Atherogenesis in Mice

Another day, another plug for the diet-heart hypothesis in BBC Health, even when the study being reported on Scientists pinpoint fats danger is really about molecular genetics(Thorp et al.,Reduced Apoptosis and Plaque Necrosis in Advanced Atherosclerotic Lesions ofApoe and Ldlr Mice Lacking CHOP, Cell Metabolism ,Volume 9, Issue 5, 474-481, 6 May 2009, subscription required). The study showed that mice lacking a gene (CHOP) which helps to trigger cell death (apoptosis) had a 35% smaller area of plaques and 35% less apoptosis and 50% less necrosis (dead tissue) in plaques. To quote the researhers directly (as reported by the BBC):

Lead researcher Dr Ira Tabas said that previous research had suggested that this mechanism might be involvedin plaque rupture, but the magnitude of the effect uncovered in the latest study was a surprise.
He said: "The fact that we were able to isolate one gene encoding one protein with such a profound effect on plaque necrosis (death) was a big surprise."
Dr Tabas said the finding raised hopes of new drugs which could act on the key gene, or the associated mechanism, to cut the risk of dangerous plaques.
"Just about everybody in our society has atherosclerosis (thickening of the arteries) by the time we reach 20," he said.
"So the wave of the future in treating atherosclerosis will be in preventing harmless lesions in young people from becoming dangerous ones, or soothing dangerous plaques so they don't rupture as we age."

Never mind what effect such a treatment might have on necessary cell death (e.g. to deal with emerging cancers) in other parts of the body.

Anyway, what does this have to do with diet and the heart? Well, again from the BBC article:

Scientists have identified a genetic mechanism which appears to determine which fatty deposits in the arteries have the potential to kill us. Most of these plaques pose no risk to health, but a minority burst, forming blood clots, which can cause heart attacks or strokes. .....
Fatty deposits begin to form in the arteries of most people in their teens, but the vast majority are harmless.

Here we see the perpetuation of the myth that fat just floats around in the bloodstream clogging up our arteries like it would a drainage pipe. Plaque formation is a much more complex process than that and its genesis is still not fully understood (see for example, extensive discussion here or here).

But, ah you say, just read on ...

The researchers bred mice prone to develop plaques, and fed them a high-fat diet for 10 weeks.

So what was this high-fat diet? It was the TD.88137 Western Diet (Teklad Lab Animal Diets, Harlan Laboratories, Madison, WI) which consists of:

	g/kg
Casein	195.0
DL-Methionine	3.0
Sucrose	341.46
Corn Starch	150.0
Anhydrous Milkfat	210.0
Cholesterol	1.5
Cellulose	50.0
Mineral Mix, AIN-76 (170915)	35.0
Calcium Carbonate	4.0
Vitamin Mix, Teklad (40060)	10.0
Ethoxyquin, antioxidant	0.04

(Data from this pdf.)

This diet is 17.3% protein, 48.5% carbohydrate and 21.2% fat by weight, but 15.2% protein, 42.7% carbohydrate and 42.0% fat by energy, thus approximating a typical Western-style diet which is high in fat and simultaneously high in carbohydrate. Note that of the carbohydrates 70.4% by weight is sucrose! The mice are eating 30% of calories as sucrose. Now mice are not little people, but what does that kind of intake do to people?

How does this compare to a mouse's real diet?

From The Mouse in biomedical science (James G. Fox, Stephen W. Barthold, Muriel T. Davisson, Christian E. Newcomer, 2nd ed., Academic Press, 2007) p. 28 we learn that it is still debated whether mice are granivores, eating a wide range of cereals, oilseeds, and a variety of grass and plant seeds, or whether they live on a mix of plant and animal sources. However from the evidence presented in this book it appears that in many environments, mice eat small invertebrates for at least part of the year (i.e. when seeds are in short supply) or to supplement plant seed diets.

