A Guest Post on Prof. Grant Schofield's Blog

This is just a short post to direct readers to my guest post here: http://profgrant.com/2014/07/30/all-that-fat-a-guide-for-the-perplexed/

Which contains all my thoughts about dietary fat recommendations and the lipid hypothesis, without too many distracting details.

I also want to supply a link to a most enjoyable book, Bertha M. Wood's "Foods of the Foreign-born in Relation to Health" from 1922.
https://archive.org/details/cu31924003579756
I think this is the first record of "dietary transitions", adverse changes to the traditional diets of migrants in a new land. It was written at the height of U.S. xenophobia (in the immediate aftermath of the Great War and the Bolshevik revolution) and can also be seen as a response to prejudice. Though the Hungarian child's diet below might not have helped much.


In 1922, diabetics were treated by restricting starch, especially from grains and legumes; this was replaced with non-starchy vegetables. Fat was not generally restricted (though this is said to be necessary in some cases, perhaps because sugar doesn't seem to have been reduced).
I learnt about Bertha M. Wood's book from The Old Foodie blog.

Epidemiology can be Interesting

      Hat tip to Nigel Kinburn for pulling up two studies from Siri-Tarino et al.’s 2010 saturated fat meta-analysis that did show correlations with heart disease. These were also the studies with the widest range of intakes. So what can they tell us?
      The first is by Jim Mann and colleagues from 1993, and straight up I am surprised that this has been included in any meta-analysis, because it uses a self-selected vegetarian cohort, with friends and family standing in for the rest of the population.
      “The study differs from previous prospective studies of diet and IHD in that the volunteers were individuals whose self-selected diet resembled, in nutrient content, current dietary recommendations rather than the relatively high saturated fat diet typical of most affluent societies. The findings may not only help to explain which attributes of a vegetarian diet protect against IHD but also which foods and nutrients are important in the aetiology of IHD in populations who modify their diets along the lines of present guidelines.”
      It’s odd that such high-bias methodology isn’t excluded from meta-analysis, and makes me wonder what else is included.
      What does Mann et al. tell us?
“Results—IHD mortality was less than half that expected from the experience reported for all of England and Wales. An increase in mortality for IHD was observed with increasing intakes of total and saturated animal fat and dietary cholesterol—death rate ratios in the third tertile compared with the first tertile: 3.29, 95% confidence interval (CI) 1.50 to 7.21; 2.77, 95% CI 1.25 to 6.13; 3.53, 95% CI 1.57 to 7.96, respectively. No protective effects were observed for dietary fibre, fish or alcohol. Within the study, death rate ratios were increased among those in the upper half of the normal BMI range (22.5 to under 25) and those who were overweight (BMI over 25) compared with those with BMI 20 to under 22.5.
(Relative risk figures have been converted from 100 to 1.0)

      IHD was significantly associated with higher consumption of eggs, cholesterol, animal fat, and saturated fat.
      But, here’s the surprising finding; none of those dietary factors was associated with any increase in total mortality, significant or non-significant. People who avoided dying of IHD by following the healthy eating guidelines were dying at the same rate – the same ages - as their less health-conscious friends and family. This wasn’t pinned down to any particular cause of death.

      The fact that BMI under 20 was associated with as much increased risk of overall mortality as BMI over 25 (“total mortality was significantly higher in those with an initial BMI under 20, and a similar though not statistically significant trend is apparent for IHD mortality.”) wasn’t mentioned in the abstract, and is underplayed in the text (if it can be explained by undiagnosed pre-existing disease, so can the correlation with higher BMI). A bit like this dodgy AHF BMI calculator. Set this to BMI 7 (maximum height, minimum weight) and you still look healthy; muscular or curvy depending on gender. Results in real life may vary.

      The main dietary finding pertaining to all-cause mortality in Mann et al.;
“all cause mortality for all subjects was significantly lower in the middle and highest intakes of green vegetables (0.62, 95% CI 0.46–0.83; and 0.74, 95% CI 0.56–0.99) and among those consuming the highest intake of nuts (0.76, 95% CI 0.60–0.97) compared with the lowest intakes of these foods.”

     The second paper is by Bonniface et al., and unfortunately doesn’t supply all-cause mortality data.
      “Not consuming alcohol, smoking, not exercising and being socially disadvantaged were related to high saturated fat intake and CHD death. Cox survival analyses adjusting for these factors found that a level of saturated fat 100 g per week higher corresponded to a relative risk for CHD death for men of 1.00 (0.86-1.18) and 1.40 (1.09-1.79) for women. This difference between the effects of saturated fat in men and women was statistically significant (P=0.019).”

     Mean intakes of SFA in Bonniface et al. - Men: 47.0 g/d Women: 34.4 g/d. A respectable ~20%E (similar to the consumption by Indians eating food prepared with ghee in Raheja et al. 1995).
“The cut-off points for the quintiles of saturated fat in grams per week were 220, 276, 337 and 427 for men and 159, 202, 252 and 319 for women. There was a clear trend to higher CHD death rates associated with higher total and saturated fats and Keys' fat difference in women.”

      Keys' fat difference? This is the ratio between SFA and PUFA.
      “The result for the Keys statistic indicates that a higher level of saturated fat can be compensated by a lower level of polyunsaturated fat, in the ratio 2:1.”
      PUFA by itself showed no correlations, but the Keys difference did. In fact, the correlation between Keys' difference and CHD in table 3 is pretty striking.

