sandeep in their respective childhoods, for whatever reasons. Priti had more SAT hyperplasia than Sandeep, so she has more storage capacity for dietary fat than Sandeep does. Priti can gain more SAT, which protects her from developing T2DM. Sandeep can't, so he gains VAT, which has limited storage capacity and is more metabolically-active than SAT.

See also Adipocyte Hyperplasia - Good or Bad? and A *very* special dual-fuel car analogy for the human body that I just invented.

A tale of the unexpected & an analogy.

The tale.

A friend had a faulty lap-top mains adaptor. It was one of these:-

From http://www.pchub.com/uph/laptop/46-33769-9191/Toshiba-Common-Item-Toshiba-AC-Adapter-Laptop.html

I offered to fault-find it. I measured the output voltage with my multimeter.

The output voltage was 0V.

I felt the lead where it exited the connector. It didn't feel right, so I cut the connector off & stripped-off some insulation. Lo and behold, the inner conductor (it was co-axial cable) was broken. I prepared the conductors, tinned them, soldered them and powered the adaptor, with a sense of impending triumph.

The output voltage was 0V.

I tested the continuity from conductors to connector. That's when I discovered that there was a short-circuit between the inner and outer conductors. I snipped-off the connector and confirmed that it was the connector that was short-circuited, not the adaptor or cable. I fitted a replacement connector and powered the adaptor, with a sense of impending triumph.

The output voltage was 0V.

At this point, I decided that the adapter was Beyond Economic Repair and advised the friend to buy a new one, which subsequently worked perfectly.

So, how did the adapter get to have not one, not two but THREE faults on it? It turned out that the lead had been yanked sideways, which bent the connector. The friend had straightened the connector with pliers (!). This short-circuited the connector, resulting in an internal fuse blowing in the adapter. The friend then "jiggled" the connector in the socket, in a vain attempt to make it work. This broke the inner conductor of the co-axial cable.

The analogy.

 

Some health problems are multi-factorial. Fixing only one, but not all of the problems, results in not fixing the problem. So, if you try "A" and there's no improvement, either "A" isn't one of the problems, or "B", "C"......"Z" need fixing, too.

This post was inspired by Effects of 12 weeks high dose vitamin D3 treatment on insulin sensitivity, beta cell function, and metabolic markers in patients with type 2 diabetes and vitamin D insufficiency - a double-blind, randomized, placebo-controlled trial.

Taking an effective dose of Vitamin D3 for a reasonable length of time didn't make a significant difference to insulin sensitivity or beta cell function. It did for me, as my main problem was Vitamin D insufficiency. I got lucky.

Calcium shift: An interesting hypothesis.

More serendipity! Billy the k left a comment that piqued my curiosity.

From http://www.health-heart.org/acceuil.htm The atheroma 'junk' in the media is cholesterol + calcium in older people.

From Aging and calcium as an environmental factor. (emphasis mine)
"The consequences of calcium deficiency might thus include not only osteoporosis, but also arteriosclerosis and hypertension due to the increase of calcium in the vascular wall, amyotrophic lateral sclerosis and senile dementia due to calcium deposition in the central nervous system, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to diabetes mellitus, immune deficiency and others.

I highlighted amyotrophic lateral sclerosis in red, as many Facebook friends have been having buckets of water & ice cubes tipped over themselves to raise money for research into this horrible & ultimately fatal condition.

So, what prevents & reverses migration of calcium from hard tissues to soft tissues?
Clue: It carboxylates osteocalcin in bone matrix Gla proteins. Yes, it's Vitamin K2.

See also Calcium, parathyroids and aging. N.B. 50iu/kg bodyweight/day of Vitamin D3 significantly lowers parathyroid hormone.

Dear ItsTheWoo, how do you do?

This post is attacking what I consider to be faulty reasoning. It's not a personal attack on ItsTheWoo, who I like (even though she drives me up the wall, sometimes!).

From http://hypetrak.com/2011/10/mayer-hawthorne-how-do-you-do-full-album-stream/

See What I believe and what I don't.
The basic The Energy Balance Equation:- Change in body stores = E_in - E_out
For a detailed mathematical analysis of weight change, see Completing the trine: vive la différence!

From Back to black, CIAB, pharmaceutical drug deficiencies & nerds:-
Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.


The faulty reasoning is in Dear Nigel and other CICO zealots: you are ignorant. Charming!

I'll quote passages from it and refute them, one by one.

