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.

What are the action and reaction forces when a hammer hits a nail?

Diabetics 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 carbohydrate intake to a minimum keeps blood glucose levels within reasonable limits (between 3 & 7mmol/L) most of the time.

For people with type 2 diabetes and a fat belly (~85% of type 2 diabetics), that's not fine. Their disease is a disease of excess, causing dyseverythingaemia (hyperglycaemia, hypercholesterolaemia, hypoHDL-cholesterolaemia, hyperNEFAaemia, hypertriglyceridaemia, hyperuricaemia, etc). However, because the only tool in their box is a blood glucose meter, their disease looks like a disease of high blood glucose level (hyperglycaemia) only. Applying Bernstein's Law of small numbers by reducing carbohydrate intake to a minimum keeps blood glucose levels within reasonable limits, but makes everything else worse if energy from carbohydrates is replaced by energy from fats.

EDITED to include information in the comments: Only if energy from carbohydrates is reduced to a minimum AND energy from fats isn't increased to compensate (i.e. eat a PSMF or a Modified PSMF), 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

Type 2 diabetes: which are the safest carbohydrates?

In my previous post, I stated that people with type 2 diabetes should eat ~100g/day of carbohydrate.

Beans means...

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 type 2 diabetics, as it "barges its way" into the liver via Glu-T5 and fructokinase. Type 2 diabetics who have a high fasting serum glucose level almost certainly already have full liver glycogen stores, so adding to them isn't advisable.
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 a laxative effect in large quantities.
Sorbitol has a virtually zero GI and 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:

Don't overcook starches, as that raises their GL. Al-dente is best.
Gram dhal a.k.a. chana dal.
Long-grain rice. Refrigerating cooked rice for 24 hours slightly lowers the GL by forming resistant starch. See item 275 in the table in the first link.
New potatoes. Refrigerating cooked new potatoes for 24 hours drastically lowers the GL by forming resistant starch. See item 605 in the table in the first link. Old potatoes can be used, but they probably won't taste as good.
Bürgen Soya & Linseed bread has 11.9g of carbs/slice.
Pearl barley.
Sweet corn.
Beans.
Chickpeas.
Lentils.
Peas.
Fettuccine.
Egg noodles.
Starchy nuts e.g. peanuts , cashews and chestnuts.
Vegetables.
Root vegetables.
Raw carrots.

The above lists also apply to people with Type 1 diabetes who are having difficulty keeping their blood glucose between 3 and 8mmol/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 (~100g/day of carbohydrate) halves serum glucose fluctuations compared to a higher-carb diet (~200g/day of carbohydrate). A very-low-carb diet (~50g/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's a deficiency in "X", taking supplement "X" will correct the deficiency in "X".
If problem "Y" is caused by a deficiency in "X", then taking supplement "X" will fix problem "Y".

If there's no deficiency in "X", taking supplement "X" won't do anything.
If problem "Y" isn't caused by a deficiency in "X", then 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 probable that they will not be deficient in Vitamin D3. Therefore, supplementing with 5,000iu/day of Vitamin D3 will highly probably do nothing.

If the above person has type 2 diabetes, supplementing with 5,000iu/day of Vitamin D3 won't fix their type 2 diabetes.

Not exactly...

Rocket Science!

There will be some people for whom all of the supplements & exercise that I recommend don't help 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!

Can very-low-carb diets impair your mental faculties?

I wanna tell you a story...

In 2006, I had a test done on my pituitary gland*, called an Insulin Shock Test. It was pretty much what it said on the tin. I laid on a hospital bed, I was injected with an overdose of insulin and I was monitored for blood glucose and growth hormone levels every 30 minutes.

My blood glucose fell and fell and fell and fell until it reached ~1.5mmol/L (~27mg/dL). What happened was interesting. I came out in a cold sweat and developed a tremor. Apart from that, I felt fine. The consultant in charge was chatting to me and I was chatting to him. Eventually, I was given a sandwich, a yoghurt and a banana to eat.