     Both populations were in Britain. Perhaps the take-home is, that in Britain, at least at a certain point in time, you could choose how you wanted to die to some extent by choosing your diet around heart guidelines. Or by watching your Keys' ratio if you were female (women today, with vegetable oil diets, would not have ideal Keys' ratios by these tables). But living longer than those around you by restricting saturated fat is not a prediction supported by this epidemiology, or by any meta-analysis, as was discussed by Simon Thornley, Grant Schofield and I in our letter to the NZMJ.

     Diet epidemiology is interesting stuff. It’s incredibly hard to do well, and the things we can take away from it are sometimes unexpected. The papers that go into meta-analyses, even for something like SFA, are wildly heterogeneous in design and in quality. Jim Mann et al.’s 1993 paper told me just about everything I wanted to know that it was possible to tell from the data collected. Bonniface et al. were more obscure; critical data points for the Keys' difference were not included. What use are quintiles without means or cut-offs?
      I was surprised, as I said, that the Mann et al. paper, good though it is, is being included in meta-analysis, because of the self-selection bias (so, self-selection in Paleo or LCHF diet studies shouldn't be a barrier to being taken seriously either). That it was included speaks to the impartiality of meta-studies like Siri-Tarino et al. 2010 that exculpate saturated fat. Meta-studies give the overall truth that is relevant for public health planning, but miss the finer details of what is happening in specific communities at specific times. For example:
      In Mann et al., nuts are protective. This is a common finding, e.g. in Hu et al. 1998. In Bonniface et al. PUFA is not associated with harm, but the Keys' difference is. In Britain at the time of this study, among the mainly middle and upper classes, perhaps vegetable oils were not in common use. Perhaps nuts were a major source of linoleic acid, enough to attenuate its relationship with disease. And in Bonniface et al., with its more working class catchment (and this being Britain, class distinctions do matter), perhaps the ideal Keys' difference of 2:1 is what you get closer to eating nuts and fish with meat and dairy fat, and the adverse lower and higher ratios are what you get either not eating nuts and fish, or using vegetable oils and spreads instead of animal fats.
(the mean PUFA intake of 63.1g/week for women is ~4%E).
     Because it may turn out that when diet-heart epidemiologists one day separate PUFA in nuts and fish from PUFA in oils they will get very different values, as these AMD researchers did.

     Take home: For someone who has the disease of CHD, especially someone following a moderate fat, higher carbohydrate diet like most of the population (the dietary pattern at the heart of all epidemiology) it makes sense to follow these clues, as well as recognising the modern risk factors of sugar and refined flour; eat some nuts, fish, don’t eat red meat every day, eat only a few eggs per week, eat some full-fat dairy, and so on.
      On the other hand, for the average person to eat a pleasurable diet that has been designed around avoiding CHD risk factors from animal foods risks inviting in a host of other diseases that they may be susceptible to in ways they were never susceptible to CHD. Advice to the general population should be limited to recommending those protective factors for CHD that a) supply micronutrients, and b) are also protective factors in a wider sense (nuts, fish, fruit and vegetables, and full fat dairy), instead of messing with Keys' difference based on theories about blood lipids, as opposed to consistent findings based on real food inputs and hard endpoints.

Another Reason why the Lipid Hypothesis is Bunk

The lipid hypothesis, as evry fule kno, predicts that eating saturated fat causes elevation of serum cholesterol or LDL which then plays a causal role in cardiovascular heart disease. How or why no-one knows but the feeling out there is that saturated fat causes bad cholesterol and heart disease. The notion is, as they say, entrenched; it is a meme more widely believed now than any religious dogma.

Unlike the unknowable nature of God, the lipid hypothesis can be disproved by multiple lines of evidence. Here is one.

Animal fat is a blend of saturated fats, monounsaturated fats, and polyunsaturated fats. Polyunsaturated fats lower serum cholesterol, monounsaturated fats have no effect on serum cholesterol, and some saturated fats also have no effect on cholesterol. William Barendse describes the set-up eruditely and eloquently in his epic review “Should Animal Fats be Back on the Table? A critical review of the human health effects of animal fat” as follows;

“As an example from one of the hardest animal fats, approximately only 27% of tallow from pasture-fed beef is cholesterol-increasing saturated fatty acid (CISFA) (Yang et al. 1999b), i.e. chain length of 12–16 carbons, and which would raise serum cholesterol, 1% is polyunsaturated, ~4% is conjugated linoleic acid (CLA), and the rest is either MUFA or is the saturated fatty acid (SFA) stearic acid that causes the same effect on total serum cholesterol (TSC) as MUFA (Keys et al. 1965; Grande et al. 1970; Bonanome and Grundy 1988; Tholstrup et al. 1994a, 1994b; de Roos et al. 2001; Mensink et al. 2003). By comparison, in butter from pasture-fed cows, 42% of the fat is CISFA (Couvreur et al. 2006) and would raise serum cholesterol despite butter having a total of more than 60% SFA.”
(FYI, butter also supplies twice as much cholesterol as tallow.)

Therefore, if the lipid hypothesis were true, we would expect butter and other forms of dairy fat (of which butter is merely the concentrate) to cause, or at least be associated with, more heart disease than meat fat, especially considering that most meat fat is less saturated than tallow.

