Amazing results challenge guidelines in new study

  • A new study challenges the dietary guidelines for heart health
  • MUFAs and omega 6 PUFAs not effective at reducing atherosclerosis risk
  • Omega 3 fish oils reverse triglycerides and weight gain in an animal model of insulin resistance, despite increased calories

Read time: 9 minutes (1400 words)

Guidlines for prevention of heart disease have shifted in recent years away from a simplistic ‘reduce total fat’ message towards a more nuanced emphasis on the type of fat. The current American Heart Association (AHA) recommendation is to ‘replace saturated fats with monounsaturated (MUFA) and polyunsaturated (PUFA) fats.’

For the purpose of this post, I am going to put aside my objection to the demonising of saturated fats and instead focus on the MUFA / PUFA alternatives recommended by the AHA. Similarly, I am not going to challenge the cholesterol hypothesis nor debate the merits or otherwise of lowering LDL cholesterol here. Instead I am going to look at a recent paper that studied the effects of MUFAs and PUFAs on atherosclerosis risk.

Note the terms n-3, n6- and n-9 in the title of this paper; these are just shorthand for omega-3 polyunsaturated fatty acids (ω3 PUFAs), omega-6 polyunsaturated fatty acids (ω6 PUFAs) and omega-9 monounsaturated fatty acids (ω9 MUFAs). I’ve made a quick reference guide for these below, showing typical foods high in each kind of fat:

The role of triglycerides in cardiovascular disease

Cardiovascular disease is often preceded by insulin resistance during which changes to the cholesterol delivery system increase the risk of atheroma formation in the artery wall. One of the hallmarks of insulin resistance is an increased production in very low density lipoproteins (VLDL) which are high in triglycerides.

The following is a quick explanation about triglycerides which you can skip if it’s a bit too much or you are already familiar with the subject…

The relevance of triglyceride-rich VLDL

VLDL is a carrier protein, produced by the liver, which transports triglycerides from the liver to the adipose (fat) tissue. It is important to note that these triglycerides are primarily endogenous i.e. manufactured by the body, rather than coming directly from dietary sources.

VLDL and triglycerides are raised principally by (1) Excess caloric intake from any source and (2) Carbohydrates (and especially fructose). In the former case the formation of VLDL can be seen as the body packing away and storing excess calories which are transported to the adipose tissue where they can be stored for a rainy day as fat.

In the case of carbohydrates, triglyceride rich VLDL is manufactured as a response to overwhelming surges in blood glucose that cannot be dealt with sufficiently by insulin induced uptake by the organs, especially muscle and liver glycogen stores. Indeed some have said that raised blood triglycerides are a reliable marker of carbohydrate consumption.

If cells become insulin resistant they stop taking up glucose effectively, increases the need for diversion of calories into the endogenous VLDL pathway. Hence insulin resistance is characterised by raised triglycerides.

Fructose has some unique metabolic problems as it does not trigger insulin, so cannot be taken up by cells as quickly as glucose. Instead it has to be processed by the liver, which can easily be overwhelmed, turning the excess into triglyceride rich VLDL.

It should not be surprising then, that the rats used in the study I am reviewing here, were made insulin resistant by feeding with sugar water (30% sucrose water) for 12 weeks. Sucrose is equal parts glucose and fructose, so their water contained 15% of each of these sugars.

So the aim of this study was to see how different dietary fats affect the dislipidemia associated with insulin resistance, especially the triglycerides. To do this the rats in this study were split into 5 groups: A control group on standard diet, whilst the other four were all made insulin resistant by feeding 30% sucrose water for 12 weeks. Of the four insulin resistant groups one was supplemented with n3 PUFAs, one with n6 PUFAs and one with n9 MUFAs.

It’s a pretty obvious experiment to undertake, and at this point you might rightly be asking why? Hasn’t this has all been done before? Surely the science on such a basic question is settled? With 60 years of American Heart Association advice you would think they had the science to back up their assertions and advice, wouldn’t you?