Some time later, when I had stopped sweating and shaking, the consultant returned and told me that I had become confused. My brain had ceased to function correctly due to a lack of blood glucose (the insulin had totally suppressed serum FFAs and ketones, so there were no other brain fuels available), but I was too mentally-impaired to know that I was mentally-impaired. As far as I was concerned, everything was fine & dandy. This is the Dunning-Kruger effect.

Referring to Blood Glucose, Insulin & Diabetes, as blood glucose falls due to either starvation or a lack of dietary carbohydrate, insulin falls and glucagon rises, stimulating the liver to convert liver glycogen into glucose for export to the blood. Eventually, liver glycogen becomes depleted and blood glucose falls again. The pituitary gland notices this and secretes AdrenoCorticoTropic Hormone (ACTH) which stimulates the adrenal cortex to secrete cortisol. The adrenal glands are also stimulated to secrete adrenaline (a.k.a. epinephrine). Cortisol increases the conversion of amino acids and other substrates into glucose by the liver and kidneys. If blood glucose continues to fall, the pituitary gland secretes growth hormone (GH), which has an anti-insulin effect.

From http://anthonycolpo.com/boosting-growth-hormone-with-diet-training-fact-or-fiction-part-2/:-
"after the zero-carb phase, subjects reported symptoms of hypoglycemia that included weakness, irritability, mental confusion, nausea, hunger, cold sweating and disturbed co-ordination. GH levels were higher during exercise after the low-carb phase, but so too were levels of other fuel mobilizing hormones such as epinephrine, glucagon, and cortisol." Epinephrine, glucagon, and cortisol are stress hormones. Chronically-high blood levels of stress hormones disrupt sleep and cause irritable, aggressive behaviour.

Ethanol inhibits gluconeogenesis in the liver (possibly also in the kidneys) resulting in worse hypoglycaemia. Worse hypoglycaemia results in more ACTH & adrenaline secretion and worse hypercortisolaemia, which can adversely affect the hippocampus, impairing memory.

In conclusion, if you want to eat a very-low-carb diet, long-term:-1) Don't do much high-intensity exercise. See "Funny turns": What they aren't and what they might be.
2) Don't drink much (if any) booze.

See also Can Low-Carb Diets Make You Crazy?

*My pituitary gland failed the test by secreting only 40% the amount of GH that it was supposed to. For six months, I was given GH to inject using a special pen with a 8mm x 0.3mm needle. By the end of the six month trial, I had perfected the art of painless injection. The trial was discontinued due to lack of any noticeable benefit (17 days supply of GH @0.3mg/day cost £120!).

Type 2 diabetes in the UK.

From Insulin usage in type 2 diabetes mellitus patients in UK clinical practice: a retrospective cohort-based analysis using the THIN database:-

"Importantly, this analysis has been conducted using routine data from UK clinical practice, which allows an insight into how patients are managed in current UK practice. In summary, this study demonstrates a persisting delay both in oral therapy escalation and insulin initiations in patients with type 2 diabetes, with a relative reduction in the effectiveness of oral therapy escalation. There is an apparent threshold HbA1C of > 8.5% beyond which additional oral therapy in routine practice appears unlikely to achieve an HbA1C target ≤ 7.0%.
This study thus highlights the need for more timely escalation of glucose-lowering therapy, including insulin initiation, in order to limit unnecessary patient exposure to hyperglycaemia and associated serious consequences, such as macro-vascular and micro-vascular complications."

An HbA1C of 7.0% still results in macro-vascular and micro-vascular complications. If someone develops type 2 diabetes in the UK, the NHS isn't going to save them. They have to save themselves.

See also Having Diabetes and Car Insurance and Applying for a Driving Licence and Informing the DVLA. Basically, developing type 2 diabetes in the UK sucks.

People who have Impaired Glucose Tolerance need to take action to prevent their condition from deteriorating into full-blown Type 2 diabetes. See http://nigeepoo.blogspot.co.uk/search/label/Diabetes.