To the contrary, the 2012 epidemiological analysis, Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis, one of the few studies to separate saturated fats according to their dietary sources, found a strong protective (inverse) association between dairy fat and CVD, and a weaker positive association with the less saturated fat from meat, across a multi-ethnic population (this ruling out the possibility of the results being unduly influenced by genetic factors);

“When we evaluated risk across quintiles of SF consumption from each food source, a significant inverse association was seen for dairy SF [HR (95% CI) for extreme quintiles: 0.56 (0.38, 0.82); P-trend = 0.01], whereas meat SF was not statistically significantly associated with risk [HR (95% CI) for extreme quintiles: 1.40 (0.94, 2.08); P-trend = 0.12] (Figure 1). Butter and plant sources of SF were not associated with CVD risk, but ranges of SF consumption from these sources were quite narrow, which limited our ability to detect differences in risk across quintiles.”
“In sensitivity analyses in which angina was excluded from CVD endpoints, inverse associations of total, dairy, and plant SF with hard CVD were somewhat stronger, whereas the positive association of meat SF with hard CVD was slightly attenuated (data not shown).”

In case it is thought that the sample size in the MESA study (5,209) was too small, it is a common finding that dairy fat is either not, or is inversely, associated with CVD incidence.

An argument could be made that some factor associated with dairy fat, such as (hypothetically) calcium, reverses the harmful effect of saturated fat. If such were in fact the case, how nugatory would that harmfulness then need to be?

There may be things that raise cholesterol and that are associated with CVD. Industrial trans fatty acids seem to meet this case, as well as various organic toxins and heavy metals that are not fatty acids, and that are likely to be bad for you quite independently of any perturbations of your lipids. Sugar and high-GI starches are other potential candidates, which takes us into the intricacies of lipoprotein classes beyond the cartoon characters of cholesterol and LDL. There are also bound to be fatty acids, as well as other factors, which can increase CVD risk while lowering cholesterol. There have certainly been enough trials of cholesterol-lowering drugs, and cholesterol-lowering diets, where more people have died in the treated group, and sometimes died with lower cholesterol.

Yet people still believe this thing. It is nonsense. There are other things that better deserve the energy that has been poured into making people worry about saturated fat, and about the influence of dietary fats on cholesterol. The lipid hypothesis, and consequent pious attempts to respect or enforce the magical 10% saturated fat limit, have had a mischievous influence over the modern diet. Belief in it has not made us, in the majority, healthy, wealthy, or wise. It has made us saturate our bodies in polyunsaturated fats without considering whether they are omega 6 or omega 3, cis or trans, oxidised or unoxidised, or how far they are in fact necessary, or whether they bring anything in the way of nutrition to the diet to make up for the choline, carotenoids, cholesterol, retinol, menaquinone, and cholecalciferol we miss out on by not eating as much butter or fatty animal parts as our ancestors did. We have been fools, and we are making our society sick. It is time to stop.

Diabetes as an Iatrogenic Disease - the Second Hit

Why does dairy fat, and perhaps other similar fats like tallow and coconut, seem to prevent diabetes?
A broken omega 6:3 ratio becomes more likely with higher PUFA intakes. There is something about having a low PUFA intake that preserves the balance, even at relatively low omega 3 intakes.
We can see this in the recent fatty liver study comparing olive oil with canola oil and soy/safflower oil (control). For 6 months 20g of oil per day was used to cook food; this is not much (and it seems likely to me that many participants would have used more than they were directed to, if only to increase the palatability of their meals). There was no change in fatty liver and insulin resistance scores in those using soy/safflower oil, which is presumably what all subjects cooked with before.

The pre- and post-intervention difference in liver span was significant only in the olive (1.14 ± 2 cm; P 0.05) and canola (0.66 ± 0.33 cm; P 0.05) oil groups. In the olive and canola oil groups, post-intervention grading of fatty liver was reduced significantly (grade I, from 73.3% to 23.3% and from 60.5% to 20%, respectively [P 0.01]; grade II, from 20% to 10% and from 33.4% to 3.3%, respectively [P 0.01]; and grade III, from 6.7% to none and from 6.1% to none, respectively). In contrast, in the control oil group no significant change was observed. 

So canola oil and olive oil were about equally good for reversing steatosis; this might be an expected effect of supplying fats with an omega 6:3 ratio of 2:1 for six months. But when it came to glucose and insulin, there was a marked difference:In a comparison of olive and canola oil, a significant decrease in fasting insulin level, HOMA-IR, HOMA-βCF, and DI (P 0.001) was observed in the olive oil group.
In fact, fasting insulin and blood glucose were normalised in the olive oil group, but not in the canola oil group. With regard to these measures of glycemic control, a 50% lower intake of linoleic acid (with substitution of MUFA from oleic acid) produced more benefit than a 20-fold increase in alpha linolenic acid.

