[Yes, this one took a long time to write]
When I started looking at heart disease, or cardiovascular disease (CVD) it was initially because I was interested to know why the Scots and the French had such different death rates. I had also just finished a book by James le Fanu called ‘Eat your heart out’ in which he made it very clear, or at least he did to me, that fat/saturated fat in the diet had nothing to do with CVD in any way shape of form.
However, at the time le Fanu was very much a voice crying in the wilderness. The experts had a very different song, or dirge. Namely that the Scots diet was terribly unhealthy, and this fully explained why they kept keeling over from heart attacks. Their bad diet raised cholesterol levels and…. thud (sound of Scots person falling over dead).
This is still very much the case. All of our medical authorities still announce the absolute truth of the ‘terrible Scottish diet’ with adamantine confidence. They usually bring out the almost mythical ‘deep fried mars bar’ as the perfect example as to why the Scots die of heart attacks, and strokes, and suchlike. ‘Well, what can you expect of a nation that eats deep fried mars bars… ho, ho.’
The truth is that hardly any Scotsman, or women, has ever eaten such a thing. And if they did it once, they will most certainly never do it again (I was certainly put off for life after one drunken foray on a Saturday night). Of course, there is also a perfect irony here. A mars bar is almost entirely made up sugar (not fat). When you fry it, it will be in vegetable/polyunsaturated fat – as saturated fats have been virtually banned in deep fat fryers. So, in theory, a deep fried mars bar should be somewhat more heart healthy than a ‘virgin’ mars bar. As it now contains a mass of hot sugar plus some heart ‘healthy’ polyunsaturated fat.
I suppose this example, at least to me, highlights the complete lack of any consistent logic or thought in the diet heart world. A fact that I became very painfully aware of, over many years. Indeed, I came to realise that there is no area of human existence where more nonsense is spouted than the ever-changing beliefs about what constitutes a healthy, or unhealthy diet. Frankly, it is almost entirely wall to wall rubbish.
At one point I made an effort to look at the classical ‘risk factors’ for heart disease between France and Scotland. This was done some years ago as part of a paper I wrote called ‘Does Insulin Resistance cause atherosclerosis in the post-prandial period?’ Something which I still think is at least part of the picture of CVD.
Here is the table I put together from a number of different sources – there was no single source for the data I was looking for. [I could not find separate UK and Scottish figures for a number of the factors, so I had to look at the UK as a whole. In addition, at there were no clear cut data on saturated fat, so I used animal fat as a proxy – which is almost the same thing]
| Risk factors and death rates from CHD in the UK and France per 100,000/year (men 55 – 64) | ||
| France | UK | |
| Animal fat % total energy intake | 25.7% | 27% |
| Fruit/veg % total energy intake | 5.0% | 4.3% |
| Percentage smoking | 32% | 29% |
| Total cholesterol level | 6.1mmol/l | 6.2mmol/l |
| HDL level | 1.3mmol/l | 1.3mmol/l |
| Systolic BP | 150 | 148 |
| Prevalence type II diabetes | ~2% | 2% |
| Percentage who never exercise | 32% | 24% |
| Mean BMI | 26.6 | 26.6 |
| Death rate from IHD (IHD 410-4) | 128 | 487 |
As you can see, there was virtually no difference in the classical risk factors for UK men and French men. Despite this, the French had one quarter the risk of death from ischaemic heart disease [what you or I would tend to call heart disease]. Since that time the French rate of heart disease has continued to fall, as it has also done in the UK, whilst the French consumption of saturated fat has risen. Interestingly total cholesterol levels have fallen in both countries.
So, whatever was going on had very little to do with diet. And if it had very little to do with diet, then it also had little to do with cholesterol either. If your hypothesis is that eating saturated fat increases cholesterol, or LDL cholesterol levels, which then causes CVD then how can two countries with exactly the same saturated fat consumption and cholesterol level (and all other risk factors equal) have such a different rate of CVD? And how could France, whilst continuing to eat more saturate fat, have a falling cholesterol levels? And how does the Ukraine, which currently has the lowest saturated fat intake in Europe, end up with the highest rate of CVD etc. etc. etc.
When you start looking at facts like this you must start to question the diet-heart cholesterol hypothesis. Or at least I thought you must. How wrong I was. Virtually the entire medical profession was wedded to the diet-heart cholesterol hypothesis – still is. Facts appear to have no impact whatsoever on this belief system.
Anyway, once I started to look at CVD in more detail, I was confronted with a choice. Accept that I must be wrong. After all, how can all the researchers and experts and Nobel prize winners be wrong. They must surely be seeing things that I cannot. Or, accept that the diet-heart cholesterol hypothesis was wrong. The blue pill, or the red pill.
Dear reader, I chose the red pill, in the sure and certain knowledge that rejecting the conventional thinking was certainly not going to be an easy path to follow. I also knew that if I was going to reject the diet-heart/cholesterol hypothesis, then I had to try and find out what does actually cause CVD. When I looked around at first there, were few alternative voices, or hypotheses out there. If truth be told, there seemed to be none (at least initially). But if not cholesterol, then what?
Over time, as I looked around, some ghosts in the machine began to emerge. I was aware of a doctor (whose name I cannot even remember) who firmly believe that fibrinogen was the main cause of CVD, and I went to a talk that he gave on the subject – not paying it much heed in truth. Then the Scottish Heart Health Study was published, and the single most powerful risk factor that emerged for CVD risk was… fibrinogen. A blood clotting factor. Aha. Could CVD actually be due to blood clotting abnormalities?
This was a time before the internet, before search engines, before finding information was so easy. This was an era when you had to traipse down to the medical library and pull actual books from actual shelves if you wanted to find out stuff. After pulling a lot of books off a lot of shelves I learned of Duguid, a Scottish doctor, who argued that blood clotting was the cause of CVD (I paraphrase).
His work was published shortly after the second world war, and has remained mostly unread. Then I went all the way back to Karl von Rokitansky who, in 1852, felt that atherosclerotic plaques were, in fact, just blood clots – in various stages of repair. An observation which, from time to time, other researchers have noted. Most particularly a doctor called Smith, from Aberdeen. He is no longer active in this area of research.
Here is the abstract from his paper ‘Fibrinogen, fibrin and fibrin degradation products in relation to atherosclerosis’. I have quote the abstract in full, for those who like to see a bit more detail. Others may glaze over, or skip to the last sentence:
‘Many human atherosclerotic lesions, showing no evidence of fissure or ulceration, contain a large amount of fibrin which may be in the form of mural thrombus on the intact surface of the plaque, in layers within the fibrous cap, in the lipid-rich centre, or diffusely distributed throughout the plaque. Small mural thrombi are invaded by SMCs (smooth muscle cells) and collagen is deposited in patterns closely resembling the early proliferative gelatinous lesions. In experimental animals, thrombi are converted into lesions with all the characteristics of fibrous plaques, and in saphenous-vein bypass grafts, fibrin deposition is the main cause of wall thickening and occlusion. There seems little doubt that fibrin deposition can both initiate atherogenesis and contribute to the growth of plaques.
Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease. Fibrin may stimulate cell proliferation by providing a scaffold along which cells migrate, and by binding fibronectin, which stimulates cell migration and adhesion. Fibrin degradation products, which are present in the intima, may stimulate mitogenesis and collagen synthesis, attract leukocytes, and alter endothelial permeability and vascular tone.
In the advanced plaque fibrin may be involved in the tight binding of LDL and accumulation of lipid. Thus there is extensive evidence that enhanced blood coagulation is a risk factor not only for thrombotic occlusion, but also for atherogenesis. Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.’ 1
For those whose eyes did glaze over, concentrate only on the last sentence. ‘Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.’
Here, ladies and gentlemen, lies my little secret. My evil twin brother who I have kept in the attic for the last twenty years, gnawing at the floorboards. The terrible truth that there is an association between LDL levels/familial hypercholesterolemia and CVD. Something which I appear to have argued against for many, many, years.
Does this mean that the experts have been right, all along? High LDL cholesterol levels do cause CVD? Well maybe, maybe not. At this point I need to take you back to the statement again. ‘Enhanced blood coagulation frequently coexists with hyperlipidaemia.’
Does this mean that hyperlipidaemia actually causes enhanced blood coagulation? Or does it mean that something else causes both. Here is the old ‘yellow fingers and lung cancer’ discussion.
‘People with yellow fingers are more likely to die of lung cancer.’
Why… because people with yellow fingers smoke, and smoking causes lung cancer. Ergo yellow fingers are simply a sign of smoking, they do not actually cause lung cancer.
‘People with raised LDL are more likely to die from CVD’
Why… because people with raised LDL are also more likely to have enhanced blood coagulation. Ergo, raised LDL levels are only associated with enhanced blood coagulation, they do not actually cause CVD. It is the blood coagulation factors.
Alternatively, raised LDL may actually enhance blood coagulation, all by itself.
Where does the answer lie? In truth the answer has been very difficult to tease out. Even now, after many years, I do not feel that I can fully disentangle the data. Here for example, is a paper called ‘Maternal familial hypercholesterolaemia (FH) confers altered haemostatic profile in offspring with and without FH.’
‘Children with (n=9) and without (n=7) FH born of mothers with FH, as well as control children (n=16) born of non-FH mothers were included in the study. The concentrations of tissue plasminogen activator, plasminogen activator inhibitor (PAI-1), tissue factor (TF), TF pathway inhibitor (TFPI), thrombomodulin, fibrinogen, prothrombin fragment 1+2 and von Willebrand Factor were measured. Our findings show i) higher levels of PAI-1 and TFPI in children with and without FH born of mothers with FH compared with control children, ii) lower levels of thrombomodulin in children with FH compared with control children, and iii) significant correlations between maternal PAI-1 levels during pregnancy and PAI-1 levels in the offspring.’2
What this tells us is that, if a mother has Familial Hypercholesterolaemia, she passes on abnormalities of blood coagulation to her children. Both those that have, and those that do not have FH. [Not all children of mothers with FH will end up with the FH gene]. Some of this may be epigenetically modulated. In short, it is not the LDL that is important, it is simply the mother’s genes….
Or is it? Here is a paper suggesting that the LDL itself, independently of anything else, makes platelets more likely to stick together (a key step in blood clotting).
‘The interaction of platelets with lipoproteins has been under intense investigation. Particularly the initiation of platelet signaling pathways by low density lipoprotein (LDL) has been studied thoroughly, since platelets of hypercholesterolemic patients, whose plasma contains elevated LDL levels due to absent or defective LDL receptors, show hyperaggregability in vitro and enhanced activity in vivo. These observations suggest that LDL enhances platelet responsiveness….’ 3
However, maybe these researches misinterpreted what they were seeing. For example, another paper found that the level of LDL in those with FH was not related to their risk CVD. It was purely the level of clotting factors that was related to CVD. This paper entitled: ‘Coronary artery disease and haemostatic variables in heterozygous familial hypercholesterolaemia.’
‘Haemostatic variables were measured in 61 patients with heterozygous familial hypercholesterolaemia, 32 of whom had evidence of coronary heart disease. Age adjusted mean concentrations of plasma fibrinogen and factor VIII were significantly higher in these patients than in the 29 patients without coronary heart disease, but there were no significant differences in serum lipid concentrations between the two groups. Comparisons in 30 patients taking and not taking lipid lowering drugs showed lower values for low density lipoprotein cholesterol, high density lipoprotein cholesterol and antithrombin III, and a higher high density lipoprotein ratio while receiving treatment. The results suggest that hypercoagulability may play a role in the pathogenesis of coronary heart disease in patients with familial hypercholesterolaemia.’4
So it is not the high LDL? It is the raised blood clotting factors that are found in some, but not all of those with FH. As you can see, it is not straightforward at all.
Just to complicate the picture further, here is a paper strongly suggesting that HDL is directly anti-coagulant.
‘Native HDL prevents platelet hyperreactivity by limiting intraplatelet cholesterol overload, as well as by modulating platelet signalling pathways after binding platelet HDL receptors such as scavenger receptor class B type I (SR-BI) and apoER2′. The antithrombotic properties of native HDL are also related to the suppression of the coagulation cascade and stimulation of clot fibrinolysis. Furthermore, HDL stimulates the endothelial production of nitric oxide and prostacyclin, which are potent inhibitors of platelet activation. Thus, HDL’s antithrombotic actions are multiple and therefore, raising HDL may be an important therapeutic strategy to reduce the risk of arterial and venous thrombosis.’ 5
And what about VLDL?
‘There is a considerable body of evidence supporting an association between hypertriglyceridaemia (high level of VLDL), a hypercoagulable state and atherothrombosis. A disorder of triglyceride metabolism is a key feature of the metabolic syndrome that increases risk of both ischaemic heart disease and type 2 diabetes approximately 3-fold. An increasing prevalence of obesity and metabolic syndrome is likely to contribute markedly to the prevalent ischaemic heart in the foreseeable future, and therefore it is crucial to understand mechanisms linking hypertriglyceridaemia and a hypercoagulable state. Activation of platelets and the coagulation cascade are intertwined. VLDL and remnant lipoprotein concentrations are often increased with the metabolic syndrome. These lipoproteins have the capacity to activate platelets and the coagulation pathway, and to support the assembly of the prothrombinase complex. VLDL also upregulates expression of the plasminogen activator inhibitor-1 gene and plasminogen activator inhibitor-1 antigen…’ 6 etc.
You can go back and forward in this area, finding research that contradicts itself upside down and inside out again. What I think I know for certain is the following:
- High LDL levels/familial hypercholesterolemia is closely associated with increased blood coagulation (in a high percentage of those with FH, though not all) – through many different interrelated mechanisms. Some genetic, some possibly directly due to LDL itself.
- VLDL (triglyceride) seems to increase blood coagulation – and this seems a very consistent finding
- HDL has anticoagulant effects
I don’t know how powerful these different pro and anti-coagulant effects are, but they certainly exist. To an extent I could just say what does it matter if LDL does, or does not increase blood coagulation directly – but is simply associated with blood clotting abnormalities. It all fits within the processes that I have outlined in this series of blogs. Namely, anything that increases the risk of blood clotting increases the risk of CVD. And LDL (directly, or through genetic association) does increase the risk.
However, I thought it would be dishonest of me not to highlight the fact that there could well be a causal association between LDL (and VLDL) and CVD. Also there does seem to be a causal protective mechanism provided by HDL.
Or, to put this another way, perhaps all the experts were (a bit) right all along. Even if they have consistently promoted a process that does not make any sense at all i.e. LDL leaks into artery walls causing inflammation and plaque growth etc.
A further proviso is that I cannot see that the LDL/VLDL/HDL effects are very strong. After all I just co-authored a paper showing that higher LDL levels in the elderly are associated with increased life expectancy and a slight reduction in CVD risk. [There are many other factors clouding the issue here – too many to discuss in one go]. Confused yet… welcome to my world.
So where did I get to. I think I got to the point where I accept that:
- LDL is pro-coagulant and – at very high levels e.g. in FH – increases the risk of CVD [though it is difficult to disentangle this from intertwined genetic pro-coagulant factors]
- VLDL is pro-coagulant, and increases the risk of CVD
- HDL is anticoagulant and protects against CVD
Which then brings onto statins, and how they work. First to re-iterate that statins do reduce the risk of CVD [Something, I have never disputed]. However, they do it not by lowering LDL, but because they have anticoagulant effects. Not that potent, about the same as aspirin, but the effect does exist.
Here from a paper entitled ‘statins and blood coagulation’:
‘The 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A (CoA) reductase inhibitors (statins) have been shown to exhibit several vascular protective effects, including antithrombotic properties, that are not related to changes in lipid profile. There is growing evidence that treatment with statins can lead to a significant downregulation of the blood coagulation cascade, most probably as a result of decreased tissue factor expression, which leads to reduced thrombin generation…. Treatment with statins can lead to a significant downregulation of the blood coagulation cascade….’ 7 An effect confirmed by their protection against DVT.
‘Venous thromboembolism (VTE) includes both deep vein thrombosis (DVT) and pulmonary embolism. The 2009 JUPITER trial showed a significant decrease in DVT in non-hyperlipidemic patients, with elevated C-reactive protein (CRP) levels, treated with rosuvastatin.’ 8 Yet, the experts continue to tell us that statins work, purely, by lowering LDL levels. Ho hum.
Whilst I could have written this series and simply pushed LDL, VLDL and HDL to one side. I thought I needed to bring them into the discussion. Not to dismiss them but, I hope, to explain what their role within CVD may actually be – pro and anti-coagulant agents. Here is where they fit, and make sense. Looking at lipoproteins in the light also helps to explain how statins actually work.
References:
1: http://www.ncbi.nlm.nih.gov/pubmed/3524931
2: http://europepmc.org/abstract/med/23199546
3: http://www.ncbi.nlm.nih.gov/pubmed/16877876
4: Br Heart j 1985; 53: 265-8
5: http://www.ncbi.nlm.nih.gov/pubmed/24891399
6: https://www.karger.com/Article/Pdf/93221
7: http://www.ncbi.nlm.nih.gov/pubmed/15569822
8: http://www.ncbi.nlm.nih.gov/pubmed/22278047
Dr. Malcolm Kendrick 
very good
Thank you Dr Kendrick for another fascinating, and thought-provoking article.
The comparison data between France and the UK was particularly striking – I wondered if you’d been able to come up with any possible explanations for the massive difference in the IHD death rates? Are there possibly classification issues here, and how do the all-cause death rates compare?
Having lived in France, I know that the French in general reject mass produced foods. They eat lots of fatty meat, but nearly always have a salad plus other vegetables at meal times. They like deserts, but shun those that aren’t home made. They drink wine, but mainly at meal times. They appreciate taking a long time over meals. Hence the usual 2 hour lunch break. If you add to that the natural vitamin D they are soaking up in their sunny country. I think you can explain the discrepancy.
Interesting. But why do the French have only one quarter the risk of death from ischaemic heart disease compared with Brits?
