Giant Puff Ball with Garlic and Rosemary


…served here with scrambled eggs and smoked salmon.

✓Gluten-free ✓Grain-free ✓Sugar free ✓Low-carb ✓Dairy-free option

Here’s one for the hunter-gatherers amongst you: If you are lucky enough to come across this excellent wild-mushroom, it’s easy to cook, mild flavoured, melt in the mouth and looks pretty on the plate…

First catch your puffball…

When you first stumble upon the fruiting body of the giant puffball fungus (Calvatia gigantea) it can be a little unsettling. These are one of the largest edible fungi in the UK and are found most often in rough grass or pasture.

We thought ours was some rubbish left in the countryside and went to pick it up – only realising what we were dealing with after dislodging it from its tiny umbilical earth-stalk. We found three others close by, but just took the one we had detached, which was the size of a small football.

Despite a little slug damage, the puffball was in good condition – firm, white – at its peak for eating. At their best the flesh is a consistent texture all the way through and squeaks a little as it is cut. Once they start to go over they lose their solidity, and become yellow or brown – not so good. Really old ones are like a dried up brown bag and puff spores like some gothic talc dispenser at the slightest touch, which is what they are really all about as a fungal reproductive organ.

Cooking Giant Puffball

Once home, the puffball needs only a quick wipe over to remove dirt. It can be stored in the fridge until you are ready to use it.

Collect the other ingredients: Fresh garlic and rosemary (ours came straight from the garden), olive oil, salt and pepper and your favourite oil for frying (I used goat’s ghee which burns less readily than with olive oil).

Crush the peeled garlic cloves with a little salt to make a paste. Add a little olive oil.

Cut the puffball into half inch (1cm) thick slices. Each slice may need cutting in half to fit in your pan, but they do shrink a little during cooking.

Spread the crushed garlic paste on both sides of the puffball slices. Add chopped fresh rosemary. Small sprig tips can be pushed into the flesh.

Heat a large pan with plenty of butter, ghee or other fat of your choice. Fry for a few minutes on medium heat.

Turn and fry on the other side for another minute or two. They should develop a nice colour. Don’t overdo it or you will burn the garlic.

That’s it! They are ready to serve.

I made scrambled egg to go with them, along with some smoked salmon. We had it for Sunday brunch for two. Delicious.

The remaining 3/4 of the puffball went in the fridge and was cooked in a similar way over the next few days with our evening meals: once as a side dish interleaved with sliced fried aubergine (egg plant), and today with roast duck and salad.

Tomorrow I’m going to try the last of my giant puff ball with fried halloumi. I think they will go together really nicely.

After that. Who knows how long I’ll have to wait to come across another Jiggly-puff ball. But I’ll be ready to catch it when I do…

 

 

Low fat (but not full fat) dairy associated with increased risk of Parkinson’s disease

Read time: 4.5 minutes (850 words)

Intro

MedPage Today [full article here] drew my attention to a recent Harvard study published in the journal Neurology [abstract herewhich took a closer look at previously identified associations between dairy products and Parkinsons Disease. Their analyses were based on data from two large prospective cohort studies, the Nurses’ Health Study (n = 80,736) and the Health Professionals Follow-up Study (n = 48,610), with a total of 26 and 24 years of follow-up, respectively. An previous study (see below) found an increased risk of Parkinson’s with higher levels of dairy protein consumption.

The latest study looked more carefully at the different types of dairy product. They found that among those who ate 3 or more portions of low fat dairy per day (skimmed milk, low fat cheese and yogurt etc) 4 in 1000 went on to develop Parkinson’s disease, whereas among those who ate no portions of low fat dairy only 3 in 1000 developed the disease.

Comparing the two groups that equates to a roughly 33% increased relative risk. Of course that is only a rather piffling 0.1% absolute risk increase – hardly anything to worry about in the grand scheme of things. What makes this study interesting, however, is that the association did not exist for full fat dairy products only low fat ones.

Uric acid and Parkinson’s disease

The study’s authors speculate that the increased risk seen in the low fat milk group may be due to the ability of milk protein (casein and lactalbumin) to reduce uric acid levels. Parkinson’s disease and uric acid? I wasn’t aware of this link, so started digging into the research…

A particularly helpful review in Practical Neurology [Uric Acid’s Relationship with Stroke and Parkinson’s Disease: A Review] filled me in on the background.

It turns out that there is a growing body of evidence demonstrating an association between low uric acid levels and incidence of Parkinson’s disease. Not only do Parkinson’s sufferers tend to have have low levels of uric acid, but those with higher levels have slower and less aggressive progression of the disease. Importantly, some studies have identified that low uric acid levels four years prior to the onset of Parkinson’s symptoms has a stronger association than levels at onset of symptoms, suggesting that uric acid is linked to the  pathogenesis of Parkinson’s.