Here we have a paper that compares the effect of LA restriction (from 8%E to 4%E) with the effect of DHA in immune-deficient mice bearing human breast cancer cells;
Tumor prostaglandin E2 concentrations were reduced by feeding the lower LA level; further dose-dependent decreases occurred in the DHA dietary groups and were accompanied by reduced levels of 12- and 15-hydroxyeicosatetraenoic acids.
According to Raheja et al. (1993) "prostaglandin E2 is a potent inhibitor of first-phase insulin release, whereas an arachidonic acid lipoxygenase product, possibly 12-hydroxyeicosatetraenoic acids (12-HETE) sustains increased second-phase insulin release". A pattern also known as insulin resistance, or if sufficiently elevated, NIDMM or type 2 diabetes. These elevated prostaglandins are also seen in type 1 diabetics.
And, what do you know, ghee reduces PGE2 in Wistar rats:Ghee, the anhydrous milk fat, is one of the most important sources of dietary fat in India. Male Wistar rats were fed diets containing 2.5, 5.0 and 10 wt% ghee for a period of 8 weeks. The diets were made isocaloric with groundnut oil. The results showed that serum thromboxane levels decreased by 27-35%, and 6-keto-prostaglandin F1alpha by 23-37% when ghee was incorporated at level of 10% in the diet. Prostaglandin E2 levels in serum and secretion of leukotrienes B4, C4 and D4 by peritoneal macrophages activated with calcium ionophore decreased when increased amounts of ghee from 2.5 to 10% were included in the diet. Arachidonic acid levels in macrophage phospholipids decreased when incremental amounts of ghee were fed to rats. These studies indicate that ghee in the diet not only lowers the prostaglandin levels in serum but also decreases the secretion of leukotrienes by macrophages.

(I haven't seen fulltext for that, but control, groundnut oil, is around 30% LA, and 10 wt% will be more than 10%E).

With regard to ALA, this epidemiological paper on prostate cancer, while perhaps  irrelevant, has an interesting line:ALA intake was unrelated to the risk of total prostate cancer. In contrast, the multivariate relative risks (RRs) of advanced prostate cancer from comparisons of extreme quintiles of ALA from nonanimal sources and ALA from meat and dairy sources were 2.02 (95% CI: 1.35, 3.03) and 1.53 (0.88, 2.66), respectively. The multivariate RR of advanced prostate cancer from a comparison of extreme quintiles of the ratio of LA to ALA was 0.62 (0.45, 0.86).
Do you have any idea how much dairy fat it takes to get into a high quintile for ALA? Anyway, just another epidemiological paper where animal fats come out safer than their vegetable equivalents. One of the ones you don't hear about.
As I mentioned previously here, in New Zealand per capita weekly butter consumption at the beginning of the Second World War was 415 grams. It is now 112 grams, which is half of the reduced 1940s wartime ration. Not much Type 2 diabetes in New Zealand prior to the Second World War. Not much consumption of heart-healthy oils either, but plenty of consumption of sugar and white flour.

The second hit: In children and young individuals, a high intake of n-6 PUFA is correlated with fasting hyperinsulinaemia, and dietary supplementation with n-3 PUFA leads to an improved lipid profile but not insulin sensitivity. In adults, high-carbohydrate meal consumption was reported to cause hyperinsulinaemia, postprandial hyperglycaemia and hypertriacylglycerolaemia. (Misra, A. 2009).
Take a child, and raise them on this high-LA, vegetable oil diet (because saturated fat and high cholesterol, don't you know, cause heart disease in toddlers). By the time they reach adulthood, they'e primed for the second hit:

Refined grain consumption and the metabolic syndrome in urban Asian Indians (Chennai Urban Rural Epidemiology Study 57).

Compared with participants in the bottom quartile, participants who were in the highest quartile of refined grain intake were significantly more likely to have the metabolic syndrome (odds ratio, 7.83; 95% confidence interval, 4.72-12.99). Higher intake of refined grains was associated with insulin resistance and the metabolic syndrome in this population of Asian Indians who habitually consume high-carbohydrate diets.

That's grains, by the way, not sugar, not HFCS.

Dairy fat intake is associated with glucose tolerance, hepatic and systemic insulin sensitivity, and liver fat but not β-cell function in humans.

Diabetes as an Iatrogenic Disease - the Indian Experience

Diabetes and dairy fat in India.

     The epidemics of diabetes, cardiovascular disease and related conditions in India have been called iatrogenic (Raheja B.S. 1994), a product of diets high in linoleic acid as a result of “chasing the phantom of cholesterol” (Raheja et al. 1993). The traditional Indian diet (39% fat) supplied 20.3%E as saturated fats, mainly from ghee, with 5% from linoleic acid. Concerns that this diet is atherogenic have resulted in replacement of ghee with high-linoleate oils; the modern urban diet being 31.9% fat, with 5.6%E as saturated fat, and 16.9% linoleic acid (Raheja, B.S. et al. 1993).
   
     In children and young individuals, a high intake of n-6 PUFA is correlated with fasting hyperinsulinaemia, and dietary supplementation with n-3 PUFA leads to an improved lipid profile but not insulin sensitivity. In adults, high-carbohydrate meal consumption was reported to cause hyperinsulinaemia, postprandial hyperglycaemia and hypertriacylglycerolaemia. (Misra, A. 2009).


The association of ghee consumption in the Indian diet with a lower rate of diabetes is consistent with the correlation between serum markers of dairy fat consumption and reduced diabetes risk (Mozaffarian et al. 2010, 2013). The NZ Ministry of Health currently recommends a wide range of linoleic acid and alpha-linolenic acid in the diet; the lower recommended intake of LA being 4%, the upper being 10%, and the lower recommended intake of ALA being 0.4%, the upper 1% (the omega 6-3 ratio at median intakes thus being 10:1). Saturated fat intake below 10%E is recommended. (Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. 2012 MOH).

