Low-carbohydrate High-fat 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

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-carb (~100g/day), highish fat 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 ~100g/day. N.B. As ~50% of dietary proteins can be converted into glucose by gluconeogenesis, ~100g/day of slow-digesting proteins such as meats, eggs & cheeses can contribute ~50g/day of glucose towards the ~100g/day total.

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 http://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)."

"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, transition to a diet based on whole, minimally-refined animal & vegetable produce.

See also http://www.fend-lectures.org/index.php?menu=view&id=94

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 IR/IGT/Met Syn/T2DM, a bit like replacing a failed circuit-breaker by sticking a nail in its place, to allow the house to function while you fix the problem by buying a new circuit-breaker. Although the house functions fine with a nail in place of a circuit-breaker, you wouldn't want to spend the rest of your life without a working circuit-breaker protecting the house.

So, why do low-carbers seem to want to spend the rest of their lives using a temporary patch to ameliorate their IR/IGT/Met Syn/T2DM?

Long-term use of very-low-carb, very-high-fat diets is not recommended.

1. Cortisol level can gradually increase, resulting in increasing fasting BG level. See How eating sugar & starch can lower your insulin needs.

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. Some people seem to gradually go bat-shit crazy. See Can very-low-carb diets impair your mental faculties? Read the comments in https://www.facebook.com/TheFatEmperor/posts/1633434020253792. Do the behaviours of Ivor Cummins & Gearóid Ó Laoi seem normal to you?

4. Insulin Resistance is bad, mmm-kay? See Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

5. Dyseverything elseaemia isn't addressed. See Type 2 diabetes: between a rock and a hard place , Type 2 diabetes: your good signalling's gonna go bad and When the only tool in the box is a hammer.

6. Dietary deficiencies may develop. See Rigid diets & taking loadsa supplements to compensate for them.

7. High-fat diets with no energy deficit result in high postprandial TG's. Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

There may be more but I'm knackered, so I'm Publishing!

Fun with maths: How many grams of "X" does it take to achieve "Y" mmol/L of "X" in the blood?

There are ≤3 fuels in blood - Glucose, Palmitic acid (FFA) & Beta-HydroxyButyric acid (Ketone body).

From http://www.medbio.info/horn/time%203-4/homeostasis1.htm#Sources%20of%20blood%20glucose:

Taking blood volume as 5L (a petite woman has less):-

5mmol/L of Glucose ≡ 4.5g of Glucose.

1mmol/L of Palmitic acid ≡ 1.28g of Palmitic acid.

6mmol/L of Beta-HydroxyButyric acid ≡ 3.12g of Beta-HydroxyButyric acid.

Instead of going on a ketogenic diet (with all of the health hazards associated with it), why not just add Beta-HydroxyButyric acid to your drinks?

There's a problem. All metabolic fuels produce an insulin response (from functioning pancreatic beta cells) - this is one of the ways the level of each fuel is regulated in a NFB loop. Therefore, drinking more than 3.12g of BHB (more than 2.76mL) produces a large insulin response, which results in sleepiness. Ditto for GHB.

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:-

Did you know that Human erythrocytes (red blood cells) are loaded with cholesterol and that 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.

Metabolic Inflexibility: What it really means.

Here's a picture from Metabolic Flexibility and Insulin Resistance.

The Metabolically-Inflexible (MI) & Insulin Resistance

Here's another picture.

Fig 2. ● = Metabolically-Flexible (MF). ○ = Metabolically-Inflexible (MI).

Salient points:
1) Excess serum FFA a.k.a. NEFA is bad.
2) Respiratory Quotient (RQ) a.k.a. Respiratory Exchange Ratio (RER) changes due to dietary changes are more sluggish in the MI than in the MF.
3) Under Insulin Clamp conditions, RQ/RER is lower in the MI than in the MF, due to impairment of glucose oxidation and non-oxidative glucose disposal.

I have posted this because of Danny Roddy's post Is Supplemental Magnesium A Surrogate For Thyroid Hormone? , which leads onto A Bioenergetic View of High-Fat Diets.

In the first article, Danny Roddy writes:-
"Additionally, taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient (e.g., high-fat diet, light deficiency, excessive exercise) seems pretty silly. For example, as a rule, diabetics have a reduced respiratory quotient (Simonson DC, et al. 1988), tend to have higher levels of free fatty acids or NEFA (Kahn SE, 2006), and are often deficient in magnesium (De Valk HW, 1999)."

The second sentence (diabetics have a reduced respiratory quotient...and are often deficient in magnesium) seems to contradict the first sentence (...taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient seems pretty silly).

Simonson DC, et al. 1988 is Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin-dependent) diabetic patients.
"In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal."

Impaired glucose oxidation with normal lipid oxidation lowers RQ/RER. Therefore, lower RQ/RER must be bad, right? Wrong. From the above study:-
"...euglycaemic insulin clamp studies were performed..."
Remember Salient point 3)? Simonson DC, et al. 1988 is an insulin clamp study, the results of which don't apply to free-living people (who aren't insulin clamped).

See also Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. RER/RQ increases & decreases with increases & decreases in exercise intensity. This is Metabolic Flexibility (MF). Sorry, Danny.

No fat belly: no rocks and no hard places.

I finally defeated Google Image Search!

 Boo-Ya, Google!

I've been blogging about the problems associated with having a fat belly. It therefore figures that not having a fat belly is advantageous. I was asked whether "skinny-fat" people might have problems with high serum NEFAs when on a very-low-carbohydrate diet (≤50g/day of carbohydrate).

In my opinion, if fat cells in the belly area aren't stretched to the max, they won't be spewing NEFAs into the blood. Therefore, even "skinny-fat" people can safely go on a very-low-carbohydrate diet and stay on it indefinitely.