• "With a zero caloric deficit, there is zero weight change"

"FACT: Calories neither determine weight OR body composition with certainty. Nigel / some CICO zealots may agree body composition changes are privy to nutrition, but wt is 100% controlled by calories. This is something they pretty much made up and biological science does not at all support this idea. Calories neither control body composition OR body weight/mass with any certainty. The bulk consumed with fork and spoon does not need to stick on your body in the form of a mass laden tissue, ever."
Calories determine weight change. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned). It would have been nice if Fig. 6 had contained a plot of "Effect of energy intake on change in body weight", but it didn't.
LBM = Lean Body Mass
FM = Fat Mass = Body Fat
Weight change = LBM change + FM change
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36
∴ A calorie IS a calorie (where weight change is concerned).
∴ Insufficient protein can result in loss of LBM (bad).

The main thrust of ItsTheWoo's argument is that inter-personal variations in weight gain from subject to subject, invalidates Bray's conclusion. It doesn't.
Some subjects become more energetic on a 40% caloric surplus, which increases their NEAT & TEA, which increases their Eout, which reduces their weight gain.
Some subjects don't change their energy on a 40% caloric surplus, which doesn't change their NEAT & TEA, which results in intermediate weight gain.
Some subjects become less energetic on a 40% caloric surplus, which decreases their NEAT & TEA, which decreases their Eout, which increases their weight gain.

I believe that the Insulin Sensitivity (IS) of the subject determines which category they fall into and by how much. The higher the IS, the higher the energy, as high IS results in low serum insulin, which minimises sedation. Energy Balance always applies.

I've never stated that Calories exactly determine weight change. That's a strawman.
I've never stated that Calories determine body composition. That's a strawman.

•  " Every subject [in bray's overfeeding study] gained weight (mostly fat mass) during the 40% energy excess overfeeding period. "

"Again, making crap up. There is NO RULE IN BIOLOGY which states all consumed energy must be retained as body mass. Indeed most typical people gain fat during overfeeding (with great resistance/inefficiency of fat gain), but it is indeed possible to hardly gain any or none at all as in constitutional thinness. What happens during calorie consumption among different people (and perhaps, different DIETS and different TIMES and different ENDOCRINE situations...) is a wild card determined by the biology i.e. neuroendocrine functions of the animal in question. There is NOTHING about physics which reflects / informs physiology other than the basic fact the latter exists within the former (which, again, tells us NOTHING ultimately). How organisms process consumed nutrition is not a physics question. There is no freakin' law of physics or physiology for that matter which states nom nom time = thigh chub. You don't have to wear that pizza as a popeye's muscle or as a shelf butt."
Somewhere within all of the irrelevant waffle about rules & laws, ItsTheWoo raises an interesting point. Although a caloric surplus is always required for weight gain, eating more Calories can sometimes result in zero weight gain. How so? From ItsTheWoo's link:-
"Conclusion: This data is the first to demonstrate a resistance to weight gain in constitutional thinness (CT) population in response to 4-week fat overfeeding, associated with an increase in resting energy expenditure and an emphasised anorexigenic hormonal profile.
In CT people, their energy expenditure increases in line with their energy intake. Therefore, even though they're eating more Calories, there's no caloric surplus, therefore there's no weight gain. Energy Balance always applies.

• "Yes, kcals do get wasted. You don't understand things quantitatively i.e. how many kcals get wasted."

"I know anxious/obsessional people like the safe feeling of balancing calories. The fact reality is more complex and you can't just enter things in a phone app and be ASSURED of what is going on in your body, doesn't invalidate the truth of the fact metabolic reactions are more complex THAN CALORIES.

Just because it is *impossible* for a reasonable free living human to quantify all of the metabolic, endocrine, nervous system factors influencing adipocyte growth changes does not mean they don't fucking exist."
ItsTheWoo left out my calculations. Here they are:-"if I eat 2000 calories of a ketogenic diet in 3 hrs, most of it is wasted as heat, physical energy (I know, because I am EXTREMELY warm/energetic) and then the rest of time i am using a relatively greater percent of stored fat."
Do you know at what rate you're burning-off extra energy intake as heat energy output when you're "EXTREMELY warm/energetic"? Here's an estimate:-
If the mean TEF for your meal is 11% (assuming your meal is 50%E protein & 50%E fat), that's 220kcals (921kJ) "wasted" as heat energy. That'll make you feel EXTREMELY warm, as 220kcal raises the temperature of 57kg of water (your body) by 3.84°C.