     The message from the Indian researchers into the causes of their diabetes epidemic is that higher consumption of dairy fat protected marginal dietary omega-3 intake from abrogation by excessive intakes of omega-6 fatty acids. Replacing highly saturated dairy fats with diets higher in linoleic acid and refined carbohydrate, which is the same effect that the campaign against saturated fat has had among more disadvantaged New Zealanders, has increased the rate of diabetes, which is consistent with the New Zealand experience, suggesting that the increased incidence of diabetes in New Zealand has been in large part an iatrogenic phenomenon.

     "The present epidemic of DM and ACVD in Asian indians and possibly in other communities is iatrogenic resulting from what may be called modern malnutrition due to increased intake of total and n-6 fats and decreased intake of n-3 fat and antioxidants. Such a diet induces oxidative stress and activates the immune system. Imbalance between n-6 and n-3 fats result in inappropriate immune response. It also leads to increased and unbalanced biosynthesis of metabolites of n-6 fats. These are immune suppressive, proinflammatory and thrombogenic. They also contribute to insulin resistance and dyslipidemias. This makes DM and atherosclerosis as malnutrition related oxidative immune inflammatory disorders. Various risk factors are also the result of the same inappropriate response. Our intervention studies give considerable support to this hypothesis. It is suggested that simple correction of diet defects can reverse the disease process and thereby offer a simple, practical therapeutic option not only for the primary prevention of each of these disorders or their complications but also for the so called risk factors for these diseases. It is suggested that the real remedy for DM, ACVD and all the risk factors lies not in drugs or surgery but in the kitchen."
- B. S. Raheja

Misra, A. et al. (2009). South Asian diets and insulin resistance. Br J Nutr. 2009 Feb;101(4):465-73. doi: 10.1017/S0007114508073649

Mozaffarian, D. et al. (2010). Trans-Palmitoleic Acid, Metabolic Risk Factors, and New-Onset Diabetes in US Adults. Ann Intern Med. Dec 21, 2010; 153(12): 790–799. doi:  10.1059/0003-4819-153-12-201012210-00005

Mozaffarian D. et al. (2013). Trans-Palmitoleic acid, other dairy fat biomarkers, and incident diabetes: the Multi-Ethnic Study of Atherosclerosis (MESA). Am J Clin Nutr. 2013 Apr;97(4):854-61. doi: 10.3945/ajcn.112.045468.

Raheja B.S. (1994). Diabetes and atherosclerosis as immune-inflammatory disorders: options for reversal of disease processes. J Assoc Physicians India. 1994 May;42(5):385-90, 395-6. PMID:7829439

Raheja, B.S. et al. (1993). Significance of the N-6/N-3 Ratio for Insulin Action in Diabetes. Annals of the New York Academy of Sciences, 683: 258–271. doi: 10.1111/j.1749-6632.1993.tb35715.x

Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. (2012) New Zealand Ministry of Health.
http://www.health.govt.nz/system/files/documents/publications/food-and-nutrition-guidelines-for-healthy-children-and-young-people-p4.pdf

Uffe Ravnskov, Zoe Harcombe and Aseem Malhotra on the New Censorship

This is just a bookmark for three responses to two recent incidents of press censorship.
ABC withdrew the two episodes of "Heart of the Matter" Catalyst show, despite nothing substantial in the complaints being upheld, and the BMJ retracted some comments critical of statins, including those of Dr Aseem Malhotra, which were opinion based on his clinical impression, and had been presented as such.

[EDIT: This BMJ comment thread supplies all the information anyone might need to know about statin side effects. The patients' stories in particular.]

This is from Uffe Ravnskov's newsletter:

Why are the media afraid of revealing the greatest medical scandal in modern time?

In my October 2013 Newsletter I told you about the Australian TV program "Heart of the matter" produced by Maryanne Demasi, a PhD in medical science and a science reporter and presenter with  Australian Broadcast Corporation (ABC)¨s catalyst. In the program she interviewed several experts about their view on the effects of cholesterol-lowering diets and statin treatment. As far as I know this is the first TV program in the western world where critics of the cholesterol campaign have been allowed to present their view in detail. The shrewish reactions from the National Heart Foundation and from the drug companies were therefore predictable. 

In accordance with their Code of Practice and the editorial policies ABC asked the Audience and Consumer Affairs (A&CA) to examine the critical comments. Eleven critical points were examined, but although ten of them were cleared of bias, the ABC declared that the programs have been removed from the ABC website, because the A&CA has concluded that some parts of the program breached ABC standards on impartiality. 

Their decision is most curious because the A&CA did not find any factual information wrong. For instance, in their report you can read the following about the first episode “The dietary villains”:



1. The factual information in the program was accurately presented and the reporter has demonstrated that she diligently sought and considered a variety of views on the subject. No material inaccuracy has been demonstrated by any complainant.

2. The principal perspectives were presented.

3. Neither position was endorsed by the program.

4. Neither perspective was misrepresented.

5. The nature of the program necessitated that the unorthodox theory was given more time and explanation. The Code does not require that they receive equal time, nor that every facet of every argument is presented. 

With one exception similar conclusions were made about the second part. I shall come back to the exception that breached the ABC standards. 