Uric acid BTW is an intriguing endogenous antioxidant which although primarily synthesised by the body is also influenced by diet. Excess levels can lead to the formation of crystals which is the basis of the painful condition gout, but can also contribute to kidney stones and kidney damage. Foods containing purines, such as shellfish, offal, meat and beer, can raise uric acid levels, as can alcohol and fructose, so should be avoided if you suffer from gout or kidney stones. The idea that such foods may be protective against Parkinson’s is interesting (although clearly one would not want to go as far as to cause gout!) On the other hand, dairy, cherries and vitamin C are associated with lower risk of gout and are classed as hypouricemic foods as they reduce uric acid levels.

It is believed that uric acid may exert a neuro-protective effect through it’s antioxidant action:

It has been hypothesized that uric acid reduces oxidative stress on neurons. This may have a significant bearing on therapeutic management of disease, as many neurological disorders are believed to result from oxidative stress. As a potentially modifiable risk factor, the prospect for uric acid and its derivatives to play a role in disease modification or prevention has great potential. – Pello et al, 2009

Studies looking at dietary associations with Parkinson’s disease have identified that uric acid lowering foods (e.g. dairy) are always associated with an increased risk of Parkinson’s, except for one. Vitamin C is the only uric acid lowering nutrient associated with reduced Parkinson’s risk: possibly because it is a powerful anti-oxidant itself.

Results from an earlier analysis of the Health Professionals Follow-up Study found clear trends indicating reduced incidence of Parkinson’s disease with increasing consumption of fructose and alcohol (uric acid raising foods) and an increased risk with higher levels of dairy protein consumption (a uric acid lowering food) Adapted from Xiang Gao et al, 2008

Full fat dairy

In the new study the increased risk for Parkinson’s disease was only associated with low fat dairy, not full fat. Why wasn’t full fat dairy associated with an increased risk of Parkinson’s?

For now there is no clear answer, but according to MedPage Today the authors of the study say “The lack of association with full-fat dairy products could be due to a countervailing effect of saturated fats. I think more research is needed to better understand the mechanisms involved in this association,”

The benefits of dairy fats have come up time and again, yet I still know many people who avoid full fat milk, cream, cheese and butter. See our posts:

Bottom Line

The size of the increased absolute risk of Parkinson’s disease associated with consuming low fat dairy products (0.1%) is too small to make it a reason in and of itself to avoid low fat dairy – unless of course, you have a family history of the disease in which case every bit of risk reduction helps.

For all of us, however, this study adds to the evidence of the benefits of full fat over low-fat dairy.

References

  • Intake of dairy foods and risk of Parkinson diseaseKatherine C. Hughes et al, Neurology, June 2017 [Abstract]
  • Low-Fat Dairy Linked to Small Increased Risk for PDKate Kneisel, Contributing Writer, MedPage Today, June 2017 [Full article]
  • Uric Acid’s Relationship with Stroke and Parkinson’s Disease: A Review Scott Pello et al, Practical neurology, Jul/Aug 2009 [Full article]
  • Diet, Urate, and Parkinson’s Disease Risk in Men, Xiang Gao et al, American journal of epidemiology, 2008 [PMC full text]

In the News

  • Why you’re better off eating FULL fat dairy: Consuming three or more portions of the low fat variety of yoghurt, milk or cheese raises the risk of Parkinson’s disease, Daily Mail [Online Article]
  • Low-fat milk linked to Parkinson’s risk, The Times [Online Article]

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.

Results

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.

Conclusion

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

References

Gluten-free diet MAY be unhealthy and MAY increase risk of heart attack (or not)

OK, so I made up the quote above, but it captures a certain zeitgeist that’s in the air right now. The media is all too keen to uncritically give gluten-free and clean diets a kicking at the moment, wagging fingers at all those ‘silly people’ who fell for the anti-gluten message even though they don’t have coeliac disease – what fools!

Except, as we have explained in multiple articles on this site, gluten has a far greater reach than that 1% who have classic coeliac disease. Non coeliac gluten sensitivity (NCGS) is a recognised and studied condition, with an estimated prevalence of up to 6% of the population.

And even a cursory look behind these dismissive headlines shows that the studies they are based on add almost nothing to our understanding of gluten pathology, and indeed contradict themselves. Continue reading

Paleo veggies (video and infographic)

MODERN WILD FOOD GATHERING. When you know what to look for there are plenty of edible wild plants out there. How do they fit into a paleo diet?