And what about the Brits living in France?? Or any other country with CVD risk much lower than the UK. Would be interesting to have some data on how they are doing, if they have changed diet/lifestyle, and how that affects their health outcomes.(Just to clarify – I do not think that simply crossing the border changes anything).
Emigration is often very bad for CVD risk. But this greatly depends on a number of factors. The Rosetta community in the US had no CVD at all. First case of a heart attack was in 1968. The Rosetta community was basically an entire village transplanted from Southern Italy to the US, retaining lifestyle, religion, cultural ties etc. However, Asian Indians moving to South Africa, US, UK etc. have fared very badly. Japanese moving to the US rapidly ended up with US rates of CVD [apart from those who retained a more traditional Japanese lifestyle].
“Emigration is often very bad for CVD risk. But this greatly depends on a number of factors. The Rosetta community in the US had no CVD at all. First case of a heart attack was in 1968. The Rosetta community was basically an entire village transplanted from Southern Italy to the US, retaining lifestyle, religion, cultural ties etc. However, Asian Indians moving to South Africa, US, UK etc. have fared very badly. Japanese moving to the US rapidly ended up with US rates of CVD [apart from those who retained a more traditional Japanese lifestyle].”
I read somewher this was only true until olive oil was replaced by sunflower oil, advocated on the basis that it decreased cholesterol. Then the Italian Rosetta community started to americanise its diet , and cardiovascular diseases started to incfrease.
I think it is from this book (in modern Latin)
Thanks.
Small point – in para. 4 you state that animal fats are virtually banned in deep fat fryers. Here in South Lincolnshire.they don’t seem to have heard that one – pretty much all use beef dipping. Tough luck if you are a Hindu!
Beef dripping makes the best chips – sorry 😦
I had chips fried in beef dripping in Suffolk last week. Delish.
Lucky you! I wish our local F&C did the same
So, why do you think the British and the French have such different death rates from CVD if it’s not dietary fat and it’s not excercise? Are they just happier?
They always seem pretty grumpy to me. However, they have retained their social structures far better than, most, of the UK.
Maybe it’s just stress. We could check cortisol levels. Also, my gripe with all this diet data is that it is really very crude. As someone mentions here, if the french have produce from pasture fed animals there will be more vitamin K2 in the diet, maybe more omega 3 as well. The fat consumption looks the same but these vital microscopic ingredient quantities will be different. Here we could check CV calcification (CT scan for coronary calcium) of Scottish and French people as K2 makes a big difference to this. I am now rambling here, but I wonder what the arterial calcification looks like for people on statins as another bad statin side effect is inhibition of gut K2 synthesis. Have there been comparisons of statins against aspirin or clopidogrel for CVD reduction?
Anyway, this blog has been a wonderful series of insights – I hope this is not the end.
Statins markedly increase calcification. Recent articles on Medscape/Medpage proudly indicate this. The ploy is that calcification stabilizes plaque. So, if you have a high CAC score, you necessarily (I would say NOT necessarily) have heart disease. Therefore, the treatment is statin – iINCREASING your calcification. I went along with this for a while before side effects and this whole calcification question provoked my quitting.
I could find the links if you really needed.
To JD Patten,
Yes please, I am in a lazy phase. If you can easily find the the articles on statins & calcification that would be useful.
Robert,
Here’s the report that alerted me to the issue:
http://www.medscape.com/viewarticle/842499
Easy to use PubMed. Go to “Advanced”, choose Title, abstract from the drop-downs, and enter your choice of search terms:
http://www.ncbi.nlm.nih.gov/pubmed?term=(statin%5BTitle%2FAbstract%5D)%20AND%20calcification%5BTitle%2FAbstract%5D
In ‘The Great Cholesterol Con’ Dr Kendrick suggested the different death rates may be due to the fact that the Brits stuff down lunch at their desks or on the motorway whilst the French take two hours for lunch with a nap often thrown in.
…time spent off the treadmill
France… closer to the equator, better sunshine leading to higher Vitamin D levels, coupled with more Vitamin K in the diet (soft cheese, butter, etc)… seems a likely candidate as to the differences in CVD rates to me.
Always keep in mind that distance from the equator (and elevation!) make less difference than the kind of clothing you wear and the SPF you slather on.
You realize that the northern boarder of the US is about the latitude of Southern France? If available vitamin D played any role, the Americans should be at least at healthy as the French.
Attempts to ascribe differences between the Pas de Calais region and the Gascogne (or as Chris Masterjohn does, between northern and southern Israel) to latitude alone aren’t all that contvincing.
Higher levels of Vit D in France?
The more I read and think about it, the more astounded I become how things are simplified and generalized in so many (if not all) areas of medicine and nutrition. Simple one-fits-all solutions (eat less, exercise more; high sat fat=high cholesterol=high risk of CVD=statin prescription) – no (or hardly any) room for individual thinking on either the expert or patient side …
Thanks again Dr K for constant opening eyes and minds.
As I understand it from my little biology knowledge, potassium chloride joins with albumin to form fibrin. If this is out of balance in the system, because albumin is a cloying substance, would this contribute to the problem. And I believe potassium chloride thins the blood.
Dr Kendrick, a really gripping exciting article. It is making me delve into my old grey matter and discover again, that surely must be good for my Transient global amnesia of which I hope to never experience again. I confess I am out of date and may be wrong with my biology.
Thank you, I so look forward to your fabulous missives.
Dear Dr Kendall
You mentionned earlier, there would be some what not do tips?
Also why do clots break off and go swimming around?
Need to bring some (mice) microbes in:
Adaptive immunity against gut microbiota enhances apoE-mediated immune regulation and reduces atherosclerosis and western-diet-related inflammation (Saita, 2016)
http://www.nature.com/articles/srep29353
“Common features of immune-metabolic and inflammatory diseases such as metabolic syndrome, diabetes, obesity and cardiovascular diseases are an altered gut microbiota composition and a systemic pro-inflammatory state. We demonstrate that active immunization against the outer membrane protein of bacteria present in the gut enhances local and systemic immune control via apoE-mediated immune-modulation.
(…)
Thus suggesting that intestinal microbiota have a crucial protective effect against the formation of atherosclerotic plaques, that as we show in this paper may be, at least in part, mediated by the adaptive immune response against gut microbes.”
Interesting paper but unclear what the practical implications for humans is apart from encouraging us too eat a peck of dirt.
Wish I knew. But eating “a peck of dirt” is probably not enough.
Anna: I suspect one of the clues, in regard to food, is variety. And eating entirely organic, as glyphosate is ubiquitous now in the food supply, and it blocks the shikimate pathway which our gut bacteria use to make nutrients such as folate. Having pets probably helps, too.
Like the other Commenters, I would like to know what causes the difference in the French and Scottish death rates from heart disease? You commenced the article by describing the huge difference between the death rate from CVD of the 2 countries and then made no further mention of it in the article?
…he doesn’t know, that’s why.
The way I see it, though I’ve studied this less than 1% as much as Malcolm, is that the epidemiological results are too weak to reveal much at all about the disease. While whole-country studies give crude results with significance, chopping up population data into sub-populations does not seem to lead to any particularly convincing results or even much in the way of useful hints.
Of course this kind of study should only be used to raise hypotheses which can then be tested in a better way, but those tests are either underpowered (small RCTs for what is after all a relatively rare effect in most healthy populations) or probably full of confounders (observational trials like WHI which come up with little in the way of significance).
So we end up not far from where we started. Human populations are likely not genetically diverse enough to explain much of what is observed, and so it has to be environmental. Best bet seems to be a mix of lifestyle (stresses, poverty, migration …), nutrition (plus sun exposure) and toxins. I doubt that we know much at all about the relative importance of those factors, either overall or on a population by population basis (it would be unwise to expect the same relative importance of these factors in different populations).
On the other hand it is possible to experience positive changes based on nutrition, perhaps the easiest of the variables to manage. I moved from eating a usual UK diet to real food. My teeth were soft, now they are hard and decay has essentially stopped and gingivitis is under control. My blood insulin is much more stable and less on average than it used to be (indicated by mild ketosis). I suspect if I were to get an e-beam CT my CAC score would suggest lower risk than if I had remained on the standard diet.
Ken
Love your newsletters, but “Which then brings onto statins, and how they work. First to re-iterate that statins do reduce the risk of CVD [Something, I have never disputed].”
Malcolm, do they really realy really reduce any risk? Only in 0 – 2,6%, according to The NNT.com:
http://www.thennt.com/nnt/statins-for-acute-coronary-syndrome/
– 100% saw no benefit
– None were helped by preventing death, heart attack, stroke, or heart failure
http://www.thennt.com/nnt/statins-for-heart-disease-prevention-with-known-heart-disease/
– 96% saw no benefit
– 1.2% were helped by being saved from death
– 2.6% were helped by preventing a repeat heart attack
– 0.8% were helped by preventing a stroke
http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/
– 98% saw no benefit
– 0% were helped by being saved from death
– 0.96% were helped by preventing a heart attack
– 0.65% were helped by preventing a stroke
Like you said, statins do reduce the risk of CVD, great!
I never said I thought the reduction was impressive, or even worthwhile.
The harm statins cause is far more impressive! From the 100% that saw no benefit: “An unknown number were harmed by medication side effects/adverse reaction” to “1% were harmed by developing diabetes, 10% were harmed by muscle damage” for the 96 and 98% patients that saw no benefit. Why did they ever approve statins?!? Money Maker?
The trouble with small effects, is not only that they are not worth exploiting, but also that they are much easier to produce by skulduggery!
The harm caused by statin muscle damage has been compounded by the fact that seemingly no research has been done on fixing that damage. They couldn’t really research a phenomenon that they always described as trivial.
As some people have reported here, the damage doesn’t always clear up after stopping the statin!
It is something I have objected to for many years. The use of ODDs/HRs ratios. While for demonstrating significance these are acceptable they grossly inflate the risk to the individual patient, something the medical establishment has forgotten in its concentration on herd statistics. Big Pharma is known to support these inflated relative rates because, as pointed out by
Gigerenzer, in his book Risk Savvy: How To Make Good Decisions. Also the use of an algorithm that in fact is circa 90% wrong compounds the problem (I am assuming the algorithm is “diagnostic” in that is used to prescribe drugs)
PHARMACOGENETICS OF SLCO1B1: POPULATION GENETICS AND EFFECT ON STATINS
Marja Pasanen
can be downloaded in full at:
http://ethesis.helsinki.fi
https://helda.helsinki.fi/handle/10138/17738/search?scope=&rpp=10&sort_by=0&order=DESC&query=Marja+Pasanen
In this thesis, the SLCO1B1 c.521T>C variant allele was associated with
substantially increased exposure to certain statins, suggesting that it could increase the risk of
statin-induced myopathy in patients with the SLCO1B1 variant genotype.
And
It has been suggested that avoiding high-dose simvastatin administration to patients carrying the c.521C allele (approximately 32% of the Finnish population in our studies) could reduce the incidence of simvastatin-induced myopathy by nearly 60% (Nakamura 2008)
but elsewhere
Alternatively, simvastatin could be avoided in patients with the c.521CC genotype (approximately 4% of the Finnish population)
A bit confusing perhaps but this dissertation has been signally ignored. Usually anything genetic gets promoted except as in this case it may be useful but would reduce “profit”,
The French paradox is interesting, I did not notice an attempt at explanation though.
Being a wine lover self interest leads me to ponder on this.
I agree the polyphenol/resveretrol component may have something to do with it. But I am thinking of calling myself the FIBRE EMPEROR because of my faith in the fiber-SCFA-SCFA receptor-GLP1-Treg-anti-inflammatory connections. The short chain fatty acid ACETATE is increased substantially and immediately with alcohol consumption and via acetate SCFA receptors and increased adenosine levels must have important immune system cell signaling consequences. Question is who consumes more alcohol in a moderate fashion the UK or France?
France
but alcohol increases blood pressure does it no.
Jane,
It is worth reading this (very cheap) book about alcohol consumption and health:
The book is written in the Kendrick style – i.e. it is readable, but explores the results of actual studies and is fully referenced.
It would seem that if you are not in danger of becoming addicted, there is a substantial health benefit associated with drinking regular moderate amounts of alcohol – particularly wine!
That is not what the medical authorities tell us, but that no-longer surprises me!
Bought it immediately
Thanks for recommendation
Concerning alcohol: it matters what and how much you drink, and how it is prepared. The coolest paper ever:
Shaken, not stirred: bioanalytical study of the antioxidant activities of martinis (Trevithick, 1999)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC28303/
Wow, thanks for sharing! Looking at the last half page above the 007 article, was that a special issue for mischievous research?
Looks a little like a special issue:
http://www.bmj.com/content/319/7225
Diana,
The only trouble is that my impression is that there isn’t much evidence that anti-oxidants – as distinct from the plants that contain them – actually give health benefits. Maybe my impression is wrong, but is there a study of the actual health benefits, as opposed to the test-tube ability to destroy hydrogen peroxide?
David
a great question. Actually both pro- and anti-oxidants are needed and used by the body. Low level / temporary pro-oxidants generate hormetic stress which is positive. On the other hand, longer oxidative stress that is not dealt with may be detrimental. I think your comment referred to some studies showing no positive (actually negative) health effect of antioxidants taken as supplements.
P.S. I think the positive effects of whisky do not come only from its “antioxidative” properties.
That was fun from the NIH. Thanks
Nice piece once again
Dr. K. – “Dear reader, I chose the red pill, in the sure and certain knowledge that rejecting the conventional thinking was certainly not going to be an easy path to follow.”
…
“Where does the answer lie? In truth the answer has been very difficult to tease out. Even now, after many years, I do not feel that I can fully disentangle the data.”
Sadly it’s very hard to trust the data at this point, as you well know. Much of it is compiled from manipulated studies that are designed to prop up preconceived notions. This is anti-science and it saddens and frustrates me, as a lover of truth. Yet I know the truth remains for all eternity, waiting patiently to be discovered by courageous men like you Dr. K.. Men who are willing to ask tough questions and seek inconvenient answers for the sake of knowing the truth.. Answers that often times give cause to question lifelong beliefs and premises… Answers that justify taking a sledge hammer to foundational “knowledge” that entire careers and billion $$$ industries are built upon.. The easy path would indeed be to go along with the herd..
This is why I see you as courageous. It’s not a word I toss around lightly. I believe this courage stems from an overwhelming love and respect of the truth. Is this the value that sets men like you apart from the consensus-minded herd? I think so. But I can’t be entirely sure. I can not know what is in another man’s heart..
Anyway. If my suspicions are correct, I thank you. In a crazy world where sometimes I find myself wondering if truth even matters, to stumble upon thinking men like you refreshes and encourages me.
This is not to say that I entirely agree with you. I’m not sure that I have the knowledge to make that decision quite yet – I’m a simple man with a curious mind who reads and thinks a lot.. What I am saying, is that I appreciate you..
Does this mean I’m one up on CVD because I’m taking apixaban?
Possibly.
Malcolm,
Statins stimulate atherosclerosis and heart failure (Okuyama et al) 2015. They are mitochondrial toxins, effective in lowering LDL but ineffective in preventing CHD.
And the rate of decline of CHD has slowed since statins were introduced.
But they do reduce the risk of CVD? How does your statement square with the above paper?
Yes, increasingly confused and no more likely to swallow a statin!
Well, they do reduce the risk of CVD in the clinical trials that have been done. According to the statisticians employed by the companies than ran the trials. I have yet to get to the point where I completely dismiss pharma sponsored research. Though, at times, I am sorely tempted. P.S. I would never take one, and encourage people not to take them.
Dr Kendrick,
I take your point But the HPS study the probability of NO BENEFIT approached certainty in a year (p = 299/300 = 1.00 to two decimal places). Remember the trumpet claim “treat 3 million, save 10,000 lives a year? Also 156 lives (unidentified) saved in 5 years in a group of 10,269 post MI or very seriously at risk, statin tolerant patients (1 in 300+ again)?
There were some comparisons that were ignored such as the dead treated cholesterol levels compared with those of the dead placebo group. Surely that comparison would be very interesting as would the TC levels of the two survival groups and the within group comparisons of dead and survived. That data was obviously very “confidential”
I am afraid that I have less confidence in Big Pharma trials than your good self, thanks to you, Prof Goetzsche and JP ioannidis and my own assessment of studies such as the HPS
I agree, almost entirely. But there is still, I think, a wafer thin benefit that does exist.
Does that include people who have had a heart attack? If so, what would you recommend in place of statins?
As a patient advocate, patient peer reviewer (BMJ) and diabetes reseacher I have long been perplexed by the REAL cause of CHD. I’m pretty sure that eating fats of animal origin has little to nothing to do with it, otherwise our primitive hunter-gatherer ancestors wouild have been falling like flies.
My pet theory is that by shunning sources of nutrients and macronutrients that are present in animal foods and natural dairy products we have laid ourselves open to all forms of heart disease and likely cancer. Vitamin D and Vitamin K seem to me to be at least worthy of indictment as by consuming foods that are high in the D2 (synthetic) and K1 varients instead of D3 (cholecalciferol) and K2 (Menaquinone 7) we have lost the ‘balance’ that previously existed in our intake of foodstuffs. In essence K2 works in synergy with D3 to concentrate calcium in our skeletons and teeth, and purges it from our bloodstream where it can concentrate in plaques and stiffen arteries. K1 is largely a clotting agent, so a diet that that does not balance the intake can end up a higher predominance of K1.
As we feast on our ‘healthy’ diets and ‘five-a-day’ we largely eliminate these important vitamins that were and still are (in a more depleted form) present in a diet that embraces fats and proteins from animal sources, that are eating plenty of lush grasses (not grains and soya in a confined space). Societies that ate little meat made considerable use of their by products such as butter and hard cheeses as well as eggs (yolks), fish and bi-valves to make up this deficiency of meats. And by meats, I stress that we used to eat ‘nose to tail’ with the offals and bones (high in K2), being the most eaten and today’s prized ‘cuts’ of sirloin and fillet being largely fed to the dogs.