Well, shockingly, you would be wrong. As the authors note:

To our knowledge no studies have addressed the impact of dietary n-3, n-6 and n-9 fatty acids on VLDL composition and size in the [insulin resistant rodent] model.

There are several reasons why this basic question has not been answered before:

  1. Many previous studies looking at the effects of PUFAs on insulin resistance have applied n6 and n3 together, with only a few addressing n6 alone
  2. Previous studies evaluating n3 fish oils have used cod liver oil, which contains high levels of vitamin A, D and cholesterol, which could affect the findings.
  3. Assessment of MUFAs (n9) have usually used olive oil, which contains a broad range of phytochemicals which may be responsible for the beneficial heart effects observed in those studies, rather than the actual monounsaturated fats it contains.

To get round these problems ithe researchers used the following oils:

  • n3: fish oils from pressing whole fish, hence low in vitamin A and D.
  • n6: linoleic acid rich sunflower oil, low in phytonutrients
  • n9: high oleic sunflower oil

Rodent diets contained 15% w/w of each oil, which represents about 35% by calories i.e. similar to a standard western diet.


What they found was striking and deserves some careful reflection.

To make the findings a little easier to appreciate I have made a graph of some of the key results, but tables with all the study data are provided at the end of the post.

Data is expressed as mean percentage differences compared to the standard rodent chow diet (Reference). All four insulin resistant diets (IR) were sucrose rich; the three intervention diets consisted of supplementing with 15% w/w with n-3: deepwater fish oil; n-6: sunflower oil; n-9: high oleic sunflower oil.

Triglycerides ()  and Liver fat ()

The effects of the high sucrose feeding, as expected was a jump in triglycerides, which can be seen between the Reference and IR results above. Dramatically, supplementation with n3 fish oils almost completely reversed this dyslipidemia, returning VLDL particles to normal. Whilst remarkable, this is in line with previous epidemiological, human and animal studies that have shown n-3 PUFA have positive physiological effects on IR and lipid metabolism.

n6 and n9 oils, however, only weakly attenuated these harmful changes, failing to reverse the atherogenic state of the VLDL particles. This casts doubt on the validity of the American Heart Association recommendations.

In the case of the MUFA (n9), previous studies using olive oil have shown greater improvements in insulin resistance parameters, but as already noted, olive oil contains a broad range of bioactive phytochemicals (e.g. sterols and polyphenols). By using high oleic sunflower oil this study has been able to show that MUFAs do not of themselves produce these beneficial effects.

In relation to MUFAs this is particularly important as many processed food uses high MUFA oils that are low in phytonutrients as these can impart undesirable flavours.

Accumulated liver fat follows a similar pattern to plasma triglycerides. Again, n3 oils produce the best reductions in damage caused by insulin resistance.

Weight gain () and Calorie intake ()

Some of the most surprising results were seen in relation to caloric intake and weight gain. All groups of rats could eat ad libitum, yet in the n3 fish oils and n9 MUFA groups caloric intake was considerably raised. Extraordinarily, despite this those fed the n3 fish oils had no weight gain during this trial, whilst those fed the n9 high oleic oil had the most weight gain.

Rats fed the n6 sunflower oil supplemented diet had lower caloric intake than the n3 and n9 groups, but still gained more weight than the n3 group.


The authors of this study conclude:

In insulin resistance, while n-3 PUFA showed expected favorable effects, supplementation with n-6 PUFA and n-9 MUFA did not prevent atherogenic alterations of VLDL. Thus, the recommendations of supplementation with these fatty acids in general diet should be revised.

The authors seem somewhat nonchalant about the n3 fish oils, but it is worth reflecting for a moment just what those fish oils did: the rats were drinking insane quantities of sugar, eating a hyper caloric diet, yet avoided most of the effects of insulin resistance and weight gain. That’s a pretty impressive feat as far as I can see!