There have recently been a number of articles making pronouncements on the original paleo diet, as eaten by our paleolithic ancestors. At the end of last year, December 2016, we had…

  • Ancient leftovers show the real Paleo diet was a veggie feast (New Scientist)
  • Secrets of the paleo diet: Discovery reveals plant-based menu of prehistoric man (Eureka Alert)

Then in March this year…

The more recent articles appeared following a paper by Laura Weyrich et al. published in Nature, March 2017, titled Neanderthal behaviour, diet, and disease inferred from ancient DNA in dental calculus. Afifah has written a post about the herbal medicines these Neanderthals were using, and we are going to publish a guest post addressing the vegetarian claim shortly.

The December articles on paleo veggies were prompted by an Israeli study (Melamed et al. PNAS) which identified the remains of a wide variety of plant food remains in a cave in the Levant (modern Israel). The 780,000 years old remains are unusual as plant materials are rarely preserved at such sites, so this paper provides some insight into the plants resources used by our ancient ancestor homo erectus.

The remnants include no fewer than 55  different species including roots, seeds, nuts, fruit and leaves. Many of these resources were seasonal and some required simple processing and cooking. Here is the New Scientist Video that accompanied their article, which, I think you will agree, has a touch of the Blue Peter about it:

You would think from the headlines that evidence that our ancestors ate a wide variety of plant foods is new or somehow overturns Paleo Diet thinking. The media portrays the Paleo Diet as consisting largely of red meat, but that is wrong. Since its inception, proponents of the modern Paleo Diet such as Professor Lauren Cordain have argued that we should be eating more like hunter-gatherers. That has always meant both the gathering part (eating plant foods) as well as the hunting bit (eating animal products).

What is strange about the recent media pronouncements is that the research that stimulated them is perfectly in accordance with Paleo Diet principles. It seems as if the media are spinning these stories for the sake of headlines, which makes them, in the lingo of the day, fake news does it not?

Paleo Veggies

A careful reflection on the details of the foods identified in the Melamed study suggest a number of subtle paleo principles we might all like to take on board:

1. Increase the range of plant foods eaten

Few of us eat as wide a variety of plant foods as these ancient hominids. Modern hunter gatherers also tend to eat a far wider range of plant foods than typical modern humans. Not only does eating a range of plant foods increase the range of phytonutrients ingested, but it also reduces the exposure to the anti-nutrients found in any one plant source.

2. Eat seasonal food

This is really part of eating a wider range of plant foods and means we give our body a rest from any anti-nutrients when that food is out of season. Another plus is that seasonal foods can be higher in nutrients than those that are grown out of season under artificial light: that’s why winter tomatoes and early season strawberries often taste so insipid (taste being evidence of nutrients. Read ‘The Dorito Effect’ for more info on this amazing area of science).

3. Grow your own

Our ancient ancestors couldn’t preserve foods by canning and freezing. The freshest foods you can eat are those that you have just picked from your own garden, minutes before eating them. Here at Rosemary Cottage we grow a lot of our own fruit, berries, and veg (in fact we have a blog just about this here). They are packed with flavour and much higher in nutrients than supermarket varieties which are often picked under-ripe and have sat around for a couple of days on the shelves or have been flown half way round the world in a low oxygen ‘protective atmosphere’. If you haven’t got a garden or allotment you can buy living salads, mustard and cress, or growing herbs which provide the same fresh-food benefits.

4. Eat wonky, small, damaged  and organic veggies

Studies have shown that fruit and veg that have been exposed to harsh environmental conditions often have higher levels of nutrients as these compounds are primarily plant defence compounds. The perfect, class 1 fruit and veg we are offered in the supermarket have been overly pampered, sacrificing nutrients for looks. Many of the phytonutrients in veggies are concentrated in the colourful skins. Cherry tomatoes therefore pack more nutrients per kilo than their larger cousins as they have a larger surface are to volume ratio. Another benefit is that buying wonky veg increases farm profits and reduces food waste.

Organic fruit and veg tends to be less perfect, more blemished, usually class 2. Possibly for this reason they often have higher levels of nutrients (European Journal of Clinical Nutrition)

5. Include close-to-wild foods

It is a fact that many modern fruit and veg have been bred to increase water, sugars and starches and to be less bitter or sour – all of which has diluted the phytonutrients. Consequently, some of the most nutrient dense plant foods are those that have had the least selective breeding such as the following.