K2 then chimes with your anticoagulent theory quite nicely Dr. Kendrick, and is to some extent proven by the Japanese lack of CVD and Osteoporosis if they consume ‘natto’ which is very high in K2 as MK-7. Whilst being one of the most unpleasant eating sensations I have ever tried it is also the K2 variant with the longest half life in the human gut. Dried natto is the only type that would be palatable to the western taste and I use that to supplement a diet depleted often of the sources we used to have available to us.
It also seems to me that the trick of the French may be that they eat the same overall content, but it is higher in macronutrients like in their ‘blood pudding’, raw steak, higher quality butter and love of cheeses as their source of many saturated fats.Their carb intake is also moderated by the making of many bread products with butter and eggs, so although the content can look the same overall, the devil may be in the detail.
Weston Price did an enormous amount of investigation way back in the 1930’s and he is said to have found K2 and called it Vitamin X, but I have no evidence that this is true but it is plausable. He placed great faith in the use of butter oil for the restoration of health in the children he treated in remote communities and combined it with cod liver oil; a potent but likely quite awful tasting concoction.
A small point about frying fish and chips commercially: hydrogenated oils have effectivelky been banned in catering. The seed oils now used have wrought chaos with commercial fryer units due to oxidising and smoking (a carcinogen hazard), so a number of traditional outlets (mainly in ‘gods own country’) have reverted back to the use of beef dripping or lard, suitably clarified of course. One outlet I particularly frequent even renders their own dripping from the carcases they buy in for the restuarant and fries their chips in it. Delicious.
Thanks, Ernie. I’m about to order some natto and intend on forcing it down. I can pretty much do this with anything (remember “vegemite”? Rice cakes? I’ve eaten it all). What I find happens is that it’s difficult for a while, then you decide you like it. Sort of like eating real, fermented sauerkraut or kimchi (or even scotch whiskey) – tastes terrible at first, but grows on you.
Scotch whisky does not have an ‘e’. That would be Irish whiskey.
Lots of good stuff in Scotch whisky, and perhaps, possibly, who knows, in Irish whiskey too…
Note the copper pots, there is a role of copper in the formation of organic complexes during whisky distillation.
Dr K
The Irish told us that the only thing Scotch whisky is fit for is rinsing out the mouth before you drink Irish whiskey. Do you have a retort?
Choose a window, you’re leaving.
I did not know that about the e, and whiskey/whisky. I always thought that was colloquial and not related to origin.
BobM: I add some chopped green onion, soy sauce, and Dijon mustard; makes it slightly less revolting. As for kimchi and kraut, I make my own, and thoroughly enjoy them.
Regarding Scotch and Irish whisky/ey, this table from Dr. Yellowlees in a 1977 letter to the editor is instructive http://bjgp.org/content/bjgp/27/178/317.1.full.pdf :
Taking the UK as 100, cirrhosis of the liver for England and Wales is 96, for Northern Ireland is 109, and for Scotland is 137.
Looking at that table, Scotsmen are sick, and Scotswomen sicker.
I visited Scotland for Hogmanay in 1974. I got smashed over the head with a whisky bottle and kicked senseless, just off the Royal Mile in Edinburgh. I still bear the scars.
My stepfather was born in South Africa of Scots parents. Very proud of his Scottish roots. Would put on his tartan trews and drag us off to Caledonian evenings. He got cirrhosis of the liver.
Scots! *shaking my head*
I got some natto (locally made, non-GMO, but not organic, made in the state next to mine), and I do not think it’s bad plain. It’s not great, but I can eat it plain. It’s better with soy sauce (naturally brewed, no wheat, organic) or Butt Kicker hot sauce (a quite hot red hot sauce, which pretty much kills the taste of anything and makes you drink a lot of water).
I did not whip the beans 50 times, which I’ve read you should do. I just took some and ate it. This natto comes in 4 ounce cups, with a serving size of 2 ounces (56 grams). For anyone on a low carb diet, 2 ounces of natto has 120 calories, 6g fat of which 2g is saturated (doesn’t list MUFA or PUFA), 8g carbs, 3g fiber, 10g protein. It supposedly has a high bacteria content, and they can survive being frozen (which is good, as the fresh stuff doesn’t last too long, and I ordered so much I have to freeze it; it came packaged overnight in a cooled box).
What amount of this do people eat? I ate nowhere close to 2 ounces; I was thinking averaging maybe 1 ounce per day or so. Is that reasonable?
This study used 100 grams/day, which is an entire 4 ounce cup (about 112 grams):
http://www.ncbi.nlm.nih.gov/pubmed/10874601
(Of course, this study is basically useless, as it says if you eat natto…your concentration of K2 in your blood goes up. Duh! Too bad it wasn’t done for five years with a lot of people and with heart disease rates.)
BobM: I buy 50g containers from the frozen foods section of our Japanese store, imported from Japan, so I assume they are non-GMO. This is as much as I could eat at one time, and the label calls it one serving.
Totally my experience. There is a suggestion that what we like is influenced by the gut flora & fauna. If we change diet the old flora & fauna don’t like it and signal that. However with time the balance of flora & fauna changes to those that like the new food and they then signal that it is delicious. I found this effect when I ceased to accept that FDA food pyramid many years ago after reading Uffe Ravnskov’s first book. I now find even the look of a mound of carbs discomforting.
Hi Gary, after eating natto for a few days, I find if I add soy sauce to it, I actually like it a lot. Dare I call it “delicious”? I guess when you used to eat rice cakes (basically, cardboard), vegemite, protein powders, individual proteins, etc., your taste buds have deteriorated. 😉
I’m trying to stay in ketosis, for health reasons, so I’m trying to eat a little natto per day, only about an ounce. If I had to eat the four ounce cup I have, I might need more than just soy sauce.
Eating a nutrient rich diet seems like a good idea.
Ernie Berry,
I entirely agree with you and as a kindred BMJ patient reviewer it seems to me that there is a lack of nutritional knowledge within medicine and medical research with the result that vitamins and other essential nutrients are ignored. As individual components, their potential is limited but overall, they result in a healthy body; the last thing in Big Pharma’s business model. For example it seems to me that there is a step function philosophy; the patient has not got scurvy, ergo the patient is sufficient in Vit C. Likewise not “rickety” means sufficient in Vit D and so on.
What year was the Le Fanu book? The only thing I can find on Amazon is a bunch of ghost stories.
The LeFanu book (The Rise and Fall of Modern Medicine) was first published back in 2002 if memory serves andwas updated and re-published circa 2012. It can be obtained from Amazon as a paperback or Kindle edition. I can strongly recommend the book. It is very insightful and should be on every doctor’s desk
Please ignore my question. Found the book under Le Fanu. The ghost person is LeFanu.
I join other readers in asking – why then do the French have such a low risk of CVD compared to the British?
Sit at a cafe in France for a couple of hours. The answer is all around you.
plus, having spent a lot of time in France, way better attention to quality food as a way of life especially compared to the USA where I am now where sugar is added to everything and the pasteurisation paranoia. The diet here and UK is so ‘processed carb’ rich. A high fat and high carbs regime is a guarantee for poor health. Also, the regular but mild (not like the UK binge attitude to alcohol) consumption of Red wine helps to make a more mild atmosphere.. In my opinion just cut the Carbs to the minimum, use coconut oil as the only oil or grass fed butter and lots of good proteins. Works for us.
What, the girls are more chic?
Better cuisine, in my opinion (resulting in more balanced micronutrient intake).
Diana,
You are lucky. I even tried to get a reprint from Hall but the email address given on the journal abstract failed.
If, as you say, it was designed to test a theory in the healthy, where the general metabolism would be very robust to short changes in diet, the duration of the study (however sophisticated and technically advanced) was simply too short; our weeks on each diet; a holiday change inn diet. Frankly I am surprised that they found anything. If the study had been conducted over a minimum of 6 months for each treatment, it might have proved something important
What’s your opinion of Zetia?
Not much above zero
Malcolm, have you looked at the CVD risk reduction of ACE inhibitors vs statin? I believe they’re fairly similar and of course blood pressure reduction is the reasoning. But NO production could very well be the main benefit beyond just <BP. Thoughts?
Agree completely
Might ARBs have a similar NO benefit to ACE inhibitors?
Good afternoon Dr Kendrick
It was good to see you on national tv recently.
However, regarding the heart disease topic..rather than blame the firemen at tne scene for the cause of the fire, have you ever considered the gluten (pro inflammatory) position? Poorer people (that would include the Scots) eat a diet high in gluten (bread, pastries, biscuits, cake etc) and The French have their French sticks and croissants for an unhealthy breakfast.
We now know that gluten is indigestible by humans and the resulting gut inflammation causes permeability, thus allowing large food molecules to get through causing further inflammation in the brain (as dementia, depression, anxiety etc), the skin (psoriasis, acne etc), the joints (arthritis etc).
If you want to know more you could read up on Dr David Perlmutter, Dr Tom O’Bryan, Dr Hyman and Dr Peter Osborne.
You could simply google gluten and heart disease to start, but I’d suggest reading what Dr Hyman says about it first:
http://drhyman.com/blog/2011/03/17/gluten-what-you-dont-know-might-kill-you/
I first discovered at the age of 30 that it was gluten and dairy that had made me sick for such a long time. That was over 32 years ago and I’m so pleased to finally see modern Drs research and publish on the subject (usually because they’ve been sick from gluten themselves) and so I’m able to keep up to date. I’ve also been able to transform the health of many people over the years but, sadly, you can’t get everyone to change their diet.
Kind regards.
Jackie
Sent from my iPad
>
This I find very interesting as my daughter aged 35 has had Pleuro Pericarditis which hospitalised her for 10 weeks during her pregnancy 2 years ago. She has had 2 recurrences since, and its now thought that she has an Auto Immune Condition. I’m wondering if Gluten is to blame but she’s been told by her Rhumatologist that her blood tests are all normal, and her condition is Idiopathic.
We are all very very concerned about her health and she doesn’t want to be on drugs like Steroids, large doses of anti inflammatories, and even as was suggested yesterday Immune suppressants.
Desperate for any advice.
Jennie,
Sorry to hear all your daughter is dealing with. Have you looked into an an autoimmune protocol (AKA autoimmune paleo) diet? My antibody levels are better since starting the diet. And I’m not on any of the drugs.
It looks like you’ve other family members with gluten issues, it’s definitely worth looking into. The drugs the rheumatologists want us on are no joke.
Thank you for your reply, and all other replies.
After seeing Rhumatologist yesterday my daughter is being referred to a specialist centre in London. It seems likely now that she has a Genetic Auto-Inflammatory disorder, which Im given to understand is not the same as an Auto Immune disorder ( help me out here Dr K!)
We are very pleased she is being referred, and have been told there will be a lot more testing taking place, which will probably involve ‘blood relative’ members of our family too, to try and identify the problem .I’m afraid in the mean time she is taking a lot of medication, but without it she would be back in hospital I have no doubt.
Thank you for your replies. It now seem after seeing her Rhumatologist on Monday that she possibly has a rare Genetic condition. Not ‘Auto Immune’ but ‘Auto Inflammatory’ there is a difference I’m given to understand, ( help me out here Dr K)
He’s referred her to a Specialist Centre in London for further tests which may include other blood relatives in our family being tested . The small bowel biopsy has been discussed too, as blood tests show no inflammatory markers for Gluten , but it hasn’t been ruled out.
In the mean time however she is taking numerous medications, to keep her ‘stable’
Without which I have know doubt she would be back in hospital.
Can’t reply to Dee in the usual way for some reason?
Thank you for your replies.
My daughter has seen Rhumatologist this week and has been referred to a Specialist in London who deals with Rare Genetic disorders. It seems that she has an ‘Auto Inflammatory’ condition rather than an ‘Auto Immune condition’
There is a difference but Dr K will have to help me out on this one!!!
There will probably be some family testing to try and get to the bottom of her illness.
A small bowel biopsy has been discussed too, even though her blood tests are showing negative to Gluten.
For her, Pleuro Pericarditis has become quite debilitating.
In the mean time however she is on numerous medications to keep her stable, without which I have no doubt she would be back in hospital
A report on the actual percentage of the US population that might have trouble with gluten.
The percentage is small. Digestion is complex, but trouble free for about 93% to 94% of us.
http://health.usnews.com/health-news/blogs/eat-run/2015/06/11/think-youre-sensitive-to-gluten-think-again
The links are interesting too.
I’m sure that for those who do have trouble, it’s a serious business.
Various foods can be problematic for some of us. I, myself, am in serious danger around kiwi fruit. Go figure.
Don’t let mass paranoia frighten you. Be rational. Seek real information. Act accordingly.
re: …gluten. … Digestion is complex, but trouble free for about 93% to 94%…
Anyone wondering can just quit gluten-bearing grains (wheat, rye, barley) for 30 days and see what happens. Caution: withdrawal symptoms are possible. As needed, replace the eschewed calories with foods that don’t provoke BG; perhaps some cheese.
«Don’t let mass paranoia frighten you.»
It’s not paranoia when the threat is real, and gaining on us.
Gluten-free, in isolation, is a fad, and the majority of the GF products on the market are junk carbs with junk fats and other toxins common in many processed food-like substances. It’s hard to say what informs those who buy this stuff.
Gluten-free as part of a spectrum of dietary and microbiome corrections is not a fad. Celiacs and those with NCGS frankly need to do more than just avoid gluten. Many of the anecdotes here from other readers point in useful directions.
In the context of the present blog, one of the main advocates of grain-free living is a US cardiologist, who, about a decade ago, stumbled into the connection between wheat and CVD (and a huge list of chronic non-infectious ailments).
Bob Niland: I have to agree with you. I had no apparent problem digesting gluten or any other component of rye (my preferred sourdough grain) or any other grain, which I ate for decades, but giving them up had two benefits: My digestion is clearly improved, and I lost my belly fat. I think there is much more to the problems with grains than meets the eye, certainly more than the small percentage of folks diagnosed with celiac.
Fully appreciate what you say, and I know these ‘diet crazes’ are all the fashion , but as my brother has Herpetiformis Dermatitis (gluten allergy)
And HIS daughter is has been diagnosed as Celiac after a small bowel biopsy I just wonder!
The figures you give for French and English CVD – are they for male/female or combined?
Those figures were for men only. Usually female figures are about x3 less in both countries.
The fact that man and women in the same households have such vastly different rates of heart disease must point to some conclusions?
1) Food plays a very small role. I would imagine that the French men and women would eat a similar diet?
2) Sunshine would be similar for both?
The difference between men and woman’s disease rates is so huge it has to be that something about being a man is bad for our hearts.
Of course. Unless, you are a diabetic woman.
I am surprised that you are so flippant about the difference between CVD rates in men and woman. You are being given magnificent epidemiological studies on a plate.
Scottish men/women eating similar foods, similar UV exposure, similar pollution exposure, similar eating habits, perhaps drinking the same wine, etc etc.
French men/women the same.
By comparing men and women in the same countries you are taking out a huge amount of variables.
The question still remains – why such a huge difference between them?
I gather that testosterone is a contributor to CVD – is it as simple as this?
The Scots are bursting out with the stuff?
Dr Kendrick, when you say usually female figures are about x3 less, do you mean before menopause or overall?
Before menopause
As regards the French paradox, there has been some interesting work done by Roger Corder
(professor of experimental therapeutics at the William Harvey Research Institute).
Dr. Corder began looking at French longevity statistics in detail and discovered that they
are not distributed evenly throughout all regions. In fact the longevity distribution is
especially high in South Western part of the country. Looking at nutritional factors and
red wine consumption, it turns out that the red wines produced in this region are high
in procyanidins (a type of flavonoid polyphenol) and he feels that this is the cognizant
factor in the French paradox as these substances have a particularly beneficial effect
on arterial health.
Could it be that procyanidins also have a positive effect on the clotting cascade?
In any case he wrote a book – The Red Wine Diet – published in 2006 – which is not a
tongue-in-cheek “Drinking Man’s Diet” type book but represents a serious piece of work
based on his research. His web site (the-red-wine-diet.com) contains a summary of what’s
in the book.
Certain red wines = positive effect on blood clotting. Could it be?
I am always wary of the red wine protects hypothesis. It only ever existed because it was used as a way of explaining the ‘French paradox.’ There never was a paradox, only the fact that the diet/heart-cholesterol hypothesis was – and is – wrong.
Malcolm,
The book that I referenced above:
Does claim that there is some evidence that moderate wine consumption is slightly better than moderate beer consumption, but that they both increase life expectancy and reduce CVD. Do you agree with this?
France is also obviously a lot more sunny than Scotland – how much of an effect do you think this has?
The south of France would get more sunshine than the north, and much more than Scotland.
As Dr. Kendrick himself said in https://drmalcolmkendrick.org/2016/03/23/sunbathing-is-good-for-you/ : “I would further add that sun exposure is the best known way of increasing NO synthesis throughout the body. This protects the endothelium and, as you would expect, lowers blood pressure (the natural way). So, you are far less likely to die from CVD.”
Fascinating article, yet again – thought provoking, but leaving me even more confused.
“Facts appear to have no impact whatsoever on this belief system”.
Perhaps this is an inevitable effect of the mind’s preference for clear-cut paradigms, as urged by Thomas S Kuhn in his classic book “The Structure of Scientific Revolutions” (which is currently celebrating its 50th birthday). Kuhn makes a strong case that many people – maybe almost all – find it close to impossible to reject an old paradigm, no matter how obviously faulty, until they have found a new one that is clearly better in every way.
So, until someone comes up with a convincing explanation of CVD that is very hard to poke holes in, the current official theory will continue to command loyalty among those who need some theory to cling to.
