Science and zealots: How to detect bad science and how to detect zealots.

Last night, I got banned from Zoë Harcombe's blog. More on that later. Meanwhile, this...

From http://capisho.blogspot.co.uk/2013/07/science-vs-faith.html

I re-read It's all about ME, baby! (1997 - present) and there's something important missing.

In 2005, I discovered Lyle McDonald. Before this happened, I had the following beliefs:-
1. If something works for me, it must work for everyone else.
2. If someone with qualifications states a fact, it must be true.
3. If someone without qualifications states a fact, it must be false.
4. If a study confirms my beliefs, it must be true.
5. If a study contradicts my beliefs, it must be false.

Sound familiar?
1. is a "Hasty generalisation" fallacy.
2. is an "Appeal to authority" fallacy.
3. is an "Ad hominem" fallacy.
4. & 5. are a "Cherry-picking" fallacy.

Suffice it to say, Lyle bitch-slapped the fallacies out of me. Thank you so much! Read Lyle's site, if you want to learn.

How can studies conflict with each other so much?

Having read a number of conflicting studies, here are some of the tricks that bad studies use:-

1. Fudge the methodology:-
In a meta-study (a study of studies), to make something that's bad (e.g. some saturated fats/fatty acids) look harmless or to make something that's good (e.g. Vitamin D) look useless, fudge the inclusion criteria so that only studies using low intakes or a narrow range of intakes are used, so that the RRs are either close to 1 or have 95% CI values above & below 1. In addition, include studies that show both positive and negative effects (due to them looking at different types of saturated fats/fatty acids, say), so that the overall result is null.

In a study, use a different type of the thing being studied (but bury this fact somewhere obscure so that it's easily missed) to get the opposite result. E.g. To make "carbs" look bad, use a test "carb" that comprises 50% simple carbs (sugars) and 50% complex carbs (high-GI starches, preferably), thus guaranteeing a bad result.

2. Fudge the statistics:- e.g. Regression toward the mean. I'm not a stats nerd, but there are many ways to lie with statistics.

3. Make the abstract have a different conclusion from the full study (which you hide behind a pay-wall), by excluding the methodology and results.


Back to Zoë Harcombe: I left some comments on Jennifer Elliott vs Dietitians Association of Australia.

My M.O. for detecting zealots is by using a slowly, slowly, catchee monkey approach. I left a comment supportive of low-carb diets, because:-

For people with Insulin Resistance, low-carb diets DO ameliorate obesity, postprandial sleepiness and postprandial hyperglycaemia.

Was that loud enough?

I added that I thought the first priority should be to tackle the causes of the Insulin Resistance, because reversing a condition is better than ameliorating it.

My comments were helpful, with links to blog posts showing the above and how to reverse T2DM in 8 weeks. I then went for the throat, criticising Jennifer Elliot, as the article she wrote contained cherry-picked references. I included three more links to my blog as supportive evidence. This resulted in the removal of all but one of my comments (and the comment that remained had the link removed) and the addition of the following:-

"Zoë Harcombe says:

October 23, 2015 at 8:55 pm

Nigel – too many comments purely trying to get traffic to your site – link above removed; other comments spammed. You’re now spammed.
Best wishes – Zoe"

The correct word is "banned", Zoë! Low-carb zealot successfully detected.

It's not a problem if a lay person becomes a low-carb zealot, but it is a problem if a Health Professional/Fitness Trainer becomes one. Cognitive bias and a refusal to accept contradictory evidence are not good traits for someone who's supposed to be practising evidence-based health/fitness.

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

See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people get more weight loss on low-carbohydrate diets than on high-carbohydrate diets, and insulin sensitive people get more weight loss on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes' carbohydrate/insulin hypothesis of obesity was correct, everyone would get more weight loss on low-carbohydrate diets. This isn't the case, therefore Gary Taubes' hypothesis is not correct.

Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies"!

The Aragon Insulin Fairy

The Energy Balance Equation

Change in Bodily Stores = Energy in - Energy out, where... 

Energy in = Energy entering mouth - Energy exiting anus, and... 

Energy out = BMR/RMR + TEF + TEA + SPA/NEAT

See The Energy Balance Equation to find out what the above terms mean.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. Trust me, I'm a retired Electronic Engineer. I've observed this (too) many times!

1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting massive postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Bodily stores increase. There are also accusations of sloth & gluttony!

2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Bodily stores decrease.

In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.

There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587

P.S. In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.

P.P.S. Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions.

P.P.P.S. Insulin Resistance can be fixed in the long-term. See Insulin Resistance: Solutions to problems.

Type 2 Diabetes can be fixed in the long-term. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Aim to fix the problem in the long-term. If a long-term fix isn't possible (due to excessive destruction of pancreatic beta cells), use a low-carbohydrate diet as an adjunct to medication.