Low-carbohydrate diets: Green flags and Red flags.

Fun with flags. But first, a poem!
Atkins Antidote
 
Eating low carbohydrate what threat that poses?
Do my friends think I’m suffering from halitosis?
I’ve got these sticks for measuring ketoacidosis
I’m taking supplements but I don’t know what the dose is

I’m trying hard to keep in a state of ketosis
I’m not sure what the right amount of weight to lose is
I’m sure I’ve put on a pound just through osmosis
Is eating this way risking osteoporosis?

Are my kidneys wrestling with metabolic acidosis?
My store of liver glycogen I don’t know how low is
Who knows what the glycemic load of oats is?
Does anyone know if I can eat samosas?

Ian Turnbull (whose poetry is better than his science!)

I do. The answer's "No!" :-D

From https://forum.nationstates.net/viewtopic.php?f=23&t=13567&start=8925

The Green flags... 

1. For a person with Insulin Resistance, an ad-libitum low-carb diet results in more weight loss than an ad-libitum high-carb diet.

See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes , for an explanation.

2. For a person with Type 1 Diabetes Mellitus (T1DM), a lowish-slowish-carb (~150g/day) diet results in minimal disturbances to blood glucose levels and minimal bolus insulin doses.

See Diabetes: which are the safest carbohydrates? , to see which foods should comprise the ~150g/day.

3. For a person with LADA or MODY, see 2.

4. For a person with Type 2 Diabetes Mellitus (T2DM), a LCLF 600kcal/day Protein Sparing Modified Fast can normalise BG in 1 week and reverse T2DM in 8 weeks (provided there are sufficient surviving pancreatic beta-cells). See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/
"After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003)." and
"Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2)."

After 8 weeks, the diet is gradually changed to a healthy balanced diet containing carbs.

See also https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)33102-1/fulltext and Roy Taylor - Reversing the irreversible: Type 2 diabetes and you. 4th Oct 2014

Compare the above results with the inferior results obtained in A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, which is 10 weeks of VLCVHF Nutritional Ketosis.


As Insulin Resistance is multi-factorial, ALL of the potential causes need to be addressed. Once this has been done, IR should be reversed, allowing restrictions on dietary carbohydrate intake to be lifted. See also Can supplements & exercise cure Type 2 diabetes?

The Red flags...

The low-carb diet is a temporary patch to ameliorate the symptoms of IR/IGT/Met Syn/T2D, a bit like replacing a blown fuse by sticking a nail in its place, to allow the house to function while you fix the problem by fitting a new fuse. Although a house functions with a nail instead of a fuse, it's not a good idea to spend the rest of your life without a fuse to protect the house from fire in the event of a short-circuit.

So, why do LCHF'ers want to spend the rest of their lives using a temporary patch to ameliorate the symptoms of their IR/IGT/Met Syn/T2D?

Long-term use of very-low-carb, very-high-fat, low protein diets (a.k.a. Nutritional Ketosis) is not recommended.

1. Cortisol and adrenaline levels increase due to insufficient glucose production from dietary protein, resulting in gradually-increasing fasting BG level. See How eating sugar & starch can lower your insulin needs and Survival of the Smartest (part 2) - Dr Diana Schwarzbein.

2. If you do too much high-intensity exercise, you may momentarily black-out, fall and hurt yourself. See "Funny turns": What they aren't and what they might be.

3. Insulin Resistance is bad and should be reversed, if at all possible. See Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

4. T2D causes carbohydrate intolerance and fat intolerance, resulting in high postprandial BG and high postprandial TG. See Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity.

5. Dyseverythingaemia isn't fixed. See When the only tool in the box is a hammer.

6. High-fat diets with no energy deficit result in high postprandial TG & high LDL-c. Postprandial lipaemia & high LDL-c are atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

7. Permanently-high NEFA (a.k.a. FFA). See Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, very-low-carbohydrate diet.

This raises the RR for Sudden Cardiac Death.

This also depletes beta cells causing loss of the 1st phase insulin response. See Chronic Exposure to Free Fatty Acid Reduces Pancreatic b Cell Insulin Content by Increasing Basal Insulin Secretion That Is Not Compensated For by a Corresponding Increase in Proinsulin Biosynthesis Translation.