Implications for diet

This study looked at the effects of fat choice in the context of insulin resistant animal models. The results support and extend previous research in humans and epidemiological studies. Taken together these point to certain food choices: fish, seafood and olive oil are good choices based on these results; Omega 6 vegetable oils such as sunflower, safflower, corn and soya oils are best avoided, as are low-polyphenol MUFAs like high oleic oil and possibly filtered rapeseed (Canola) oil. A high quality fish oil supplement seems prudent too.

Based on the ideas suggested by this study cold pressed rapeseed oil is potentially interesting as like extra-virgin olive oil, it contains high levels of phytonutrients, but unlike olive oil it has significant levels of alpha linolenic acid (ALA), a short chain n3 fatty acid. Based on the results above I would expect it to have beneficial metabolic effects possibly similar to or slightly better than Olive oil. Well that’s my prediction. So lets see…

I searched Pubmed for “rapeseed cardiovascular”. Sure enough, in one of the first studies I found [Baxheinrich et al, 2012] patients with metabolic syndrome (which is just one step down from full blown insulin resistance), were placed on a low calorie diet enriched either with olive oil (high n9 MUFA, low n3 ALA) or cold pressed rapeseed oil (high n9 MUFA high n3 ALA) for six months. Although both groups improved similarly on many metabolic measures (body weight, systolic blood pressure, cholesterol, and insulin levels), the cold pressed rapeseed group had significantly lower triglycerides. That said rapeseed oil is probably less suitable than olive oil for high temperature cooking as the ALA it contains is very heat sensitive. Still, its a good choice for salad dressings and mayonnaise!

Additional data

For those of you who like to dig into the data here are some key tables from the study:

(1) Composition of diets; (2) Intakes and body weight; (3) Effects on adipose tissue/liver and serum parameters


The three wise herbalists brought… Gold, Frankincense and Myrrh




Everybody knows the story of the three wise men bringing gifts of Gold, Frankincense and Myrrh to the infant Jesus in the Christmas nativity. There is plenty of symbology around these iconic gifts allowing a host of interpretations. What I want to focus on here are some very real medical uses of the herbs Frankincense and Myrrh, and if you allow me a little bit of poetic licence, Saffron (as gold)…



Whilst the metallic element, gold, does have some medical uses, as a Medical Herbalist I do not use it, so I am going to talk about the golden herb saffron, which can literally be worth its weight in gold. [Daily Mail: How an ounce of saffron is more expensive than gold: Cultivation of exotic spice returns to Essex for the first time in 200 years]

Saffron is made from the stamen of the saffron crocus (Crocus sativus). Each crocus produces just three of these delicate strands per year, and they must be laboriously picked by hand before drying, at the right temperature and duration.

When used in cooking – such as saffron loaf or saffron rice – it adds a strong golden colour and has a distinctive aroma and flavour. I always add half a dozen strands of Kashmiri saffron when making a small pot of special gunpowder green tea. When used medicinally it has serotonergic (mood enhancing) effects, is an antioxidant, anti-inflammatory, anti-convulscent, has anti-timor effects, neuro-endocrine (hormone engaging) influence and has neuro-protective properties [ref].

Here is some evidence of medical efficacy:

  • Depression
    A 2014 review of the scientific literature [ref] identified six high quality studies that demonstrated  a positive effect, similar to that seen with anti-depressants drugs, and without the dependence or side effects.
  • Psychological and behavioural
    An excellent 2015 review paper from an American research team [ref] concluded: “Findings from initial clinical trials suggest that saffron may improve the symptoms and the effects of depression, premenstrual syndrome, sexual dysfunction and infertility, and excessive snacking behaviors.”
  • Cardiovascular
    It is reported that regions of the world that regularly consume saffron have lower levels of heart disease. The anti-atherosclerotic, antioxidant, anti-diabetes, hypotensive, anti-ischemic, anti-platelet aggregation effects of saffron suggest it is cardio protective and animal studies show this to be the case. [ref]
  • Diabetes
    Saffron has a hypoglycaemic effect and has been shown to raise insulin levels in diabetic rats with low insulin, whilst enhancing glucose uptake. Its antioxidant properties may reduce diabetic vascular complications too [ref].
  • Obesity & Weight Loss
    Saffron has been shown to reduce body weight in rats, whilst in humans it has been shown to reduce appetite and increase satiety [ref] “After 2 months, the subjects using the saffron extract reported a decrease in snacking and lost more weight than the control group”

