Saturday, 14 March 2009

He who pays the piper calls the tune.

There’s a new food-police force on the block, trying to stop us from eating real, healthy, natural food. Believe it or not, it’s called The Fat Panel. Here is ‘the clinical evidence’ against saturated fat, according to the website.

It's all right - I'll wait while you take a peek at it...

No, you’re not missing something – there is no evidence there. None at all. And so I asked for the evidence, and received a paper, entitled Saturated fatty acid consumption: outlining the scale of the problem and assessing the solutions, which, I was informed, is “copy write” (sic.) to the British Nutrition Foundation, although the paper’s authors are the eight Panel members

The Panel claims to be independent, but almost the first thing I noticed was the acknowledgement:

“The Fat Panel is supported by an unrestricted educational grant from the Margarine and Spreads Association.”**

Oh that’s all right, then – it’s sure to be a balanced, unbiased review... isn’t it?

Contradictions abound in the paper; contradictions between referenced studies, and between the report itself and current nutritional advice. For example:

Lauric, myristic, and palmitic acid raise serum cholesterol but stearic acid has no effect

The first three are found in coconut or palm oil, and in dairy products, but where do we find stearic acid? In meat fat, dairy products and chocolate ... but aren’t we told not to eat meat fat, and only this week Scottish doctors wanted to tax chocolate!

On page three I found precisely what I expected, under the heading of Saturated fatty acids in the UK diet:

Data from the 1997 and 2000–2001 National Diet and Nutrition Surveys (NDNS) show that adult males, females and children (4–18 years) derive 13.4%, 13.2% and 14.3% of their food energy from SFA, respectively.

Yes, once again those flawed food surveys are relied upon by people claiming to be experts – people who really should know better. But then we must remember who is paying the piper!

It goes on:

The main sources of SFA in the UK diet are milk and milk products, meat and meat products, cereal and cereal products and potatoes and savoury snacks

Now, unlike the authors, I’m no nutritionist, but I have been dieting for a good many years, and reading nutrition tables, and I know of no potatoes that contain fat – saturated or otherwise - and aren’t we now being exhorted to eat more grains?

If grains aren’t cereals, then what on earth are they?

Eventually we get to the supposed links between saturated fats and disease, beginning with some bold statements.

“The UK recommendations for intake of total fat and different fatty acids are based on the evaluation of the scientific evidence relating to risk of cardiovascular disease (CVD).”

“It is well recognised that dietary SFA causes atherosclerosis in animals ...”
“... and that certain SFA raise blood cholesterol levels which are key risk factors for CVD”

Then comes a fascinating sentence,

“The evidence from intervention trials is less convincing but does indicate that replacing SFA with PUFA and cis-MUFA does reduce the risk of cardiovascular events“

“... and there is now convincing evidence that trans fatty acids increase risk of CVD.”

Hallelujah! At last a statement with which I can agree. However, weren’t we urged to eat trans fats just a few short years ago??

Coronary heart disease

Here we have our first inkling of the quality of some of the studies used in the review:

There is good evidence that SFA (C12–C16) increase serum cholesterol levels by raising both LDL- and HDL cholesterol concentrations (Keys 1957).

Good evidence? Good grief! Did you notice who the study was by? None other than Ancel Keys, who started the whole low-fat diet bonanza all on his own, by using just the data that fitted his hypothesis. The data was available for twenty countries, but Keys chose just the seven that ‘proved’ his theory, and the Western world has got fatter and sicker ever since.

SFA intake is positively related to an increase in ...mortality from CHD. (Hu et al. 2001a)

Hu's study opens with an astonishing admission:

It is now increasingly recognized that the low-fat campaign has been based on little scientific evidence and may have caused unintended health consequences.

followed by:

A higher intake of total and saturated fat is widely believed to contribute to the development of CHD.

And the source for that belief? Ancel Keys again!

Hu et al admit the low-fat campaign was based on little scientific evidence, and then cite that same ‘evidence’ to show how unhealthy saturated fats are!

But does the Hu study conclude that SFA intake is positively related to an increase in mortality from CHD? Nope – it’s a comparison between the various fats that could or should replace saturated fats in the diet.

The Panel's paper continues:

Although the replacement of SFA with carbohydrate reduces energy intake and total and LDL-cholesterol concentrations, it has a TAG-raising (Berglund et al. 2007) and HDL-lowering effect (Turley et al. 1998), both of which increase the risk of CHD.

So, replacing saturated fats with carbohydrates increases the risk of coronary heart disease?

Why the blazes is Dr Susan Jebb and her cronies telling us we should reduce saturated fat and increase whole grains [carbohydrate] in our diet? Ah yes! She's the wolegrain and Slimfast lobby, isn't she!

Next the review asserts:

... a reduction in the male population SFA intake from the current levels of 13.4% to the recommended level of 11% of food energy, by replacement of SFA with PUFA, would be expected to reduce LDL-cholesterol levels by 0.13 mmol/l (2.4 ¥ 0.052) (Sorkin et al. 1992)

However, the study that’s based on is Cholesterol as a risk factor for coronary heart disease in elderly men so were its conclusions relevant?

Serum total cholesterol shows a positive association with CHD morbidity and mortality in men aged 65 years and above. This may, however, not hold true for persons aged 80 years and above.

And what sort of research was carried out by Sorkin et al?

A MEDLINE search of all published studies that evaluated the association between high cholesterol levels and CHD in persons aged 65 years and above

So the evidence that men should replace their saturated fat intake with polyunsaturates is based on a Medline search of published studies – good, bad, indifferent, or hopelessly biassed – which may, or may not have had something to do with PUFAs or men under pension age?

