Dr David L. J. Freed, MB, MD, MIBiol
This is probably the case of greatest intrigue for me. Apart from its intrinsic interest, I am the patient.
My story begins 24 years ago when I was still working as an immunologist at Manchester University. I was already making myself unpopular by taking an interest in food allergy, and my attention was engaged by a paper from the late David Davies, a Welsh pathologist, who reported the startling finding that fatal heart attacks were statistically associated with the possession of circulating antibodies against cow milk [1]. I asked my postgraduate student, Janet Ditchfield, to see if she could replicate this work and she accordingly copied Davies's assay. When establishing the normal range for these antibodies we went around the Medical School taking blood samples from whichever staff were willing to allow us, and to my surprise we found the highest titre of all in my own blood. I was then aged 34, and apart from some dust-mite rhinitis I had never had an allergic symptom in my life, and certainly no hint of milk allergy or intolerance. I considered myself entirely fit and well.
About a year later I was at a meeting together with the late Keith Eaton. We were given a splendid lunch by the sponsoring drug company and as Keith held the table spellbound with his usual eloquence I felt myself becoming unaccountably drowsy. As I fought to keep my eyes open I also became aware that my heart was pounding uncomfortably in spite of the fact that I was sitting (slumping) in my chair at complete bodily rest. It popped into my mind that the delicious dessert we had just consumed had contained cream, and I remembered my high titre of anti-cow-milk antibodies. I resolved that I would thenceforth avoid milk and its products, and I kept fairly faithfully to that resolve through the years (and obsessively so for the last 15).
Fast-forward to age 57. Apart from some middle-age spread, and an occasional tendency to hypertension when under work pressure, I still considered myself pretty healthy, although I also had a tendency to rheumatism which I held at bay by keeping strictly to a stone-age diet during the week. My one indulgence was on Saturday, the Jewish sabbath, when we are traditionally expected to consume bread and wine. Admittedly, our religious law only requires us to eat a small piece of bread the size of an olive, but like all devout wheataholics I treated that as carte blanche to indulge liberally in my wife’s delicious home-made bread, not to mention her even more delicious home-made cakes and sticky sponge puddings.
In November '02, one Saturday afternoon, I was coming downstairs from a post-prandial nap when I was suddenly afflicted with severe chest pain. It did not feel tight or constricting, it did not radiate, and I was discomfited but not frightened. Margaret Moss and I had just published a paper suggesting that the single biggest cause of heart attacks was milk [2], and as I had avoided the stuff for many years I was confident that I must be immune to heart attacks. I supposed the pain must be due to oesophageal dysmotility brought on by a too-hearty sabbath lunch. I took a book and sat in a chair, and after about 25 minutes the pain went away.
But next week it recurred, and after a few weeks I noticed a pattern. The pain would hit me after the first sabbath meal on Friday night, then return the following afternoon after lunch, and was often severe on Saturday night, coming on at rest. Sunday would be a bit better, Monday better still, and by Wednesday or Thursday it would be completely gone. In the 'danger period' between Saturday and Tuesday the pains were distinctly related to exercise, as well as coming on at rest. Walking up a gentle slope near our home, especially if there was a chilly wind, brought on the pain, bad enough to make me stop and rest. On the other hand, far greater exertion on a Thursday or Friday caused no pain at all.
The treadmill/ECG result was equivocal, though the BP was worrying, hovering around 160/100. I still attributed the pains to oesophageal dysfunction, or possibly allergic coronary spasm not caused by atheroma [3], and being an allergist it didn't take me long to put two and two together. It must be something I was eating on the sabbath, I reasoned, and that could only be wheat or wine. It didn't take long to test the idea. Stopping wine made no difference (to my relief) but when I cut down the wheat to the mandatory olive-size nibble at each sabbath meal, the chest pains stopped within ten days (after an initial aggravation).
Months later, the long-awaited angiogram appointment arrived. I went along just for the satisfaction of proving myself atheroma-free, but to my surprise and dismay, there was indeed coronary narrowing, of the LAD artery. The typical chest pain hit me unexpectedly, just as the cardiologist injected the contrast medium,. I watched it on the monitor, and felt the pain simultaneously. I had in the same moment discovered that I had angina, and also (inadvertantly) how to control it.
But by this stage I was, by dint of wheat-avoidance, virtually pain-free. Clearly there must be a significant element of coronary spasm, caused by food allergy/intolerance, on top of the narrowing shown on the angiogram. But having just published a strong causal link between coronary disease and the one foodstuff I had avoided for years, I found the wheat connection rather difficult to swallow. As I remarked to my GP, if the heart disease didn't kill me, the embarrassment probably would!