A 2,000kcal meal (a whole day's worth of food) takes a lot longer than 3 hours to digest & absorb. I'll guesstimate it as 24 hours. 921kJ of extra heat power over the course of 24 hours = 10.7W, which is an increase of 17.7% over your normal Metabolic Rate of ~60W heat power (~1kcal/minute).
It's easy to "prove" something by being vague. That's PSEUDOSCIENCE. I do science. If you do the maths, you can see that, of the 2,000kcal ketogenic meal, most of it isn't wasted as heat, because if most of it is wasted as heat, ItsTheWoo would spontaneously combust!

• "Dr. Robert C. Atkins made the same fundamental cock-up when he said that humans pissed-out loads of kcals of ketones each day, giving a Metabolic Advantage to ketogenic diets."

"1) The advantage of a ketogenic diet (non-fasting) does exist, so it's not a 'cock up", even if his mechanism was wrong.
2) If atkins was wrong (you pee out all LCHF food) who cares? That was 30+ years ago. He was a cardiologist who observed a VLC diet made him slim. He used his medical education to hypothesize a reason why. His hypothesis was wrong, but his observations were right. This happens all the time in science or basic human reasoning; make observations, form hypothesis. The hypothesis may be wrong, the findings are STILL RIGHT (i.e. low carb diets DO make slim, just not via peeing away ketones)."
1) There is no Metabolic Advantage to ketogenic diets. See https://www.jbc.org/content/92/3/679.full.pdf
2) Atkins' observations were wrong. See The Battle of the Diets: Is Anyone Winning (At Losing?)
a) Low-Carb diets work better than High-Carb diets for people who are Insulin Resistant.
b) Low-Carb diets work worse than High-Carb diets for people who are Insulin Sensitive.
c) Low-Carb diets work the same as High-Carb diets for everybody in Metabolic Ward Studies.
If there's a Metabolic Advantage to ketogenic diets, they would work better than high-carb diets all the time. They don't. See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes for my hypothesis, which explains a), b) and c).

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

From https://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet → ↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So? T2DM is a disease of chronic excess. Chronic over-consumption was caused by Food Industry marketing, not carbohydrates.

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleading. Siri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat → ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

Why you really can't outrun your fork.

Hat-tip to Yoni Freedhoff.

From http://www.blacksheepfitness.co.uk/you-cant-outrun-your-fork.html

See Effect of school-based physical activity interventions on body mass index in children: a meta-analysis.
"Meta-analysis showed that BMI did not improve with physical activity interventions (weighted mean difference -0.05 kg/m², 95% confidence interval -0.19 to 0.10). We found no consistent changes in other measures of body composition."

Some people believe that if going to the gym isn't making them lose weight, they're not exercising hard enough. Chronically over-exercising can chronically raise serum cortisol, which makes the kidneys retain water, causing a stall in weight-loss, as well as causing raised fasting blood glucose, irritability, poor memory and a slower metabolic rate, due to the reduced conversion of thyroxine into tri-iodothyronine.

Don't over-exercise!

A healthy body weight is made in the kitchen, not the gym. Buy produce, cook it and eat it!

Although I totally support the use of low-carbohydrate/calorie diets for people with insulin resistance or Type 2 diabetes, now that I'm no longer insulin resistant, I can eat natural carbohydrates, without any problems.

A medium-sized (orange-fleshed) Sweet Potato takes only 4 minutes to bake in its jacket in a 700W microwave oven. The flesh is moist & sweet, unlike that of a Yam or potato.

I eat the whole thing, including the jacket. It's very filling and I'm still able to lose weight. For active and insulin sensitive people, a Kitavan-style diet is absolutely fine.

How low & very low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people lose more weight on low-carbohydrate diets than on high-carbohydrate diets and insulin sensitive people lose more weight on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes's carbohydrate/insulin hypothesis of obesity is correct, everyone would lose more weight on low-carbohydrate diets than on high-carbohydrate diets. This isn't the case, therefore Gary Taubes's hypothesis is not correct.

Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies".

The Aragon Insulin Fairy

The Energy Balance Equation

Change in Body Stores = Energy in - Energy out, where... 

Energy in = Energy entering mouth - Energy exiting anus, and... 

Energy out = BMR/RMR + TEF + TEA + SPA/NEAT

See The Energy Balance Equation to find out what the above terms mean.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. See Control of overshoot for more information.

1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Body stores increase. There are also accusations of gluttony & sloth!

2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Body stores decrease.

In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.

There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587

In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.

Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Insulin Resistance can be fixed. See Insulin Resistance: Solutions to problems.