The objections reveal that either the complainants have an alarming lack of knowledge or that they consciously try to mislead. Here come a few examples; in a complicated 49 pages document from ABC you can read all of them. 

“The hypothesis that eating saturated fats can increase cholesterol levels which in turn can cause heart attacks is widely accepted by the medical community.”

It is true that it was accepted many years ago, and most doctors and lay people still think it is true. However, more and more researchers have realized that it is totally wrong. Furthermore they would have known it already sixteen years ago if they had read my review about this issue, or my review from 2010  or a more recent one by Robert Hoenselaar or the recent meta-analysis by Chowdhury and coworkers“

Sadly, as it appears from the following, the complainants seem to be unfamiliar with the most simple facts of biochemistry. 

"It was mentioned that those molecules which contain long chains of single carbon bonds are more stable than those containing numerous double bonded carbon groups. Students doing high-school chemistry will be able to tell you the fault in this statement.”

As I told you in my February 2013 newsletter this is a fact. Any well-informed student will also be able to tell you that, and if anyone still thinks that the authorities cannot be wrong, any textbook in biochemistry can tell you that they are. 

Several complainants argued that the viewers were misled because some of the interviewees “had businesses promoting nutrition based products, diets, books and supplements that constitute conflicts of interest”.

But as Dr. Demasi pointed out, everyone interviewed had a conflict of interest including Ass. Professor David Sullivan who is a member of several advisory panels within the pharmaceutical industry and he has also received research grants from several statin-producing drug companies. Furthermore Dr Robert Grenfell, another supporter of the cholesterol campaign who was interviewed in the program, is Director of the National Heart Foundation, which has received millions of dollars from pharmaceutical companies for research, scholarships and fellowships.

“The pharmaceutical industry was accused of ‘criminal’ conduct akin to ‘organised crime’. Medicines Australia strongly rejects such accusation and feels that it is unfair (sic) characterisation of Australia’s medicines industry.”

Haven´t they read Peter Gøtzsche´s book Deadly Medicines and Organized Crime? Or the recent article in The Independent? Have they forgotten the VIOXX scandal? Have they forgotten the criminal behavior of Pfizer? 

Most pages were about the questioning of the benefit of statin treatment. As one of the complainants wrote: It is a fact that appropriate cholesterol interventions are very powerful in preventing cardiovascular disease. And in a letter to Dr. Demasi the National Heart Foundation wrote: The mass of evidence suggests that…statins reduce the risk of death or cardiovascular events in populations without a history of CVD, irrespective of age and gender and across a wide range of cholesterol levels.

If you think this is a fair statement, read my newsletters from May 2013, August 2013, September 2013 and November 2013 The simple fact is that no statin trial has been able to prolong the life for women or for people without coronary heart disease. Therefore, if you are a doctor and you have a heart-healthy patient who want to lower jhis/her cholesterol, tell the patient the following: “Your chance not to get a non-fatal heart event during the next five years according to Cochrane is about 97 per cent. You can increase your chance to 98 per cent if you take a statin every day. But then your risk of suffering muscle problem is at least 20 per cent unless you never exercise; your risk of becoming sexually impotent is about 20 per cent; your risk of suffering from diabetes is about 4 per cent, and you also run a risk of memory loss, liver damage, peripheral neuropathy, cataract, and even cancer, but we do not yet know how large these risks are. And don´t forget than many non-fatal events may heal with little future discomfort or none at all.”

Now to the reason why the program was removed.

One of the rules in ABC´s Code of Practice is the following: Do not unduly favour one perspective over another. But how could Dr. Demasi be able to do otherwise???  I mean, if the members of A&CA acknowledge that all the critical remarks from the opponents of the cholesterol campaign were true, and If the proponents are unable to present any relevant counter-arguments, how could A&CA state, as they did, that some parts of the program breached ABC standards on impartiality?


 A&CA suggested that Catalyst should add extra information to the website to provide more balance. They did not recommend to strip the stories off the website. This decision was made by ABC management. The question is why? Some speculate that it was political pressure from the drug industry or the Heart Foundation or it was an action to avoid more controversy.Fortunately both programs are still available on Youtube. Here is part one, and here is part two.

Uffe Ravnskov, MD, PhD, independent investigator

Spokesman of THINCS, The International Network of Cholesterol Skeptics

Magle Stora Kyrkogata 9, 22350 Lund, Sweden

Assem Malhotra's response to the BMJ statins censorship is here:

And Zoe Harcombe's analysis of both matters is here: 

Saturated fat IS good for you, but how much polyunsaturated fat do you need?

Working on the "Real Food" AUT dietary guidelines submission it became clear that neither the epidemiology of the lipid hypothesis nor the RCT experiments testing it were designed to separate the supposed artery-clogging effect of saturated fat from the purported heart-healthy effect of polyunsaturated fat.
What we had was a series of comparisons of higher SFA and lower PUFA vs. lower SFA and higher PUFA. There were no investigations of either higher SFA in a diet with optimal PUFA, or of deficient PUFA in a diet also low in SFA.
The former of these, higher SFA in a diet with optimal PUFA, is what the low-carbohydrate, high-fat (LCHF) diet supplies. The latter is a danger on a low-fat diet, so "let them eat margarine".