To be on the safe side I have started walking short journeys instead of driving, and now go to the gym weekly where some intense exertion causes impressive tachycardia but not the slightest twinge of pain (and the BP has normalised and I feel better and fitter than I can ever remember), but I still have no doubt that the biggest factor is food allergy.
I know that angina is still waiting in the wings because I now notice subtle associations that I did not previously. Short-lived chest pains, which I now recognise, are also provoked by other grains such as rice, also by egg (but not, intriguingly, free-range egg) and sometimes by beef. My blood 20 years ago contained antibodies not just to milk but also wheat and many other foodstuffs. I am coming to think that any allergenic food can cause coronary spasm, whereas milk is the chief cause of coronary atheroma, being the most allergenic foodstuff and also possessed of uniquely unfavourable biochemical and nutritional characteristics [2].
To those of us brought up on the conventional paradigm of "coronary disease equals excess cholesterol " this talk of allergy must be bewildering, but it need not be. All pathologists agree, and have agreed for over a century, that the initial lesion of atheroma is inflammation of the arterial endothelium, breaching its barrier function and allowing access to the intima for molecules and cells normally confined to the lumen. References are cited in [2]. The importance of this initial inflammation, while never denied, has rather dropped out of fashion in medical thinking because no aetiological agent has been unequivocally identified. Situations like this are of course like a red rag to a bull to the enquiring allergist, and raise suspicions that the initial insult could be an antigen or antigens introduced daily to the body via the trojan horse of food.
Angina can be caused either by atherosclerosis (long-term, fixed) or by coronary spasm (short-term, variable), and the latter is one of the conditions AEN medicine is good at (see the BSEM website). Perhaps my coronary stenosis dates back 20-odd years to my milk-drinking days (I was a big milk fan back then, and had xanthelasma in my 20's) and only the spasm element is new?
My current hypothesis of atheroma is that type III allergy due to circulating food antibodies (mainly milk) causes inflammation of arteries (a known consequence of circulating immune complexes [4]), allowing cholesterol to diffuse in depending on its circulating concentration. Cholesterol might even serve to reduce the arterial inflammation, even though at the same time it is also contributing to stenosis. If the atheroma is bad enough there will be angina every time the heart has to work hard. Coronary pain due to spasm, on the other hand, can occur even in the absence of significant atherosclerosis if the spasm is tight enough, and will not necessarily occur every time the heart works hard, only when the spasm is bad. In my case I seem to have both, hence the confusing picture. Had it not been for the spasm I would never have discovered the atherosclerosis.
More recently a further observation clarified my thinking, again following a religious occasion. There is a widespread Jewish custom, on our festival of Pentecost in early June, to eat cheese and milky foods. Naturally I have banned that custom for many years from our house, but on this occasion my stepson was visiting, and my wife insisted on making his favourite cream cakes, with lashings of real cream. I am very fond of this boy and watched him with pleasure, eating one after the other. Until, that is, I noticed my chest pains again. All in the mind? Once the table was cleared the pains disappeared, only to re-appear three times throughout the evening. On the third occasion the penny dropped – on each revisit of pain, my stepson had been sitting close to me.
We have all met patients with such severe food allergy, at least of the IgE, Type I variety, that merely being in the same room as the food, or coming close to someone who has recently eaten it, causes symptoms, and this can be provoked double-blind. Cream has no odour at that concentration, at least not one that I could detect, but it seems that that tiny dose was enough for me. [For the immunologically-minded, this is apparently not a Type I allergy since my anti-milk antibodies are not IgE; it is probably type III and I think it would be the first recorded case of this mechanism causing such extreme sensitivity]. It also explains three puzzling contradictions that I noted 20 years ago.
One is the heart attack suffered by one of our pathologists around then. Newly enthusiastic about the milk-coronary link, I advised him to give up milk. He answered, to my bafflement, that he had not touched the stuff for years, because of an extreme cow-milk allergy. The second is our finding, back then, that even vegans who have not touched milk for decades can still have extremely high anti-cow-milk antibody levels (most irregular - antibody levels usually wane fairly quickly once the antigenic stimulus is removed). And thirdly, Peter Elwood, a Cardiff epidemiologist, found a negative correlation between the amount of milk consumed and heart attacks – the less milk a man consumes, the more likelihood of heart attack [5].
But if, as it seems, milk allergy can be provoked merely by smelling the stuff, that answers all three contradictions. None of us in milk - consuming countries can avoid milk because we constantly inhale airborne traces. Elwood's high-milk-consumers are simply not allergic to milk, they absorb all of its nutrients without ill-effect and live long healthy lives. His low-milk-consumers, on the other hand, are allergic to it. They probably try to avoid it because they subliminally associate it with feeling unwell, but they are inhaling traces, willy-nilly, every time their workmates have a tea break (just as my pathologist colleague was, and just as vegans do).