  • Leaves: Water cress, rocket, parsley, purslane, coriander leaf, miners lettuce, samphire, seaweed, tea
  • Fruit: Blueberries, red and white currents, blackberries, raspberries, alpine strawberries, olives, capers, sour cherries
  • Seeds: All nuts and seeds, coffee
  • Roots: Salsify, scorzonera, oca, pink-fir apple potatoes, water chestnuts, tiger nuts
  • Shoots: Sprouted seeds, mustard and cress, bamboo shoots, asparagus, sprouting broccoli
  • Flowers: Artichokes, borage, nasturtium, calendula

Many of the above need only be eaten in relatively small quantities as it is often the toxins in these plants that stimulate our immune system, so you don’t want to over do them. (See our post: The chemical warfare on your plate). For example, health benefits of tea and coffee seem to peak at 4 to 5 cups per day and the benefits of tree nuts levels off at 30g per day. In some cases over doing it can actually lead to harm: for example spinach, which if consumed every day can lead to kidney stones due to its high oxalic acid content. Daily juicing of spinach is therefore unwise, despite ‘green smoothie’ proponents waxing lyrical about it. (Read here about some of the problems with oxalates)

I’ve made a nice info-graphic of some wild-like foods you might want to try. Although they are not always easy to come by I have seen all of these in supermarkets or farmers markets over the last year or so. I have several of them in my current garden, and have eaten all of them at one time or another. How many have you tried?

Final thoughts

A little thought about the paleo veg principles above makes it clear why paleo veganism must have been a rare or intermittent occurrence. Few paleo veggies contain sufficient calories to sustain life, and due to their anti nutrients eating them in large quantities or for prolonged periods could easily lead to problems. Furthermore, the wild foods that are sufficiently high in calories (nuts, seeds and some tubers) would need to be available in quantity, year round, or starvation would be a very real risk. Changing availability and seasonality mean it is unlikely our ancestors were vegans for extended periods, although there would no doubt have been times when animal food sources were limited and they would have been forced to get by on plants alone. In short – humans are and have always been highly adaptable omnivores.

April News Round-up

This month: Great British Beef Week Ketogenic diet in diabetes Low fat foods cause weight gain MUFA’s may extend life Olive oil helps reverse insulin resistance Fewer arterial plaques with Med diet BMJ article triggers saturates fat spat The perfect cuppa Conventional thinking on salt challenged again Health benefits of cheese


St George’s Day and Great British Beef Week

I held a St George’s Day party on Sunday 23rd (which is also, rather appropriately, Shakespeare’s birthday), and I served a traditional roast beef joint with parsnips and carrots. Turns out, without knowing it at the time, I was right on the money as April 23rd was the start of the Great British Beef week!

According to the Grimsby Telegraph (April 30th) this year was the seventh annual Great British Beef Week, run by The Ladies in Beef, an organisation of female beef farmers who care passionately about British beef. It’s purpose is to support the hard working British beef farmers, which is exactly what I did by purchasing a 3.5 kg organic beef joint from Goodwood – our local producer.

My St Goerge’s day roast beef looked like the one above (but without the Yorkie puds (wheat) and taties (American originally). Interestingly, the Goodwood butcher suggested that I do not season the joint – “Let the flavour of the meat speak for itself” he said, and it certainly did! The unseasoned joint was placed on a bed of thickly sliced onions rings and popped in an oven that had been pre-heated to its highest temperature. Once in, it was turned down to 140°C for 1hr 25 minutes. My guests were full of praise … very gratifying.

If you missed out during this year’s Great British Beef Week, don’t worry, you can cook it all year round!  The Telegraph (April 26th) has a range of British Beef recipes to inspire you (just avoid the ones that use gluten)

Ketogenic diet valuable in diabetes

Diabetes.co.uk (Mar 28th) reports on a trial, conducted by Stephen Phinney and Jeff Volek who placed 262 overweight participants with type 2 diabetes on a ketogenic diet for 10 weeks (carb intake < 30g per day, increase fat, and modest protein). Key findings:

  • HbA1C levels dropped an average of 20%, with half returning to normal (non-diabetic) levels by the end of the study
  • 7.2% weight loss; 20% reduction in triglycerides
  • 60% had one or more medications reduced in number and dosage or, in some cases, discontinued altogether

A two year trial is in the pipeline.

Volek and Phinney have been working in this field for a couple of decades and have an excellent track record in low carb high fat science. They have at least two books on the subject, so please look at their work online.

Low fat foods can cause weight gain and lead to fatty liver disease

Low fat yogurt packaged as heart healthy, but it contains nearly 5 teaspoons of sugar per serving (see chart of sugar in other low fat foods)

In 2014 The Telegraph undertook a study which found that many low fat diet foods contained high levels of sugars. In one case a “low fat” meal contained almost six times the sugar levels of its “full fat” equivalent dish. Many people have suggested that the sugar may be less healthy than the fat it replaces, and now a new study reported in Medical Daily (April 26th) confirms this.