1946 Dietary Guidelines - not bad at all.

Richard Lehman described the mindset in a recent BMJ blog: 
If I despair of meta-analyses, what can I say about dietary surveys? Actually, they’re quite fascinating, though they rarely bear any definable relation to human health. Diet and religion are often closely aligned. The authors of this paper have got religion bad: “Diet is one of the fundamental risk factors for health, disease, and disability in the world. Indeed, given that trends in metabolic risk factors such as blood pressure, cholesterol, glucose, and body mass index are being largely driven by nutrition, suboptimal diet is the single leading modifiable cause of poor health in the world, exceeding the burdens due to tobacco and excess alcohol consumption combined.” They then go on to look at fat. Why, I know not. But it is quite interesting to see which countries eat what types of fat. Where people eat more saturated fat, they often eat more unsaturated fat. For all I know this may help to explain why nearly everyone everywhere is enjoying their food more and living longer.
In the paper Richard Lehman is discussing, we find the alarming statement that the Centre for Disease Control (which really should be worrying more about emergent viruses and antibiotic-resistant bacteria and less about fat) thinks that getting 13% of our energy from linoleic acid (omega 6 PUFA) will be "optimal". If that's optimal, what do they consider an excess? This crazy figure is certain to be based on the amount of linoleic acid required to reduce serum LDL to a particular "healthy" target across a Western population, with no thought given to metabolic health, and bearing no relation to any intake humans might have been exposed to for any period in their evolutionary history.

As Peter D. said in a recent comments thread, "You have a basic assumption that blood lipids cause CVD. You will make many wrong choices based on this hypothesis." Now, I don't know what causes CVD. It could be blood lipids - there are intelligent people who think that small, dense LDL particles typical of refined-carbohydrate diets rip up the arterial walls like stilettos on a ballroom floor. But I do know that the assumption that blood lipids cause CVD has led to many wrong choices. Wrong choices in the supermarket. Wrong choices in the design of experiments. Wrong choices in the interpretation of epidemiological data. Imagine what useful drugs statins might be if they were not over-prescribed on the basis of LDL counts, with results like this.

Many analyses of the "lipid hypothesis" epidemiology and RCTs failed to distinguish between omega 6 and omega 3 PUFA, or between vegetable PUFA (linoleic acid and alpha linolenic acid) and long chain polyunsaturated fats found in animal foods like EPA, DPA, DHA and arachadonic acid. This is understandable because, when Ancel Keys cooked up the lipid hypothesis, no-one knew that omega 3 fatty acids existed, let alone that they were essential nutrients. I'm not even sure if anyone realised that omega 6 was essential back then.
We are stuck with an article of faith from the Dark Ages. A diet high in saturated fats that happens to be deficient in polyunsaturated fats - say with fats supplied exclusively from tallow and hydrogenated shortening, with over-cooked boiled meat or deep-fried fish, milk, boiled greens, sugar, and highly refined grains - which was the mid-20th century diet for many in the Westernised world - can be deficient in PUFA. Smoking and drinking and the general lack of antioxidants in the diet, as well as the effect of insulin from the refined carbohydrate, will tend to squander what PUFA there is. Not surprising if this population has more CVD. What will be surprising is, if the saturated fat has anything to do with it. That diet will also be high in monounsaturated fat (beef olein is the MUFA from tallow, used in old-school chip shop fryers), but somehow MUFA gets a pass. It's all very unsatisfactory.


Is there any research that can help us sort out the difference between a lack of PUFA and an excess of SFA? Well, maybe. We can at least see the difference between an excess of PUFA, and a lack of SFA.This study by Amin A. Nanji and Samuel French is an ecological study comparable to Ancel Key's "7 Countries" study, except that it includes 17 countries.
Mortality from cirrhosis in many countries deviates markedly from that expected for a given per capita alcohol intake. We investigated the possibility that dietary factors might explain the deviation expected and actual mortality rates in different countries. Deviations from expected cirrhosis mortality was calculated as a percentage for 17 different countries, all of whom had carrier rates for hepatitis B virus of less than 2%. The percentage of deviation was correlated with dietary intake of saturated fat, polyunsaturated fat, cholesterol, and also with mortality from ischemic heart disease. The percentage of deviation correlated inversely with dietary cholesterol (r= -0.86, p 0.001) and saturated fat (r= -0.80, p 0.001) and positively with polyunsaturated fats (r= -0.55 p 0.05). This suggests that both saturated fat and cholesterol protect against alcoholic cirrhosis while polyunsaturated fats promote cirrhosis. The correlation between percentage of deviation and ischemic heart disease (r= -0.78, p 0.002) suggests that those factors that promote ischemic heart disease protect against alcoholic cirrhosis.


