Resistance is useless!

...said the Vogon guard. If that means nothing to you, watch this...


You probably know all about Insulin Resistance (IR) if you've read my blog for some time, as I may have mentioned it once or twice ;-) There's also Leptin Resistance (LR) in the brain, which reduces the amount of appetite suppression that leptin is supposed to produce. Robb Wolf's just written about Adrenaline Resistance (AR?) and chronically-high serum cortisol seems to induce Cortisol Resistance (CR?) in the hippocampus, resulting in poor short-term memory.

When the level of "X" in the blood is low most of the time, "X" receptors in the body up-regulate, so when the level of "X" in the blood goes high, it has an effect. When the level of "X" in the blood is high all of the time, "X" receptors in the body down-regulate, so when the level of "X" in the blood goes higher, it has a reduced effect.

The above suggests that regularly "grazing" on food is not a good idea, as this results in a fairly constant slightly elevated serum insulin level. Eating a meal, not eating for a few hours then eating another meal results in high serum insulin while the meal is being absorbed and low serum insulin for the rest of the time.

Gizmag: Injectable nanoparticles maintain normal blood-sugar levels for up to 10 days.

Fascinating technology featured in Gizmag & posted by someone HERE.

The nano-network that releases insulin in response to changes in blood sugar

"The injectable nano-network is made up of a mixture that contains nanoparticles with a solid core or insulin, modified dextran (which is commonly used to reduce blood viscosity), and glucose oxidase enzymes. When exposed to high levels of glucose, the enzymes convert glucose into gluconic acid, which breaks down the modified dextran to release the insulin. The gluconic acid and dextran, which are biocompatible, dissolve in the body, while the insulin brings the glucose levels under control.

The nanoparticles are given a positively or negatively charged biocompatible coating so that when they are mixed together, they are attracted to each other to form a “nano-network.” The positively charged coatings are made of chitosan, a material found in shrimp shells that has also found applications in self-healing car paint, while the negatively charged coatings are made of alginate, a material normally found in seaweed."

Wow! Cool bananas!

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.

Type 2 diabetes: your good signalling's gonna go bad.

A little bit of Tammy Wynette.

 

Good signalling:

There's a famine. You've got nothing to eat. Your body's glycogen stores have just run out. What happens next? As food intake is zero, serum insulin level is minimised, so lipolysis (fat mobilisation) is maximised. Serum NEFAs are maximised. High serum NEFAs provides fuel for tissues that utilise NEFAs and a "stop utilising glucose!" signal, in conjunction with low serum insulin. High serum NEFAs also increase ketogenesis in the liver, to give the parts of the brain that can utilise ketones an alternative choice of fuel, to reduce glucose utilisation to a minimum. Glucose utilisation must be minimised during a famine, as it's generated by the liver & kidneys from glucogenic amino acids, obtained from lean body mass (LBM) by hypercortisolaemia.

Gone bad:

You're a type 2 diabetic with a fat belly. For reasons that I don't understand (blood supply? Proximity to liver?), belly fat deposits spew NEFAs into the blood at a much higher rate than arm, boobs, love-handles, bum & thigh fat deposits. On a very-low-carb diet (50g/day carbs), serum insulin level is minimised, so lipolysis (fat mobilisation) is maximised. Serum NEFAs are maximised. High serum NEFAs provides fuel for tissues that utilise NEFAs and a "stop utilising glucose!" signal, in conjunction with low serum insulin. A type 2 diabetic with a fat belly already has underlying insulin resistance, due to over-full muscle, adipose and/or liver cells (making the liver spew glucose into the blood at too fast a rate and the muscles & adipocytes take it out of the blood at too slow a rate). The very-low-carb diet makes the underlying insulin resistance worse and high serum NEFAs in a milieu of caloric sufficiency wreak havoc. Serum fasting glucose level increases. Serum LDL-c level increases. Serum TG level increases. Serum just about everything level increases, except for serum HDL-c level, which decreases.

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."

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.

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.