Type 2 Diabetes can also be fixed. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Aim to fix the problem. If it's impossible to fix the problem, a low-carbohydrate diet as an adjunct to medication is fine.

Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Julianne Taylor of Paleo & Zone Nutrition posted the following excellent lecture on Facebook:-

Eating Through The Myths: Food, Health and Happiness - Taylor, Prof. R., Berlin, 28-Sep-12
EDIT: The link above needs Flash. If Flash isn't available, see YouTube video below.

Salient points:

1) It's a chronic calorie excess (of carbohydrates and/or fats) that causes problems.
2) Motivation, motivation, motivation!
3) Both diet and exercise are important. See Move More: Solutions to problems.
4) You can't outrun your fork. See The 5th Myth of Modern Day Dieting: You Can Outrun Your Fork.
5) Underlying Insulin Resistance needs to be addressed. See Insulin Resistance: Solutions to problems.

See also Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol, and Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause (PDF).

For more information on Prof. Taylor's work, see Reversing Type 2 Diabetes.

EDIT: Long-term results are now in. See Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The full study is behind a pay-wall, but here are a couple of Figures from it.

86% of participants who completed all 3 phases of the trial maintained over 15kg of weight loss and achieved remission from diabetes. Participants who dropped-out at various points achieved less weight loss at the 1 year point and achieved a lower % of remission. It's not easy for people who are consuming 15% fewer kcals/day of healthy foods to maintain motivation when they're constantly being bombarded by persuasive marketing encouraging them to eat yummy Food Products.

If beta cells have been irreversibly damaged and the above approach doesn't work, improved glycaemic control can be achieved using a LCHF diet.

Carbs, Carbs, Carbs, Carbs and Carbs.

Carbohydrates seem to get the blame for everything nowadays. "Carbohydrates made me fat". "Carbohydrates burned-out my pancreas". "Carbohydrates raised my blood glucose". "Carbohydrates raised my blood triglycerides". "Carbohydrates stole mer jerb!". O.K, I made the last one up!
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.

Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.

Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.

The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!

1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.

2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.

3. There are oligosachharides e.g. FOS.

4. There are polysaccharides e.g. inulin.

5. There is soluble fibre/fiber e.g. cellulose.

Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.

It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.

I'm back with some miscellaneous ramblings.

I'm not dead! Who knew?


I saw https://twitter.com/JimJohnsonSci/status/468745252170248192 and read Modeling type 2 diabetes in rats using high fat diet and streptozotocin.

What I find a bit sad is the "cure > prevention" attitude. The cause of pre-diabetes & type 2 diabetes is pretty well known now, i.e. it's basically the inability of body stores (liver/muscle glycogen stores & fat masses) to accommodate any more, resulting in excessive amounts of various things (e.g. glucose, fat, cholesterol, NEFAs etc) in the blood, with varying degrees of beta cell dysfunction.

The degree of fatness at which body stores become full depends on the degree of adipocyte hyperplasia, so it's possible for slim people to become type 2 diabetic, though ~85% of type 2 diabetics are over-fat. Some slim people are misdiagnosed with type 2 diabetes, as they have LADA or signalling abnormalities. Some have acquired endocrine abnormalities.

I've been pre-diabetic twice to my knowledge, the most recent occasion being last year when I became slightly manic after mum died and got into a large number of arguments on various blogs. I "took my eye off the ball" diet-wise and ended up gaining too much body-fat, even though my belt didn't feel noticeably tight. I blogged about feeling too hot last year. When I had blood tests in September to find out why I was overheating so much, the results revealed hyper****aemia, where **** = glucose, total cholesterol & triglycerides. The doctor recommended that I take a statin. I declined, stating that I knew what had caused the problem and that I would deal with it. I was told to have repeat blood tests in 3 months time.

I subsequently "kept my eye on the ball" diet-wise (using bathroom scales to monitor progress), lost 8kg (some of it fat mass & some of it muscle mass) and when I was retested 3 months later, the previously abnormal blood test results were back to completely normal. That's twice I've gone from pre-diabetes to normal, which suggests that deterioration from pre-diabetes to type 2 diabetes is not inevitable, provided that the cause is dealt with before excessive irreversible beta cell dysfunction occurs.

The main reason why the incidence of over-fatness & type 2 diabetes is increasing is the overconsumption of "Crap in a bag/box/bottle" by increasing numbers of people. How to reverse this trend? Damned if I know!

We are all just prisoners here, of our own device.

If you don't recognise the words in the title, here's the classic song from which they came.