Low-glycaemic diet seen to reverse diastolic dysfunction of diabetes.

From http://www.medscape.com/viewarticle/802947?nlid=30763_1301&src=wnl_edit_dail (Medscape log-in required):-

"Of 32 overweight or obese diabetic patients (mean body-mass index, 34) without cardiac disease who were engaged in a "rehabilitation program in order to lose weight" that included two hours of supervised aerobic exercise per day, half followed a low-glycemic diet (25% carbohydrate, 45% fat, 30% protein) and the other half a low-fat diet (55% carbohydrate, 25% fat, and 20% protein) for three weeks. The diets provided the same amount of calories. Those on the low-fat diet then switched to the low-glycemic diet for an additional two weeks"

"....the two diets led to about the same declines in weight and waist circumference..."

The diet was 25% carbohydrate, 45% fat, 30% protein.
It was a low-carbohydrate/low-glycaemic load diet.
It was not a very-low-carb diet.

Weird filters, Part 2.

Here's that weird picture again.

Why is it that some people see the world through weird cognitive bias filters? It makes discussion with them impossible, as what I write is remixed with weird filters into something completely different. They then argue against something completely different, not what I wrote. This is the classic Straw Man argument.

Here are some more examples of remixing with weird filters:-

"I can eat whatever I want" is remixed into "I can eat as much as I want". I actually meant "there are no banned foods".

"Inject some insulin" is remixed into "Shoot-up insulin to cover the 400g of carbs that I never even mentioned!"

To all intents & purposes, I had T2DM. Another 0.2mmol/L on my fasting serum glucose and I would have been diagnosed as having T2DM. As my fasting serum glucose was slowly increasing, it would have soon gone over 7.0mmol/L, had I not got lucky and fixed the underlying problem.

In January 2003, I had impaired Glucose Tolerance (fasting serum glucose = 6.8mmol/L on one OGTT, and 2 hours post-75g glucose load serum glucose = 8.7mmol/L on another OGTT). A sandwich used to send me to sleep.

By September 2008, I had normal Glucose Tolerance (fasting serum glucose = 5.0mmol/L & 2 hours post-75g glucose load serum glucose = 3.7mmol/L on the same OGTT). I also no longer suffered from hyperinsulinaemic drowsiness. I was approximately the same weight that I was in 2003, so the improvement was not due to weight loss.

P.S. Information about ways to tackle Insulin Resistance can be found in Insulin Resistance: Solutions to problems.

N.B. If someone has a valid medical reason for being on a very-low-carb or ketogenic diet, that's fine by me. I don't think that it's necessary for people with T2DM to be on a very-low-carb or ketogenic diet. In fact, eating more carbohydrate allowed Jason Sandeman to reduce his insulin dose for good BG control.

Dr. Richard K Bernstein on insulin for type 2 diabetics, and some definitions.

Dr. Richard K Bernstein:-

Dr. Richard Bernstein, the world's leading low-carb diabetologist, says in Diabetes: The Basics:-
"Many people (including the parents of diabetic children) view having to use insulin as a last straw, a final admission that they are (or their child is) a diabetic and seriously ill. Therefore they will try anything else - including things that will burn out their remaining beta cells - before using insulin. Many people in our culture have the notion that you cannot be well if you are using medication. This is nonsense, but some patients are so convinced that they must do things the “natural” way that I practically have to beg them to use insulin, which is as “natural” as one can go. In reality, nothing could be more natural. Diabetics who still have beta cell function left may well be carrying their own cure around with them - provided they don’t burn it out with high blood sugars and the refusal to use insulin."

Some definitions:-

From Low-carbohydrate diet:-
"The term "low-carbohydrate diet" is generally applied to diets that restrict carbohydrates to less than 20% of caloric intake, but can also refer to diets that simply restrict or limit carbohydrates."
A typical woman consumes ~2000kcals/day. A typical man consumes ~2,500kcals/day. Therefore...