Strength and insulin resistance

In all the discussions about how different diets may or may not promote insulin resistance, one thing that often gets missed out of the discussion is the role of the muscles.  Empty the muscles of glycogen through hard exercise and they will get more insulin sensitive to suck up the sugar out of the blood.  (Nigel has been trying to explain this but that is a different topic)

It is something that I talk about in Hillfit as a side benefit of strength training and an issue that Doug McGuff and John Little go into in Body by Science. 

Anyway, interesting to see this study come through this morning - at least some association between strength levels and markers of insulin sensitivity

Muscular strength and markers of insulin resistance in European adolescents: the HELENA Study

The aim of the study was to examine the association of muscular strength with markers of insulin resistance in European adolescents. The study comprised a total of 1,053 adolescents (499 males; 12.5–17.5 years) from ten European cities participating in the Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) Cross-Sectional Study. Muscular strength was measured by the handgrip strength and standing long jump tests. Cardiorespiratory fitness was measured by the 20-m shuttle run test. Fasting insulin and glucose were measured and the homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) indices were calculated. Weight, height, waist circumference and skinfold thickness were measured, and body mass index (BMI) was calculated. In males, the handgrip strength and standing long jump tests were negatively associated with fasting insulin and HOMA (all P < 0.05) after controlling for pubertal status, country and BMI or waist circumference. When skinfold thickness was included in the model, the association became non-significant. In females, the standing long jump test was negatively associated with fasting insulin and HOMA (all P < 0.001) after controlling for pubertal status, country and surrogate markers of total or central body fat (BMI, waist circumference or skinfold thickness). Findings were retained in males, but not in females after controlling for cardiorespiratory fitness. The findings of the present study suggest that preventive strategies should focus not only on decreasing fatness and increasing cardiorespiratory fitness but also on enhancing muscular strength.

A comment, a simile and insanity.

A lot of my recent titles contain three items.

1) The comment: I'm just about to leave the following comment on Peter (Hyperlipid)'s blog post Insulin and the Rewards of overfeeding. I thought that it was so good at summing-up, I'll post it here first!

"All,

Insulin increases the amount of glucose & FFAs entering fat cells, muscle cells & the liver.

Insulin decreases the amount of glycerol & FFAs exiting fat cells & the amount of glucose exiting the liver.

Hyperinsulinaemia (which can produce sedation) results when one or more of the following tissues loses insulin sensitivity:- fat cells, muscle cells & the liver.

So, why do people keep saying that hyperinsulinaemia locks nutrients away in fat cells only, thus robbing other cells of nutrients, thus causing lethargy?

The relative insulin sensitivity of tissues determines the relative partitioning of nutrients into those tissues.

When tissues lose sensitivity to insulin, blood glucose control becomes impaired. This results in a roller-coaster blood glucose level after eating high-glycaemic carbohydrates. A rapidly-falling blood glucose level can cause ravenous hunger. I have experienced this during medically-monitored tests (OGTTs & an insulin shock test).

Low-carb/ketogenic diets don't result in a roller-coaster blood glucose level and therefore don't cause ravenous hunger. Simples!

Over-eating due to ravenous hunger is NOT gluttony, just as under-moving due to sedation is NOT sloth.

THIS is gluttony."

EDIT: This didn't go in my comment but should have:- "Low-carb/ketogenic diets result in the avoidance of moreish & calorific foods such as sweets, chocolate, cake, biscuits, pizza, Pringles etc. A single bite of such foods has a negligible effect on blood glucose & insulin levels, but encourages another bite and another and another ad nauseam due to Food Reward.

2) The simile: I use similes. I used the simile "As happy as a pig in shit" in a comment somewhere on Woos blog. Now, you may (or may not) have noticed that my user-name is Nigeepoo. We Brits are obsessed by two things - The weather and our bowel movements. I find things to do with poo and farting amusing (schoolboy humour, I know!). I used the simile "As happy as a pig in shit" because it is amusing to me.