An increasing number of people are becoming like birds in gilded cages. See The perfect crime.
"What's fascinating is this: the marketing is so powerful that some of the people being hurt actually are eager for it to continue. This creates a cultural feedback loop, where some aspire to have these respected marketing jobs, to do more marketing of similar items. It creates a society where the owners and leaders of these companies are celebrated as risk-taking, brave businesspeople, not as the modern robber barons that they've become."

Did I ever mention?...

When the only tool in the box is a hammer...

Everything that needs fixing looks like a nail.

People with diabetes mellitus are issued with blood glucose meters - and nothing else.

For people with type 1 diabetes, that's fine. They lack insulin, so they have to inject insulin in the right amounts & types to keep their blood glucose levels within reasonable limits. Applying Bernstein's Law of small numbers by reducing glycaemic load to a minimum keeps blood glucose levels within reasonable limits (between 3 & 7mmol/L) most of the time. See also The problem with Diabetes.

For people with type 2 diabetes and excessive visceral (belly) fat (~85% of people with type 2 diabetes), that's not fine. Their disease is a disease of chronic excess intake relative to oxidation, causing fasting dyseverythingaemia
(hyperglycaemia, hypercholesterolaemia, hyperNEFAaemia, hypertriglyceridaemia, hyperuricaemia, etc). People who have type 2 diabetes don't have only postprandial hyperglycaemia - they also have postprandial hypertriglyceridaemia. See Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity. Postprandial hypertriglyceridaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

However, because the only tool in the box of someone with type 2 diabetes is a blood glucose meter, their disease looks like one of only hyperglycaemia. Applying Bernstein's Law of small numbers by reducing carbohydrate intake to a minimum keeps blood glucose levels within reasonable limits, but makes other things worse if energy from carbohydrates is replaced by energy from fats.

Only if energy from carbohydrates is reduced AND energy from fats isn't increased to compensate (i.e. eat a LCLF PSMF or Modified PSMF until sufficient visceral fat has been lost), does carbohydrate restriction help people with type 2 diabetes.

A little moderate to vigorous physical activity does more than you think.

There are others!

Hat-tip to Bill Lagakos for tweeting this:- The Influence Of Physical Activity On Vascular Complications And Mortality In Patients With Type 2 Diabetes Mellitus.

"RESULTS: Forty-six percent of participants reported undertaking moderate to vigorous physical activity for >15 minutes at least once in the previous week. During a median of 5 years of follow up, 1,031 patients died, 1,147 experienced a major cardiovascular event and 1,136 a microvascular event. Compared to patients who undertook no or mild physical activity, those reporting moderate to vigorous activity had a decreased risk of cardiovascular events (HR 0.78, 95% CI 0.69-0.88, p < 0.0001), microvascular events (HR 0.85, 95% CI 0.76-0.96, p0.010) and all-cause mortality (HR 0.83, 95% CI 0.73-0.94, p0.0044)."

A HR of 0.83 is a reduction of 17%. That's quite impressive, for at least 15 minutes of moderate to vigorous physical activity at least once a week. Must. Get. Off. This. Sofa. More. Often.

Impaired Glucose Tolerance: also between a rock and a hard place.

A high percentage of people with excessive visceral adiposity (belly fat) have Impaired Glucose Tolerance (IGT). This post is about them.

Image from http://carbsanity.blogspot.co.uk/2013/03/insulinproinsulinetc-in-normal-igt-and.html

IGT is caused by excessive NEFAs spewing into the blood and/or deficiencies and/or sedentariness.

If nothing is done about it, IGT will progress to full-blown Type 2 Diabetes, which will get worse and worse as per the graphs to the right of the IGT one.

To do something about it, see http://nigeepoo.blogspot.com/2011/02/insulin-resistance-solutions-to.html

Diabetes: which are the safest carbohydrates?

In my previous post, I stated that people with T2DM should eat ~150g/day of carbohydrate.

Soak & cook your own beans al-dente, for slowest release carbs.

See International table of glycemic index and glycemic load values: 2002. Below is a list of carbohydrates that have a low glycaemic load, or GL (GL = glycaemic index * grams of carbohydrate in the serving).

Non-nutritive sweeteners:

It's often claimed that non-nutritive sweeteners produce a cephalic phase insulin response. The mere anticipation of eating produces a cephalic phase insulin response. See How neural mediation of anticipatory and compensatory insulin release helps us tolerate food. An insulin response suppresses serum NEFAs, so it's not all bad.