My friendly cardiologist, needless to say, doesn't think much of all this dietary nonsense. He attributes the symptomatic improvement to weight loss and exercise. I timidly suggested to him that since I was now out of pain, perhaps I was also out of danger? He pursed his lips and shook his head slightly. "I want you on the maximum dose of a strong statin," he said, "plus a beta blocker, aspirin and clopidogrel, for life. If you like, you can have a balloon angioplasty as well."
I was expecting that answer, and I think I might agree with his assessment of the risk. Presence or absence of cardiac pain is one thing; risk of infarction could well be another. I've probably had the coronary atheroma for many years, whereas the coronary spasm is a new and perhaps separate thing. The fact that I can control the latter proves nothing about the former. Thornton Crouch, while a single-handed GP in Newquay, put 44 of his angina patients on a milk-free, egg-free diet for six months, and observed that in 43 the angina got progressively better. Most of them also got slimmer and more normotensive as well - but three died of heart disease nevertheless (albeit all three were persistent heavy smokers) [6].
I've consulted my homoeopath and taken the remedy he prescribed, and with some misgivings I started on daily aspirin, but I'm dubious about the wisdom of an angioplasty and the thought of long-term conventional medication horrifies me and I'm not taking any. I stopped the aspirin when it gave me gout. I'm awash with magnesium and other supplements that my nutritionist gives me, but the conventional drugs stick in my throat. I'd appreciate advice from you guys out there.
And lastly. When I cut down my wheat consumption I gradually lost about two stone of weight. I made no other attempt at weight loss, which is not an issue that much bothers me (my wife prefers me cuddly!). I don't believe my calorie or carbohydrate intake is any lower - if anything it's probably higher as I still eat heartily of meat and potatoes, with lots of saturated fats (and my blood lipids remain fine).
It may not therefore surprise you that I attribute the weight loss to one of the lesser-known effects of wheat lectin, which has an insulinomimetic effect on adipocytes. That is, wheat and other lectins stimulate fat cells to take up glucose and convert it into fat, just as insulin does [7]. We've all seen obese patients who complain bitterly of lacking energy. But their bodies are literally larded with energy, all the calories locked away in their adipose tissue. Three months of stone-age diet and they're slim and energetic again. Perhaps their fat cells are no longer driven by dietary lectins into excessive glucose uptake, and this allows them to utilise blood sugar for its proper purpose instead. My chest pains stopped, incidentally, long before any weight loss, so the relief was not due to that.
And another thing, wheat lectin, curiously, sticks to endothelium, damages its integrity, and activates platelets [7-8]. Even more curiously, human anti-cow-milk antibodies also cause platelet agggregation [2] - the combination of anti-milk antibodies and wheat lectin must be quite strongly thrombogenic. I've still got the antibodies but I don't need to compound them by adding wheat lectin. I reckon I should be able to survive a normal or even raised cholesterol level if I can hold intimal inflammation and platelet activation at bay, without (I hope) recourse to aspirin or clopidogrel.
I tell you what though. The knowledge that you've got coronary disease, and have a moderate but real risk of sudden death, doesn't half change your view of the world. The knowledge that you might not be here next year "concentrates the mind wonderfully", as Defoe noted, and imposes a different order of priorities.
REFERENCES
1) Davies DF, Johnson AP, Rees BWG, Elwood PC, Abernethy M,
Food antibodies and myocardial infarction,
Lancet 1974, i: 1012-14.
2) Moss M, Freed DLJ, The cow and the coronary:
epidemiology, biochemistry and immunology.
Int J Cardiol 2003, 87: 203-216.
3) Anthony H, Birtwistle S, Eaton K, Maberly J.
Environmental Medicine in Clinical Practice, 1997,
BSAENM Publications, p286.
4) Roitt I, Brostoff J, Male D. Immunology (4th edn) 1996,
Mosby, London, ch 24 (24.1-24.12)
5) Elwood PC, Pickering JE, Hughes J, Fehily AM, Ness AR.
Milk drinking, ischaemic heart disease and ischaemic stroke II:
Evidence from cohort studies.
European Journal of Clinical Nutrition 2004, 58: 718-724.
6) Crouch TH. Symptomatic improvement of chronic heart disease on a milk-free, egg-free diet.
The Practitioner 1984, 228: 623-4.
7) Freed DLJ. Lectins in the food: their importance in health and disease.
J Nutr Med 1991, 2: 45-64.
8) Northover AM, Northover BJ.
Lectin-induced increase in microvascular permeability to colloidal carbon in vitro
may involve protein kinase C activation.
Agents Actions (1994) 41: 136-9.