Very-low-carb diet = <10% energy from carbs ≡ <~50 or ~62.5g carbs/day.
Low-carb diet = <20% energy from carbs ≡ <~100 or ~125g carbs/day.
"Healthy eating" = >55% energy from carbs ≡ >~275 or ~344g carbs/day.

It’s the Calories, Stupid.

I thought I'd mark my return to blogging by taking the piss out of a certain Diet Doctor for his post It’s the Insulin, Stupid, who takes (and tweaks) Fig 7A from Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production.

At first glance, Fig 7A looks like a CIH believer's dream come true (apart from the words "High Fat Diet").

Hyperinsulinemia → Obesity.

Obesity is caused by too much insulin. Game, Set and Match to insulin.

Not so fast! Let's take a look at the rest of Fig 7.

Figure 7. Revisiting the Current Model of Obesity and Type 2 Diabetes(A) The most widely accepted model of the pathogenesis of obesity and type 2 diabetes posits that a high-fat diet leads to obesity and insulin resistance (there is debate about the relative order and causality of these). In this widely held view, insulin resistance then leads to hyperinsulinemia, which is followed by β cell exhaustion, and then type 2 diabetes. The accepted model is incompatible with our results that put the insulin hypersecretion genetically upstream of obesity.(B) Our data support a model whereby insulin levels must be kept low to maintain energy expenditure in white adipose tissue via the expression of Ucp1. Our data do not address the order of subsequent events after obesity (outside the yellow box), such as insulin resistance and/or type 2 diabetes, since they were not observed in our studies. In other words, the effects of insulin gene dosage on obesity are independent of sustained changes in glucose homeostasis or insulin resistance.

↑ Peripheral Hyperinsulinemia → ↓ Uncoupling Proteins (WAT) → ↓ Energy Expenditure → ↑ Obesity.

Obesity is caused by a reduction in energy expenditure. Game, Set and Match to The Energy Balance Equation. It’s the Calories, Stupid. In the mice in this study, energy expenditure is strongly influenced by insulin levels. In humans, not a lot. In humans, insulin can act as a stimulant and as a sedative.

I'm not an insulin denier as is obvious from my other blog posts. I'm still controlling my carbohydrate intake.
I'm not a food reward denier and I've been using food reward principles to lose some more weight.

The above post will probably annoy some people. Before wasting your time writing a comment, please note my Moderation Policy.

Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

Another techie post.

From http://en.wikipedia.org/wiki/Negative_feedback_amplifier

There's been some arguing discussion over whether Hyperinsulinaemia (HI) causes Insulin Resistance (IR). My answer is...Yes and No.

HI increases IR long-term. See Downregulation and upregulation: The Insulin Receptor and Insulin oscillation.

HI doesn't increase IR short-term. How can I claim this? The above diagram represents a Negative Feedback Control System, which is how Blood Glucose is regulated.

"Input" represents Glucose from digested sugars and starches. The arrow pointing at AOL represents Blood Glucose (BG). The triangle containing AOL represents pancreatic beta cells. "Output" represents Insulin Secretion (ISec). More BG = More ISec.

The box containing ß represents three things that work in parallel to reduce Blood Glucose.
1) The Liver. More ISec = Less BG Production.
2) Muscle mass. More ISec = More BG imported to Muscle mass, via Glu-T4.
3) Fat mass. More ISec = More BG imported to Fat mass, via Glu-T4.
The three things aren't of equal strength, but they provide overall negative feedback.

If overall negative feedback is halved due to doubling of overall IR in the above three paths, ISec doubles. If you don't believe me, see Idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha. Double the value of resistance 2 (the negative feedback resistor Rf) from 10,000ohms to 20,000ohms and the output voltage on the inverting amplifier doubles from -10V to -20V.

The idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha is interesting in that an idealised op amp (the triangle with + and - inputs) has infinite gain and infinite voltage on its power supplies. As a result, there is zero volts (output voltage divided by infinity) between the idealised op amp's + terminal and its - terminal. If the idealised op amp's + terminal is connected to 0V (a.k.a. "Earth"), its - terminal is at 0V (a.k.a. "Virtual Earth") and has zero variation, whatever the input voltage. An actual op amp has a voltage gain of ~140dB (~10,000,000), so an output voltage of -10V can be achieved with a voltage of 1uV (one millionth of a Volt) on its - terminal.

If pancreatic beta cells had a zero threshold and infinite gain like an idealised op amp, BG would be zero and have zero variation with varying Glucose input. Pancreatic beta cells actually have a positive threshold and low gain, so BG is positive and has significant variation with varying Glucose input.

If ISec becomes zero (as in type 1 diabetes), there is zero negative feedback and BG goes up a lot. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are 0V instead of infinite.

If ISec becomes insufficient (as in type 2 diabetes), there is insufficient negative feedback and BG goes up a bit. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are 5V.

Having established that ISec is proportional to overall IR, what would happen if overall IR was proportional to ISec? If ISec doubled, overall IR would double, which would double ISec, which would double overall IR, ad infinitum. ISec would increase to maximum. THIS DOESN'T HAPPEN. Therefore, IR doesn't increase in proportion to ISec, short term.

Long-term, increased ISec increases IR for a variety of reasons, one of them being that increased ISec increases the rate at which cells fill with glycogen. Once full of glycogen, cells must down-regulate their import by down-regulating Glu-T4 and Glu-T2 (fat and liver cells also up-regulate their export of stuff) or rupture.

So, deplete your cells of glycogen by eating a diet that results in you unconsciously eating less and moving more. Also, do some higher-intensity exercises. Chris Highcock emailed me a link to Muscular strength and markers of insulin resistance in European adolescents: the HELENA Study.

Fiber and Insulin Sensitivity.

Bluddy Americans. It's Fibre! But anyway....

Stabby the Raccoon posted the following study in a comment on CarbSane's blog. I thought that it was so interesting that I am linking to it here.

Fiber and Insulin Sensitivity.

This study has built-in cognitive dissonance.

The first Fig. suggests that cereal fibre is associated with a much lower RR for Type 2 Diabetes Mellitus (T2DM) and that fruit & veggie fibre aren't.

Schulze et al. 2007: Cereal Fiber RR = 0.6 - 0.7. Fruit Fiber RR = 0.9 - 1.05. Vegetable Fiber RR = 0.95 - 1.15 approx.

The next table suggests otherwise.

Andersson et al., 2007: Whole grain diet contained 112 g/d of whole grain, 18 g fiber. No effect of whole grains on insulin sensitivity.

Ebeling et al., 1988: 5 g/d granulated guar. No effect on insulin sensitivity.

Johnston et al., 2010: Resistant starch supplement -40g/d. Improved insulin sensitivity with resistant starch.

Landin et al., 1992: 30 g/d granulated guar, given in 3-10 g doses. Improved insulin sensitivity with guar diet.

Maki et al., 2011: High-resistant starch diet- 30 g/d, Low-resistant starch diet- 15 g/d. Improved insulin sensitivity with both resistant starch diets, but effect only reached statistical significance for men.

Nilsson et al., 2008: White bread enriched with barley fiber and 8g resistant starch, Barley kernel based bread. Improved glucose tolerance with resistant starch.

Pouteau et al., 2010: 28 g/d acetogenic fibers (acacia gum and pectin). No effect on insulin sensitivity.

Robertson et al., 2003: High-resistant starch diet- 60 g/d. Improved insulin sensitivity with resistant starch.

Weickert et al., 2006: Fiber-enriched with 31.2 g insoluble fiber. Improved insulin sensitivity with increased insoluble fiber.