Sugars and Sugar alcohols:

Fructose is not recommended for people with T2DM, as it "barges its way" into the liver via Glu-T5 and fructokinase. People with T2DM who have a high fasting serum glucose level almost certainly already have full liver glycogen stores, so adding to them isn't advisable. Whole fruits (not juices) are fine.
Lactose has a virtually zero GL, isn't very sweet and has/hasn't a laxative effect in large quantities (lactase-dependent). Heating lactose turns it into lactulose.
Lactulose has a virtually zero GI, is sweet and has a laxative effect in large quantities.
Galactose is not recommended, as large amounts may accelerate ageing.
D-mannose has a virtually zero GI, is sweet and doesn't have a laxative effect in large quantities. It can be used to treat urinary tract infections (UTIs) caused by e.coli, due to the fact that the kidneys filter it out of the blood and pass it out in the urine. Mannose in urine reduces the adhesion of e.coli to the inside wall of the urinary tract. See Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex.
Trehalose has a virtually zero/moderate GI, is sweet and has/hasn't a laxative effect in large quantities (trehalase-dependent).

Lactitol has a virtually zero GI and has a laxative effect in large quantities.
Sorbitol has a virtually zero GI and has a laxative effect in large quantities.
Xylitol has a virtually zero GI, minty overtones and reduces dental plaque. However, it has a laxative effect in large quantities.
Erythritol has a virtually zero GI, minty overtones and is wee'ed-out like D-mannose, so it doesn't have a laxative effect in large quantities.

Starches:

Note: Tinned starches are usually overcooked, so cook your own. Don't overcook starches, as that makes them faster-absorbing. Al dente is best.

Gram dhal a.k.a. chana dal.
Long-grain rice. Refrigerating boiled rice for 24 hours lowers the GL, by forming resistant starch. See item 275 in the table in the first link.
New potatoes. Refrigerating boiled new potatoes for 24 hours lowers the GL a lot, by forming resistant starch. See item 605 in the table in the first link. You can boil old potatoes, but they're probably not as good.
Pearl barley.
Sweet corn.
Beans.
Chickpeas.
Lentils.
Peas.
Starchy nuts e.g. peanuts , cashews and chestnuts.
Vegetables.
Root vegetables.
Raw carrots.

If even low-GL carbs spike BG too much, this indicates severe IR in liver and/or skeletal muscle. See Insulin Resistance: Solutions to problems.

The above lists also apply to people with T1DM who are having difficulty keeping their blood glucose level between 3 and 7mmol/L.

Type 2 diabetes: between a rock and a hard place.

About 85% of type 2 diabetics have excessive visceral adiposity (belly fat). This post is about them.

Which is better - the rock or the hard place?

 

1) The rock:

This is serum glucose. People with type 2 diabetes can measure their own serum glucose. Eating carbohydrates makes serum glucose increase, the rate of increase being proportional to the glycaemic index and the magnitude of the increase being proportional to the grams of carbs consumed. By limiting the intake of dietary carbohydrates, large spikes in serum glucose can be avoided. The occasional spike above 7.8mmol/L (140mg/dL) doesn't hurt. It's spending long periods of time above 7.8mmol/L that's harmful (by glycation).

A low-carb diet (~150g/day of carbohydrate) halves serum glucose fluctuations compared to a higher-carb diet (~300g/day of carbohydrate). A very-low-carb diet (~75g/day of carbohydrate) further halves serum glucose fluctuations compared to the low-carb diet. This seems like an improvement, at first glance.

2) The hard place:

This is the invisible "elephant in the room", as it's not measured by doctors and people with type 2 diabetes can't measure it themselves. It's serum Non-Esterified Fatty Acids, or NEFAs (a.k.a. Free Fatty Acids, or FFAs). Serum NEFAs are high when fasting and fall after eating foods that raise serum insulin (carbs & certain proteins). People with type 2 diabetes and excessive visceral fat (belly fat) have higher-than-normal serum NEFAs due to adipocyte insulin resistance (IR). See Insulin Resistance: Solutions to problems.

Just like with serum glucose, there's nothing wrong with serum NEFAs going up & down. It's chronically-high serum NEFAs that's harmful (except during periods of caloric restriction). See Showing posts sorted by relevance for query NEFA "type 2 diabetes" .

See Fig. 1 in Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. On a very-low-carb (less than 50g/day carbs) diet that's not calorie-restricted, serum insulin remains low all of the time. To insulin-haters, that sounds like a good thing. Unfortunately, it means that there is no insulin spike to suppress serum NEFAs by shifting the balance of NEFAs going in/coming out of fat cells. Serum NEFAs stay high all of the time, which is harmful.