3) The insanity: According to Woo in the following comment:-

"Re: the comment...Sorry, not convinced.
You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap."

Woo, you are as mad as a March hare. IMO of course, like everything I write. Duh!

Testing hypotheses - a rant.

My brain just exploded! On Why conventional view of obesity / FR is wrong, ItsTheWoo wrote "...there is not a doubt in my mind obesity is entirely 100% an illness, a disorder... "

According to ItsTheWoo's hypothesis, the increasing incidence of obesity all around the world since 1970 is 100% caused by the increasing incidence of illness all around the world since 1970. Seriously, WTF?

According to Nigeepoo's hypothesis, the increasing incidence of obesity all around the world since 1970 is significantly caused by the increasing influence of Crap-in-a-Bag/Box/Bottle (CIAB) manufacturers on the population by cunning marketing and on the Government by bribery lobbying since 1970.

The former results in increasing consumption of CIAB and the latter results in increasing subsidies on the raw materials used for manufacturing CIAB, making CIAB cheaper (also more profitable) than natural foods, thus increasing consumption of CIAB. See Why are Twinkies cheaper than carrots?

There are other factors causing increased obesity e.g. increasing numbers of towns/cities which discourage walking. See also Determinants of the Variability in Human Body-fat Percentage.

Highly-engineered and highly-calorific CIAB encourages subconscious over-eating via Food Reward. The hyper-secretion of insulin (compensatory hyperinsulinaemia) caused by the subconscious over-eating of CIAB causes subconscious under-moving by inducing drowsiness and lethargy, sometimes followed by the munchies if blood glucose goes too low. Insulin is just a hormone that is secreted for the storage of stuff and a reduction in the burning of stuff. Don't blame insulin for doing its job. If you have zero insulin (e.g. untreated type 1 diabetes), your body stops storing stuff and starts burning stuff uncontrollably. Before the invention of insulin injections, people with type 1 diabetes usually died within 2 years.

Subconscious over-eating is good for the profits of CIAB manufacturers. An increasing number of dyslipidaemic/hypertensive/depressed/diabetic/demented/w.h.y. people is good for the profits of health-care providers and drug manufacturers. These organisations currently make huge profits, so it's not going to be easy to change anything that will reduce them.

I deleted the last part of my rant as it was a bit too ranty, but I'm reinstating it in a toned-down form as I've mentioned it in the comments.

ItsTheWoo continually conflates subconscious over-eating and under-moving with conscious over-eating and under-moving (gluttony and sloth). The vast majority of over-fat people become over-fat due to subconsciously over-eating and under-moving. A tiny minority of over-fat people are gluttonous and slothful.

Telling people to consciously Eat Less, Move More doesn't work. This doesn't mean that Eat Less, Move More doesn't work. It means that Eat Less, Move More has to be done subconsciously. This is where low-carb/paleo/real food diets come into their own.

Rant over.

How eating sugar & starch can lower your insulin needs.

This is a bookmarking post. Jason Sandeman is a chef who has a couple of web-sites at Well Done Chef! and Jason Sandeman — Real Food For Your Life. He has Latent Autoimmune Diabetes of Adulthood (LADA), which has resulted in a total loss of his pancreatic beta cells which means that he has to take insulin.

Now, it's generally believed in low-carb circles (and by myself) that people with Type 1 Diabetes Mellitus (T1DM) should minimise their intake of sugary & starchy carbohydrates as these promote wild fluctuations in blood glucose. See The problem with Diabetes.

Jason wrote the following comment on Richard Nikoley's blog. The relevant part is as follows:-
"Even more weird – now that I have introduced the starches into the diet – I have actually got better control now. I thought my insulin needs would go up – but they haven’t. They’ve gone down."

To which I replied:-"How about this for an explanation? You now have a well-controlled glucose input to your circulation via diet, which has suppressed the poorly-controlled glucose input to your circulation via hepatic glucose production."