Loss of the 1st phase insulin response causes Impaired Glucose Tolerance (IGT). See β-Cell dysfunction vs insulin resistance in type 2 diabetes: the eternal “chicken and egg” question

IGT causes high postprandial blood glucose after eating incidental carbohydrates. This is Metabolic Inflexibility, which isn't good.

8. Natural selection increases the incidence of a genetic impairment in the Inuit which reduces ketosis, inferring that reduced ketosis is an evolutionary advantage. Watch Inuit genetics show us why evolution does not want us in constant ketosis.

That's all for now.

Ketogenic Diets and Sudden Cardiac Death.

Last night, thanks to comments on my previous post, I stumbled across The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism, then a Google search led me to Sudden Cardiac Death and Free Fatty Acids.

The following graph is Figure 1 from Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet.

Nice Insulin, shame about the FFAs.

From the first link above:-
"Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins."

From the third link above:-
"Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs."

See also Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography, and Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population.

I think that's quite enough bad news for a Friday afternoon.


EDIT: So much for fat being a "clean-burning" fuel for the heart. Some people believe that, because dietary fats pass from the small intestine, via the Lacteals, to circulation at the Subclavian vein, this means that the heart prefers to burn fatty acids.

From Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD:-

Human erythrocytes (red blood cells) contain cholesterol and it can contribute towards atherosclerosis. See https://twitter.com/Drlipid/status/496625195738619904.

See also Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects. This is more evidence that very high fat meals are atherogenic, which is relevant to Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

Why do some people have trouble doing things in moderation?

This is related to my previous post.

From http://www.kindredcommunity.com/2013/01/xtreme-eating-awards-2013-extremism-running-amok-at-americas-restaurant-chains/

Some people take low-carbing to an extreme, 'cos if reducing carbohydrate intake has benefits, reducing it to zero must be better. Oy!


We're told that eating 5 portions of fruit and vegetables a day is good for us. One patient who was admitted to St George's with malnutrition, had been eating more than 50 portions of fruit and vegetables a day, 'cos if 5 portions of fruit and vegetables a day is good for us, 50 portions of fruit and vegetables a day must be better. Oy!


People who are taking the anti-clotting medication Warfarin need to maintain an accurate balance between their warfarin dose and their Vitamin K intake to keep their INR between 2 and 3, as warfarin antagonizes vitamin K₁ recycling, depleting active vitamin K₁.
"Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice. Data establishing a causal relationship is still lacking, and a 2006 review found no cases of this interaction reported to the FDA; nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility. The mechanism behind the interaction is still unclear." Here's a clue...

From Possible interaction between warfarin and cranberry juice (emphasis, mine):-
"After a chest infection (treated with cefalexin), a man in his 70s had a poor appetite for two weeks and ate next to nothing, taking only cranberry juice as well as his regular drugs (digoxin, phenytoin, and Warfarin). Six weeks after starting cranberry juice he had been admitted to hospital with an INR (international normalised ratio) > 50. Before, his control of INR had been stable. He died of a gastrointestinal and pericardial haemorrhage. He had not taken any over the counter preparations or herbal medicines, and he had been taking his drugs correctly." Cranberry juice contains no Vitamin K. Oy!

"The Committee on Safety of Medicines has received seven other reports through the yellow card reporting scheme about a possible interaction between warfarin and cranberry juice leading to changes in INR or bleeding. In four cases, the increase in INR or bleeding after patients had drunk cranberry juice was less dramatic. In two cases, INR was generally unstable, and in another case INR decreased. Limited information is available about whether patients complied with their treatment in these cases.

Cranberry juice (Vaccinium macrocarpon) is popular and is also used to prevent cystitis. Interaction with warfarin is biologically plausible, because cranberry juice contains antioxidants, including flavonoids, which are known to inhibit cytochrome P450 enzymes, and warfarin is predominantly metabolised by P450 CYP2C9. The constituents of different brands of cranberry juice may vary, and this might affect their potential for interacting with drugs. Whether the constituents of cranberry juice inhibit CYP2C9 and therefore the metabolism of warfarin or interact in another way needs further investigation. Until then, patients taking warfarin would be prudent to limit their intake of this drink." Oy!