In short, the typical composition of a diet of invertebrates is high in fat and protein e.g. from p.41 in Marsupial nutrition, (Ian D. Hume, Cambridge University Press, 1999) it can range from 20-60% fat and 10-75% protein (by weight of dry matter) for typical things that a mouse might eat (insects and insect larvae). Cereals are typically 68-79% carbohydrate, around 10-15% protein and 2-7% fat, legumes are as much as 25% protein, typically 50-60% carbohydrate and only 1-2% fat whereas nuts (e.g. hazelnut) and oilseeds (e.g. sunflower) are typically about 15-25% protein, 50-60% fat and 15-20% carbohydrate (from various tables in On Food and Cooking, H. McGee, 1st ed. Unwin Hyman, 1984).

From this we can conclude that a typical wild mouse would for part of the year eat a diet that was mainly protein and fat and for another part of the year eat a diet that was high in carbohydrate - at least if it ate cereals, but not so much if it ate other types of seeds - but low in fat. It would not however be eating a lot of sucrose. The carbohydrate in grains and seeds is starch which is a polymer of glucose and does not contain fructose. As further support of this analysis here Peter of Hyperlipid considered data on what wild-type mice eat when given free choice: about 12% protein, 6% carbohydrate and 82% fat (all as proportions of energy).

A final note about the mice. The mice used in the experiment were either apoe or ldlr mice. Apoe mice lack a particular lipoprotein (apolipoprotein E) which is important in both the HDL and vLDL cholesterol transporters, in particular:

ApoE mediates high affinity binding of chylomicrons and vLDL particles to the LDL receptor, allowing for specific uptake of these particles by the liver, preventing the accumulation of cholesterol rich particles in the plasma
.....
Mice develop normally, but exhibit five times normal serum plasma cholesterol and spontaneous atherosclerotic lesions

Ldlr mice lack a proper LDL receptor and essentially mimic (familial) hypercholesterolaemia with a very high circulating LDL level and an increased propensity to develop atherosclerotic lesions amongst other things.

Does this not indicate that fat is the root cause? Well not necessarily.

vLDL is made in the liver to transport triglycerides (made from excess carbohydrates intake) to the tissues for use and storage. At this stage, it does not contain apoE: it has to pick that up from HDL on the way. ApoE contributes to its recognition and re-uptake by the liver after it has performed its delivery task or it loses its apoE and becomes an LDL particle and is taken up by body cells with an LDL receptor. So, this process will become disrupted in an apoe mouse which does not have a proper apoE protein. No wonder it ends up with excess blood cholesterol (which really means excess circulating lipoproteins). Similarly as ldlr mice lack the LDL receptor, they cannot remove the LDLs left at the end of the described process. On the other hand, after digestion, fat is absorbed either directly into the bloodstream - if the molecule is small - which gets it to the liver (where it may contribute to triglyceride production) or, for larger molecules, as chylomicrons which go via the lymphatic system into the bloodstream and from there directly to fat tissue for storage or to the liver to be used to provide fuel.
So which is more likely to contribute to the problem - the 21.2% of food (by weight) that comes as fat (most of which doesn't go straight to the liver anyway) or the 48.5% of food (by weight) that comes as carbohydrate - three-quarters of which is sucrose and half of that is fructose (i.e. 17% by weight of the total food intake) which goes straight to the liver and comes out as triglycerides.

Mediterranean Diet Score - What else does the model tell us?

A further analysis of the expected (from the model) vs the observed numbers within each diet score category and eating particular amounts of each food group throw up more interesting observations. This doesn't mean that we are claiming that people should behave like the model and that we expected that their food choices would not be internally correlated in some way. In fact, we expected that they would be (so do these researchers which is why they are trying to describe a dietary pattern); this data gives us information on what these correlations are.

We have already noted that meat & poultry intake is actually largely independent of the diet score. So, when researchers claim that a Mediterranean diet is low in meat, we will know that that is not borne out by this data.

Comparison of expected vs actual numbers in the low score (0-3) group shows that there are more people getting a low score because they score 0 for vegetables, fruit & nuts, legumes or fish consumption (i.e. they don't eat 'enough' of these). Conversely, in the high scoring group (6-9) there are more people than expected scoring a 1 in these same categories. There are also more people than expected scoring a 0 for meat & poultry, dairy and cereals in the high scoring group, i.e. they get a high score while still eating 'bad' amounts of these food groups. The suggestion here then is that the diet score is mainly a reflection of vegetable, fruit & nut, legume and fish consumption and is much less related to dairy and cereal consumption as well as being independent of meat consumption.

