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

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

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

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

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

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

3. He plays the Shill Gambit card.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

A *very* special dual-fuel car analogy for the human body that I just invented.

The human body is like a very special dual-fuel car.

From http://www.aa1car.com/library/alternative_fuels.htm

In this very special dual-fuel car:-

Glucose is represented by Ethanol, 'cos Ethanol is a carbohydrate, according to Robert Lustig ;-)
Glucose is C₆H₁₂O₆. Ethanol is C₂H₆O. 3(C₂H₆O) = C₆H₁₈O₃. It's not very close, but it'll do!

Caprylic acid is represented by Octane, 'cos fatty acids are hydrocarbons, don'tcha know? ;-)
Caprylic acid is CH₃(CH₂)₆COOH and Octane is CH₃(CH₂)₆CH₃, which is actually pretty close.

Storage depots:

 

Carbohydrates:

For Ethanol, there's a large storage tank (≡ muscle glycogen) and a small storage tank (≡ liver glycogen). The contents of the large storage tank cannot be used to top-up the small storage tank, but the contents of the small storage tank can be used to top-up the large storage tank. The contents of the small storage tank are used to fuel a generator (≡ Hepatic Glucose Production) to keep the ECU (≡ brain) working at all times. The contents of the large storage tank are used to fuel the engine.

Fats:

For Octane, there's a large storage tank (≡ subcutaneous adipose tissue) and a small storage tank (≡ visceral adipose tissue). The contents of the small storage tank are used to produce hormones etc. The contents of the large storage tank are used to fuel the engine.

Substrate Utilisation:

When the car is driven at low speed, the engine burns mostly Octane (≡ RQ=0.7).
When the car is rapidly accelerating or driven at high speed, the engine burns mostly Ethanol (≡ RQ=1).
When the car is being driven intermediately, the engine burns a mixture of Octane & Ethanol.

Overeating/Undereating:

 

Carbohydrates:

If the large Ethanol storage tank becomes full, excess Ethanol overspills to the small storage tank.
If the small storage tank becomes full, a gizmo kicks-in and converts excess Ethanol into Octane (≡ De-Novo Lipogenesis).
It also shifts fuel usage of the engine towards Ethanol, to deplete Ethanol as quickly as possible.
If the small storage tank becomes full, the car malfunctions (≡ fatty liver).

Conversely, if the small storage tank becomes nearly empty, it shifts fuel usage of the engine towards Octane, to conserve Ethanol.

Fats:

If the large Octane storage tank becomes full, excess Octane overspills to the small storage tank.
If the small storage tank becomes full, the car malfunctions (≡ insulin resistance/metabolic syndrome/type 2 diabetes).

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.