In the study mice that were fed a high-sugar, low-fat diet had an increase in liver fat, body weight, and body fat, despite consuming the same amount of calories as the control mice. Compared to mice fed a high fat diet, sugar calories were found to cause twice as much fat accumulation as the fat calories they replaced.

“Most so-called diet products containing low or no fat have an increased amount of sugar and are camouflaged under fancy names, giving the impression that they are healthy, but the reality is that those foods may damage the liver and lead to obesity as well,” said the study’s lead investigator, Krzysztof Czaja

Monounsaturated fats extend life in animal study

Eureka Alert (April 5th) reports on an intriguing study from Stanford University published in Nature, of longevity in roundworms which found that feeding them monounsaturated fat increased lifespan in a similar way to calorie restriction, despite the fact that they put on weight.

Monounsaturated fats are found in high levels in olive oil, rape seed and avocado oils, and also in beef fat and lard. Whilst mentioning olive oil a recent study has also shown that…

Olive oil helps reverse insulin resistance

The Express (April 11th) reports on a mouse study that showed a compound found in olive oil (hydroxytyrosol) can reverse insulin resistance and fatty liver induced by an obesogenic diet. This adds to research published in December 2016 that showed this compound also reduced oxidative damage in cells and may contribute to explaining some of the benefits of a Mediterranean diet…

Fewer arterial plaques with real-world adherence to Mediterranean Diet

Adherence to a Mediterranean-style diet showed a dose-dependent protective association with the presence, number, and thickness of atherosclerotic plaques independent of other risk factors, in a new study (Medscape, April 26th).

BMJ article triggers saturated fat spat

The Guardian (April 25th) gives a good account of the controversy taking place amongst scientists over recent claims and counterclaims over the health credentials surrounding saturated fat. Worth a read: Good for a laugh.

The Perfect Cuppa

The Mail Online (April 18th) reports on a study that found the beneficial compounds in tea are most available when the tea has been brewed for longer. The study author also found that adding milk does not reduce the availability of these compounds. He recommends drinking three cups per day.

Conventional thinking on salt challenged again… and again.

We have written several posts challenging conventional thinking on the supposed harms of salt (see here and here). So we were interested to read in The Independent (April 17th) that a study investigating a simulated mission to mars which kept 10 men sealed in living quarters and given a strictly controlled diet for a period of 205 days. Unexpectedly, when given a high salt diet the participants drank less but were also hungrier. The results were confirmed in mice too. It appears that although salty food leads to an initial thirst (hence salted peanuts in the pub) over the long term the total intake of water is less.

More news on salt front came in on April 26th, in The Express, with an article on a recent study looking at blood pressure and sodium intake. The researchers found the participants who consumed less than 2,500 milligrams of sodium a day – about the equivalent of 6g of salt, had higher blood pressure than participants who consumed higher amounts of sodium.

“We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure. Our findings add to growing evidence that current recommendations for sodium intake may be misguided.”

Salt – good or bad?
Seems that worrying about it is more likely to raise your blood pressure than eating it!

Health Benefits of Cheese

Wow. April 2017 was quite the month for cheese news. Goggle (April 28th) celebrated the 256th birthday of Marie Harel, the creator of Camembert in 1791, with a Google Doodle which provided a slideshow showing the steps involved in making this famous cheese (take a look here). As an aside, I think Brie and Camembert are the same thing, just in different shapes. Any comments anyone…?

Meanwhile, yet another study showing the benefits of cheese made the headlines with The Mail (April 24th) claiming “Eating cheese could prevent you from getting liver cancer – and it may even help you to reach 100!” – weirdly due to it containing spermidine (?!?)

Spurred on by the spermidine The Telegraph (April 25th) went further, pushing out the cheese boat with ‘5 surprising health benefits of cheese’. Here are their headings to tempt you to read more…

  1. Boosts your immune system
  2. The secret to longer life?
  3. Prevents tooth decay
  4. Helps with weight loss
  5. Makes you smarter

Finally, The Huff Post UK (April 25th) went just a bit too far with “7 Perfectly Valid Reasons To Eat More Cheese”. But really, that’s just showing off. Lets just gaze at a picture of lots of lovely cheeses…

An important and often overlooked benefit of cheeses, is that many – especially aged varieties – contain the precious vitamin K2, also known as menaquinone 7. This is not the same as vitamin K which is found in green vegetables, but is bacterially produced in cheeses during fermentation, and is particularly high in Brie and Gouda.

In the body K2 functions to guide calcium to the skeletal tissue, and prevent it being deposited, or rather, dumped, in soft tissues such as the aorta and other blood vessels where it contributes to atherosclerosis (sclerosis means hardening)Calcium in the wrong place leads to ‘calcification’ and having enough K2 to prevent this is one of the reasons for cheeses being a ‘top food’ in my reckoning.