What about the predicted correlation between meat & poultry, dairy and the monounsaturated/saturated fat ratio? Whether this has any impact is very hard to determine. The main reason for this is that the postulated effect is obscured by the data presentation. To see why consider this thought experiment:

Let's assume our subject has a score of 6 so far and we have meat & poultry, dairy and the fat ratio still to determine. If either meat & poultry or dairy score 0 (i.e. greater than median consumption), this increases the chance that the fat ratio will also be scored 0, giving a final score of 7; if both meat & poultry and dairy score 0, then there is an even greater chance of fat ratio being 0, giving a final score of 6. But, we can't see the difference (i.e. that there are proportionally more scores of 6 and 7 and fewer of 8 than expected) because all scores 6-9 are lumped together. The same argument works in the other direction, making the scores 2 and 3 potentially more frequent than scores of 1, but again this effect is obscured when the low score includes 0-3. Perhaps this is why?

Data Patterns in the Mediterranean Diet Score

The original construction of the edifice known as the Mediterranean Diet began with a paper which used a scoring system to handle the mass of data that results when you give thousands of people food frequency questionnaires. The data manipulation is roughly like this: People say how often and how much they eat of typical dishes and foodstuffs; these quantities and frequencies are converted to daily food group consumption for which a score is given. RESULT massive amounts of data reduced to one number.

Let's recall the basics: the food groups were: vegetables, fruits & nuts, legumes, meat & poultry, fish, dairy products, cereals, monounsaturated to saturated fat intake ratio and alcohol intake. The bad score was 0 for eating more of the bad groups (meat & poultry, dairy, low mono to saturated fat ratio and alcohol) and not enough of the good groups (vegetables, fruit & nuts, legumes, fish, cereals) and the good score was 1 for doing the opposite. When these scores are added up, the lowest possible score (bad) is 0 and the highest (good) is 9.

Now, it turns out that the pattern of scores expected can be modeled by a mathematical probability distribution known as the binomial distribution. Strictly speaking, to adopt this model of the situation we need to make two assumptions about the behaviour of the participants. Firstly, we assume that each participant is operating (i.e. choosing foodstuffs and quantities of these to eat) independently of (i.e. not influenced by) each other participant (this is quite likely) and secondly, we need to assume that a participant's scoring on each food group is independent of (i.e. not influenced by) the score of other food groups. This second assumption is not entirely true, for example, it is clear that there would be some correlation between both dairy products and meat & poultry consumption and the monounsaturated/saturated fat ratio. However, for now, let's make this assumption and then we can check whether the actual data support this view.

With this model for the scoring process, it becomes possible, given the total number of participants, to calculate the expected numbers with different scores. It is quite easy to see that, given the way the scoring system has been constructed, there will be a full spread of scores, because on every food item, there is a 50-50 chance of scoring 0. Another point to consider is that, with the exception of scores 0 and 9, there are multiple ways of obtaining the other scores. For example, a score of 1 may be obtained by being above the median on one and only one of the 9 food groups - which means there are 9 different ways of getting this score. Whereas a score of 2 may be obtained by combining a score of 1 from 2 out of 9 groups: there are 36 ways of doing this. For the most likely scores of 4 and 5, it can be shown that there are 126 different ways to obtain each of these scores.

Table 2 (and you should look at this table while reading the next bit) in the paper shows the individual food group scores versus the Mediterranean diet score. This table is important because it gives some insight into the raw results of the scoring process which is otherwise obscured because score results for the individuals are grouped into three categories: low diet score (0-3), medium (4-5) and high (6-9). This is distinctly unhelpful and does not let us see how many got each individual score. However we can see – within each diet score category – how many people scored 0 or 1 for a particular food group (i.e. how many people ate more than the median amount and how many ate less than it - or vice versa).