So, one man's inadvertent (his doctor should have warned him about eating next to nothing while taking warfarin) dietary extremism resulted in his own death and the restricted intake of cranberry juice for everybody else taking warfarin. Oy. :-(


P.S. It's about time an alternative to warfarin was found. It's difficult to maintain an accurate balance between warfarin dose and Vitamin K intake.

Jumping through hoops, and my Blog List.

I'm seeing a curious thing. The VLC "camp" seems to be "jumping through hoops" to prove a point.

From http://davidbressler.com/2013/08/26/easier-harder/

From Neuron fuel and function (emphasis & formatting, mine):-
"Ketones and lactate do not drive reverse electron flow through complex I. Glucose can. Palmitate certainly can. What you want from a metabolic fuel depends on the remit of your cell types. Neurons within the brain preserve information by their continued existence.

This is best done by burning lactate or ketones. NOT glucose and, of course, not FFAs.

Anyone who claims that glucose is the preferred metabolic fuel of the brain has not though (sic) about what a neuron has to do and what an astrocyte actually does do. Or much about the electron transport chain."

Basically, glucose is bad mmm-kay. Also, anyone who claims that glucose is the preferred metabolic fuel of the brain is a dumb-ass. Damn our livers & kidneys churning out glucose! Are they trying to kill us?

∴ Carbohydrates are bad and must be avoided at all cost! This, of course, is utter nonsense.

Glucose can drive reverse electron flow through complex I. Can means that it's possible. Is it probable?

On a hypercaloric Western diet of excessive crap-in-a-bag/box/bottle, yes.

On a Kitavan diet of ~70%E from tubers, no.

On a diet of Basmati rice & beans, no.

On a diet of whole fruits, no.

See also Another crash and burn on low carb paleo and CrossFit. Enough of the 'carbs are evil' nonsense. Carbphobia is hurting a lot of people.

I have a list of blogs that I read on a regular basis. As a result of the bad science & cherry-picking displayed in various VLC blogs, I have deleted them from my Blog List.

See also Guest post: Denialism as Pseudoscientific Thinking.

Defending the indefensible: Gary Taubes and *that* statement about gluttony.

Here's another "video" (it has sound and static images only). As I haven't learned how to embed a YouTube video that starts at a specific time, here's a link to it and a picture of it:- Gary Taubes' "Why We Get Fat" IMS Lecture On August 12, 2010 (Part 8 of 8), starting at 8 minutes and 13 seconds in.

To quote: "You can basically exercise as much gluttony as you want, as long as you're eating fat and protein."

Itsthewoo told me that Taubes was being ironic i.e. he was joking. I call bull-shit on that, for the following reasons.

1) You don't joke about something as important as diet, in a video that's likely to be heard by many people.

2) If you are foolish enough to joke about something as important as diet, you make 100% certain that listeners know that you're joking, by stating in the very next sentence that the preceding sentence was a joke. Taubes didn't do that.

3) I didn't hear chortling or any other audible clue that Taubes was joking. Did you?

I therefore conclude that itsthewoo is hearing (and seeing) the world through "cognitive bias" Weird Filters , resulting in her hearing what she wants to hear. Sorry!

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.

Ketogenic diets - when they're not ketogenic.

High in the Arctic, Eskimo!

It's generally assumed that eating less than 50g/day of carbohydrate results in ketosis. Assume makes an ass out of "u" and "me". From Lyle McDonald's book The Ketogenic Diet:-

The Ketogenic Ratio (KR) = K/AK, where K = Ketogenic stuff and AK = Anti-ketogenic stuff.

K/AK =  (0.9*Fat + 0.46*Protein)/(1.0*Carbohydrate + 0.1*Fat + 0.58*Protein) where Fat, Protein & Carbohydrate are in grams.

For the treatment of epilepsy (very strongly ketogenic), K/AK must be greater than 1.5. For people who want to get into benign dietary ketosis, K/AK can be lower.

Eskimos eat a diet containing virtually zero dietary carbohydrate (~50g/day as muscle & liver glycogen). However, they are not in ketosis. See STUDIES ON THE METABOLISM OF ESKIMOS.