Although some people are allergic to cows milk, many find they can tolerate goat and sheep milk cheeses which are increasingly available. The true unfortunates are those that cannot even tolerate these dairy products and they will need a regular K2 supplementation. Without sufficient K2 osteoporosis and calcification will occur. Clearly not a good state of affairs, so bring on the cheese trolley!

Gluten Update April 2017

The effects of gluten are not confined to just the 1% of the population that suffer with Coeliac Disease and the estimated 6% who suffer with Non-Coeliac Gluten Sensitivity, but can have detrimental effects in everyone. In these updates we share some of the latest research.

  • Effects of gluten on gluten-tolerant mice
  • Relatives of coeliacs often have gluten related disorders
  • NCGS persists even after 8 years on gluten free diet
  • Gluten free diet prevents progression of potential coeliacs
  • Coeliac disease may be triggered by a common virus
  • Coeliac disease and joint and bone problems

Read time: 11 minutes (2000 words)

Effects of gluten in otherwise gluten-tolerant mice

Dietary gluten causes severe disorders like celiac disease in gluten-intolerant humans. However, currently understanding of its impact in tolerant individuals is limited.

A ground breaking study has undertaken the first detailed investigation into the effects of gluten on metabolism and microbiome in gluten tolerant mice. The purpose of the study was to identify the effects of an obesogenic diet with or without gliadin (a key, immunogenic component of gluten).

The team from The National Food Institute, Denmark (Li Zhang et al, 2017) analysed a huge array of parameters, including insulin resistance, histology of liver and adipose tissue, intestinal microbiota in three gut compartments, gut barrier function, gene expression, urinary metabolites and immune profiles in intestinal, lymphoid, liver and adipose tissues.

Using tightly controlled diets the researchers found that a relatively small change (exchanging casein for 4% gliadin) resulted in a considerable impact on the host response in the mouse model. The levels of gliadin used were comparable to that found in bread. The remainder of the diet was, however, higher in fat than a typical human meal (35g fat/100g).

The headline findings include:

  1. Gliadin Intake Affected Glucose and Lipid Metabolic Homeostasis
  2. Gliadin Intake Altered Gut Microbial Composition and Activity
  3. Gliadin Intake Caused Lower Expression of Gut Barrier Function Related Genes in Ileum
  4. Gliadin Intake Changed the Metabolic Signature of Urine
  5. Gliadin Did Not Affect Systemic Inflammatory Markers but Altered Immune Cell Composition in Liver and Inflammatory Phenotype of Visceral Adipose Tissue

The changes were predominately negative, but there is a huge amount of detail to unpack in this research, cetainly more than I want to go into in this post. That said, I will look a little more into the changes to the microbiome as they are particularly fascinating. If you are interested in going into the other areas more deeply then check out the full free text.

Changes to the intestinal microbiome

After nine weeks on the 4% gliadin diet levels of lactobacillus had fallen by more than 90%. (These are generally considered beneficial bacteria). Conversely, bacteria associated with detrimental health changes including Clostridium XI, Dorea and Coriobacteriaceae increased in abundance by more than ten fold.

Strains belonging to Clostridium XI, including also the opportunistic pathogen C. difficile, are associated with compromised health. Dorea spp. are found to be overrepresented in irritable bowel syndrome patients, and patients with non-alcoholic fatty liver disease. Coriobacteriaceae spp. have repeatedly been shown to be involved in host lipid metabolism, and many bacteria within this group are considered as opportunistic pathogens

One apparently positive change observed in the gliadin consuming mice was an increase in Akkermansia in the colon. This species is usually associated with beneficial effects on metabolic health and inflammation. However, it feeds primarily on mucin secreted from the gut wall, and the researchers suggest its proliferation may be due to increased turnover of the small intestine mucosa due to disrupted gut barrier function.

Another recent paper (The gut–kidney axis in IgA nephropathy: role of microbiota and diet on genetic predisposition, Coppo, April 2017) underscores the importance of gluten-microbiome interaction, in this case to the development of IgA nephropathy (Berger’s disease).

The importance of this research is that it is a major piece of work exploring the effects of gluten relevant to the ‘normal’, apparently gluten-tolerant population. It has shown a large range of measurable effects which will need to be investigated further, particularly to establish their relevance in humans. In terms of the gluten iceberg these researchers are undertaking the deep sea diving necessary to establish the extent of the sub surface portion of the gluten phenomena. I am sure we will see more research like this in the coming years.