Using the binomial distribution and the total number of individuals, it is possible to predict how many people should score 0 or 1 for each food group in the three diet score categories under our assumptions outlined above. (But note that we will get the same prediction for each and every food group because the model makes no distinction between these.) For example, for men in the category of low diet score (0-3), we would expect 2257 individuals and to see only 643 (28%) scoring 1 but 1616 (72%) scoring 0. In the category of medium diet score (4-5) 4378 individuals are expected, with equal numbers scoring 0 and 1 and in the category of high diet score (8-9), we would expect to see 643 of 2257 (28%) scoring 0 and 1616 (72%) scoring 1.

How does the prediction compare to the actual values? Quite well in fact for legumes and fruit & nuts (both 23%/77% and 50/50 in the medium score category) and dairy products (31%/69% in the low and high categories and 50/50 in the medium category) not quite so well for fish, vegetables and fat ratio where the ratios are actually 'more extreme' than predicted (18%/82% or 20%/80% in the low and high score categories). Cereals (36%/64%) and meat & poultry show the worst correspondence where the ratios are 'less extreme' than predicted. Overall we slightly overestimate the number in the medium score category (actual number 3808) and underestimate the numbers in the low and high categories.

There are some foodstuffs included in Table 2 which are not included in the calculation of the Mediterranean diet score: eggs, potatoes and sweets. As they are not used to calculate the score, it can be expected, that any participant in any diet score group would be equally likely to be above as below the median consumption of these items and so there would be approximately a 50%/50% split in the consumption in each diet score category. A sizeable departure from these figures would suggest that the participant's consumption of these non-scoring foodstuffs is in some way dependent on or linked to consumption of a scoring food group. However, this is clearly not the case, except possibly for potatoes, which show about 16% deviation from the expected 50-50 split in favour of (unsurprisingly) vegetables.

This leads to the most notable find in this table - a point which was completely unmentioned in the original article. The distribution of meat and poultry consumption appears to be essentially independent of the Mediterranean diet score. Within each scoring category, the distribution of above and below median consumption for meat and poultry is much more like that of eggs and potatoes and sweets than it is of the other items making up the diet score. Whatever the diet score group, there is close to a 50-50 split in the distribution of individuals' meat consumption. On a Chi-sqared test on the actual versus the expected values, the meat and poultry item shows the strongest result for independence in common with the foodstuffs which are independent of the diet score (e.g. eggs, potatoes, sweets) because they are not used in its calculation. It is interesting that this result is not remarked upon in the paper. In fact, to the contrary, when giving an example based on the link between a 2-point increment in the diet score and improved survival, it is mentioned that such an increment could be achieved by `making a substantial reduction in meat intake' despite the evidence that many high scorers score highly in spite of an above median meat intake!

When epidemiology works

Sometimes epidemiology produces a reasonable result. Take this recent story.

Researchers note that somewhere has a very high rate of a relatively rare condition. In this case a province of Iran with a high rate of oesophageal cancer. The first step in such a situation is often the case control study. This is a study done on the basis of matching people already diagnosed with the condition as closely as possible with controls who do not have the condition and then attempting to find significant ways in which the cases and the controls differ. Case control studies can be problematic because the results can be manipulated by choice of the controls. Also this type of study is purely observational and it is after the fact observation. You are relying on people's recall and what they recall may be influenced by their present condition - particularly when they have a serious disease. However in this study the results were quite striking:

Compared with drinking warm or lukewarm tea (65C or less), drinking hot tea (65-69C) was associated with twice the risk of oesophageal cancer, and drinking very hot tea (70C or more) was associated with an eight-fold increased risk.

The speed with which people drank their tea was also important.

Drinking a cup of tea in under two minutes straight after it was poured was associated with a five-fold higher risk of cancer compared with drinking tea four or more minutes after being poured.

There was no association between the amount of tea consumed and risk of cancer.

Compare this with the purported increase in risk of death from eating red meat (based on the responses to one labyrinthine food frequency questionnaire ten years earlier) of about 0.31 times (men) to 0.36 times (women).