Hepatic glucose production (HGP) is increased by Glucagon, Cortisol & Adrenaline/Epinephrine. These are secreted as blood glucose level falls below certain values in order to keep our brains alive. See Blood Glucose, Insulin & Diabetes.

As keeping our brains alive is rather important (!), the mechanism is fairly crude in operation and blood glucose can overshoot in a positive direction, as a bit of glycation is less harmful than brain death. See "Funny turns": What they aren't and what they might be. Hyperglycaemia requires insulin to lower blood glucose back to the normal range.

Therefore, eating some (but not too much) sugar & starch can result in lower blood glucose level and lower insulin secretion. Eating fibre/fiber (a carbohydrate) is also good for keeping blood glucose low, as only just mentioned in Fiber and Insulin Sensitivity. Ain't the human body weird?

How stuff works, Part 2.

I'm the kind of person that likes to analyse everything to death (and make lists).

1) Here's what I wrote on Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count:-
"I’m going to stick my neck out here and state that fat, sedentary people do better on low-carb diets because:-

Fat, sedentary people have severe muscular insulin resistance.
This results in chronic hyperinsulinaemia and acute hyperinsulinaemia on eating carbs (which causes lethargy & increased sedentariness).
Chronic hyperinsulinaemia impairs the Phase I insulin response.
This impairs the stability of the blood glucose control system, resulting in large fluctuations in blood glucose level on eating carbs.
A rapidly-falling blood glucose level causes severe hunger pangs (I’ve experienced this under medical supervision).
Severe hunger pangs cause overeating, resulting in increased fatness.
GOTO 1

Low-carb diets reduce the large fluctuations in blood glucose level. Once normal blood glucose control has been restored by bodyfat loss & exercise, low-carb diet is no longer required."

I added a hot-link that wasn't in the original comment. Thanks to Sam Knox for linking to that study.

Lethargy & increased sedentariness result in very few calories burned (BMR/RMR + TEF). Eliminating (lethargy & increased sedentariness) greatly increases calories burned without conscious effort (BMR/RMR + TEF + TEA + NEAT/SPA). This is why people on low-carb diets can eat more and still lose weight. The Energy Balance Equation still applies.


2) I've noticed that people conflate Food Tastiness with Food Reward. Here's my opinion:-

Excessive reward = Moreish. What your food tastes like is only vaguely relevant. Avoid eating moreish foods, unless you're a body-builder who's trying to bulk.

Here's what I wrote on Food Reward: “There’s Always Room For Dessert”:-
"I believe that obesity is physiological AND neurological (the proportions varying from person to person).

For example, one chocolate doesn’t disturb my blood glucose & insulin, but I still crave another. And another. Ad nauseam."

Physiological cravings take hours to kick-in.
Neurological cravings take seconds to kick-in.

Emily Deans wrote:-
"Multiple times I’ve used naltrexone (an opiate blocker) to stop binge eating. The cravings go away. It only takes a few weeks. It’s a nice way to undo addiction/reward without starving someone… not FDA approved."

That's pretty damning evidence for the existence of Food Reward. How can naltrexone block something that doesn't exist?

Finally Monsieur, a waffer-thin mint.

Bias.

All lies and jest. Still, a man hears what he wants to hear and disregards the rest. Here's a lovely song by Simon & Garfunkel.



I watched the Paranoia video from my last post a few times and I couldn't help but notice how balanced it was. The Labour party (Roy Jenkins) was praised, the Conservative party (Margaret Thatcher) was praised and capitalists (Rupert Murdoch) were praised. Nixon's politics were never mentioned. He was simply power-mad. The more power/influence/money that someone has, the more they have to lose and therefore the more distrustful & paranoid they become.

Since the Hutton Inquiry, the BBC has bent over backwards to appear balanced and impartial. There's probably still bias in it, but I can't see it. That's because I'm biased!

I see a lot of Confirmation bias. There are various theories out there which try to explain the recent huge rise in rates of obesity and morbid obesity, as these conditions are occurring in ever-younger people. Morbid obesity in childhood is a disaster, as it leads to fat mass hyperplasia, (rather than fat mass hypertrophy), which leads to hypoleptinaemia when significant fat mass is lost and a lifetime of low metabolic rate & excessive hunger.