Eskimos eat so much protein that the Anti-ketogenic effect of Protein offsets the Ketogenic effect of Fat + Protein. Table IV is interesting, as it shows how much energy is lost as ketones on the third day of successive fasts in non-Eskimos (Subject #1 fasted once only). Note:- Beta-hydroxybutyric acid  produces 5kcals/g.

Subject #1:- 10.5kcals. ?kcals, ?kcals.
Subject #2:- 100.5kcals, 7.0kcals, 2.75kcals.
Subject #3:-  9.75kcals, 0.0kcals, 0.0kcals.

The answer is "not a lot" (except for Subject #2 on the first fast).

Continued on Ketogenic diets - when they're not ketogenic, Part 2.

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 like 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.

*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!).

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.

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.

Everyone is Different, Part 2.

Cont'd from We are not all the same.

A long, long time ago...


I learned that Everyone is Different, thanks to a study by Julia H. Goedecke, Alan St Clair Gibson, Liesl Grobler, Malcolm Collins, Timothy D. Noakes and Estelle V. Lambert.

Well, stone the flamin' crows! Timothy D. Noakes' name just popped up in Alan Aragon's article 2013 NSCA Personal Trainers Conference: Looking Back at my Debate with Dr. Jeff Volek. Dr. Noakes has had problems with his blood glucose level and has adopted a very-low-carb/ketogenic diet.

What also caught my eye in Alan Aragon's article was (Note: TTE = Time To Exhaustion):-
"However, the authors’ conclusion is misleading since 2 of the 5 subjects experienced substantial drops in endurance capacity (48 and 51-minute declines in TTE, to be exact). One of the subjects had a freakishly high 84-minute increase in TTE, while the other increases were 3 and 30 minutes."

I expect that the subjects with 84 and 30 minute increases in TTE would be praising ketogenic diets, whereas the subjects with 48 and 51 minute declines in TTE would be cursing them and the subject with 3 minutes increase would be "Meh". Vive la difference!

Also note that sprint capability...remained constrained during the period of carbohydrate restriction. As mentioned in It's all in a day's work (as measured in Joules), exercise above a certain intensity (~85%VO2max) burns significant amounts of carbs, no matter how fat-adapted someone is.

Cont'd on Everyone is Different, Part 3.

Not exactly rocket science, is it?

If Paul (astrophysicist) Jaminet met Jack (neurosurgeon) Kruse ;-)

The paleo diet was recently ridiculed as a food fad in Natural’s Not In It. It also came last in a US News Best Diets survey.

Ways of eating such as very-low-carbohydrate, low-carbohydrate, low-reward, paleo, primal, ancestral, just eat real food etc discourage the consumption of manufactured food products and encourage the consumption of produce. If a large percentage of the population stop filling their shopping baskets with manufactured food products and start filling them with produce, who suffers? Not exactly...

This is why the food manufacturing industry tries to ensure that the population gets the best nutritional and dietetic advice that money can buy. See also New study: Big Food’s ties to Registered Dietitians.

While libertarians and anarchists moan about freedom from government interference, the food manufacturing industry has the freedom to crap all over the aforementioned diets and influence people to buy manufactured food products. Morbidity is also very profitable for healthcare and drug companies.

I think that I've now flogged this particular horse to death!

A comment, a simile and insanity.

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 roller-coaster blood glucose levels after eating high-glycaemic carbohydrates. A rapidly-falling blood glucose level causes 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!

Overeating 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.


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!

Look after your brain, Part 5.

This is another bookmarking post.

I spotted an article by Emily Deans M.D. called Nutritional Brain Bomb - Thiamine Deficiency.

So there's yet another way to knacker the brain, resulting in Wernicke's encephalopathy and in severe cases, Korsakoff's psychosis. Both of these conditions are partially irreversible due to neuron death. Both of these conditions are partially reversible by high-dose thiamine therapy.

Thiamine 500mg/day is one last therapy to try mum on after I've got her back on Vitamin K2 (hopefully today).

Continued on Quality >> Quantity.

New beginnings, cot'd.

As a result of New beginnings. , I've demolished my wall and I now want to start a new relationship. I've got a lot of love to give and I want to find that special lady to give it to. Here's the ideal music video.


I won't be blogging so much in future.