And what was also nice was that having asked people to estimate how hot they drank their tea, they then went and measured the actual temperature.

Calorie Restriction and Memory - Low-Carb wins again, actually...

This study is the latest to make headlines around the world as it is claimed that modest calorie restriction in elderly people can result in an improvement in memory. From the abstract:

Animal studies suggest that diets low in calories and rich in unsaturated fatty acids (UFA) are beneficial for cognitive function in age. Here, we tested in a prospective interventional design whether the same effects can be induced in humans. ......We found a significant increase in verbal memory scores after caloric restriction .... which was correlated with decreases in fasting plasma levels of insulin....No significant memory changes were observed in the other 2 groups. This interventional trial demonstrates beneficial effects of caloric restriction on memory performance in healthy elderly subjects.

However, what caught my eye in reports of the study was this:

However, care was taken to make sure that the volunteers, despite eating a restricted diet in terms of calories, carried on eating the right amount of vitamins and other nutrients.

Now, this is an important point - it was even - implicitly - used as an objection to the approach by an anonymous dietician who said that:

....people, particularly those already at normal or low weight, should be "extremely careful" about attempting such a diet. She said: "There is other evidence that, far from enhancing memory, dieting or removing meals can interfere with memory and brain function.

presumably because it follows that if you just cut calories by 30% you cut nutrition by 30%.

But these people claim they didn't reduce the subjects intake of vital nutrients, how did they manage this?

The truth is revealed in the (rather limited) data in the Table S2 in the supplementary information package.

For individuals in the caloric restriction experimental group the mean calories fell from 1843 to 1630, the mean protein intake went from 77g to 71g (all numbers rounded to nearest whole number), the mean fat intake from 70g to 57g and the mean carbohydrate intake from 192g to 74g!! Converted to percent energy measures, this means the mean values went from 17% protein, 35% fat and 43% carbohydrate to 24% protein, 43% fat and 25% carbohydrate (the values don't add to 100% because alcohol intake was included). In other words caloric restriction was achieved, without compromising nutrition, by restricting carbohydrates (especially one imagines typical nutritionally empty carbohydrates like products made mainly of white flour and white sugar).

Interestingly, the individuals in the second experimental group which increased its unsaturated fat intake (to 68% of total fat intake on average - that's 36% mono-unsaturated fat which didn't actually increase (baseline for that group was 36%) and 32% polyunsaturates (from 15%)) didn't show the memory improvement, although they also appeared to have achieved a conversion to 'low-carb'. However, in their case the standard deviation for carbohydrate intake was bigger than the mean value (and much larger than the baseline value), which suggests a huge variation within the group.

Another caveat is that while taking the mean values of consumption and converting to calories reproduces (to within 40 calories or better) the reported mean caloric intake for the before case in all the groups, it is does not do so for the after case (the discrepancy is as much as 400 calories - and in all cases the mean nutrient data (in grams) result in an under-estimate of the mean calories). A better model - using a normal distribution for each parameter - might give an idea as to why this is so. Another interesting fact related to this is that - apart from the unsaturated to saturated fat ratio for the unsaturated fatty acid experimental group, none of the reported differences in before and after macronutrient mean intakes were reported as significant.

To sum up: the calorie restriction appears to have been mainly achieved by restricting carbohydrates. The researchers claimed that they had achieved calorie restriction without reducing nutrient content of the diet. The only way to do this is by removing or significantly reducing nutritionally empty carbs e.g. see here. Mean dietary data reported from the study lends support to this theory. The results observed in the subjects e.g. reduced insulin levels also support this theory.

Lark Rise - Discussion

The book Lark Rise documents the apparent good health and long lives of nineteenth century rural labourers despite a physically demanding lifestyle, a life of considerable material poverty relative to today and less medical support than is available today. The testimony of this book is backed up by my own observations of mortality and lifespans while doing family history research. What could be the explanation?

The first that springs to mind is that the author is simply mistaken; that her recollection is clouded by time, by the rosy glow of the good old days. However, the author herself seems aware of this possibility and her own seeking for an explanation suggests that, as far as she can tell, she is recalling fact and not invention.