What great advice from our Government bodies!

Then the Panel gets to deciding which types of SFA are the best:

... lauric acid, myristic acid and palmitic acid are known to be the most hypercholesterolaemic SFA (Mensink et al. 2003)

It doesn’t sound good, does it? But hang on one minute. What were Mensink’s actual findings ?

... lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and
stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations.

In other words, contrary to the Panel’s statement, myristic and palmatic acids had little effect, and carbohydrates made things worse.

... stearic acid appears to be neutral in relation to total cholesterol concentrations, but not in relation to the progression of atherosclerosis or risk of CHD (Hu et al. 1999).

Do the study’s conclusions support this statement? No!

A distinction between stearic acid and other saturated fats does not appear to be important in dietary advice to reduce CHD risk ...

And after all the verbiage about the effects of different types of fats that might or might not be good/bad for us, we have this statement from the Panel:

... the difficulty in sourcing highly enriched sources of individual SFA makes it difficult to conduct meaningful intervention trials to compare their individual impact on the blood lipid profile and CHD risk.

We have a situation where the Panel admits that meaningful trials to prove what they want proving would be difficult, so it has relied on extremely thin, misleading, and unrelated evidence from other sources instead!

Type 2 Diabetes mellitus

As summarised in recent reviews (Vessby 2000; Hu et al. 2001b), results from large epidemiological studies are inconsistent, with studies reporting both positive and negative associations between intake of SFA and risk of impaired glucose tolerance, type-2 diabetes and insulin

Well, Vessby’s conclusions are negative:

... controlled dietary intervention studies in humans investigating the effects of different types of fatty acids on insulin sensitivity have so far been negative.
Hu’s 2001 studies must be very important as they have been cited 949 times. As Vessby’s was negative, Hu’s must be the positive one, right? So does this one show a positive association between SFA and diabetes? No it does not!

Nineteen epidemiological studies on dietary fat and carbohydrate in relation to hyperglycaemia and Type 2 diabetes are listed. There is no consistency whatsoever between the results. Some associate carbohydrates, some total fat, some saturated fat, some meat, while four of them show no associations at all.

As Hu says, "the findings are inconclusive" and struggles for possible reasons, ranging from methodology to false reporting by participants. He does, however, report:

“A purported benefit of a low-fat diet is weight loss. But the association between dietary fat and obesity is not clear and
long-term clinical trials have not provided convincing evidence that reducing dietary fat can lead to subsequent weight loss.”
and he concludes

“Although it is generally agreed that dietary modification is an important means of preventing Type II diabetes, there exists no general consensus about the role of dietary fat and carbohydrates.”

So it would seem that neither Vessby nor Hu bear out the Panel’s statement.

The Panel concludes that further evidence is needed and is awaiting the results of the RISCK and LIPGENE trials, both of which are very likely to be badly flawed, as they seem to be using the same food groupings as the NDNS 2000-20001, except that LIPGENE has removed the healthy fats and replaced them with polyunsaturates provided by Unilever Best fods UK Ltd.

Other diseases linked to SFA intake

... studies investigating the relationship between SFA intake and obesity have reported inconsistent results ...

Hmmm... now that’s interesting, isn’t it?

... increased intake of animal fat, particularly as meat products, may be related to increased risk of colorectal cancer (Gonzalez 2006) and breast cancer (Sieri et al. 2008); however, there is little evidence to suggest that different classes of fatty acids (i.e. SFA vs. MUFA vs. PUFA) are associated with differential effects on risk.

Both references are from the EPIC study data, and Barry Groves has cast sufficient doub on both to render them meaninglesshere and here.

A moderate intake of SFA was found to increase the risk of dementia and Alzheimer’s disease, but this association was found only in those with the Apolipoprotein (Apo) E4 polymorphism (Laitinen et al. 2006)

In other studies, a high intake of SFA was associated with neither dementia (Engelhart et al. 2002) nor Parkinson’s disease (de Lau et al. 2005).

Then comes admission number two:

In epidemiological studies, it is difficult to distinguish between different fatty acids as all dietary fat consists of
mixtures of fatty acids and it is often not possible to adjust for intake of other fatty acids.

Saturated fatty acids and public health

The evidence linking SFA intake with increased risk of CHD and other diseases highlights the importance of implementing strategies to reduce population SFA intake in the UK and thereby associated morbidity, mortality and economic costs.

Pardon?! Remind me again - the evidence linking SFA with CHD and other diseases is what, exactly?

Let's see what we have gleaned from the studies referenced in the Panel's paper:

CHD? No evidence
Dementia? No evidence
Parkinson’s? No evidence
Breast cancer? No evidence
Obesity? Inconclusive evidence
Colorectal cancer? No evidence
High cholesterol? None – unless you count Ancel Keys
Alzheimer’s? Some, but only in a very specific group of people.

Do you know what really p*sses me off most about all of this? We’re paying for these so-called experts to sit around and produce papers that do not stand up to even amateur scrutiny.

** The Fat Panel comprises Unilever (Flora), Dairy Crest (Clover), and Kerry Group (Move Over Butter).


  1. Well done! I am sick of being bombarded with the 'low fat' message. People look at you as though you are mad if you say anything different like 'low-carb high fat' is best. The way the Government carries on about food etc makes me so cross!

  2. Excellent post. Thanks for all your hard work. None of these studies tracked the amount of carbs eaten and I suspect if they did, it would show that carbs are the cause of cancer and heart disease.

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  4. What a surprise - an anti-fat website with absolutely no scientific evidence to back it up. Just like the FSA's dreadful 'eatwell' website and countless charity websites. Well done Megan, keep up the good work!


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