There's Taubes' (Wrong) Insulin & Carbohydrate Theory Of Obesity, which makes the acronym TWICHOO.

There's Guyenet's Food Reward Theory Of Obesity, which doesn't make an acronym.

There are opposing camps of people who believe that one theory is right and the other is wrong, and they cherry-pick evidence to "prove" it. However, the two theories are not mutually exclusive. I believe that refined carbohydrates (and thus insulin) have a large influence on fat mass in people with poor blood glucose control, due to roller-coaster blood glucose & insulin levels causing lethargy and subsequent overeating. I believe that food reward has a large influence on fat mass, due to it causing overeating.

That's why I'm in favour of REAL food diets, as they reduce both blood glucose & insulin fluctuations and food reward. Please note that reward is not the same thing as deliciousness. Fries/chips aren't delicious but they are moreish. Real foods can be delicious without being moreish.

Insulin Resistance and brain health

Watching my Dad's dementia, brain health is becoming a real interest.  Here is a study which shows that reduced insulin sensitivity is linked to smaller brain size and deteriorated language skills in the elderly. 

"We found that in elderly whose insulin sensitivity was still high, the brains were larger, and they had more grey matter in regions that are important for language skills, compared with those who had diminished insulin sensitivity. We also observed that higher insulin sensitivity was associated with better scores on the language test. Our findings offer a possible explanation for why methods that improve insulin sensitivity, such as exercise, are promising strategies for counteracting cognitive aging late in life," says Christian Benedict.

Of course insulin resistance is complex - not just about eating too many carbs - and Stephan's series is a great outline of the issues.  Again, environment, genetics, gut flora are all kicking around but a real food diet, rest, exercise and reducing stress all help keep you sensitive to insulin.

What I believe and what I don't.

First, some soothing music...


I've been getting into arguments on the Internet again! People assume that I believe certain things and "put words in my mouth". As we all know, assume makes an ass out of u and me. I am therefore "laying my cards on the table", so that you have no excuse for being ignorant.

I believe that human beings are extremely complicated creatures both physiologically and psychologically. Our weights are influenced by a humongous number of factors, some of which I will list below.


Physiology

Calories count (but don't bother counting them)! If we eat more than we use, we store the excess in fat mass and muscle mass. If we eat less than we use, we draw the deficit from fat mass and muscle mass. Insulin is involved in the storage of stuff, as is acylation stimulating protein (ASP).

Moving too little makes our skeletal muscle insulin resistant, as inactive muscles have virtually zero requirement for glucose and fatty acids, so down-regulate the uptake of them. See also The effects of high-intensity intermittent exercise training on fat loss and fasting insulin levels of young women.

Eating too much and moving too little has sweet-F/A to do with gluttony and sloth.

Our weights are regulated by our brains, which are influenced by a large number of hormones & chemicals, including insulin. There is no "set point" weight.

In the winter, when it's cold and dark, we eat more, sleep more and move less so we gain body fat. Subcutaneous fat acts as heat insulation, so having more of it in the winter makes sense.

Our weights can be affected by water balance, which is controlled by our kidneys.

How much of a particular food we eat is influenced by reward. Some foods can be addictive (or moreish, as we say in the UK) due to excessive reward. Deliciousness and moreishness are not the same thing. Reward theory and set-point theory are not the same thing.

Rapidly-falling blood glucose level in the normal range can stimulate appetite. I have had personal experience of this on three occasions where my blood glucose level was being monitored. As eating a load of high-glycaemic carbohydrates can result in rapidly-falling blood glucose later, this is another good reason to not overeat refined carbohydrates.


Psychology

The exercise paradox. Exercise decreases appetite*. So, why do some people eat more when they exercise more? See Normal Weight Men and Women Overestimate Energy Expenditure – Research Review and Discrepancy between self-reported and actual caloric intake and exercise in obese subjects.