It's likely that one of the reasons the doctor was seen so rarely was due to the cost. In those days there was no NHS. A doctor's services had to be paid for although it is claimed that wealthy doctors also treated patients who were unable to pay for free and many hospitals were charitable institutions and free to the poor (see for example, discussion in the following books: Sociology as applied to medicine by Graham Scrambler, Elsevier, 2008 and Social policy and welfare by Walsh, Stephens and Moore, Nelson Thornes, 2000, both available on Google books). However, it seems likely that the doctor was only called in when absolutely necessary. People might have treated less serious complaints themselves and put up with chronic conditions and pain such as arthritis.

Assuming then that this does show that serious disease - such as cancer - was largely absent what is the reason for this generally robust health and long life?

First and foremost, probably vitamin D: - children were sent outside to play every day, labourers worked outdoors. Pork meat and fat was a major component of the diet and the pigs were kept outside and fed a diet of scraps, milk and vegetable matter which would have been notably deficient in soy and corn (i.e. maize, because in nineteenth century England, corn meant wheat)! Thus, the lard obtained likely would have been as high in vitamin D as it is possible for lard to be and probably lower in omega-6 polyunsaturates than today's. Thus the diet would have been better balanced in the omega-6/omega-3 ratio.

Meat was eaten daily and, even if only once a day, because of the way nothing was wasted and everything cooked in one pot, the goodness (minerals, gelatine) from meat and bone juices would have been eaten up by the children, soaked into the bread or pudding. In addition, it appears that fish was eaten weekly (the fishmonger called weekly) and fish roe was prized and preferentially given to children.

Although many fruits and vegetables we habitually eat today (oranges, bananas, tomatoes) were absent. Other, native green plants (e.g. sorrel, nettle, dandelion, goose grass and many more are all edible) were taken from the wild and eaten. (It is in fact to this that the author herself attributes the good health of the hamlet.)

Finally, the bread was made from stoneground wheat. It is widely believed that this is more nutritious than today's refined white flours. But, it's not as clear cut as it seems.

On the one hand, white flour is very low in nutrients compared to wholemeal (see here for the effects of modern processing on flour). From Fitday, all-purpose white wheat flour unenriched has the following micronutrient profile (as a percentage of daily allowance)

Vitamin A	0	%
Calcium	2	%
Vitamin D	0	%
Thiamin	10	%
Niacin	8	%
Vitamin B6	3	%
Phosphorus	14	%
Selenium	61	%

Vitamin C	0	%
Iron	8	%
Vitamin E	0	%
Riboflavin	3	%
Vitamin B12	0	%
Manganese	43	%
Copper	9	%
Magnesium	7	%
Zinc	6	%

whereas whole wheat flour has much more Iron, B vitamins and other minerals.

Vitamin A	0	%
Calcium	4	%
Vitamin D	0	%
Thiamin	36	%
Niacin	38	%
Vitamin B6	20	%
Phosphorus	42	%
Selenium	121	%

Vitamin C	0	%
Iron	26	%
Vitamin E	5	%
Riboflavin	15	%
Vitamin B12	0	%
Manganese	228	%
Copper	23	%
Magnesium	41	%
Zinc	23	%

But without neutralization of the phytate content of the wholemeal flour, much of this nutritional content, particularly the minerals, cannot be absorbed [1] (see also the discussion of White Flour vs Whole Wheat here). There is also the question of its effect on teeth. There are also other 'anti-nutrients' in whole grains - see for example here.

However, it's possible that, as the bread was made at home, it was actually a sourdough bread. In this case the effects of anti-nutrients (lectins and leptins) and phytate would have been partially neutralized by the longer fermentation. (Stephan on Whole Health Source has many posts on this issue.)


[1] McGee, H. On Food and Cooking, London: Unwin Hyman Ltd, 1984.