A minor quibble. While I think that animal fat percent is a good marker for saturated fat (at least in populations not eating a lot of coconuts), most animal fat is around 50% monounsaturated fat, with the rest mainly saturated fat and a (relatively) small amount of polyunsaturated fat. For instance, lard (pork fat) is over 50% monounsaturated fat, of the same type found in that Angelic Olive Oil:
http://nutritiondata.self.com/facts/fats-and-oils/483/2
This is another reason why demonization of saturated fat makes no sense: real meat has all types of fat and you can’t simply separate one type of fat from another.
As always, another thought-provoking article. Could I ask you to add “(Bob: you’ve already read this one)” to the title? 😉 I keep getting confused as to which of these is new or old.
Having had a high cholesterol level of around 8 for some time I have always been interested in your blogs. Unfortunately I find them very confusing & being left no wiser ! It would be so much more helpful for everyone reading if you could simplify it all ie., what does cause heart disease ? What can one do to prevent it ? Instead of waffling on in jargon that not many can understand. I know you mean well but I am yet to read a blog that makes any sense !
Julie, I would disagree that Dr Kendrick waffles. He is trying to explain complex issues, so there has to be detail. If you read his blogs, you will appreciate that there are no simple answers – if there were, no one would die of CHD anymore!!!!
Julie,
I think perhaps you have to choose between the simplified information the NHS (or equivalent) put out, which is simple but wrong, and the ‘waffle’ that you get here, which reflects the fact that the orthodox picture is clearly wrong, but there is uncertainty as to what exactly does cause CVD. If you are willing to plough through a few tables, you can reassure yourself that people with high cholesterol seem to live a bit longer (on average) than others:
http://vernerwheelock.com/179-cholesterol-and-all-cause-mortality/
You might also want to read “The Great Cholesterol Con”, which is easy reading in places, less so in others.
My understanding of what I read here (I am not a medical doctor), is don’t worry about your cholesterol, cut down on sugar but don’t worry at all about fats , don’t take statins (I know what they can do first hand), drink in moderation, and take plenty of exercise. Try to avoid stress.
Thank you David for your reply. Yes I have read the Cholesterol con & no I don’t worry about my cholesterol any longer having read so many articles which, like you say, people with high cholesterol live longer. I have tried to read between the lines of Dr Kendricks blogs & am watching my sugar intake as it now seems sugar is now our enemy. I am just very simplistic & find some of these blogs extremely confusing & not to the point. It would be so much easier if someone would come out with the clear statement like you have that…..Cholesterol is nothing to worry about, eat everything in moderation, don’t eat too much sugar, keep yourself reasonably fit don’t smoke & drink alcohol in moderation & enjoy life ! If only everything was put as simple as that but hey ho it never is. I think you have said exactly what most worried people want to read. I just wish the NHS would state this instead of scare mongering people into taking statins & worrying about everything they put in their mouths. I’m glad someone else thinks like me !
Julie, I understand your concerns, and am too searching for simple answers to what makes us sick… However, this seems to be an incredibly complex area, and I don’t think there is a simple ‘one fits all’ answer.
For example, cholesterol – it does appear that it has some role in CHD, but probably not the role that the mainstream puts forward (increase HDL and/or reduce LDL and you’ll be OK). Plenty of people with low cholesterol get heart disease, and vice versa – the type of (LDL) cholesterol is probably important (large fluffy particles being the least damaging, small dense particles the most damaging). And the ratio of triglycerides to HDL seems to be one of the main factors in the risk of CHD.
And eating meat – which is a fantastic source of many of the nutrients that we need. But most of the meat we buy is grain fed, which means it is high in Omega 6 (rather than grass fed meat, which is higher in Omega 3), which is thought to be pro-inflammatory… Which has links with cancer and CHD…
So nothing is simple – and also, we’re all different, so the diet that works for one person, may be completely wrong for someone else.
However, there are many things that we do know help us live longer (you’ve mentioned many of them) – don’t smoke, exercise and keep moving, avoid excessive sugar/carbs, stay trim, avoid stress (as far as is possible!), get plenty of sleep…
Good luck in your search for answers!
Julie, I think everyone wants simple explanations, and that’s why half-baked theories end up getting popular. But it’s not surprising that the truth would be extremely complicated because nature had eons to invent and tweak the human body to get it to the point we’re at today.
But if you want for simpler guidelines, I recommend you read about the Blue Zones around the world where people live unusually long, active, healthy lives with little dementia. One does not need to understand the science of nutrition, disease, the microbiome, etc. to understand that if people in all 6 of these especially healthy regions (which are scattered around the world and include Asians, Hispanics, Europeans, etc.) thrive while eating lots of legumes (for ex) – then legumes are probably good for most humans – or at least not bad!
You will find the usual: Fresh whole foods, little sugar/junk food, exercise (especially walking on hilly terrain and gardening) as part of daily life, lots of sunshine, ample social connections, relatively low stress. Nothing surprising. There are doubtless factors we have not yet figured out to explain the unusual health and longevity of these people, but I think that actively imitating their lifestyles and diets (the particular diets, except for legumes, differ, so you have lots of choices) is as reasonable (and evidence-based) an approach as following any of the regimes that public health experts and doctors have come up with using scientific studies.
There are no figures for carbohydrate / sugar consumption in France vs UK.
re: And what about VLDL?
What VLDL is the data based on? Here in the US, when VLDL is reported on the standard lipid panel, it’s often merely:
VLDL = TG ÷ 5
which means both that:
☤ VLDL, like LDL-C, is a fiction, and that
☤ what we’re really talking about is TG (triglycerides),
TG being one of the two actually useful numbers from a lipid panel (the other is HDL).
Any historical epidemiological data on VLDL may therefore highly suspect, with respect to VLDL per se.
If, on the other hand, we consider VLDL numbers of unknown provenance to be surrogates for TG, then the data becomes more interesting, as TG appears to be quite responsive to available carbohydrates in the diet. Anyone with a TG higher than 60 mg/dL might want to look into the matter of de novo lipogenesis.
As I argued at:
If very low density lipoproteins matter (and they do), then they need to be directly measured, and rarely are.
I suspect there’s a dearth of historical epidemiological data which includes direct VLDL measurement, and if there is, it may be complicated by the test technology used (NMR, electrophoresis, the dear departed VAP, perhaps others), as some of the numbers can’t trivially be normalized to each other for comparisons and correlations.
Thanks Bob, that was one question on my mind how reliable the LDL and VLDL numbers in those studies were.
The other question: how did they define FH? At the more traditional levels of about 600 mg/dL or at the ever lower thresholds recommended for primary stating treatment?
And lastly, how did they discern high VLDL from FH vs from eating too much fructose?
Here’s a little puzzle piece. I have PCOS. When I had my second child (conceived thanks to a low carb diet and Metformin) 16 years ago, I read a lot of medical literature, since it was rather “cutting edge” at that time to use a low carb diet and Metformin to help PCOS, and my question was whether or not to continue Metformin during the pregnancy.
So I came across some literature suggesting a higher miscarriage rate in women with PCOS because of elevated levels of the blood clotting factor PAI-1. And there was a doctor at Cleveland Clinic recommending that women with PCOS SHOULD stay on Metformin during pregnancy because it regulated PAI-1 levels. Somewhere there is his paper, but I’ll have to hunt for it, not remembering his name but I know it started with a “G” and may have been Gelb. This would have been published around 1999 or 2000. A connection between insulin metabolism and blood clotting factor.
I stayed on Metformin (had to really convince my doctor about that!) and had a healthy, full-term pregnancy. Nobody was watching my cholesterol levels at that time, but my low carb diet aimed at reducing insulin has kept my LDL and triglycerides in a good range. I see connections.
So, aspirin would be a reasonable treatment for DVT, and eating plenty of HDL would also help?
How would you eat HDL?
Very carefully
That’s exactly the answer to the question of how hedgehogs make love!
It was a serious question nonetheless.
Bob, not a specialist myself, but HDL is a lipoprotein ferry in the blood. I don’t think you could actually find a food that contains HDL.
The only thing I know of that will increase HDL is to eat fewer carbohydrates. In general, a high carb diet decreases HDL and a low carb diet increases HDL. This likely is not true for all people (is anything ever?), but works for many.
Alcohol raises HDL
That’s good then. but alcohol isn’t so good for high blood pressure is it.
when I increased my red wine consumption, my HDL went way up
French versus Scottish rates of CHD. Sunshine. Vitamin D. I believe that even people in northern France have higher rates of CHD than those in southern France – there was a comparison of CHD in Lille (northern France), Strasbourg (more or less central France) and Toulouse (southern France): “Coronary disease in France: data from the MONICA registers (1985-1991)”: http://www.ncbi.nlm.nih.gov/pubmed/8935864 The sunshine/vitamin D hypothesis makes sense.
How does Subbotin’s recent review fit with what you know?
http://www.sciencedirect.com/science/article/pii/S1359644616301921
Yes! I’d really like to know. Multi-layered endothelial intima, yet “normal”? Lipids delivered from adventitious vasa vasora?? That’s nothing like a single layer of endothelial cells covering a clot sealed injury, lipids coming from red cells.
Is a resolution forthcoming?
Dr. K, Great article, I have a better understanding of what may or may not cause CVD. The best part is your disecting the truth from fiction. Thank you
Phew! That was a long one! And we’re still not there yet, so we still have more to look forward to…
This interesting post reminds me of the eminent physician and physicist John Gofman, University of California, who was the first scientist to be able to correctly analyse lipid profiles in the blood in the early 50-th with his ultracentrifuge where he could sort out the lipids of different density but to the disinterest of the medical community.
Gofman demonstrated that saturated fats could raise the amount of LDL in the blood but that it was the cabohydrates that elevated the VLDL. He also pointed out that the measurement of total cholesterol was a “false and highly dangerous guide” to the effect of diet on heart disease.
Another eminent scientist in the field of lipid metabolism at that time was Pete Ahrens, Rockefeller University, was of the same opinion as Gofman. When he gave lectures he would show photos of two test tubes of serum obtained from the same patient – one when the patient was eating a high carbohydrate diet and one on a high fat diet. One test tube would be milky white indicating lipemia. The other would be absolutely clear.
The milky plasma was obtained on the carbohydrate rich diet and the clear plasma on the high fat diet. What made the serum white was the VLDL particles who mainly carry triglycerides but also some cholesterol.
If FH increases the risk of CVD due to its higher fibrinogin association, why does the more elderly FH population live as long as or longer than the average age? And why did a Dutch study find that, historically,the FH gene produced inidviduals who survived and lived longer than those without the gene?
Is the FH population in France higher or lower % than the UK? Does the Ukraine have a higher level of FH than France?
How many of our UK population have undiagnosed FH? If there are potentially a significant number of inidentified FH individuals because they present no symptoms, does could this unknown FH element affect statistics?
http://www.bmj.com/rapid-response/2011/11/02/benefits-familial-hypercholesterolaemia
Could the fact that in the UK, eating heavily processed food is the norm for a large percentage of the population whereas in France, cooking a meal from basic ingredients is more likely? Could that have an effect on nutrients, minerals, vitamins?
I think it definitely does!
Not necessarily, judging by what is available and ends up in people’s carts in French hypermarches, and judging by what street and restaurant food people eat, it is not siginicantly healthier than average German fare. But then, I haven’t been to the UK in 25 years, so I have no idea what things are like there nowadays.
If HDL is anticoagulant and protective against CVD, why do studies that raise HDL artificially show no benefit? Do the types of HDL that are raised matter?
So complex. Hang in there. You’ll find the answer, I know. Thanks for this series
Probably because they raise HDL through drugs, which have their own effects. You can disentangle the effect of the drugs from the increase in HDL. I’d like to see a long term study where people raised their HDL through diet (basically, the only way to do this is to reduce carb count). However, this type of diet would also decrease insulin, blood sugar, insulin resistance, etc.
Using a low carb diet, I’ve increased my HDL by about 40% or so, although that’s over two years. Will it help? It’s unclear. But I’ve also lost 50+ pounds, reduced my blood pressure, and had many more positive effects. Too many things have changed.
Really splendid Doctor.
There is no point being entirely sceptical about such phenomena as LDL and statins. They have their bit to contribute, and you have in my opinion brought them into something like a proper relation.
I just want to say, there was a “Scottish diet”, it is recorded here.
http://journeytoforever.org/farm_library/medtest/medtest_iftl.html
It is a story not of macronutrient imbalance, but of micronutrient depletion.
The CHD epidemic of the 20th Century coincided with the greatest removal of vitamins and minerals from processed food, and was followed by a flood of increasing supplementation and food variety.
This is not the only meaningful correlation, but it is a very important one.
“The main feature of the modern Highlander’s diet is the absence of fresh vegetables and salads, the absence of wholegrain cereals, and the massive intake of refined carbohydrates.”
I think this is an example of one of the pitfalls of dietary analysis. This person had a preconceived notion of what is healthy and then noticed absence of some of those foods. He didn’t comment on “an absence of papaya” or “a lack of rice” or “a lack of bone marrow.”
He was a doctor. Hiis patients were eating white bread, jam, and tinned meat. Their teeth were falling out from scurvy and they were dying of CVD and related ailments. The locals eating more nutritious food weren’t ill.
This isn’t rocket science.
“These diseases are common in the modern Highlander. Here is no haven of health. The people appear to be plagued by modern diseases no less than town dwellers. The 3,500 patients in our area require the services of three doctors. Dental decay, diabetes, obesity, varicose veins, disordered bowel function, peptic ulcer, coronary heart disease, high blood pressure and, above all, cancer are encountered daily in the surgery.
General practitioners have a unique opportunity of observing the daily lives of their patients and to a student of human nutrition this tale of woe comes as no surprise. When visiting patients at mealtimes I have been repeatedly appalled at what I saw on the family table: tinned meat, tinned vegetables, very seldom any salads; masses of white bread, scones, biscuits, cakes, sweet drinks, packeted milk puddings, margarine instead of butter, and, in place of porridge, the ubiquitous packeted, sweetened breakfast foods.”
If you want to be sceptical about this, you are welcome to live on these foods, but you will have to find the 1950s version of them which will have less in the way of supplementary vitamins minerals and antioxidants than today’s. Good luck.
http://journeytoforever.org/farm_library/medtest/medtest_yelsl.html
Dr. Yellowlees was so very right, decades ago. Nothing to disagree with. Agriculture and “food” distribution system is still governed by greed, in the same way as Big Pharma.
Co-signining this:
“Unfortunately I fear I do not share his optimism that such a future will come. Possibly because as a family doctor I have spent so much of my time wringing my hands over the lunacies and perplexities of the human lot. ”
“Although we have seen in recent decades a tremendous expansion of human knowledge of material things, I doubt if we have matched our increase in knowledge with a deepening of our wisdom.”
Compare:
700-year-old West African soil technique could help mitigate climate change
Ancient farming practice could be the answer to offsetting carbon dioxide emissions, preventing food shortages
https://www.sciencedaily.com/releases/2016/06/160616105901.htm
Dr Dawit Solomon, the lead author from Cornell University, said: “What is most surprising is that in both Africa and in Amazonia, these two isolated indigenous communities living far apart in distance and time were able to achieve something that the modern-day agricultural management practices could not achieve until now.
Gretchen, the phrase ‘Scottish cuisine’ doesn’t quite have the same appeal as ‘French cuisine’.
The characteristics of modern English food seem to be splodge, starch, sweet stuff and lots of bread, margarine and potatoes with Scottish food seeming to be a poor cousin of that, versus the French being sticklers for high quality ingredients well prepared plus lots of real butter and cheese.
This is changing with the rise of the celebrity chefs but even Jamie O., no matter what you think of his dietary ideas, has been having a struggle in his campaign to improve the nutritional qualities of English school food.
That’s a great piece, thank you puddleg58. Was it really written in 1978? Have we all been wandering around with our eyes shut since then (apart from Dr K or course)?
My opinion too. Micronutrients matter more than any macro ratio.
Yes, and there’s more from Dr Walter Yellowlees here
http://journeytoforever.org/farm_library/medtest/medtest_yelsl.html
Yellowlees was a defender of Yudkin against Keys, he wrote a book about his experiences in real wars, the Highlands, and the diet wars.
He died in 2014
http://www.edinburghnews.scotsman.com/news/obituary-dr-walter-yellowlees-97-1-3437539
“In advocating the prevention of illness through exercise and sound nutrition, he devoted his energy to promoting to his patients the value of eating fruit and vegetables, reducing their sugar intake, choosing wholemeal bread instead of white, and butter instead of margarine.”
These things matter, perhaps not as much individually as taken together. Of course wholemeal bread today is not what it was, but this is a preventive prescription, not a treatment plan.
Not everybody. Here’s some proof:
http://www.wsj.com/articles/SB10001424052702304447804576414202460491210
I am surprised that no-one that I’ve noticed in any of this series has mentioned pollution. Afaik serious, industrial strength, air soil and water pollution has been reducing in western Europe in perhaps the same time frame as the decline in chd levels. Smoke and other particulate levels in air are thought to be significant risk factors for heart disease, emphysema etc. Hopefully somone here will have access to air quality statistics and be able to compare them to those for all cause mortality.
Exactly. Clean air acts date from the 50s but only started getting strict around 1970, smoking started to drop around that time, and Silent Spring was published in 1963, with environmental legislation following in the late 60’s-early 70’s.
I think pollution was mentioned before. Given the latest NIH study on how EDTA chelation reduces RR in CVD by 30-40%, I wouldn’t be surprised if taking lead out of gasoline had some effect on declining CVD rates.
Neither would I. I would point out that the agent used for ‘chelation therapy’ is basically, an anticoagulant agent, often used to stop blood clotting in blood sample bottles.
Very interesting, I didn’t know that about EDTA.
I thought it was significant that EDTA chelates primarily lead and cadmium (at least it did in the NIH study) hence my thoughts about the dangers of leaded gasoline. I also think puddledeg58 is right about Silent Spring and the environmental changes it caused as possibly contributing to the decline in CVD incidence.