P.S. Mum had a Mini Mental State Examination today. She got a score of 12 (out of 28 things that she was physically capable of). 6 months ago, she got a score of 9 (out of 27 things that she was physically capable of). Ketogenic Diet For The Win.

She'll be tested again next year. I found out on Wednesday 23rd March that she is being given 5,000iu/day of D3. I didn't expect that to happen.

Mum's Proposed Ketogenic Diet for Dementia.

The following diet is not intended to induce deep ketosis. It's intended to be a trade-off between ketosis, palatability & simplicity.



Feedback from the nurse on duty:- "Eggs shouldn't be in the "unlimited" list. You're not supposed to eat more than two eggs a week because of the cholesterol". God Bless the NHS! The British Heart Foundation doesn't impose a restriction on egg consumption.

Eggs can be eaten as part of a balanced diet.

Mum's currently eating two eggs a day in her cooked breakfasts.

Effect of dietary egg on human serum cholesterol and triglycerides.

Old people have the lowest mortality when their serum cholesterol is higher than average.

Total cholesterol and risk of mortality in the oldest old.
Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study.
Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging.
Higher total serum cholesterol levels are associated with less severe strokes and lower all-cause mortality: ten-year follow-up of ischemic strokes in the Copenhagen Stroke Study.
Serum total cholesterol levels and all-cause mortality in a home-dwelling elderly population: a six-year follow-up.
Lipid-lowering treatment to the end? A review of observational studies and RCTs on cholesterol and mortality in 80+-year olds.

Paul Jaminet has done a series on ketogenic diets.
Ketogenic Diets, I: Ways to Make a Diet Ketogenic
Ketogenic Diets 2: Preventing Muscle and Bone Loss on Ketogenic Diets

Also: See Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.

Polite Requests.

I delivered a large wad (0.25"/6mm thick) of studies with a covering letter to my mum's new GP on Monday 17th Jan 2011. Here's what I wrote in the covering letter:- Personal information deleted.

"Dear Sir/Madam,

I have some requests concerning Mrs *****.

1) Please monitor Mrs *****’s serum B12 & homocysteine. Until Jan 31st 2010, Mrs ***** was receiving 1,000ug/day methyl B12. This was stopped by the management of Lashbrook House after I complained too much. Long-term use of PPIs in old people can adversely affect B12 absorption (evidence attached).

2) Please advise the staff at Acacia Lodge to walk Mrs ***** using the 3-wheeled rollator that I bought for her as often as she is able. Prolonged inactivity results in Insulin Resistance (IR) in skeletal muscle (evidence attached). IR results in hyperinsulinaemia on eating sugars & starches. Hyperinsulinaemia results in drowsiness and stupor (which makes it more difficult for Mrs ***** to do anything).

3) Please advise the staff at Acacia Lodge to reduce Mrs *****’s intake of sugars & starches. A low-carbohydrate/ketogenic diet is beneficial for people with impaired cognitive function (evidence attached). I have recently persuaded Acacia Lodge to give Mrs ***** cooked breakfasts and have supplied Acacia Lodge with Burgen Soya & Linseed bread (12g carbs/slice). This has resulted in improved cognitive function in the mornings.

I don’t want to impair Mrs *****’s quality of life, so she can still have chips or mashed potato (not both in the same meal as happened on Fri 10th Jan, after which I found Mrs ***** asleep in her wheelchair slumped over with her nose squashed against the arm of the chair). She can also have desserts and the occasional chocolate and/or biscuit.

4) Please allow Mrs ***** to have 5,000iu/day Vitamin D3 (provided by me), as UVB cannot penetrate window glass. 5,000iu/day is much greater than the RDA of 600iu/day but it’s a safe amount (evidence attached). That amount of Vitamin D3 has many beneficial effects (rather a lot of evidence attached!) other than bone health (for which 600iu/day is sufficient).

Thank you,

Nigel Kinbrum (son & attorney)
01252 ****** (24-hr Ansafone)
07768 ******"

The GP phoned me on Friday 21st Jan. He's taking my requests seriously and has asked for a week to read all of the evidence that I provided. Here's hoping!

We are not all the same.

Cont'd from Everyone is Different.