Safety: The widespread use of saffron as a culinary spice suggests it is safe at those doses. This superb paper, published in 2012 by an Italian team of researchers reviews the known biological effects of this amazing herbal medicine [ref] and it concludes: “To date, very few adverse health effects of saffron have been demonstrated. At high doses (more than 5 g per day), it should be avoided in pregnancy owing to its uterine stimulation activity.” Well that’s fine, as it is therapeutic well below that dose. It is a significant antioxidant and anti-inflammatory, and since these processes a known to be the drivers of most major diseases I think it worth revisiting the use of this herb more widely. The problem is just the cost!



As well as being burned for incense in religious ceremonies this gum distinctly medicinal. Chewing on bobbles of frankincense is good for mouth ulcers and gum disease, but tastes like soap or turpentine. Mostly it is therefore used either as an essential oil or powdered and encapsulated. One can also concentrate the 5-Loxin component to optimise the anti-inflammatory properties, as in one of the products I stock.

This traditional medicine of the Middle East has expectorant, antiseptic, and even anxiolytic (i.e. calming) and anti-neurotic effects as well as the well recognised anti-inflammatory ones. Indeed recent studies have shown it has analgesic, tranquilising, anti-bacterial and anti-tumour effects too, which gives it a role in the treatment of quite a range of common conditions. [ref]

The following medicinal effects come from a 2016 review:

  • Gastro-Intestinal
    Its anti-inflammatory effect gives it a place in inflammatory bowel disease (i.e. ulcerative colitis and Crohn’s disease), irritable bowel syndrome, bronchitis and sinusitis. In human studies of colitis patients, the resin was far more effective than the standard drug: “Out of the patients treated with Boswellia gum resin, 70% went into remission while in the case of sulfasalazine [the standard drug it was compared to] the remission ratio was 40%”
  • Anti-fungal
    Frankincense is strongly anti-fungal towards candida species. As well as many other moulds including food borne moulds. (One wonders if it would be effective burned as incense to reduce mould spores in houses… )
  • Asthma
    Severity and risk of asthma attacks is reduced by consumption of Frankincense gum, or by inhalation of the smoke when burned.
  • Rheumatoid arthritis Multiple lines of evidence suggest that frankinscence could help via anti-oxidant and potent anti-inflammatory effects. One researcher noted that “at a dose of 200 mg/kg, B. serrata extracts shift the balance of cytokines towards a bone-protecting pattern”

Memory, Dementia, Alzheimer’s
There is considerable interest in the role of Frankincense gum in cognitive impairment as it has been shown to improve memory in animal models of Alzheimer’s [ref]. In fact recent studies have shown that it increases neurone formation in the hippocampus [ref], i.e. that part of the brain that is essential for new memory formation. A recent human study of cognitive impairment in multiple sclerosis found that it “showed significant improvement in visuospatial memory, but had no effect on verbal memory and information processing speed.” [ref]. I would not be using simply frankincense for dementia, as there are other very valuable measures that should be employed, but this resin, depending on the case, could play a significant role in a rounded treatment approach.

In my clinical practice I find Boswellia particularly useful in autoimmune disorders, and when inflammation suddenly occurs, such as polymyalgia rheumatica, for example, which can come on over night and cause severe joint pain, disability and exhaustion. The usual drugs used by doctors have real problems associated with them, as they are aimed at suppression of the immune system, which you cannot do without negative consequences, whereas taking a deeper look at what may have triggered the condition, and treating in a more thoughtful way with medicinal herbs, including frankincense, has been very successful to date with no long term adverse effects.



