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
resistance.

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).

Red meat is a healthy food - particularly beef!

Over the last few days I've written about the dire health warnings from the World Cancer Research Fund UK and others about the dangers of 'red meat' in our diet. Despite another eight or so hours of trawling through their 1,082 references I'm still unable to find a single study that shows that red meat - real red meat - is any danger whatsoever.

As I discovered with NDNS 2000-2003 'red meat' in nutritionists' terms includes lasagne, curries, sweet and sour, meat spreads and pastes, pies, and cheeseburgers, complete with buns!

I think it's high time we all looked at what red meat in general, and beef in particular, really can do for us. As I said above, I've not been able to find any research that shows red meat is bad for us, so would I have any more luck in finding evidence that proves the reverse - that it's actually good for us? Just take a look!


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C A N C ER
Conjugated linoleic acid. A powerful anticarcinogen from animal fat sources. C, Scimeca JA, Thompson HJ. Cancer. 1994 Aug 1;74(3 Suppl):1050-4.
Conjugated linoleic acid is unique because it is present in food from animal sources, and its anticancer efficacy is expressed at concentrations close to human consumption levels. The efficacy of conjugated linoleic acid in mammary cancer prevention is independent of the level or type of fat in the diet.
Conjugated linoleic acid in animal fat can prevent cancer.

Stability of conjugated linoleic acid isomers in egg yolk lipids during frying. Food Chemistry. Volume 86, Issue 4, August 2004, Pages 531-535
The eggs, containing 4.0% CLA per gramme of egg yolk, were stored in a refrigerator at 0–4 °C for 6 months, while the egg yolks were fried in a pan at 160–180 °C for 40 s. Either storage for 6 months or frying for 40 s did not significantly change the composition of CLA in egg yolk.
Egg yolks are a good source of conjugated linoleic acid.

Role of diet on conjugated linoleic acid content of milk and meat. T. R. Dhiman*1, 1Department ofAnimal, Dairy and Veterinary Sciences, Utah State University, UT 84322-4815
Conjugated linoleic acid (CLA) occurs naturally in many foods. However, the principal dietary sources are meat, dairy products and other foods derived from ruminants. Research studies with animal models suggest that CLA reduces the risk of cancers at several sites (mammary tissue, prostrate, gastrointestinal tract, lung, and skin), reduces body fat and enhances growth of lean body mass. Fat from milk and beef contains an average 4.0 and 3.5mg CLA/g of fat, respectively.
Cows grazing on pasture had 500% more CLA content in milk compared with cows fed typical dairy cow diets containing conserved forage and grain in a 50:50 ratio. Raising beef cattle on forages and pasture with no grain supplementation can enhance the CLA content of beef.
Meat and dairy products from grass-fed cattle are high in conjugated linoleic acid, which can reduce the risk of cancers, reduce body fat, and produce a lean body.


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C A N C E R...and...V I S I O N

Role of fatty acids in malignancy and visual impairment: epidemiological evidence and experimental studies. Tsubura A, Yuri T, Yoshizawa K, Uehara N, Takada H. Histol Histopathol. 2009 Feb;24(2):223-34.
SFAs such as palmitic acid and stearic acid show little or no tumor promoting effect, and the action of oleic acid, a MUFA, is inconclusive. SFAs such as palmitic acid and stearic acid show little or no tumor promoting effect, and the action of oleic acid, a MUFA, is inconclusive.
In addition to regulation of abnormal cell growth seen in cancers, fatty acids also control cell loss seen in degenerative eye diseases, such as degeneration of lens material in cataract and degeneration of photoreceptor cells in retinitis pigmentosa. Experiments suggest that n-6 PUFAs cause deleterious effects, while n-3 PUFAs result in beneficial effects on the lens and retina. In particular, docosahexaenoic acid is known to be effective in rescuing photoreceptor cells from damage.
Saturated fats [SFAs] do not help cancers to grow, and can control degenerative eye diseases. Polyunsaturates from vegetable sources [PUFAS] injure the eyes.


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C H O L E S T E R O L

Reducing the serum cholesterol level with a diet high in animal fat. Newbold HL. South Med J. 1988 Jan;81(1):61
Multiple food allergies required a group of seven patients with elevated serum cholesterol levels to follow a diet in which most of the calories came from beef fat. Their diets contained no sucrose, milk, or grains. They were given nutritional supplements. This is the only group of people in recent times to follow such a diet.
During the study, the patients' triglyceride levels decreased from an average of 113 mg/dl to an average of 74 mg/dl; at the same time, their serum cholesterol levels fell from an average of 263 mg/dl [6.8 mmol/l] to an average of 189 mg/dl [4.89 mmol/l].
At the beginning of the study, six of the patients had an average high-density lipoprotein percentage of 21%. At the end of the study, the average had risen to 32%.
These findings raise an interesting question: are elevated serum cholesterol levels caused in part not by eating animal fat (an extremely "old food"), but by some factor in grains, sucrose, or milk ("new foods") that interferes with cholesterol metabolism?
Yes, "most of the calories came from beef fat" and blood cholesterol levels were reduced. This research has been around for over twenty years now, so why do today's nutritionists ignore it?
Could it be that there's no profit in beef fat for the diet industry or the pharmaceutical companies?



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B L O O D ...G L U C O S E

An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes.Gannon MC, Nuttall FQ, Saeed A, Jordan K, Hoover H. Am J Clin Nutr. 2003 Oct;78(4):671-2.
Total cholesterol, HDL-cholesterol, and LDL-cholesterol concentrations were essentially unchanged with the high-protein diet. However, the fasting triacylglycerol concentration decreased by 20% after 5 wk of the high-protein diet.
This is interesting, as very lean beef was used in this study, unlike the previous one with coeliacs. I'm no expert, but logic suggests that had beef with its normal fat been used, cholesterol may well have dropped as well, as in the coeliac study.

And if you live in Australia and don't have any cattle close by, kangaroo will do nicely.

Kangaroo meat - health secret revealed. Commonwealth Scientific and Industrial Research Organisation 2004 April 23.
CLA (conjugated linoleic acid) is found in dairy products, beef and lamb. CLA is produced in the stomach and tissues of ruminant animals such as sheep and cattle during the digestion process.
In trials, CLA has been shown to possess potential anti-carcinogenic and anti-diabetes properties, in addition to reducing obesity and atherosclerosis (high blood pressure).
The meat of Australia's bush kangaroo may be the highest known source of the healthy fat. Dairy milk was previously the highest known source of CLAs, followed by the fat of beef and lamb.
Conjugated linoleic acids (CLA) are polyunsaturated fatty acids. one study in humans detected an inverse (reduced) relationship between milk consumption and breast cancer risk. Many other foods contain CLA, including vegetable oils, eggs, seafood, poultry and pork but at very low levels.
Drinking milk containing conjugated linoleic acid reduced the risk of breast cancer. Although CLA is a polyunsaturate it is different to the PUFAs which are derived from vegetables.

I find it appalling that 'expert nutritionists' are forcing misleading information onto the population, when so much evidence showing the health-giving properties of beef has been steam-rollered into the ground, presumably by the powerful vegetable oils lobby, aided and abetted by the pharmaceutical companies. I have no doubt that is where the blame lies, and if you think I'm exaggerating their power, take a look at Mary Enig's articles, such as this one on coconuts.

I found no research to back up the claims that eating red meat, together with its fat, gives us cancer, high cholesterol, or high blood glucose (diabetes), but plenty to demonstrate that it actually protects us from these diseases.

I shall continue eating beef and beef fat, because I want to stay healthy.