It is a bit of a losing battle, though, since every time one chemical disruptor is taken out, they put five new ones in. I think we should just accept the fact that aliens have taken over and are now in charge of our food and meds. They knew we would be an easy race to conquer since we are so addicted to convenience.
Apart from pollution there are some other social-environmental changes over the last 60 years which would have had a large impact on longevity and disease prevalence. They might all contribute to the decline in cvd rates and the variance between regions.
Vaccination
Antibiotics
increasingly better levels of public sanitation
If social stress is so important then it is hard to understand why so many of the people who were born between the two world wars and who lived through the great depression and WW2 are living such long lives. The public health improvements seem to outweigh the
sociopolitical factors in general.
Thanks for that link puddleg, the essay is really interesting and thought provoking.
There is more detail here
http://journeytoforever.org/farm_library/medtest/medtest_yelsl.html
and a book by yellowlees here
Thanks for those links puddleg. I am going to try and pick up Dr. Yellowlees book. Here is a link to a related topic, the health of people in the Mid Victorian era, what they ate and how they worked, and what diseases they had and didn’t have with some similarities to Dr. Yellowlees experience in Scotland.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672390/
Are there any figures for homocysteine levels?
I recognise you are making a point that there is no correlation between a high sat fat diet and heart disease. I and many other GPs found that when people deliberately went on low fat diets they were not able to reduce their cholesterol levels( back in the day when we thought they mattered). If they couldn’t do that with low fat diets, they could not reduce their heart disease by avoiding saturated fat, could they? That was why we started people on statins- again for the same reason. Wasn’t it lucky that they worked for an entirely different reason- reducing inflammation- even though when they were invented no one had a clue that this might be a mechanism. The figures for days of life extended are small though, and unimpressive to me.
These days I give people the figures and let them decide what they want to do with regard to statins.
I have a few questions about the table.When is it from if the incidence of type 2 diabetes is 2% for French and UK, and the BMI of French and UK people is the same? How sure can you be that the figures are reliable? It must be from many years ago? The current incidence of diabetes is supposed to be around 5% but some of our practices report 7% with about 10% being type 1. Do the figures suggest that there is no correlation between ANY of diet, BMI, prevalence of diabetes and risk of heart disease when comparing France and UK or are they too unreliable for that? With the identical figures for BMI I wondered if it was a misprint.
The figures are nearly twenty years old. Were the diabetic figures accurate… I work on the basis that, once you question figures you don’t like (don’t seem to fit) you can then ignore anything you don’t like. At which point you can make any hypothesis fit that data. As for statins, as for most ‘preventative’ pharmaceuticals, the benefits may exist, but they are so vanishingly small that I would personally take the lot and fling them in the bin. They are just charms to ward off the devil. The identical figures for BMI are probably not correct now.
How many of your patients do you advise that there is an alternative that trumps statins hands down and that if adhered to will mean them avoiding the unpleasant side effects. I am talking about the Med’ diet which has been shown to beat Statins in terms of outcomes. If we got the nation to change its eating habits we would slash Heart Disease and Cancer rates in a way that drug companies could only dream about. To do this we need a strong voice united behind the message but alas doctors do not seem to want to be that voice despite the fact that they are the one body in which patients would sit up and take notice.
There’s no such thing as a Mediterranean diet.
I am firmly of the opinion that a lot of the “obesity crisis” is down to jersey fabrics and lycra. Sure, a lot of people are being weighed and warned, but you also see in the street sights that would not have been possible years ago. Backalong, it was not possible to get clothes that would lovingly embrace every roll of fat and the creases in between. A woman who had let herself go would have to wear the equivalent of a stout tent . Also, a lot of people go to the surgery for minor troubles which would have just merited a sigh of “It’s my age” and while they are there, they get drawn into the weighing, testing etc. And then they get handed that not-very-useful advice. We just know a lot more about what is going on, and it is on display before us.
Agreed. I don’t know about you, but I’m really, really tired of the requisite films of headless obese people strolling the sidewalk that seem to accompany every story on the obesity crisis. Enough already!
I think we should maybe call it the confirmation bias crisis.
Jean,
I agree – we live in an hysterical age – every problem is hyped, from ‘climate change’ to obesity. I also think some people are simply naturally slim, and eat well (I’m one), others are naturally somewhat more solid, and feel constantly guilty – which is sad. Women could usefully realise that they are still attractive, even well outside those BMI guidelines! That burden of guilt and dissatisfaction with the body, is yet another malign consequence of the modern medical establishment.
You will both be happy to contribute more to the NHS then to deal with the problem ?.
I suppose this example, at least to me, highlights the complete lack of any consistent logic or thought in the diet heart world.
Unfortunately this form illogical “logic” occurs in other diseases as well such as diabetes where the problem is hyperglyceamia ( a surfeit of glucose) is treated by a diet high in carbs (starch and sucrose) with an addition of metformin to block the glucose being fed from actual absorption. Always worried me.
The article is once again brilliant and indeed amusing – I am just amazed at Dr Kendrick’s ability to write it in the relatively short time that he does.
I was also very pleased to see the table comparing France with UK. There is nothing like hard basic data to make a point; so much superior to the the fancy graphs based on Odds/Hrs ratios without the basic data so common in the medical literature.
Just a thought,the one thing everyone does but is of varying quality(pollution) as a cause of cvd,the air that we breath.
As an addition to my previous comment about the “weird” fact that the fat molecules, the triglycerides, arises due to a high carb diet but not due to a high fat diet it is important to realise that it is the excess carbs that are converted to triglycerides in the liver and then put into the VLDL ‘vehicles’ to be transported in the bloodstream for proper storage in the adipose tissues and by the help of insulin concomitant with the digestion of the carbs.
Carbs on a subsistance level are used up and thus not converted into fat.
These facts were also well known 60 years ago but basically ignored by the medical establishment.
In this perspective it would have been interesting to see if there is a difference in the triglyceride levels between France and the UK. I tried a search but couldn’t find anything useful.
It is important to distinguish between starch (2x glucose), glucose, sucrose (1x glucose + 1x fructose) and fructose (and alcohol).
Glucose can be burned directly by the cells, but the insulin spike will ferry excess glucose in to the liver to be converted to VLDL and then stored in adipose tissue. Fructose is ferried directly to the liver by the portal vein and converted to VLDL in the citrate cycle and then stored in adipose tissue. Alcohol is much like fructose, but cells can burn some alcohol, hence the buzz.
The first fructose talk by Robert Lustig has all the biochemistry. Also a good primer:
http://dietheartnews.com/2013/01/is-your-breakfast-cereal-putting-fat-in-your-blood/
Glucose is converted to (prmarily) palmitici acid, which is then packed into VLDLs, along with cholesterol. Glucose is not convereted to VLDL.
You are absolutely right, I was taking a short cut that was not completely legitimate.
Check out this second talk by Lustig, interesting about the two types of body fat, Visceral and the love handle variety and why skinny people sometimes get sick
http://articles.mercola.com/sites/articles/archive/2016/06/25/excessive-fructose-consumption.aspx?utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20160625Z2_NB&et_cid=DM108857&et_rid=1544728710
Fructose can be converted to glucose if needed. I suspect that only when there is a carb overload does fructose get processed to triglycerides, and this is the situation of current consumption.
Dr. Göran Sjöberg
“high carb diet but not due to a high fat diet”
You fail to see the whole picture. By putting all the “carbs” in the same basket, you are throwing the baby out with the bathwater. Many ancestral communities thrived and were healthy on the “high carbohydrate” diet composed of tubers and legumes and cereals and veggies etc., because they were consumed whole and unrefined and unenriched, grown in healthy soil, rich in micronutrients. These people did not eat “high fat”, and were healthy. Your theory fails to explain this phenomenon.
The main microelements accompanying the storage and structural “carbs” in whole plant foods are mainly those critical for the plant growth and health: Fe, Zn, Cu, Mn, B (plus some others). These are often not in balance, or missing in sick people.
One might take into consideration that many of the tuber, root and legume starches will be of the resistant variety which gut bacteria convert to medium chain fatty acids.
Moderation probably also plays a role, i.e. 3000 calories a day of that diet might also have adverse effects.
Lastly, if grain contents such as WGAs (which are also contained in nightshades) are as bad as some say, I have to wonder how those ancestral societies coped.
WGA – so what? Lectins are plant proteins. With this approach you would be left with nothing to eat.
Diana,
My guess is that it is only that half of the worlds population who has already developed insulin resistance that really needs to care carefully about the carbs. Among us older this proportion must though be higher than among young people. And among “traditional” people, i.e. with traditional eating habits, unaffected by our industrial, processed food, if such people still exist today in any significant numbers, there doesn’t seem to be any insulin resistance and they don’t need to care about their tubers
Among diabetics and people with CVD it is probably a 100 % hit to care about the carbs and with zero carbs it seem like the pathogenic processes involved may be stopped and possibly be slightly reversed to my experience. Certainly there will be much less triglycerides and consequently fewer VLDL’s circulating in the blood if you do.
For lunch we had today in our garden charcoal grilled grass fed liver with organic butter and sauerkraut – a real treat.
If high insulin is a culprit in the pathogenic process it is certainly a strong logic involved in “my” theory about reducing the carbs among us insulin resistant people (50 %?).
Dr. Kraft has a lot of interesting things to say about insulin resistance and blood sugar control by the way.
As the recents research show, the carbohydrate-insulin hypothesis of obesity is on shaky grounds….
http://www.vox.com/2016/7/6/12105660/do-low-carb-diets-work
It is now probably far too late to test out the hypothesis that the increased number of copies of the AMY1 allele that codes for salivary amylase was selected for in populations that at a high starch/carb diet, but I would suggest that this is likely the case as we now know that obesity in individuals eating the typical high carb western diet is inversely correlated with copies of the AMY1 allele.
Why the medical establishment does not test patients for number of copies of AMY1 and then advise on diet accordingly is beyond me. Except that it is obvious that there would be no money in it for drug companies or, as Zoe Harcombe puts it, ‘food-like’ substance manufacturers.
AMY1 gene copy number variation testing: what for? Gene expression matters, not CNV. Gene expression is controlled by lots of factors. In addition, plants pack starches together with amylolytic enzymes, commensal bacteria have amylases too, which is overlooked. Some people from ancestrally “high carb” populations have low AMY1 CNV and have no problem eating starch. Gut flora genes probably matter more than your genome.
Stephen, can you explain some more? This is what I got so far: people who have few copies of the allele produce less saliva and this makes them obese?
Diana, I have my doubts about the study that debunks low-carb diets. The report states: “participants were put on a baseline diet, which was designed to be similar to what they reported they were eating outside the hospital, including lots of sugary carbohydrates.”
Look at the diet graphic. Do you see a half-dozen krispy kreme doughnuts; a couple of venti-frappi-syrupy-creamy coffees; a litre or two of sugary cool drink? Nope. In fact, the “baseline” diet is not a bad diet at all, IMO. This tells me that either the participants lied through their teeth about what their daily diet was, or those conducting the study fudged the diets to make sure the low-carb diet showed little difference to the “baseline” diet.
“it took the full 28 days on the low-carb diet for the subjects to lose the same amount of fat as they did in the first 15 days on the baseline (higher-carb) diet that wasn’t even designed to get them to lose weight.”
If on their “normal” high-carb diet they lost weight at twice the rate of the low-carb diet, it is obvious that the high-carb diet was not remotely normal. It was in fact a diet designed for them to lose weight. (It looks typical of the kind of diet you see in magazines that say “Shed those last few kilos before the big day” sort of thing.)
“These studies represent the first rigorous scientific tests of the carb-insulin model in humans,”
Yeah, right. IMO it is a rigorous demonstration of the cynicism with which “scientists” conduct these studies to get the results they want.
Martin, I don’t see how you can call the baseline diet (or low carb diet) in that study “not bad”. Both of them are total crap in my opinion.
“As the recents research show, the carbohydrate-insulin hypothesis of obesity is on shaky grounds….”
The Kevin Hall papers? Load of old rubbish to put it politely. Richard D Feinman put it much more amusingly:
Anecdotally, I get all the micronutrients I need from a diet of assorted animal parts+products and some free range eggs plus a few non-starchy vegetables. If one were to take a quick survey of the various commentators to this series, those who say how good they feel after giving up most of the starchy-carb types of foods far outweigh any other.
The holy trinity ( WheatBeansPotatoes):
Wheat:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526354/
‘In this study, we show that members of the nongluten α-amylase/trypsin inhibitor (ATI) family contained in wheat and related cereals are strong inducers of innate immune responses in human and murine macrophages, monocytes, and DCs.’
http://www.gastrojournal.org/article/S0016-5085%2813%2900615-X/abstract
NOTE: ATIs in grains are not destroyed by cooking or fermenting. They are very persistent. But you can wash out the starch and the ATIs with mildly salty water and keep just the gluten – if you are non-coeliac it is much less problematic to eat this or add it to other non-wheat starches to make bread.
Beans:
https://en.wikipedia.org/wiki/Phytohaemagglutinin
http://emedicine.medscape.com/article/1009200-overview
The Deadlies:
http://www.diagnosisdiet.com/nightshades/
Apologies if this is deemed to be too far from the actual topic of this post although I think it is still relevant.
Hi Eric,
I came across research that had been carried out over the last 5 or so years into a relationship between the number of copies of the AMY1 gene and obesity. http://www.ncbi.nlm.nih.gov/pubmed/27022442 will probably get you started if you want to do some googling.
It appears that among higher primates humans are unique in having up to 13 or more copies of the gene. As a result the amount of salivary amylase in human saliva can vary from a couple of percent to over 50%. For reason I cannot remember lower levels of salivary amylase correlate with lower levels of obesity and higher levels with higher levels of obesity – I haven’t followed this up so am not sure whether anything more has been done to examine the mechanism/s.
Diana
I checked out your VOX reference.
…. 17 overweight and obese patients to the hospital for two months….
Were they diabetic and insulin resistant?
17 is a small number w.r.t to such a complex issue and 2 months is a very short duration.
Also, if insulin important in non-diabetic overweights and the obese, why is it not routinely used in diabetics in the NHS? I would also remind you that the US CDC researcher Dr Flegal has reported on three occasions that the overweight live longer (JAMA. 2005 Apr 20;293(15):1861-7. JAMA. 2007 Nov 7;298(17):2028-37. JAMA 2013;309(1):71-82.)
What also worries me is that there is no reference to the published report. Is this a “press release”. If not why no reference. Dr Hall – has he any conflicts of interests? The NIH have in the past hidden data as I have shown in the past and have a long history of “revolving door” recruitment with commercial organizations. Sorry but I am highly cynical where “commercial benefit and status” is involved. As Max Planck is reputed to have said “research progresses funeral by funeral”
I am open to the data of the report (but it is not there) but there is a large reference base for benefit in diabetics of a low carb, hifat diet.
Mike
the study was linked in VOX article, here: http://ajcn.nutrition.org/content/early/2016/07/05/ajcn.116.133561.abstract
It was funded by NuSI, the organization founded by Gary Taubes with the mission to test his hypothesis.
Mike, there’s also evidence showing benefit to diabetics on raw food vegetarian diet or even, counter intuitively, Walter Kempner’s Rice Diet.
I think T2D can be arrested or even reversed with pretty much any whole food diet and adequate amount of exercise.
Diana,
I am intrigued about your comment “Many ancestral communities thrived and were healthy on the “high carbohydrate” diet composed of tubers and legumes and cereals and veggies etc., “.
Do you have a source for the information? I would like to learn more.
Thank you.
Traditional Japanese, traditional Hawaiians, and lots of others. Look it up.
And as far as I know, no one has been able to show that Masai or Eskimos have longer life expectancy or significantly lower rate of degenerative disease than, for example, Okinawans or Kitavans.
Brian, if you want a Western population on a high-carb diet, look at Ireland 1600 – 1835.
“The burgeoning population lived on a diet comprised mainly of potatoes and milk, which if eaten in sufficient quantity is a surprisingly nutritious, if monotonous, diet. It is also relatively tasty and easy to prepare.
It is estimated that by the late 1700s an average family of two adults and four children needed 5 tons of potatoes a year, or about 5lbs of potatoes each a day. “ — http://www.dochara.com/the-irish/food-history/food-in-ireland-1600-1835/
Diana thank you for the link – unfortunately the full paper is hidden behind a pay wall.
Downloaded the abstract
In the absence of any information to the contrary I have to assume that study patients were neither diabetics or suffering from the metabolic syndrome; in short the patients were in good health.
The basic metabolism is very robust and normally changes in diet over short periods would have marginal effects, if any, particularly where “n” is small. Indeed, the results would seem to confirm this in these healthy subjects. I was surprised that the conclusion even emphasized this:
Conclusion: The isocaloric KD was not accompanied by increased body fat loss but was associated with relatively small increases in E(nergy) E(xpenditure) that were near the limits of detection with the use of state-of-the-art technology.; pretty much as I would expect.
May I suggest that where metabolism has been severely disrupted as in diabetes with insulin resistance, the ketogenic diet, over many months, can help to reduce the disruptive effects of diabetes and insulin resistance. The study should be repeated with N >= 100 over, say 1+ years
Also the study abstract makes no mention of insulin levels or HbA1c levels, important factors in diabetes (confirming my view that the patients were healthy).
In short, it is my view that the basic metabolism in the healthy is very robust and is not subject to major changes of diet over short periods, however sophisticated the techniques. The real test is in those with severely disrupted metabolism.
mikecawdery
I have read full Hall’s paper. Its aim was not to test metabolically “disrupted” or diabetic people, only overweight and obese. It should test a simple theory: that ketogenic diet will provide some kind of metabolic advantage comparing to “high carb” diet (50% carbs). It did not happen, there was no faster fat mass weight loss. These people were locked in metabolic ward for 8 weeks, and monitored in metabolic chambers, their food intake controlled. The small increases in E(nergy) E(xpenditure) that were near the limits of detection” in people on ketogenic diet disappeared over time anyway.