If the factors that promote IHD protect against alcoholic liver disease (ALD), what are they? We can perhaps discard the red herring of cholesterol, which is a marker for animal fat, and which indicates consumption of foods (such as eggs) which are also rich in the essential hepatoprotective nutrient choline. Cholesterol does protect against ALD tested separately, but coconut MCTs (no cholesterol, no PUFA) gives the same protection as tallow (cholesterol, 1% PUFA) when the two are compared.
There has been a large body of animal experimentation designed to elucidate the link between alcoholic liver disease and dietary fats, with occasional testing of acetaminophen (paracetamol) toxicity in the same model. These papers have been analysed expertly by Victoria Prince on her blog and I will not duplicate her efforts.
http://principleintopractice.com/2012/07/23/liver-and-lipids/
http://principleintopractice.com/2012/08/02/liver-saving-saturated-fats/It can quite clearly be seen in Victoria Prince's third liver-and-lipids post below that there are mechanisms whereby saturated fats can have health benefits, distinct from the restriction of PUFA, because saturated fats from coconut and cocoa protect the liver in different ways.
"Thus it seems that dietary MCTs work in a way that maintains the expression of gut tight junction proteins, preventing endotoxin from making it into the circulation, while long chain saturated fats work in a way that increases endotoxin-binding proteins in the liver.  Both prevent endotoxin-induced damage in the liver, but in very different and distinct ways." This is not just relevant to alcoholics and people who consume paracetamol; the fact that long-chain SFAs make the liver less sensitive to LPS is relevant to the studies showing serum markers of dairy fat intake are associated with diabetes protection, because liver inflammation is a precursor to diabetes. And the fact that MCT, made from fats you can only get in significant amounts from coconut or dairy fat, maintains the integrity of the gut, is relevant to the epidemiological studies showing that children who eat margarine and drink low-fat milk have a higher rate of allergies and asthma compared to children who eat butter and drink full-fat milk.
Saturated fats are good for you. Get over it.
http://principleintopractice.com/2013/12/27/chocolate-and-coconut-for-health/


The high fat model of alcoholic liver disease was developed because rats fed normal chow plus alcohol would not develop ALD. The researchers concluded that polyunsaturated fats are "essential for the development of alcoholic liver disease", and that saturated fats are protective.
Diets enriched with saturated fatty acids protect against alcohol-induced liver injury, whereas diets containing polyunsaturated fatty acids promote liver injury (Nanji and French, 1989; Nanji et al., 1989, 1994a). Saturated fatty acids have also been reported to reverse established alcoholic liver injury (Nanji et al., 1995, 1996,1997b).
Now, the fats that promote liver injury are vegetable oils, typically in these tests corn oil and soy oil*. Thanks to the campaign against saturated fats, these are the kind of oils that the fast food eaten by drunken New Zealanders is prepared with today. This seems to be a failure in public health planning.

"You have a basic assumption that blood lipids cause CVD. You will make many wrong choices based on this hypothesis."

(*interestingly fish oil, which has a stronger association with CVD prevention than omega 6, also has a greater promoting effect on alcoholic liver disease, albeit in quantities many times greater than anyone would ever include in their diet. And deficiencies of PUFA, particularly AA, EPA, and DHA, also play a part in ALD, so Samuel French suggsts that alcoholics be advised to replenish these fats by eating "Mediterranean diet" type foods whenever they're in recovery).

The rat model of alcoholic liver disease demonstrates that in this case the effects of high PUFA, while they can be confused with those of low SFA, are not the same. It also demonstrates that the SFA/MUFA ratio of the non-PUFA fat makes little difference (olive oil is almost as protective as beef tallow against acetaminophen liver damage; it seems an oversight that olive oil has not been included in the alcohol experiments, considering how widely it is consumed).
The link between SFA and CVD disappears when SFA is considered separately ("monotonically"), rather than as a marker for PUFA deficiency. The protective association between omega 3 PUFA (the PUFA less likely to be optimal) and CVD remains about the same when these nutrients are considered monotonically, as in the 2013 Singapore Chinese Health study by Koh et al. People who ate more DHA, EPA, and ALA had significantly lower rates of CVD mortality - and they also ate more saturated fat, monounsaturated fat, and omega 6 PUFA, all increasing stepwise with omega 3 across the quartiles as CVD mortality decreased. "Where people eat more saturated fat, they often eat more unsaturated fat. For all I know this may help to explain why nearly everyone everywhere is enjoying their food more and living longer." 
The inverse association between omega 3 and CVD (0.83 OR) is seen with total omega 6 intakes of, on average, 9.9g per day, or 4-5% of energy - almost exactly the same as healthy New Zealanders ate in this paper, and much less than the crazy CDC projection of 13%. All things being equal, the people who eat the most fat, assuming they are not eating solely hydrogenated industrial fats or exclusively low-PUFA fats such as tallow, but are instead getting some fats from wholefoods, including fish, are surely eating enough PUFA to have an optimal intake for CVD prevention, regardless of any effect on blood lipids.

Polyunsaturated fats are essential nutrients, but also highly reactive and bioactive molecules. This means that the association between intake and mortality will follow a fairly steep U-curve, with a "sweet spot" in the middle. Saturated fats are inessential nutrients with low reactivity. The association curve between intake and mortality is likely so flat my dog could skate it.

(not my actual dog)

PUFA, MUFA and SFA occur together in whole foods and in traditional fats and oils. They are not easily separated, even in the laboratory. You can buy pure sugar for a few dollars in the supermarket, it's easily separated from the foods it occurs in, usually to be ladled back into some other food in excessive quantities. You can probably buy purified long-chain saturated fats like palmitic acid from Sigma Aldrich if you have the money and inclination, and MCT is a processed form of medium-chain saturated fat that is sometimes supplemented by ketogenic dieters; I've never seen it, but I've heard it's expensive.
Most people eating a LCHF diet, even those who think "saturated fat is good for you", are not going to go that far. Few are even going to use butter or coconut oil as their only fats, and anyone eating a variety of wholefoods that have been made palatable but not cooked to death is likely to have an optimal PUFA intake, whatever that is.