In conclusion, the resistant starches found in high-amylose rices such as Basmati, refrigerated boiled rice & boiled potatoes, also rye & barley breads are beneficial in terms of reducing your RR for T2DM. Watch out, though. Too much dietary resistant starch can cause colic, flatulence & diarrhoea if your intestinal bacteria are knackered. You want fermentation to short-chain fatty acids to occur, not osmotic laxation! See Genetics of Food Intolerance.

Cheapest Vitamin D3 yet.

A big thank you to Ted Hutchinson (the chap who got me interested in Vitamin D in 2007) for bringing Vitacost to my attention. Their own-brand 5,000iu Vitamin D3 mini gelcaps product is somewhat cheaper than the Healthy Origins product that I've been using ($12.99 vs $14.99). Click http://www.vitacost.com/Referee?wlsrc=rsReferral&ReferralCode=3320491 when creating a Vitacost account, to get $10 discount on orders over $30.

As imports are liable to VAT + handling charges (usually £8) if the value exceeds £15, the lower price means that I can order two pots of 365 Mini Gels for less than £15.

P&P is slightly more expensive at $7.99 vs $4. Delivery takes about two weeks.

How care homes are starving their residents to death.

Now that I have your full attention (!), care & nursing homes give their residents plenty to eat & drink, so they are not starving them to death in the conventional sense.

So, what am I talking about? Clue:- UVB cannot penetrate window glass. Watch this video.


I'm talking about Vitamin D starvation.

At this time of year, care home residents are dying like flies. My sister (who worked in a care home years ago) told me that this is normal. Three died at mum's care home in the same week recently. All of the residents have one thing in common. They're all pale.

Old people feel the cold, so if they do go outside between March and September, they're covered from head to toe in clothes. They synthesise minimal Vitamin D in their skins for their bodies to store. Then, between September and March, their bodies use up those stores. Vitamin D levels decay exponentially , with a half-life of about 60 days. As Vitamin D levels fall, the risk of getting viral infections greatly increases, mood worsens, aches and pains worsen, blood glucose control worsens, the risk of getting cancer greatly increases. Need I go on?

As Dr. Richard M. Cooper (Private GP, Harley Street) pointed out, ALL of his patients were low in Vitamin D and they were active people who could go outdoors. Many care home residents can't go outdoors. They can get a paltry 400iu Vitamin D from an Adcal-D3 chewable tablet, but they're huge things that taste like sweetened chalk and cause constipation (mum hated them).

Death by Vitamin D starvation is a long, drawn-out process that reduces the quality & length of life for care home residents. Something needs to be done about it. All care home residents should have their serum Vitamin D levels tested and be given Vitamin D3 accordingly. I have broached this subject with the manager of mum's care home.

Mum's on 5,000iu/day of Vitamin D3. Although she is now fairly non compos mentis, she still smiles a lot and laughs at my dreadful jokes. She is also infection-free.

EDIT: Here's a transcript of the important bits from the above video:-

"At this care home, they're proud of their varied menu. Even so, the Government recommends supplements for the over 65's as well as children under 3 and women who are pregnant or breast-feeding. But health charities are demanding clearer guidelines and better advice. Because research into Vitamin D deficiency has revealed associations with all sorts of conditions, including Multiple Sclerosis, Diabetes, Arthritis, Osteoporosis, Heart Disease and even some cancers."

Dr Carrie Ruxton (Nutritionist) said:-
"What I think the Government should do is promote its own policies. It had a policy for years to recommend Vitamin D supplementation for vulnerable groups, like elderly, housebound and pregnant & lactating women and children but at the moment, that's not being done. In my own example, I was pregnant twice and nobody told me to take Vitamin D supplements."

This is unacceptable. As the manager at mum's care home is not responsible for the residents' supplementation, I will be taking this up with the MP for the area.

Update: I spoke to the nurse on Friday 2nd March about mum's medical history. Before Vitamin D3, mum had a Urinary Tract Infection in the previous 9 months. Since Vitamin D3, mum has had no medical problems and she has been happy & contented. Her serum Vitamin D level is in the normal range.