Take home message: there are more ways to Rome.
An excellent quote from the site linked by puddleg58: “The concept of unity in the health of the soil, plants, animals and man seems to be beyond the comprehension of professional leaders with their passion for specialization and their consequent limited vision.”
I would also add – to be beyond the comprehension of professional diet gurus.
Thanks, appreciate this insight
________________________________
Diana,
You said,
“The main microelements accompanying the storage and structural “carbs” in whole plant foods are mainly those critical for the plant growth and health: Fe, Zn, Cu, Mn, B (plus some others). These are often not in balance, or missing in sick people.”
I am curious as to whether this is a well established fact for some definition of the word ‘sick’, or is a more general observation. It does seem to me that while Dr Kendrick is just saying that SFA’s do no harm, and can usefully displace harmful sugar from the diet, this has unleashed a host of ideas based on fairly extreme diets! Because SFA’s were demonised on such poor evidence for 50+ years, I am always cautious about the evidence base for other dietary recommendations! Copper and manganese are decidedly toxic at higher concentrations, and I also wonder how bis is the gap between beneficial levels and harmful levels!
Here a post about about copper deficiency and heart disease:
http://wholehealthsource.blogspot.com/2010/04/copper-and-cardiovascular-disease.html
David
I agree. We are back to the general attitude of the medical establishment; nutrition is generally OK but if you are sick you need a pharmaceutical. Why else would the CMO write to all doctors pointing out that in the UK, Vit D insufficiency is widespread, while the NHS does not provide Vit D testing as a routine, particularly for the elderly? ROS (reactive oxygen species) also important in many diseases (even CVD – NO deficiency) but again no test for total anti-oxidant capacity (TAC) of blood? These simply do not enter their mindset.
I live in France and just a flippant thought. Anything to do with stressful life in Scotland.
Here everyone has the two hour lunch break and appear to enjoy life more. Also the sun hours in Scotland are much less, therefore, Vitamin D or lack it.
Most people in the countryside grow their own vegetables, fruits and cook with olive oil, no butter on their bread but plenty of fermented cheese.
As I have said many times before, whilst researchers try to unravel the specific mechanism that causes HD, so that we can carry on with our god awful western diet whilst tweaking the specific mechanism or drug that will allow us to eat poorly but survive, your best bet is to look at those populations that do not get HD and adopt their diet and where possible lifestyle
This is nice!
“Conclusion: After controlling for potential confounders, siesta in apparently healthy individuals is inversely associated with coronary mortality, and the association was particularly evident among working men.”
http://archinte.jamanetwork.com/article.aspx?articleid=411678
Dear Dr K,
I have read part 18 three times, and I see two themes, the apparent French paradox and the fibrinogen /clotting activity. Are the the two linked, do the French have less malevolent clotting agents?
You mention the cafés, my experience in the cafés is groups of men, moaning about the government, football and other woes. Not for nothing are the French classified as a nation of “raleurs”
Groups of like minded individuals sharing similar opinions.
Sounds like a stress relieving supportive social structure to me.
Diana
Here is an alternative view:
https://proteinpower.com/drmike/2016/05/06/contradictions-and-cognitive-dissonance-the-kevin-hall-effect/
Now that I read more detail, I think the vox.com account of the experiment was badly reported. The experiment itself was weird. I would have thought you get a bunch of people, let them eat what they want to establish a baseline, then split them up into high-carb, high-fat, and control groups, and observe the results.
It seems that the high-fat diet resulted in a 100 calorie a day extra basal metabolism. Not a big deal. That’s about two biscuits a day. Eating decisions — to snack or not to snack; to have an extra helping; to supersize it — are much coarser-grained.
I believe a calorie is a calorie, which is what the study showed, close enough. That extra 100 calories burned off is not going to make a significant difference. If you eat too many calories you will get fat, no matter whether they come from carbs or fat. The big problem with high-carb sugary diets is that it is very easy to eat a thousand or more calories at a sitting and hardly notice it, so people on high-carb diets tend to eat too many calories. That’s the fundamental reason they get fat. There are other health issues too, of course, related to insulin spikes etc.
A calorie isn’t a calorie. 100 calories that you get from sweet potato isn’t the same as 100 calories you get from Mars bar.
A calorie is a calorie as it is a precise measure of energy. It is the energy required to heart one gram of water by one degree centigrade. (We usually talk about kcal, not calories). Ergo all calories are, must be, the same. However, the way that I see it, is that if you put one litre of petrol in a car it will not always go the same distance, because kilometers per litre is dependent on acceleration, speed, braking, tyre pressure etc. etc. When it comes to humans, one calorie can be used for other things such as repair, basal metabolic rate, percentage energy recovered etc. etc. Carbohydrates can only be used for energy production, proteins can be used for many different things etc. etc. So those who say that energy in = energy out are talking complete baloney.
The problem as I saw it in the past: “a calorie is a calorie” argument has been used to sell people on all kinds of crappy food as well as questionable diets.
“Carbohydrates can only be used for energy production, proteins can be used for many different things etc.”
This statement is not correct. Carbohydrates (mono-, oligo- and polysacharides) have many other roles too. Structural building blocks, information carriers, defense molecules… glycans have actually amazing portfolio of functions.
Martin: 100 Calories per day is a lot! More than 10 pounds per year. In 10 years you are morbidly obese. In a bomb calorimeter a calorie from fat is same as a calorie from alcohol. But in a biological system they act differently under the control of various hormones etc. Like in an electric car, when you break the cars kinetic energy goes into battery storage, whereas in a normal internal combustion engine breaks dissipate as heat.
Diana,
Your saying it makes it so? I believe that, in general, open minded readers of this blog need particulars.
I do.
‘ “Carbohydrates can only be used for energy production, proteins can be used for many different things etc.”
This statement is not correct.’
@JDPatten
I’m sorry I do not get your point. Dr. Kendrick mentioned that “Carbohydrates can only be used for energy production” and I commented that it is not correct, and mentioned briefly what else they do. What is your question?
I agree with Diana. I made a bit of a sweeping statement which was not correct.
Martin, the whole concept base of cico in relation to weight maintenance and heat output, ignoring entropy change, is a bit vague and limited by hidden problems of definition and applicability. One significant assumption is that the calory types can be assimilated eg if you were lacking some specific enzmes then you might not have the capacity to utilise some food types, granted they would then be part of the co side of the equation but perhaps would still be transformed, reduced in energy content in a non-nutritive way.
Simple cico makes no allowance for specific calory sources, mixtures, metabolic capacity or metabolic efficiency.
Here’s an article about how to feed your horse properly.
http://agriculture.vic.gov.au/agriculture/livestock/horses/management-for-horse-owners/feed-requirements-of-horses
If i were to consume the suggested 1kg of sweet meadow hay per day, the table shows that i would be consuming about 7Mj and 90g of protein. Lacking the digestive-fermentatory apparatus of a horse, I would probably lose a lot of weight. It would not give 7mj of human calories. Although i might get plenty of micronutrients.
If i were to consume the suggested amount of raw legumes for my body weight i would probably soon be dead and the calories would be going nowhere.
Dr Kendrick,
One cannot argue with that but what is the Kcal on a food label. Asked a NHS trust nutritionist that but she was unable to answer . When I mentioned digestible energy (the energy absorbed minus energy in excreta), she did not know what I was talking about. Then one has metabolizable energy which can be divided into energy used to maintain body heat and the maintenance of metabolism and then the production energy (tissue production, work etc). This energy partitioning is highly complex and is not simply a case of carb, protein, fats, fibre as I suspect the BSE epidemic in cattle demonstrated (protein from dead carcases used as “protein)
It’s a guesstimate – calorimeter measured value, adjusted for digestability, etc:
https://en.wikipedia.org/wiki/Food_energy
https://en.wikipedia.org/wiki/Atwater_system
Thanks, Diana, for that book reference.
Having followed past advice for decades, I found myself at the edge of diabetes in 2010. From that point on I’ve avoided eating anything white or anything that has a list of ingredients. I’ve backed from the edge.
Being told that potatoes and other carbs are good for me is something that I just can’t swallow without a bunch of particulars as gravy.
JDPatten
Yes potatoes can be good for you 🙂
I will use a silly example.
Mushrooms are about 20 calories per 100 grams. Is the metabolic effect of 20 calories of sugar the same as 20 calories of death cap mushrooms?
You will not get fat on death cap mushrooms.
Similarly you will not get fat on sawdust. There is more than just the energy content of the food that affects our biochemistry.
The Hall study is poor indeed. Even Hall’s understanding of his own results is woefully lacking.
As far as I understand, diabetes type two and CVD goes very close hand in hand.
Diabetes has a lot to do with poor control of of the blood glucose and is expressed by the exceedingly high blood sugar levels, deleterious not least by causing glycation of proteins (AGE’s). Another name for diabetes (T2) and especially pre-diabetes, and probably more accurate, is insulin resistance which tells that serum insulin levels turn very high in our homeostatic efforts to coop with the high glucose circulating after a carb rich meal.
But what about the high insulin levels per se?
Do we know much about any deleterious physiological effects of our most fundamental hormone at those unnaturally high levels? I know that there is a general insulin growth factor involved and perhaps this might be considered relating to CVD?
On a most fundamental physiological regulatory level I am just now stunned in my reading of the molecular biology of THE CELL where I in chapter 15 read about the cell signalling and learn how incredibly complex the internal cell response is to external signals, e.g. when an insulin molecule docks to a receptor in the cell wall.
How little we know!
And how can Big Pharma, and by the way the whole medical community, be so cock-sure that a shot of insulin is a much better treatment than reducing the carbs for the 500 million diabetics involved in the world?
In his lecture at https://youtu.be/pgMizC6sQ6w, Dr. Westman states that the quantity of blood glucose in the body under normal conditions is just 5 grams. If so, then it is easy for carbohydrate intake in just one meal (or can of soda for that matter) to multiply blood glucose level by 10-20 times, almost instantaneously, to a level that is highly threatening to health, as I understand it.
I had always thought of the insulin response as a corrective adjustment of blood sugar until I saw this video. But is this not in itself a very large impact on the body – a shock to the system? Is it not capable of triggering significant adverse effects without the subtleties of dietary composition or lifestyle coming into play?
It does seem to me that the large differences in CVD rates between generations and societies would suggest an unsubtle cause and effect, a strong force at work. There is a great volume of evidence suggesting that CVD was/is insignificant in primitive societies; the reports from physicians of the British Empire during the colonial era are really compelling on this front.
These stark differences in heart health should reflect stark differences in the general nutritional environment in my view.
Dr. K’s journey is impressive and enlightening. To me, it is exciting because he is narrowing the potential mechanisms of causation. Perhaps the answer is closer than he thinks?
Dr. K,
Is assaulting the cardiovascular system multiple times per day with a glucose flood enough, in itself, to cause the endothelial damage you describe? Is the insulin response actually rapid enough to be fully protective? Does this thinking have relevance?
I am not sure. My main problem with the (its all to do with blood glucose hypothesis) is that whilst people are consuming more sugar and presumably having more sugar spikes, CVD rates continue to fall. So, if there is an effect – which one supposes there must be – it cannot be enough of an effect to explain everything. I am more of the view that insulin is the culprit.
As an outsider, I am always puzzled by arguments as to whether the culprit is glucose or insulin, because the two are so closely coupled together.
The fact that CVD rates continue to fall is fascinating because modern man doesn’t seem to be doing anything particularly healthy – except perhaps exercising a little more.
Is it possible that there is an epigenetic effect here – a quick GOOGLE found this article:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075976/
My point is that people were subjected to great stress during and after WW2, and that may have had an epigenetic (as opposed to genetic) effect on their offspring. Now more and more people who were born to people who did not endure the stress of war (or were at least born well after the war) are entering the CVD-risk age, and that might be helping to lower the rates.
I think that it is insulin since we know that hyperinsulinemia causes vascular damage and hypertension years and decades before type 2 diabetes can be diagnosed.
Is it possible the part of the population addicted to sugar is falling? Aggregated sugar consumption statistics across nations would not reveal this but we know that awareness of the low fat fallacy is growing.
Whereas older studies suggested that there is no benefit of glycemic control in T1 Diabetics with respect to CVD, later studies suggest tighter regulation offers benefits.
http://care.diabetesjournals.org/content/29/11/2528
Malcolm,
I also think that high insulin may be a culprit but have you looked into any explanatory mechanisms?
It would be very interesting to hear your views on this subject.
Many, but I have not got my thoughts very well organised on this.
This argument works only if we assume that 39 grams of sugar in a can of Coke ends up as 39 grams of sugar in blood circulation. Are you sure this is so? I am not.
I think it pretty much is, apart from the drops that you can never quite get out.
And things are even more complicated once you look at sugar content in more complex carbohydrates and what happens to it once those carbs enter the body. That’s what LCHF proponents fail to understand, IMO.
And lo and behold the word Gluten rears its ugly head again 😂
Martin Back
Craig
RonC
I’m sorry but you will have to try a bit harder…
Still waiting for the detailed potato lecture.
It seems to me I would be wasting my time here talking about whole foods full of complex polysaccharides (potato was just an example). There are 3-4 commenters here who are willing or able to listen.
I have located a book for those who are interested.
Diana, for what it’s worth, I am very interested in what you have to say about foods. Thanks for the book recommendation!
Sasha
I am not here to lead some nutrition wars. But I think it is OK to remind people from time to time that reality is more complex and the truth is not black and white, and that something called HFLC (whatever that means, it may mean so many different things) may simply be wrong, or not so smart strategy for some/many people.
Diana, I agree. Reality is more complex and HFLC is too simplistic, IMO. Thank you for providing the links to what I always thought is a balanced nutritional approach.
Diana, had a look at Amazon comments, not read the book. I wonder if it advocates separating starches from protein, Hay diet. Hav used Hay in the past, ate everything, just give 4 hours between the food types. It works a treat. To a certain extent still eat this way. New potatoes with broad beans is a lovely dish on its own, butter or Mayo. Can’t persuade the rest of the family to eat this way. I think the Harcombe diet is a little like this. Digestion is either carbs or protein, not both. Growing children, throw everything at them, always home made, apple crumble, apples off the tree, oats and butter topping, drizzle honey. We have though, always been heavy on the vegetables, underground or above ground grown.
Sylvia
I did read the book before linking it here. It also talks about nutrient content, I even learned some new facts (I did not know that potato tubers contain kynurenic acid).
It seems people lose weight on this potato diet (and getting other benefits). Per Taubes’ theory, this should not happen.
I don’t believe Taubes said you couldn’t lose weight by eating potatoes. He’s all about insulin. It’s entirely possible for the potato diet and Taube’s theories to coexist. There are people who react better to low fat and high carb. Those people would do well on the potato diet. Others (say, most others, including me) would not. When I eat a potato (even cooked then cooled then recooked or cold), my blood sugar goes through the roof.
Now, resistant starch is different. Using potato starch, I can stay in ketosis. I can also stay in ketosis with small amounts of 86% chocolate, small amounts of tiger nuts (tubers with carbs but high in resistant starch and fat), and even small amounts of berries. The problem with a potato is that it has relatively little resistant starch and a ton of carbs. For those of us who are insulin resistant, we might as well be eating sugar as eating a potato.
I wish someone here would explain precisely what is wrong with the notion that complex carbohydrates break down in the gut into sugars – mainly glucose – when consumed. I know that some break down more quickly than others, but is there more to it than this?
Surely the additional micro-nutriments in any particular food is slightly beside the point, the main issue is how much glucose (and maybe fructose) is generated – or once again, am I missing the point?
Maybe an internet link would be better than a book reference – because fortunately I don’t need to lose weight!
Get a glucose meter and test. When I did this just after I was diagnosed with type 2, I found that all carbs including complex ones raised my glucose levels to unacceptable levels. I’m just carb intolerant as are all diabetics.
I agree, and I suspect that the posters who
argue so fervently against LCHF haven’t
checked their glucose (let alone insulin)
response to eating carbs. Yes, carbs are
just many molecules of glucose strung
together. It is a simple concept. Dr. Davis
of Wheat Belly has shown many times that
complex carbs, i.e. whole wheat, raise blood
glucose as fast or faster and as high as
straight table sugar. So stop already with
” Eat complex carbs for health.”
David
“I wish someone here would explain precisely what is wrong with the notion that complex carbohydrates break down in the gut into sugars ”
I tried to explain a bit more but none of my comments went through. Probably my comments are not welcome.
As said before. The only reason why I stop any comment is for one of three reasons. It is personally insulting, it is an advert (overt or more subtle), it is completely incomprehensible. However, there are delays. I work full time, and writing two book chapters, a paper and another book. Sometimes I get behind on things.
My apology. Thanks for the explanation.
OldTech,
So, uh . . . that would include potato carb, would it? 🙂
Just wondering if the sugar/insulin effects would be worth the nutritional value for type II.
I’m type 2 and do not eat any significant carbs for nutritional value and that includes potatoes. They are not on my list of allowed foods with one exception – resistant potato starch.
Resistant starch is starch that does not raise your blood glucose because we can not digest it, but our microbiome can use it to create short chained fatty acids which are good for colon health and may even improve glucose control. I use Bob’s Red Mill potato starch and eat it raw by mixing it in water. You do not want to heat it since that will convert it to digestible starch and that will raise your blood glucose.
@bill; re: …carbs are just many molecules of glucose strung together.
Not that simple. See the Wiki page on Carbohydrates.
re: Dr. Davis of Wheat Belly has shown many times that complex carbs, i.e. whole wheat, raise blood glucose as fast or faster and as high as straight table sugar.
Not all complex carbs. Wheat does what you describe because it is a 60% glucose polymer, in a branched form that human enzymes convert to blood glucose BG quite effectively.