Therefore, people who have type 2 diabetes and excessive visceral fat and who are permanently on a very-low-carb diet that's not calorie-restricted are harming themselves.

Not exactly rocket science, is it? Part 2

If there is a deficiency in "X", taking supplement "X" will correct the deficiency in "X".
∴ If problem "Y" is caused by a deficiency in "X", taking supplement "X" will fix problem "Y".

If there's no deficiency in "X", taking supplement "X" won't make any difference.
∴ If problem "Y" isn't caused by a deficiency in "X", taking supplement "X" won't fix problem "Y".

If a person spends a lot of time outdoors in skimpy clothing in sun that's higher than 45deg in the sky, it's highly likely that they won't be deficient in Vitamin D3. Therefore, supplementing with 5,000iu/day of Vitamin D3 won't highly likely do anything.

∴ If the above sun-worshipping person has type 2 diabetes, supplementing with 5,000iu/day of Vitamin D3 won't highly likely make any difference.

Not exactly...

Rocket Science!

There will be some people for whom all of the supplements & exercises that I recommend don't make any difference to their type 2 diabetes. Sorry about that. A low-carb (but not very-low-carb) diet will minimise your serum glucose level fluctuations without increasing your serum NEFA level excessively. See The problem with Diabetes.

Can supplements & exercise cure Type 2 diabetes?

Definitely, maybe!

From http://health-in-hand.co.uk/2013/03/24/supplements-for-the-non-supplement-takers/

According to Hyppönen and Power, in a large sample of the white British population born in 1958, 60.9% of subjects had serum 25(OH)D (the active metabolite of Vitamin D) of less than 75nmol/L in Summer & Autumn, and 87.1% had serum 25(OH)D of less than 75nmol/L in Winter & Spring. 75nmol/L ≡ 30ng/mL.

 From Hypovitaminosis D is associated with insulin resistance and β cell dysfunction, 2-hour post-load blood glucose level in an oral glucose tolerance test (OGTT) has a negative correlation with 25(OH)D concentration (Fig 1C). 25(OH)D concentration has a positive correlation with insulin sensitivity (Fig 2A). Therefore, 2-hour post-load blood glucose level in a OGTT has a negative correlation with insulin sensitivity.

"Extrapolation from the observations in the current study suggests that increasing 25(OH)D from 10 to 30 ng/mL can improve insulin sensitivity by 60%, from 3.8128 to 6.1176 (umol/L)·m-2·min-1·(pmol/L)-1. This improvement in insulin resistance could potentially eliminate the burden on cells and reverse abnormal glucose tolerance. Furthermore, the 60% improvement in insulin sensitivity that results from vitamin D treatment indicates that that treatment is more potent than either troglitazone or metformin treatment (54% and 13% improvement in insulin sensitivity, respectively). The modest effect of vitamin D on insulin sensitivity in individual persons may translate into a dramatic effect in the population as a whole because of the high prevalence of hypovitaminosis D, which, in a large population, carries an attributable risk for type 2 diabetes and the metabolic syndrome. Although a review of the literature suggests non-calcium-mediated effects, the underlying molecular mechanism remains to be elucidated."

As my 2-hour post-load blood glucose level in a OGTT became low (3.7mmol/L, from 8.7mmol/L in 2003) after supplementing with 5,000iu/day of Vitamin D3, this means that my insulin sensitivity became high. Therefore, I cured my pre-type 2 diabetes using supplements.

My fasting blood glucose level also fell from 6.8 mmol/L (> 7.0mmol/L = type 2 diabetes diagnosis) to 5.0mmol/L. I achieved this without taking any drugs for type 2 diabetes - not even Metformin, which I consider to be a safe & effective insulin-sensitiser, though it can cause gastric distress and B12 absorption issues, long-term. The supplements that I took had zero side-effects and merely corrected deficiencies.

Diabetes drugs cannot cure type 2 diabetes. However, supplements & exercise can cure type 2 diabetes, if the type 2 diabetes is caused by nutrient deficiencies and/or sedentary behaviour and if all pancreatic beta cells haven't been destroyed. Insulin injections can preserve pancreatic beta cells, while insulin resistance is being tackled. See Dr. Richard K Bernstein on insulin for type 2 diabetics, and some definitions.

Sadly, if there are no nutrient deficiencies and/or all pancreatic beta cells have been destroyed, supplements & exercise will not help.

New treatment might put Type 2 diabetes in remission.