*If exercise increases your appetite, there may be a reason for this. See Move More: Solutions to problems.

The diet paradox. People think that eating a healthy food with an unhealthy food reduces the calories, discussed in detail in The Dieter’s Paradox – Research Review.

Manipulating the masses is easier than you think.

The Coolidge Effect applies to food as well as sex. Eating one food for every meal gradually reduces reward to zero, no matter how moreish it may be initially. This is how the Potato diet worked.


I often leave very concise comments on blogs. Just because I don't mention this, that or the other doesn't mean that I consider this, that or the other to be irrelevant. I can also go on a bit. I'm a nerd!

EDIT: If I disagree with your point of view, I may try to tease more information out of you (or I may tease you just for fun). The more I disagree with your point of view, the more I'll tease you. If I utterly abhor something you stand for, I will tease you mercilessly!

Reasons to get moving...

First, a music video. What else but...?


Part 1. Get slimmer.
Insulin increases the amount of nutrients entering adipocytes, which makes us fat and hungry.

Er, just a minute!

If increasing the amount of nutrients entering cells makes us hungry, exercise (which increases the amount of nutrients entering muscle cells) would make us hungry. It doesn't. See Fig. 1. in Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.

If going for a walk outdoors makes you hungry, you're doing it wrong. Wrap up warm, as feeling cold increases hunger. Low blood glucose level also increases hunger, so don't over-exercise while on a long-term ketogenic diet.

By the way, insulin also increases the amount of nutrients entering muscle cells.
Q. What determines the relative amounts of nutrients entering adipocytes vs muscle cells?
A. The relative insulin sensitivities of adipocytes vs muscle cells.

Adipocytes are sensitive to insulin until they become full. To reduce the amount of nutrients entering adipocytes, divert more nutrients to muscle cells by increasing their insulin sensitivity. Emptying muscle cells by doing low-intensity exercise increases their insulin sensitivity. High-intensity exercise increases their insulin sensitivity.


Part 2. Prevent/reverse age-related sarcopenia (muscle loss).
See Use 'em or lose 'em. As diverting more nutrients to muscle cells increases muscle mass, increasing their insulin sensitivity results in increased muscle mass, unless you're eating way below maintenance calories. High-intensity exercise results in more muscle mass gain than low-intensity exercise.


Part 3. Make your brain work properly.
Thanks to Chris Highcock, who gave me a complimentary copy of Hillfit, I found IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition.

In plain English, this means that exercise increases both insulin and leptin sensitivity in the hypothalamus. As the hypothalamus controls appetite and both insulin & leptin are appetite-suppressing, the net result is less appetite.

Exercise and insulin sensitivity: both hard AND easy training.......

We've had material up here before on the way in which exercise can promote insulin sensitivity - even brief intense exercise.

I spotted this new study that highlights that both endurance and resistance training can have an impact, but on different elements of that sensitivity:

Insulin Sensitivity After Maximal and Endurance Resistance Training

Maximum Resistance Training (MRT) led to a greater increase in glucose uptake capacity (in muscles), whereas Endurance Resistance Training (ERT) led to greater insulin sensitivity, supporting the recommendation of both MRT and ERT as primary intervention approaches for individuals at a risk of developing type 2 diabetes.

It is something that I point to in Hillfit - intense exercise to failure that can tap into all the muscle fibres - slow, intermediate and fast twitch - lets you drain them of glucose in a way in which endurance exercise does not allow....and endurance exercise does have some benefits.

Actually it is pretty much similar to what Mark Sisson has been saying for a while:

• Lift Heavy things
• Move around alot at a slow pace

Or indeed, Clarence Bass "barbell" strategy - 

 I do a combination of high-intensity intervals and low-intensity walking—and very little of the moderate-intensity aerobics that most people do. I call this my barbell aerobics strategy because, like a barbell, it uses both ends of the intensity spectrum—with almost nothing in between. 

which is also of course Nassim Taleb's approach