The bottom line on whether a carb raises BG is the BG meter. Raw potato starch, for example, rarely budges BG in most people, and makes a great prebiotic fiber for your microbiome. Cooked potato starch is quite likely to spike BG. There are idiosyncratic variations on this. The final arbiter is the glucometer.
Anyone concerned about CVD needs to consider the matter of BG (fasting, postprandial, HbA1c and how carbs drive triglycerides), and decide what targets matter.
Bob:
Eric Westman at 1:25
Re: Glucose response: See my first sentence.
Dr. Westman is wrong. No, eating starch (potato, pasta,…) does not equal to eating a spoon of sugar.
OK – there are various different ways that glucose molecules can polymerise, but the point I would like to discover, is whether we are simply talking about the time it takes for these various polymers to decompose, or whether there is some other physiological difference between eating carbs and eating sugar (other than the fact that sucrose is half fructose).
Diana seems to be hinting that this is the case, and I am just curious. I mean, if I discuss this with people, I point out that eating carbs is just like eating glucose except for a small time delay that helps to blur out the spikes. Is anyone claiming that that description is misleading?
I think that description is misleading. Because that would mean that if you eat nothing but potatoes for a year you would get to the same place nutritionally as if you were drinking equivalent amount of sugar water for a year. I doubt that would be the case.
David
“carbs” are not only starch. Another complex carb, that is storage polysaccharide used by plants is inulin composed of – gasp – fructose. Inulin, or fructans in general, are mostly used by plants growing in below zero temperatures (sugars serve as antifreeze). Think plants like dandelion, chicory, onion, garlic, Jerusalem artichoke etc. These plants are useful source of dietary fiber we need to feed our gut flora. Gut microbiome metabolizes prebiotic fiber into short chain fatty acids (SCFAs).
Once again: carbohydrates are changed into “fat” by the action of your gut flora. You can think of these microbial metabolites, such as SCFAs, as signalling molecules, interkingdom messages from the symbionts to the host: we are here, thanks for feeding us, life is great, be healthy.
Note that SCFAs have further roles: butyrate fuels the colonocytes and care for their healthy turnover, it is HDAC inhibitor (think cancer), etc.
When you eat starchy food, first metabolites are disaccharides, like maltose. Maltose binds receptors signalling satiety in the brain (helps to prevent overeating). Some of the starch is so called “resistant” meaning it is not accessible by your own enzymes but only by microbes.
Note that plants have weapons to defend their storage carbs against hungry pathogens, such as polyphenols that block their enzymatic action. Eating high polyphenol high fiber starchy food (or their combination) is a great way to deliver most of the starch you eat in “resistant” form into your colon where it is metabolized by your gut flora. Polyphenols also selectively feed “beneficial” microbes. This is a very complex topic, there is a lot of information available if you start looking.
Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health (Ríos-Covián, 2016)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4756104/
“The gut microbiota influences our health and nutritional stage via multiple mechanisms, and a mounting body of evidence recognizes that microbial metabolites have a major influence on host physiology. Short chain fatty acids (SCFA) are volatile fatty acids produced by the gut microbiota in the large bowel as fermentation products from food components that are unabsorbed/undigested in the small intestine; they are characterized by containing fewer than six carbons, existing in straight, and branched-chain conformation. Acetic acid (C2), propionic acid (C3), and butyric acid (C4) are the most abundant, representing 90–95% of the SCFA present in the colon. The main sources of SCFA are carbohydrates (CHO) but amino acids valine, leucine, and isoleucine obtained from protein breakdown can be converted into isobutyrate, isovalerate, and 2-methyl butyrate, known as branched-chain SCFA (BSCFA), which contribute very little (5%) to total SCFA production. The aim of the present mini-review is to summarize the current knowledge about SCFA production, including bacterial cross-feedings interactions, and the biological properties of these metabolites with impact in human health.”
Diana,
Thanks for your detailed reply, and indeed you seem to be painting a much more complex picture than that which says complex carbs => sugars delayed in time!
“When you eat starchy food, first metabolites are disaccharides, like maltose. Maltose binds receptors signalling satiety in the brain (helps to prevent overeating)”
Feedback loops are clearly key to understanding almost all aspects of biology.
Does this mean that you do not support the use of LCHF diets – even for those who are diabetic?
“Does this mean that you do not support the use of LCHF diets – even for those who are diabetic?”
No, I believe that this approach works too, but I also say that it is not the only approach, and I think that the reason it works (short term) is via modulating gut flora. Microbiome helps metabolizing your food, listens to the signalling and then modulates your own gene expression. Microbes inhabiting your body (microbes – bacteria, archaea, fungi, viruses, phages etc. had enough evolutionary time to learn how).
LCHF: if people remove refined crap from their diets, then it is OK and may be helpful. My question is what is the crap replaced with, and I do not think it should be replaced with fat long term, if you are aiming for reversal. If your LCHF means high prebiotic and probiotic, and at the same time balanced micronutrients diet then I do not care how you call it. My concern is that people in their fear of carbs remove good food sources that would provide fiber and various vital micronutrients.
Some food for thought:
Effect of honey in diabetes mellitus: matters arising (2014)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3909917/
Diana: Thank you for this excellent explanation. Nutrient-dense real food. A question: Do you think there is positive value in inoculating healthy garden soil with commercially available fungi, or just let nature take its course? I suspect spores are everywhere.
Gary, I would not fall for the idea that adding commercial innoculants is beneficial. It’s like buying expensive probiotic pills with some beneficial species and forgetting to feed them with prebiotic fiber. While the probiotic bugs may do some good when passing through, they will not settle unless you support their growth with some fuel they need – supposing they manage to settle, of course, because they are immigrating invaders, in fact. The local population may not like them…
Your garden soil already contains fungal spores, waiting for their chance to grow. Feeding them (compost, plant matter, organic matter) and encouraging their growth (intercropping, less tilling etc.) is probably smarter, long term.
Interesting article about breast milk, human milk oligosaccharides, and Bifidobacteria:
“Breast-Feeding the Microbiome”
http://www.newyorker.com/tech/elements/breast-feeding-the-microbiome
Diana,
Such interesting information about bowel flora. Thank you. I was watching a talk by Dr. Stephen Phinney, about the effect of nutritional ketosis. He discusses how the Inuit (traditionally) were able to live without much if any vegetables and fibre for most of the year. Their diet was very heavy on marine animal fat and they probably were
in nutritional ketosis most of the time. He explains that the liver manufactures ketone bodies from fat, and that one of these, beta Hydroxybutyrate is preferentially used by the bowel flora over glucose from resistant starch, which was in short supply anyway. So instead of the bowel flora making beta Hydroxybutyrate from ingested resistant starch, the bowel flora can be ‘fed’ directly from beta Hydroxybutyrate manufactured by the liver. I hope I am remembering this right, feel free to correct me. I am interested in your take on this.
Maureen H
” the Inuit (traditionally) were able to live without much if any vegetables and fibre for most of the year. Their diet was very heavy on marine animal fat and they probably were
in nutritional ketosis most of the time. ”
Why should Inuits be in nutritional ketosis? That is a starvation/fasting adaptation. Inuits seem quite well fed to me (they have to be, given the cold environment.) They were definitely eating some vegetation (the Arctic is not so plant sterile as it may seem) and eating animals from nose to tail surely provided dietary glycans (sugars, fiber). So I highly doubt this claim.
“Dr. Stephen Phinney explains… that beta Hydroxybutyrate is preferentially used by the bowel flora over glucose from resistant starch, which was in short supply anyway. … the bowel flora can be ‘fed’ directly from beta Hydroxybutyrate manufactured by the liver.”
This seems rather strange, can you find the exact phrase/reference? It also seems to me you are confusing ketones (such as β-Hydroxy butyrate) and butyric acid. Gut flora is not kind of sitting in your GI tract and waiting to be fed with butyrate (or ketones, though they may use them in case of carbon shortage), on the contrary, it is producing butyrate (among other metabolites) while fermenting indigestible fibre. Complex interplay apd many bacteria species crossfeeding each other with specific metabolites. That’s your colonocytes that need butyrate as end product of the microbial action.
Diana, the Inuit diet today is not the same as their traditional diet which of course had no processed foods high in sugars, or grains. For at least nine months of the year there was no vegetation to eat, then possibly some berries and lichens in the very short summers. So in fact the traditional Inuit diet was ketogenic. Being in a state of nutritional ketosis is not the same as starvation. The Canadian explorer Vilhjalmur Stefansson lived with the Inuit in the 1920’s, eating the same diet and his experiences have been very well documented. The following Wiki link goes into some detail, it’s a long link so for the nutritional bit scroll down to “low carbohydrate diet of meat and fish”.
https://en.wikipedia.org/wiki/Vilhjalmur_Stefansson
Maureen H
No, Inuits’ traditional diet was not “ketogenic”, it could not, they could not. Have a look: https://en.wikipedia.org/wiki/Ketosis#Inuit_People
Diana, thanks for that very interesting Wiki link.
Diana: Thanks. It is as I suspected. I do all of those things, in an attempt to mimic nature. Fascinating article. I know I’ve altered my gut microbiome for the better through my dietary experimentation, but I think it was adding more plant matter, such as wild dandelions and seaweeds, to my diet, which has had the biggest impact on this transformation (and I think IF played a role). The big elephant in the room with that article is, why all these fragile preemies? We accept as normal today, in the health of our children, what, in previous generations, was unusual or rare. Methinks medical and “scientific” intervention is one of the keys to this.
“wild dandelions and seaweeds”
Diana approved 🙂
Diana,
Thanks again for your response, and the link to the fascinating article about treating Diabetes with honey! This helped to reinforce my somewhat heretical suspicion (to a former chemist) that analysing food in terms of its chemical constituents isn’t always helpful!
As is probably analyzing foods purely in terms of thermodynamics.
David, honey contains highly concentrated sugarscreating hyperosmotic environment preventing microbial growth (= honey is antimicrobial). However, when eaten, fructans, other oligos and other compounds selectively feed the beneficial microbial species (= honey is prebiotic). Not all honeys are equal, of course, the content/ratio of sugars, polyphenols, vitamins and minerals vary depending on the plant source, season etc.
Yes, honey is good medicine.
My father-in-law was in a London hospital in 2010 with a substantial abdominal surgical wound that would not heal. The physicians eventually opened it up and slathered the whole raw area directly with manuka honey. Made all the difference. A few days – good as new. (Well, almost.)
Diana,
You wrote: “when eaten, fructans, other oligos and other compounds selectively feed the beneficial microbial species (= honey is prebiotic)”.
I am not denying the evidence that honey is somehow good for diabetics, I am taking it on trust – at least for the purposes of this discussion – I am asking what that really means!
On the face of it, it means that too much glucose isn’t bad for diabetics if it is offset by certain other chemicals in the diet. Taken to its logical conclusion, one might conclude that it is the ratio of glucose to anti-oxidants in the diet that is at issue!
Furthermore, I have a disturbing hunch that if properly tested, we might find that honey is beneficial, but pills created out of its individual constituent chemicals (polyphenols, etc) might not be!
Let’s not reduce the debate about honey to glucose and polyphenols only. Looking at honey composition should be a chemist’s joy!
Diana,
I am wondering if you have a blog or website.
No, I don’t keep a blog.
Do you think the kevin hall material constitutes compelling scientific proof?
Legumes are forbidden in my house, my son in law has an anaphylactic reaction to peanuts chick peas sesame and soy and beans in general. We all carry epi-pens and pray that we never have to use them. He prospers on a diet of steak and chops and some leafy greens etc. Both my daughter and my daughter in law suffer from pcos but low carb eating makes that far less problematic. It makes family meal times interesting since I cant eat potatoes and I dont eat wheat, or seeds in general.
Chacun a son gout.
It seems apt to spend a moment reflecting on the tragedy in Nice and sharing sympathise .
Oh!
How “tired” I get by those ‘defenders’ of the existing ‘order’ who with an evident contempt for us dissidents claim to know the truth. Not very much of a scientific attitude in my eyes.
Dear Goran,
You are right about the established order. I saw my lipidist and everything I said, he started “as I have taught my students for the last thirty years………….”
I suddenly had a road to Damascus moment and realised he was not part of the solution, but the problem. He then told he is giving up consulting, and we parted with mutual, hypocritical expressions of good luck for the future
Mr Chris, isn’t that the problem? People learn something and implement it for thirty years and then it’s just too difficult to admit that you might have been wrong all along. It’s the same in other fields, but medicine seems particularly bad. In 5,10 or 20 years a whole generation of dietitians will have to admit that the low-fat diet was a colossal, misguided failure. Today’s heretics will be tomorrow’s trailblazers.
I am now and then very thrilled by my, now five year old continuos, reading of THE CELL since most of the text to me consists of hard core natural science of a kind I am used to. In this book I get glimpses of how our metabolism fundamentally works. As I mentioned above I am though completely overwhelmed by the complexity of the intricate interactions on the molecular level between our 20 000 different proteins and were some of these innumerable interactions to my amazement are disclosed in the text.
What makes this book “scientific” in my eyes in contrast to most medical literature I have come across is the humble attitude the authors display by constantly admitting how utterly little we still know about these molecular interactions.
For instance, everything in our metabolism is governed by the proteins and how they are produced and destroyed in the cells. When a specific protein is produced this is mainly done by the transcription of a proper gene in our DNA in the nucleus coding for this protein. For this to happen an extraordinary complex internal signal system is at work inside the cell after receiving an external “input”.
I just now read in THE CELL that there are various small hydrophobic signal molecules that don’t need any receptor on the cell wall, in contrast to e.g. insulin, but can diffuse directly through the plasma membrane and bind to transcription regulators. Among this type of signal molecules are steroid hormones, thyroid hormones, retinoids and vitamin D.
Here I read the following humble statement.
“The receptors are all structurally related, being a part of the very large NUCLEAR RECEPTOR SUPERFAMILY. Many family members have been identified by DNA sequencing only, and their ligand is not yet known; they are therefore referred to as orphan nuclear receptors, and they make up a large fractions of the nuclear receptors encoded in the genomes of humans …….”
I guess that it is my reading of this kind of science that makes me almost allergic towards all proponents of dogmatic knowledge and especially when they appear with arrogance in the field of nutrition. To me it is only a humble undogmatic attitude on all levels that can bring new knowledge to science.
To resubmit:
http://archinte.jamanetwork.com/article.aspx?articleid=411678
” We interpret our findings as indicating that among healthy adults, siesta, possibly on account of stress-releasing consequences, may reduce coronary mortality. We were unable to undertake a similar analysis among women because there were only 6 deaths among working women.”
This at least fits in with something we really KNOW about heart attacks. Males have needed to evolve (as fighters and protectors) to react more strongly to stress. They pump out more ACTH (Adrenocorticotrophic Hormone) and hence more cortisol – the building block of steroids. This creates the risk of accelerated growth of atherosclerotic plaque. High cortisol levels can cause problems with clotting.
There is NO SHAME in the male reaction – but far from feeling macho about it men seem not to want to acknowledge its existence let alone talk about it.
Of course what we eat matters to our health but arguing about it seems only a diversion from the most important issues. First things first.
Which is age. Evolution has no use for those over 50 ish. Under 40 you can eat what you like as long as there is nutritional balance.
50, unless you are an agouti in which case you would be lucky to live past 20. Any solid theory of what causes heart disease needs to include, as Dr K did, variations in occurrence versus age and gender. But species has a much bigger effect than that. Cvd might be thought of as a disease of aging caused by the aging process itself.
What causes aging, why do men usually age faster than women, why do agoutis age more quickly than men? What causes some individuals to age even faster than others – disease, nutrition, poisons, socio-economic hardship, …?
The closing chapters of Nick Lanes ‘power sex suicide’ are about this. Here is one of the research papers he mentions
http://www.nature.com/ng/journal/v36/n11/full/ng1448.html
But why has that balance gone so badly wrong in children? A fat child was very rare fifty years ago and now one-third of eleven year olds enter upper school overweight or obese. A fat child is nearly always a fat, unhealthy adult. It’s very sad and costing the country a fortune.
Good afternoon, again
Here’s an article which seems to confirm my thoughts about inflammation caused by food.
http://www.australiannationalreview.com/world-renown-heart-surgeon-speaks-heart-disease/
Hooe you find it interesting.
Regards.
Jackie Kay
Sent from my iPad
>
Perhaps it might be useful to examine the role of high homocysteine levels as well. Apparently it can also increase the rate of CVD . Not many doctors here in the US test for this, maybe because there is no patented drug to magically lower homocysteine levels. I will find out in my August blood test if a B12/folate supplement is doing the trick for me. Thank you for your fascinating blog!
look into adding B6
what does b12 and b6 do for you.
re: …homocysteine … Not many doctors here in the US test for this, …
That’s true for a number of other important tests as well, such as:
☤ real thyroid tests (fT3, fT4, rT3, TA)
☤ Advanced lipoprotein panels (such as NMR)
☤ CAC or CCTA scans
☤ possibly key micronutrient titers (D3, Mg, ω3, ω6:3)
☤ failing to run the routine lipid panel fasting
plus having dangerously generous consensus limits for many markers that they do test, including HbA1c.
Part of why they don’t run these tests is insurance coverage, but in too many cases, it’s also due to the MD not knowing how to interpret them (mine admitted this), not knowing how to treat for them, or having some awareness that the treatments they often prescribe sometimes aggravate them.
I have been on a very simple potato diet for about a year. I have lost about a pound a month. I know it’s not a lot but it’s adding up. All I do is boil the potatoes and freeze them so they stay fresh for about a week. I fry the potatoes for lunch with two eggs instead of a meat sandwich. That is the extent of the diet.
You may like to have a look, another very interesting theory of myocardial infarction proposed by Dr. Berthold Kern (1911-1995) for the missing piece of the coronary obstruction theory, Dr. Kern, while performing autopsies in Germany detected that the findings of these autopsies didn’t support the coronary obstruction hypothesis. His therapy, now being used by over 5000 physicians in Germany, has reportedly remarkable success.