Lyle (McDonald) brought the following study to my attention to illustrate that "We are not all the same":- Some Metabolic Changes Induced by Low Carbohydrate Diets. On a very-low-carb diet, one subject’s total cholesterol rose to 12.9mmol/L (500mg/dL in US units). The others didn't.
See also LDL cholesterol goes sky high on fatty diet.

I posted the study in various blogs to make the above point. Here are some of the replies I got:-
"Lyle? Lyle McDonald? Is that where you got that study, Nigel?" and... "I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job."
"That was a weird study (1967) what I could make of it." and... "The men did all the stages but the women only did 3 stages of the diet."
"The fats were mostly omega-6 PUFA 13-35 grams worth..."
"The report you cite is so old and out of date that it makes me cry..."

My point was well & truly missed. I got the distinct impression that people thought I was criticising very-low-carb, high-fat diets. I wasn't. The simple fact is that there is no "One True Diet" that suits absolutely everybody. In the olden days everywhere & in poor countries nowadays, people that ate/eat the wrong diet for their body died/die young. Nowadays in rich countries, they get put on drugs e.g. oral hypoglycaemics (to lower blood glucose) & hypolipidaemics (to lower blood cholesterol/triglycerides).

Please note that omega-6 PUFAs tend to lower serum cholesterol rather than raise it, as per Figure. 1 below from Individual fatty acid effects on plasma lipids and lipoproteins: human studies.

However, don't rush off and eat shed-loads of omega-6 PUFA (e.g. corn oil) in the mistaken belief that it will make you live any longer.

Cont'd on Everyone is Different, Part 2.

Look after your brain, Part 4.

Ketogenic Diet REALLY WORKS!!!
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.

The above popped-up when I Googled for "ketogenic diet" alzheimer's.

See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.

EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.

It's mum's 80th Birthday today so I'm off to see her now.

Continued on Look after your brain, Part 5.

Everybody knows.........Part 2

.........that ketogenic diets like the Atkins diet destroy your kidneys and rot your bones, right? Wrong!
.........that the Atkins diet causes ketoacidosis which is a very dangerous condition requiring urgent hospital treatment, right? Wrong!

There's a lot of nonsense spoken about ketogenic diets by people who really should know better. I suspect that they have been taught wrongly at uni or med school as per the quote in Everybody knows.........Part 1.

Benign Dietary Ketosis is NOT Ketoacidosis.

Consider the following four cases:- Note: Figures are from "Introduction to Nutrition and Metabolism" By David A Bender (Senior Lecturer in Biochemistry, UCL)

1) Healthy human, fed state: Glycogen stores are replete. Serum glucose = ~5.5mmol/L. Serum fatty acids = ~0.3mmol/L. Serum ketones = 0mmol/L. No gluconeogenesis is taking place. Amino acid pool is replete. Cortisol level is normal so there is no loss of muscle mass.

2) Healthy human, fasting for 7 days: Glycogen stores are depleted. Serum glucose falls to ~3.5mmol/L. Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is depleted. Cortisol level is high, causing slow loss of muscle mass. This is bad ketosis.

3) Healthy human, low-carbohydrate diet: Glycogen stores are depleted. Serum glucose falls to ~5mmol/L.
Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is replete (due to protein intake). Cortisol level is normal so there is no loss of muscle mass. This is good ketosis.

4) Human with untreated type 1 diabetes: Glycogen stores are depleted. Due to lack of insulin, the Glu-T4 transporters in cells cannot move to the surface so glucose cannot enter cells. Serum glucose = >20mmol/L. This causes major damage to kidneys, arteries, eyes, nerves etc by cross-linking with proteins (glycation) resulting in major disability and eventual death. As the body is forced to run on fatty acids & ketones, metabolic processes are out of control and ketones rise to much higher levels than in 2) or 3) (I don't know how high exactly) resulting in acidosis and eventual death. This is ketoacidosis.

Conclusion: Low-carbohydrate, very-low-carbohydrate & ketogenic dieting is similar to fasting in that serum glucose levels are lower than normal and glycogen stores are depleted. The body is encouraged to burn less glucose and more fatty acids & ketones, but the metabolic processes are all under control. The big difference between low-carbohydrate dieting and fasting is in the amino acid pool and cortisol levels.