From:
http://www.ctvnews.ca/mobile/new-treatment-might-put-type-2-diabetes-in-remission-1.806064
"A new study by Toronto researchers on a new way to treat type 2 diabetes shows it may cause temporary remission of the disease in up to 75 per cent of patients.
 
The new treatment involves taking four shots of insulin -- the medication required by some diabetics to control blood sugar levels -- per day for just one month. This is a change from the usual treatment, which involves daily insulin shots over an extended period of time.

Patients develop diabetes when their pancreas can't produce enough insulin to lower blood sugar levels after meals. While medications can temporarily boost insulin production, many type 2 diabetics face a lifetime of daily insulin shots. Over time, patients with the disease can go on to suffer from a range of complications including blindness, heart disease, kidney problems and nerve damage.

Dr. Bernard Zinman, the director of the Leadership Sinai Centre for Diabetes and lead researcher of the study, explained how the new treatment works to CTV News. According to Zinman, by giving type 2 diabetics concentrated levels of insulin for a month early on in their disease, their pancreas, in effect, gets a "a break."

"The diabetes in essence goes away because their own pancreas now can make enough insulin," he said.

After the month on concentrated doses, patients are required to take another type of medication to "maintain" the remission, said Zinman.

Zinman said that the period of remission may eventually wear off, and so he sees the possibility of a future "top-up" treatment, which would last another month.

While the remission period can vary in patients, the prospect of improving pancreatic function is an exciting development in diabetes research, said Dr. Ravi Retnakaran, co-researcher of the study.

"This is a very novel and exiting way of treating diabetes that could have important implications," said Retnakaran.

For patients involved in the study, the treatment has had a major impact on their quality of life. Francoise Hebert was diagnosed with type 2 diabetes in November 2010. Seven months ago she enrolled in the study, and while she found the four daily insulin doses challenging, her blood sugar levels are now normal.

Hebert now happily tells people she "no longer has the disease," and enjoys knowing she's delayed any progression of diabetes-related complications.

"It feels fabulous," she said with a laugh. "It feels absolutely wonderful."

In addition to having her diabetes go into remission, Hebert says she's also learned how to eat better and hopes to eventually be able to get her weight under control.

Type 2 diabetes is primarily caused by an unhealthy diet and physical inactivity.

The research team at Mount Sinai Hospital hopes to have study results in a year or two, as well as more safety data on the medication."

Hypoglycaemic counter-regulation at normal blood glucose concentrations in patients with well controlled type-2 diabetes.

Hat tip to Graham of the Lowcarb Team. See Hypoglycaemic counter-regulation at normal blood glucose concentrations in patients with well controlled type-2 diabetes.

"Background

Intensive treatment to achieve good glycaemic control in diabetic patients is limited by a high frequency of hypoglycaemia. The glucose concentrations at which symptoms and release of counter-regulatory hormones takes place have not been studied in patients with well controlled type-2 diabetes.

Methods

We studied seven well controlled, non-insulin treated, type-2 diabetic patients (mean HbA1 [corrected according to Diabetes Control and Complications Trial] 7·4%, SD 1·0) and seven healthy controls matched for age, sex, and body mass index with a stepped hyperinsulinaemic hypoglycaemic glucose clamp. Symptoms, cognitive function, and counter-regulatory hormone concentrations were measured at each glucose plateau, and the glucose value at which there was a significant change from baseline was calculated.

Findings

Symptom response took place at higher whole-blood glucose concentrations in diabetic patients than in controls. Counter-regulatory release of epinephrine, norepinephrine, growth hormone, and cortisol showed a similar pattern—eg, at blood glucose concentrations of 3·8 mmol/L [SD 0·4] vs 2·6 [0·3] for epinephrine.

Interpretation

Glucose thresholds for counter-regulatory hormone secretion are altered in well controlled type-2 diabetic patients, so that both symptoms and counter-regulatory hormone release can take place at normal glucose values. This effect might protect type-2 diabetic patients against episodes of profound hypoglycaemia and make the achievement of normoglycaemia more challenging in clinical practice."

What the above study shows is that, in people with "well controlled" T2DM (mean HbA1c 7·4%, SD 1·0 is poor control. Less than 6% is good control), there is counter-regulatory release of adrenaline, noradrenaline, growth hormone and cortisol at normal blood glucose levels. This is bad, as it's unhealthy to have release of counter-regulatory hormones under normal living conditions.

EDIT: Graham posted this study in support of his belief that there is low/no cortisol etc secretion due to blood glucose not falling low enough. This study actually counters his belief, as blood glucose doesn't fall low enough due to excessive cortisol etc secretion!