Lard in Lark Rise

I'm very keen on researching my family history, and recently I've been working on the predecessors of one great-grandmother who were all East Anglian 'ag labs' (agricultural labourers). I noticed an interesting thing about them: in the nineteenth century particularly, very many of them lived to a ripe old age. Even going back to individuals born in the middle of the eighteenth century, I can find more than a few - across different families - who lived into their late 70s and 80s. Why is this so? They were poor, they didn't have access to modern medical care and they worked hard physically.

One book which sheds light on this is Lark Rise to Candleford*, the first part of which was published by Flora Thompson in 1939. It is a novel/memoir of her childhood in a rural England (Oxfordshire) which even then was passing out of existence. By the 1880s, when Flora and my great-grandmother (living a similar life in Cambridgeshire) were growing up, the industrial revolution in Britain was a hundred years old, but in the agricultural sector machine power was only just beginning to replace manpower and horse-power. Hamlets and small villages were populated still by agricultural labourers, living in cottages which came with the job, and working for the local farmer. The farms were mixed farms, in the area Thomson grew up, they were mostly arable with some livestock. The weekly wage would not normally have been enough for such large families not to starve, but they survived and even thrived in the rural setting as they had the opportunity to provide for themselves: an opportunity denied to poor families in town. Indeed, Thomson notes that the general opinion of those in her village of the nearest big town, Oxford, was that although a man might earn more there, as he'd be paying more rent and would

have nowhere to keep a pig or to grow many vegetables, he'd be a fool to go there. (p. 33)

Thomson refers to the adult generation of the 1880s as 'The Beseiged Generation'. The term seems to be meant in two ways: firstly, it was a period just before enormous change. Although the social structures of the time were to hold for at least another thirty years (until after the Great War) and to a lesser extent for sixty more, not collapsing completely until after the Second World War, the big change in agriculture and the start of the inexorable decline in manpower on the land was just around the corner. Maybe it is just a coincidence, maybe it is a consequence of the initial impact of small changes, innovations, where before, for so many years, there were none, but it was a time of decaying tradition and custom. For example, she says of the herb garden:

As well as the garden herbs, still in general use, some of the older women used wild ones, ..... But the knowledge and use of these was dying out; (p. 115).

Secondly, it was a tough time economically, the agricultural wage of the 1880s was 10 shillings per week (equivalent to £258 per week today) and every way possible had to be used to feed, shelter and clothe a large family (and they did have large families, my great-grandmother was the 1oth of 11 children).

So why were they apparently so healthy? Indeed, the author herself seems somewhat pushed to explain the robust good health of the hamlet she remembers. She says:

There were two epidemics of measles during the decade, ... but, for years together, the doctor was only seen there when one of the ancients was dying of old age, or [for] some difficult first confinement... There was .... except for a few months when a poor woman was dying of cancer, no invalid. (p.19)

What They Ate
The staples of the diet were bread, lard and bacon. Every household raised and killed one or two pigs each year. The importance of the pig was shown by the amount of effort lavished on their care and feeding. They were given not only household scraps (if there were any) but specially cooked up meals of potatoes mixed with leftover cooking liquor, milk and barley meal. Children gathered weeds and grass or even snails to supplement the pig's diet. Often half the pig had to be 'mortgaged' to the baker or publican as a way of buying on credit the necessary pig fattening food.

Only one meal a day would have any meat. As an agricultural labourer's house did not have an oven, nor even a range, cooking was done in the fireplace in an iron pot slung from a rack or chain built into the lower part of the front of the chimney piece. This arrangement meant everything was cooked (boiled) together: bacon, green vegetables kept together in a net, potatoes in another net and a roly-poly pudding greased and floured and wrapped in a pudding cloth. (This last is a peculiarly English creation being a flour and suet or lard dough adaptable to either sweet, if fruit, currants or jam are added, or savoury purposes, if meat.) All that was necessary was careful timing of when to put in and take out the various components. There were no leftovers for the pig, save the vegetable and potato peelings and the cooking water.

The other two meals (breakfast and lunch) were bread and butter (rarely) or bread and lard. According to Thomson, butter was expensive, although cheaper in the summer when a pound cost tenpence, and the cheaper imitation 'butterine', presumably an early form of margarine, was not liked. Instead they collected their own lard from their pigs and flavoured it with rosemary from the garden. Rosemary did not just improve the flavour. Herbs such as rosemary and sage have anti-oxidant properties and help to prevent the unsaturated fatty acids in the lard from going rancid ([1], p.606) as it had to last until the next pig killing, an important consideration in houses which had no refrigeration.