First degree relatives of Coeliacs often have gluten related disorders despite testing negative for blood markers 

Here at the clinic we see a disproportionate number of patients who at some point in the consultation declare that one of their parents or siblings has coeliac disease, often as if this is some minor point that is hardly worth mentioning. Nothing could be further from the truth: The biggest risk factors for coeliac disease is being a first degree relative of a coeliac, with nearly four times the incidence than the general population.

The first-degree relatives (FDRs) of patients with coeliac disease are the main risk group for disease development.

– Vaquero et al, 2017

Parents, children or siblings of coeliacs should therefore have blood tests regularly, and if positive should immediately adopt a gluten free diet. A study by Nicola Imperatore et al, which I cover later in this post, has demonstrated the importance of early adoption of a gluten-free diet for anyone with positive coeliac blood tests, even when they have no  symptoms, to avoid progression of intestinal damage and immunological problems.

Some patients, however, claim that they have been screened for coeliac disease and have been told ‘they don’t have it’ – i.e. that their blood markers were negative. In many cases, however, I can tell from their symptoms that they are gluten sensitive despite the test results. Many go on to make remarkable progress once they adopt a properly gluten-free diet, but sometimes it can be an uphill struggle convincing them to give it a try. Such is the power of the medical establishment when it makes its decrees.

These clinical observations have recently received confirmation from a study published in the Journal of Gastroenterology and Hepatology (Vaquero et al, 2017), which investigated the value of a gluten free diet in first degree relatives who were negative for coeliac blood markers (anti-endomysial antibodies and raised anti-tissue transglutaminase ). In this study they invited 205 first degree relatives of known Coeliacs who were negative on blood tests to undergo genetic screening (for the HLA-DQ2/8 genes) and duodenal biopsy to check for intestinal damage. Symptoms were established by questionnaire at the start of the study, after which participants followed a three phase diet: (1) baseline diet (gluten containing) (2) gluten free diet (4 weeks) then (3) gluten ‘overload’ diet

Of 139 who completed the study HLA-DQ2/8 was positive in 78.4% of the participants (homozygous, 15.1%; heterozygous, 63.3%). Alterations to the intestinal mucosa were noted in 37.1% of participants who underwent duodenal biopsy (Marsh I, 32.7%; Marsh IIIa, 4.4%). At baseline more than half of the participants had gastrointestinal symptoms (57.6%), mainly associated with bloating (16.5%), constipation (15.1%), diarrhea (14.4%), and abdominal pain (5.8%). During the gluten-free phase this fell to just one quarter and increased agin during the gluten overload phase.

Symptom improvement during the gluten free diet was twice as common among women as men and three times as common among people with an existing autoimmune disorder. Both of these observations fit clinical patterns at Rosemary Cottage Clinic and are similar to risk factors identified in studies of Non Coeliac Gluten Sensitivity.

In conclusion: First degree relatives of coeliacs have a heightened risk of developing coeliac disease. Of those without coeliac blood markers many have intestinal damage. In addition gluten related symptoms are commonly present independent of intestinal damage. Such people would have to be classified as Non Coeliac Gluten Sensitive as they do not fit the definition of Coeliac.

Non Coeliac Gluten Sensistivity persists even after 8 years of a wheat-free diet

In a paper recently published in Gastroenterology (Carroccio et al, 2017) Italian researchers followed up 200 patients that had been diagnosed with NCGS many years earlier. 88% had experienced improved symptoms following their original diagnosis.

8 years later 148 of these individuals were still on a strict wheat-free diet, with virtually all of them (98%) reporting a continuation of symptom reduction. Among those that had not maintained a strict WFD only 58% had symptoms that were improved compared to the time of diagnosis.

The researchers repeated the double-blind placebo-controlled challenge with 22 patients, and found that 20 reacted to wheat.

This study demonstrates that NCGS is persistent, suggesting that it should be treated as a life long condition and a wheat-free diet adhered to.


A gluten-free diet prevents progression in Potential Coeliac Disease even when asymptomatic

Coeliac disease is diagnosed where patients have positive  blood tests (Anti-endomysial antibodies and raised anti-tissue transglutaminase) as well as evidence of villous atrophy on duodenal biopsy. In some cases, however, blood tests are positive, but there is little or no intestinal damage. Such situations are labelled Potential Coeliac Disease (PCD).

Until now it has not been clear whether such patients simply have a mild form of gluten intolerance, or whether they have early stages of Coeliac disease.  Furthermore, for the subset of PCD patients that have no gastrointestinal symptoms.

To answer these questions recent study an Italian team (Nicola Imperatore et al, Mar 2017) followed patients with PCD either on a gluten free diet or a gluten containing diet for a period of six years.

In short, those on the the gluten containing diet had increased intestinal damage and immune related disorders compared to those on the gluten-free diet. In addition, the asymptomatic patients who continued to consume gluten 69% developed coeliac-related symptoms, 46% developed villous atrophy and 61% immune mediated disorders.