Another aromatic resinmyrrh, (Commiphora mol mol) also comes from the Middle East, in fact Yemen originally and it has been used in the Western Herbal Medicine tradition for hundreds of years. I prefer the alcoholic extract (tincture) to the resin itself for ease of use, and offer it as part of my Home Herbal set in a dropper bottle as shown above. It is part of the Home Herbal range of medicines that I encourage my patients to keep in their medicine cupboard at all times because it is so reliable, effective and practical to use.

Ten to twenty drops added to a glass of water makes an excellent gargle for sore throats, gingivitis (inflamed gums), receding gums, loose teeth, mouth ulcers, and as a general antiseptic mouth wash which can be swished between the teeth where toothbrush bristles may not reach. A few drops can be put onto the toothbrush along with toothpaste (or my favourite alternative – salt and sodium bicarbonate). Tincture of myrrh can be dabbed neat onto small cuts or bites as it is strongly antimicrobial, antiseptic and astringent, thus helping to defend against any nasty bugs that can get in when bitten by a mosquito or whenever the skin barrier is breached, and as an astringent it helps bring swelling down [ref]. It has been used successfully in the treatment of intestinal worms, as have certain other herbs, most of which, like myrrh, taste bad (to humans and to worms, clearly)!

Myrrh has many similar properties to Frankinscence, including analgesia (pain relief), anti-inflammatory and anti-obesity properties [ref]. I find it has a vital place in the treatment of most infections, including gastroenteritis, ‘flu, colds, sore throats, bronchitis, pneumonia etc, as well as ulcers in any tissue (incl legs, stomach and mouth) and in arthritis. As an anti-inflammatory it has a role in cancer [ref] along with other herbs and dietary measures.

Apart from the above uses, myrrh has also been used in leprosy and syphilis too, which, though it may sound far fetched is quite reasonable. It is a powerful antimicrobial herb, so any bacterial infections can sensibly be treated with this age old defender of health, including common candida albicans and staphylococcal infections. They didn’t give it to the Messiah for nothing! In fact midwives used to dab myrrh onto the cut umbilical cord of new born babes in the less hygienic environment of the past [ref].

  • Gastro-Intestinal
    The anti-spasmodic and anti-inflammatory effects of myrrh are of great value when treating inflamed gut disorders [ref]. As myrrh raises white blood cell numbers it assists in ulcer and wound healing too [ref]
  • Skin
    Myrrh has been shown to be effective at treating fungal infections of the skin [ref] including ringworm, and systemic fungal problems caused by candida albicans (once treated, maintenance through a low carbohydrate diet would be wise too).
  • Liver
    Myrrh has been shown to protect the liver from lipopolysaccharides (a major gut endotoxin) and “might be sufficient to combat cellular damage caused by various conditions that resemble fulminant hepatitis” according to researchers in Saudi Arabia [ref].
  • Obesity and Type 2 Diabetes
    Myrrh “has the ability to improve insulin sensitivity and delay the development of insulin resistance… and may be used as an adjuvant therapy for patients with insulin resistance.” [ref]
  • Parasites
    Here is an in-depth paper: Myrrh: A Significant Development in the Treatment of Parasites (pdf) by a colleague of mine, the Medical Herbalist Kerry Bone. Two of the most studied areas are for the treatment of schistosomiasis (a flatworm) and fasciola (a liver fluke) – two common parasitic infections in the tropics and subtropics [ref].

So, in wishing all my readers and patients a very Merry Christmas, I also want to encourage you to use your gold, frankincense and myrrh as wisely as those three wise men. Or rather, if you have any sort of medical problem or niggle, book an appointment with me and we will see what how best to approach it using medicinal herbs and nourishing foods. Chances are you will find me to be a wise woman too.