The pig killing was an important event and was followed by a celebratory 'pig feast' to which the extended familly was invited. The feast featured "joints of pork, potatoes, batter puddings, pork pies, and sometimes a cake or two" [to take advantage of the opportunity of using the baker's oven] (p. 27) plus three or four different kinds of vegetables and a meat pudding.

At the pig feast here would be no sweet pudding, for that could be had any day, and who wanted sweet things when there was plenty of meat to be had! (p. 27).

This statement is one of the most remarkable in the whole book: it would be hard for today's children to understand.

Nothing from the pig was wasted: home-cured bacons and hams kept the family provided throughout the winter and beyond (depending of course on the size of the family and whether half the pig was already spoken for!), 'hog puddings' were also made (from the pig's blood) and the chitterlings were made into sausages after they had been rinsed under running water for three days.

Throughout the year, the main meat to be had was the preserved, salted and dried bacon and ham. Once a week, there would be a small amount of meat bought ("six-pennyworth of pieces") made go further by making a meat pudding. Even less often a small joint would be roasted "on a string before the fire" or used as a pot-roast, cooked with lard in a saucepan over the same fire. A "toad", the meat wrapped in a suet [pastry] crust and boiled over the fire would again make a small joint go farther and make sure the precious meat juices were not wasted.

Bread was bought, but the women also needed flour - to make the puddings which were otherwise the way of eking out a meagre supply of meat. This flour was obtained by the right of the labourers to the leazings: the heads of grain left behind in the field from the less efficient time before mechanical harvesting. For two to three weeks once harvesting was over, the women and children went out to the stubbly fields each day, collecting by hand the leftover ears of wheat. Once threshed by hand at home, it was taken to the local mill and a large sack of flour returned:

one bushel, two bushels, or even more, in large, industrious families. (p.28)

It would have been stone ground flour too, at least at the beginning of the decade (of which more later).

Just as the pig was home-raised, vegetables and fruits were also home-grown. The men tended allotments (parcels of land granted to them, probably as part of the cottage rental to allow them to grow food crops) where they grew potatoes and wheat or barley. In the cottage garden they grew vegetables and fruits: peas, cabbages, cauliflowers, kale, beans and potatoes, fresh greens, radishes and onions. Rhubarb, currants and gooseberries would be made into jam. They had the advantage of fresh and organic produce. They also did not waste the natural produce around them. Children went out gathering mushrooms; sloes, blackberries and elderberries could be made into jams or jellies - or brewed into wine.

Nevertheless, there were occasional variations to the diet. Eggs were eaten, but only when affordable or only by those who kept chickens. Milk was available, at very low cost, if you walked the mile and a half to the farmhouse. It was hand-skimmed, so some cream was left and it was raw. Interestingly, she says that most people did not bother and so most children did not drink milk once they were weaned.

A travelling fishmonger who also sold fruit called weekly. If it could be afforded a bloater would be bought for a penny, "but it had to be a soft-roed one, for, in nearly every house there were children under school age at home; so the bloater had to be shared, and the soft roes spread upon bread for the smallest ones." (p. 119). Oranges and, on one occasion, a tomato bought from this vendor were merely curiosities, tried out once.

Small birds were another frequent and popular addition. Older boys would go out at night and net groups of sparrows where they were nesting in the hedgerows. These could be plucked and put into a pudding. One or two would be toasted over the fire. Women and children also lured and trapped birds. To take anything bigger than a sparrow or a blackbird or thrush, even to pick up a dead hare, was poaching. But it was done, not habitually, but if the opportunity should arise.

* My edition of the book is: Flora Thompson, Lark Rise to Candleford, Penguin Modern Classics, Penguin Books, 1973.

[1] McGee, H. On Food and Cooking, London: Unwin Hyman Ltd, 1984.