This study underlines the importance of starting a gluten free diet as soon as possible following positive blood tests, regardless of symptoms and presence of villous atrophy.

Routine screening for Coeliac blood markers is not currently undertaken as many people that such tests would identify would prove to have no symptoms nor villous atrophy. It has been assumed that there would be no point in starting them on a gluten free diet as it was assumed that they would not go on to develop coeliac disease. This study challenges this position and demonstrates that many of these ‘false positives’ would indeed benefit from starting a gluten-free diet because they are at risk of developing villous atrophy and autoimmune diseases in the long term..

Coeliac Disease may be triggered by a common virus

It has long been known that the risk of coeliac disease is increased after various infections such as campylobacter, rotavirus and gastroenteritis. One hypothesis is that the presence
of both the pathogen and gluten presented simultaneously to the immune system  is enough to trigger coeliac disease.

Now a team from the University of Chicago, has found that exposing mice to a common reovirus called T1L can induce gluten intolerance. This virus was first identified in humans in the 1950s but has not been associated with any disease.

The team found that when they fed gluten to mice, those that were also infected with the virus produced two to three times as many antibodies to gluten as those that were virus free.

One of the Authors of the study Bana Jabri explained “Instead of mounting a tolerant, non-aggressive response, the immune system in the presence of the reovirus views gluten as being dangerous, promoting a destructive inflammatory response,”

The discovery has led the authors to speculate that a vaccine might be possible to prevent people from developing coeliac disease. Personally I think that’s unlikely, for a number of reasons. 1) gluten seems to cause disease by many pathways not just an aggressive immune response, 2) the researchers did not show that the mice went on to develop coeliac disease they just had a heightened immune response to gluten, 3) there is no evidence that all coeliacs had previously been infected with reovirus, and 4) physiological stressors other than pathogens appear to be able to trigger coeliac disease.

Source: New Scientist, Gluten allergy in coeliac disease may be provoked by virus (04/06/2017)

Coeliac Disease and Joint/Bone problems

In a recent letter to the journal Joint Bone Spine, Coline Daron et al report on their analysis finding 20‐30% cumulative incidence of arthralgia and arthritis among coeliac patients. They also identified an increased risk of osteoporosis:

Out of 11 case‐control studies featuring 1,008 patients with celiac disease and 13,706 controls, we noted a 2.73 [1.86‐3.99] higher risk of osteoporosis at any site in the celiac group. This increased risk was significant for femoral osteoporosis (OR=2.03 [95% CI: 1.11‐3.71]), and most of all for spinal osteoporosis (OR=7.2 [95% CI: 3.42‐15.18]. No increased risk of arthritis was noted in celiac patients compared to controls (OR=0.76 [95% CI: 0.16‐3.66]).

The authors call for physicians to undertake coeliac screening in cases of osteoporosis, arthralgia and arthritis where no obvious cause can be identified.

 

Oxtail Caserole, country style

✓Gluten-free ✓Grain-free ✓Sugar free ✓Low-carb ✓Cow-Dairy-free

This dish was incredibly easy to make, and super delicious to eat! What more can one desire when it comes to food?

The Ox tail was from Goodwood Farm and consisted of all different sizes, as you would expect, from the tail of the animal. There was thick fat round one side of the larger pieces, which can be seen in these photos, and it tasted very good indeed. Real melt-in-the-mouth fat, not chewy tough stuff at all. And all I had to do was chuck it in some hot ghee (which is great for high heat cooking as it doesn’t burn, as butter would. See how I make ghee here), add some carrot and celery sticks, some red wine and bone broth, and, Bob’s your uncle, dinner! I didn’t have much time that evening so just flung some cauliflower in a pan to accompany this classic dish, and it was a perfect match.

  • About a kilo or so of oxtail (which, at Goodwood’s wholesale prices is only £4 per kilo, or Waitrose – not organic though – £6.99 per kilo)
  • Two or three large onions, chopped
  • A handful of organic carrots, cut into thick batons
  • A few sticks of organic celery, cut into thick batons
  • Ghee – a large chunk

Season the oxtail chunks with plenty of salt and pepper. In a large cast iron pan heat the ghee, add onions and gently fry for 5 minutes. Add the seasoned pieces of oxtail, gradually turning them as they brown. Sling in the carrots and celery, and let them feel the heat for some minutes, moving it all around slowly. Crack open a jar of bone broth (I must write up how to make this… watch this space) and add it to the pan, then chuck in a glass or two of organic red wine. Stir. Cover with the lid and pop the pot in the oven at about 140°C and leave for a couple of hours.

Done.

Gone!