Steve, thanks for reminding me of those ideas. It has lead me to an interesting speculation.
How would you tie together the ideas of Dr Kern, the concepts Malcolm is explaining here and the observations of Subbotin ( and Henry Moon) plus the aging ideas of Nick Lane et al.?
Kern describes something like a necrotic catastrophe in his theory. Anaerobic stress, lactic acidosis leading to hypoxia driven cell death in heart muscle cells which are one of the cell types which have the highest metabolic demand matched very closely to their aerobic capacity.
Anything which interferes with the tension between these two leads to the ideas of Nick Lane who proposes a loss of cells through apoptosis driven by normal and inevitable free radical leakage and the constant need to get rid of cells with reduced performance as the cornerstone of the aging process. The result of this is ultimate loss of irreplaceable cells such as heart muscle, neuron, etc.
Subbotin (simplified) proposes hypoxia or glycoprotein induced thickening of the intima leading to reduced cross section. In turn this leads to increased stress on heart muscle probably in a vicious cycle and further apoptosis or hypoxia-necrosis. Its easy to completely block a narrowed artery, which leads to Malcolm, in a brief form which doesn’t do him justice – unstable plaque, a long history of damage and repair, and clots forming and breaking loose due to any one of a number of faulty repair or clot forming pathways. This all poses an elevated threat of hypoxia, cell death, necrosis etc.
Then there’s that interesting observation about heart muscle cells which become dormant?? Sounds a bit like senescence.
Its a big story and you’d need several large sheets of paper to jot down all the details.
Craig
Didn’t Dr. Kendrick remark at the beginning of the series about similarity of heart disease process and cancer? I cannot find it now.
Steve
Your tip to look at Dr. Kern has lead me to this paper:
Endogenous Digitalis-Like Factors: An Overview of the History (Buckalew, 2015)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394700
Yes, Kern, indeed.
It seems to me this question is still open here: why and how do myocardial infarctions occur in patients without significant obstruction of the coronary artery supplying the infracted tissue? In many cases the bloodclot / trombus is secondary: after the heart attack.
Kern had an answer to that question, and a drug. And apparently successfull treatments.
A summary: http://www.wrf.org/alternative-therapies/g-strophantin-heart-disease.php
Diana, atm I can’t remember. 18 major essays by Malcolm and the promise of more to come is a lot to assimilate. I think i jeed to sit down and read through them all yet again, and all the comments.
There are some similarities it seems but more harm in heart muscle cells committing apoptosis cleanly or suffering necrosis messily. Once they’re gone they are gone forever. Lots of ways that can happen accidentally – stress or disease, troubles with the plumbing etc, plus the genetic throw of the dice which leads to a preprogrammed base aging rate.
Primary heart cancer is extremely rare apparently. Metastases are more likely. Heart cells are maybe a bit like bird wing muscles? Ie super duper cells!
This, in part II. Only described as cancer-like.
“Infarction, in the case of myocardial infarction, does not mean death of the tissue. Instead, the heart muscle undergoes a complex transformation into a different cell type. One that needs far less oxygen to survive and one that cannot do the contracting thing. But it is not dead. Because dead cells become necrotic and necrotic cells disintegrate. After a heart attack do you see disintegrated areas of the heart? No, you most certainly do not. You see a form of scar tissue developing.”
Diana:
Click to access Ladich_etal_2006.pdf
15% of sudden cardiac death due to other cardiomyopathies ie non cvd. Necrosis is involved. It’s a bit academic if you’re that far gone!
Apotopsis is different to necrosis btw, probably undetectable in the short term except by chemical analysis. It is clean, programmed cell death where everything is dismantled into neat bits and pieces and recycled or disposed. It is by all accounts a normal part of the aging process in that it IS the aging process, goes on at a high rate all the time as normal cells turn over and when the tissues involved have a terminally differentiated cell type such as heart muscle cells, it results in a long term reduction in the tissue mass. eg also retinal cells, neurons.
Necrosis is a much messier process more like rotting, very unhealthy. Catastrophic. Obviously heart muscle cells are even more special than I was aware of and I’d like to know more, but still I wonder if anyone has actually counted the number of hm cells present, ‘before and after’ a major incident? If they are non functioning except as scaffolding, they might as well not be there except to plug the leaks.
Craig
an interesting paper, thanks!
Another depiction of necrotically damaged heart tissues after ischaemia and/or reperfusion. The language is a little dense for my level of understanding. I get the drift, just.
https://books.google.com.au/books?id=R3ShBQAAQBAJ&pg=PA58&lpg=PA58&dq=ischaemic+transformation+of+heart+muscle+cells&source=bl&ots=3jkWM-xPlQ&sig=4famoGGcfu-HgzyHe93lS84A82k&hl=en&sa=X&ved=0ahUKEwjI2vq73o7OAhXEnpQKHR2xDSQQ6AEILTAH#v=onepage&q=ischaemic%20transformation%20of%20heart%20muscle%20cells&f=false
supplementation with B vitamins (500 µg B12, 10 mg B6, 1000 µg folate) for 2 years lowered homocysteine levels http://www.medscape.com/viewarticle/759453_3
Pflugers Arch. 2016 Jul 14. [Epub ahead of print]
Hyperhomocysteinemia impairs regional blood flow: involvements of endothelial and neuronal nitric oxide.
Toda N1, Okamura T2.
Author information
Abstract
Increasing evidence support the idea that hyperhomocysteinemia (HHcy) is responsible for pathogenesis underlying cerebral, coronary, renal, and other vascular circulatory disorders and for hypertension. Impaired synthesis of nitric oxide (NO) in the endothelium or increased production of asymmetric dimethylarginine and activated oxygen species are involved in the impairment of vasodilator effects of NO. Impaired circulation in the brain derived from reduced synthesis and actions of NO would be an important triggering factor to dementia and Alzheimer’s disease. Reduced actions of NO and brain hypoperfusion trigger increased production of amyloid-β that inhibits endothelial function, thus establishing a vicious cycle for impairing brain circulation. HHcy is involved in the genesis of anginal attack and coronary myocardial infarction. HHcy is also involved in renal circulatory diseases. The homocysteine (Hcy)-induced circulatory failure is promoted by methionine and is prevented by increased folic acid and vitamin B6/B12. Eliminating poor life styles, such as smoking and being sedentary; keeping favorable dietary habits; and early treatment maintaining constitutive NOS functions healthy, reducing oxidative stresses would be beneficial in protecting HHcy-induced circulatory failures.
KEYWORDS:
Cerebral blood flow; Coronary blood flow; Hyperhomocysteinemia; Nitric oxide; Oxidative stress
PMID
I think most everybody following Dr. Kendrick is appreciating his deep exploration of the CVD enigma, enjoying the journey and looking forward to the conclusions. I know I am.
Personally, my interest is in learning better how to avoid the disease rather than gaining the depth of understanding sought by Dr. Kendrick who is also focused on treating those suffering from it.
Assuming the narrow goal of prevention rather than cure for the moment then the answers are clarifying rather rapidly, I think. There are several steps we can take that a) almost certainly do no harm and b) would seem to be protective of threats to the health and integrity of the endothelium.
At the risk of over-simplifying the issues, it would seem a good place to start is some level of reversion to the “natural world” of our species to which we are perfectly adapted. Dr. Kendrick has described a series of dietary, environmental and behavioral recommendations appearing to reduce the risk of CVD. Natural food, regular exposure to sunlight and clean air and adequate rest and recuperation for stress relief would appear to be a formula for CVD avoidance. All of these are characteristic of our ancestral history before the modern world intruded.
They also appear to be feasible and affordable, at least compared to engagement with the health care system for the treatment of the disease.
Am I missing something? Is this an over-simple view or insufficient?
Yes, the missing part concerns the dipping in and out of ketosis as our ancestors lived on the edge. The ability to derive our energy from stored fats allowed us to survive periods of ‘famine’ in between the ‘feasts’ – if we had not evolved this ability we could not have powered our large brains during the ‘famines’.
Much research demonstrates increased longevity when periods of starvation are common.
Or is ketosis the normal state? In Northern Europe, for example, the only year-round food supply, pre-agriculture, given harsh winters would have been fauna. Plant-based foods would have been highly seasonal. It is inconceivable that carbohydrates played much of a role in human nutrition.
This suggests that ketosis was usual albeit interrupted by bouts of glucose availability.
Not sure that starvation was so common. Man is the supreme predator and it is not clear that carnivores generally struggle to feed barring large changes in food supply, likely caused by climate change.
I think fasting (not really “starvation”, which is when you begin catabolizing your own tissue) has a large relevance. While there was meat at times, at times there was not. You just fasted through those times. Not also that while fasting, you’re in ketosis.
I do think ketosis was much more prevalent, although it depends on where you lived. If you had access to year-round tubers and fruit, you might not be in ketosis that often. I think for anyone away from the equator, those people were in ketosis more often.
Personally, I’ve lately been trying a ketogenic diet and like it. I do rotate out of it at times, though, to simulate the “feast” times. I also perform intermittent fasting, and again I rotate this — sometimes fasting days at a time, sometimes only one or two meals, sometimes eating 3+ meals in a day. Sometimes eating every day for a while. I do try to keep wheat and sugar intake low, but even those I allow myself sometimes. Good pizza is a downfall of mine, although now it’s more of an occasional treat than a trigger.
Longevity seems to be related to a more equal distribution of wealth. Even on a local basis sees some 3-4 years difference from poorer parts to more affluent areas. A study by a retired Scots Public Health chief suggested that lower opportunites to be a volunteer compared to Liverpool ( I think) explained in part the higher motality rate. ( can’t find the ref at the moment). The point is that ‘cultural’ factors play a part. I think this the major reason for the French figures – they are not equal throughout France. Its all about well being this is a good read http://www.local.gov.uk/c/document_library/get_file?uuid=bf034d2e-7d61-4fac-b37e-f39dc3e2f1f2
The other biggy is of course age. Whilst paleo people were living in their 70s if they got past 15, I think evolution has no real place for the over 50’s we are not talking social roles just physical constraints.
Oh and of course the roll of the dice.
Maybe it’s been posted here before, but it
bears repeating:
Dr. Joseph Kraft being interviewed by
Ivor Cummins. Dr. Kraft performed tens of
thousands of insulin assays and autopsies
and found a 1:1 relation between
diabetes/metabolic syndrome/ insulin resistance
and heart disease.
It’s pretty convincing to me.
Ivor also discusses the mechanism of heart
disease, its causes and possible avoidance
here:
bill,
Agree, Dr. Kraft has a lot of interesting clinical experience to me as well.
What surprises me that he stay away from the “carb issue”.
And or course we have also the prize lecture of the equally experienced diabetes researcher Professor Robert Unger who turns many things upside down relating to insulin resistance and blood sugar regulation. He interestingly also stay away from the obvious nutritional part of this subject and I just wonder why.
Ivor Cummings lectures are excellent. Such a good speaker, from his perspective as a problem solving engineer, he transfers it to medical matters so well. These celts are clever.
Concerning insulin resistance… better to have your gut flora in mind and feed it right.
“The Role of Gut Microbiota on Insulin Resistance” (Caricilli, 2013)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705322/
This may be of interest.
http://www.bbc.co.uk/news/uk-england-leicestershire-36847743
Great apes being investigated for CHD when in captivity that they don’t experience in the wild. In the article it is stated that the great apes problem cannot be associated to diet as their diet is the same as in the wild whilst reiterating the dietary link in homo sapiens and thus there appears to be a paradox. To me this is illogical as we are not too distant from our primate cousins and if there is no dietary connection for them then why should it be considered in h. sapiens? One thing that the great apes do have is a stressful environment, no matter how careful or caring the zoo is they are not in their natural habitat, their circadian rhythm must be disturbed as the UK has a wide range of daylight/darkness patterns; sunlight is reduced due to climate as well and ape physiology must be adapted to their natural environment, even if they are bred here, they cannot have evolved to be fully adapted to temperate climes; hence there will be some epigenetic influences on their development including disease processes.
In my mind the focus of this study is wrong, rather than trying to consolidate the apparent paradox between the development of CHD in great apes and humans they should forget all current theories and start afresh:
i) there’s a group of animals that are closely related to human beings that has developed CHD, how and why.?
ii) see if those same mechanisms apply to human beings
iii) develop a new pathophysiology of CHD in humans based on this animal model.
I hope this makes sense and is not too garbled.
John Collis: Thanks for this. Very good points you make. Dr. Kendrick has said something to the affect that psychosocial stress is a big culprit in the development of CHD. This would fit the bill here, as well. Epigenetic modification of gene expression may be one of those hidden factors, too.
re: …the great apes problem cannot be associated to diet as their diet is the same as in the wild…
Actually the article says “…experts do not believe the disease in great apes is linked to poor diet and lifestyle.” and repeats the “do not believe” later. That’s a wise hedging, but may bias any investigation away from discovering potential diet effects. I can think of some candidates that need to be ruled out:
◊ Are the diet solid foods really identical to wild? Are they importing wild (organic, non-GMO) produce from the native region? If so, that would tend to rule out pesticides, preservatives and genetic issues.
◊ What are they doing to compensate for no access to native soil-based micro-organisms, and any consequent effect on gut microbiome?
◊ Presumably water is provided. What’s in it? Some non-native halogens like chloramine, perchance? What’s not in it (perhaps some key trace nutrients, and important native microbes)?
◊ I’d like to think that the paddocks include some of the native plants with which these primates often have oral contact. No guesses there.
Then beyond diet:
◊ What’s done to mimic the natural circadian environment, which includes things like solar-matched truly dark night time, solar intensity and SPD-matched daytime light, sound control, etc.
I can agree that there’s very likely something to be learned here for the hairless apes. I won’t rule out stress.
Vitamin c levels? Re Pauling.
I am wondering what the “healthy” diet is for these great apes.
I remember reports from the US about great apes having CVD. Once the zoo’s switched to a diet really comparable with a diet in the wild, the CVD problem was solved.
One of the items in the original “healthy” diet was a daily whole grain biscuit.
Well, that can’t be unhealthy, can it? 😀 It was no part of the intervention diet of course.
Sorry, Í dont have links.
Yes, stress can make you ill.
One reason that conventional medicine is so sure that cholesterol causes plaques is that back in the 1970s they managed to induce and regress plaques in monkeys by controlling their diets:
“Atherosclerosis induced by the use of diets rich in saturated fat and cholesterol regressed upon cessation of these diets (references in Table 1), even after prolonged induction periods when coronary lesions had encroached up to 65% upon the lumen (Armstrong et al., 1970).” — http://circres.ahajournals.org/content/46/3/311.long
Which begs a couple of questions:
A) Do humans react in the same ways as macaque monkeys to diet? (Maybe they should give the monkeys a human fecal transplant first.)
B) Do arterial plaques cause CHD? (I’m starting to have my doubts.)
I noticed some people mentioning the Hall paper/study funded by NuSi. Like many scientists, and as is so common nowadays, I noticed the discussion section of the paper was discordant with the data presented. I think Dr. Fung does a good job addressing two of the most fallacious conclusions from the paper here: https://intensivedietarymanagement.com/heres-5-kevin-hall-go-buy-clue/
Dr. Eades addresses concerns over cognitive dissonance here: https://proteinpower.com/drmike/2016/05/06/contradictions-and-cognitive-dissonance-the-kevin-hall-effect/
And Dr. Lagakos addresses other shortcomings here: http://caloriesproper.com/the-insulin-obesity-hypothesis-is-under-attack/
stipetic,
Thank you for the link to Dr. Eades. where Halls smug performance at his poster on the conference is is brilliantly scrutinised and revealing Hall’s fundamental misinterpretation (ignorance?) of the data from his own study.
To me there seems to be a standard pattern today that when someone, as here on Malcolm’s blog is attacking LCHF as a means of our possibility to restore health, by pointing to some “debunking” study and to do this with a “besserwisser” arrogance then an alarm bell is sounding in my ears that there is something hidden and now this is so elegantly revealed by Dr. Eades.
(I guess that Dr. Fung does the same thing although I couldn’t open the link.)
It is the same unscientific, self confident arrogance that made it so hard for me to get through the book, “The Low Carb Myth”, by Whitten and Smith a while ago. Any interesting ideas and facts that could support the medical establishment resistance against LCHF and the insulin hypothesis behind our obesity epidemic got blurred by the attitude. Why do they take that stand? The aggressive smile on Ari Whitten’s face when showing he is showing his muscular torso in the author presentation is to me symptomatic for people who rather like to be in the lime light than to supporting real science.
I read the same with Dr. Guyinet.
I guess it is the actual attitude which is so revolting to me and especially when it appears together with ignorance and abuse of fundamental thermodynamics which is involved in the calorie counting, official dogma intended to “explain” obesity. In my eyes arrogance can not cover up for the actual ignorance or rather stupidity hidden in this tautological explanation.
“LDL is pro-coagulant and – at very high levels e.g. in FH – increases the risk of CVD [though it is difficult to disentangle this from intertwined genetic pro-coagulant factors]”. What are very high levels of LDL (which range of values are they in)?
At least 2 standard deviations above the norm.
Dr. Kendrick:
So…above 6.0 mmol/L?
The more I read, the worse it seems. If the converter I used was correct, I am around 12 mmol/L. Despite normal triglycerides, no blood sugar issues, being thin, and eating no processed foods, grains or sweeteners.
Can anyone else with familial hypercholesterolemia share what approach you use?
Dee,
Have you looked into this rare condition?
JD – Yes I’ve read about it before. It’s interesting. But doesn’t help me figure out my situation. 🙂
Why folic is bad and folate is good – Stephanie Seneff – start at 27 minutes https://www.youtube.com/watch?v=kj-hOG1zq_E
Thank you for sharing this. So interesting, and so very complicated. I wish what is really happening could be pinned down. Probably next to impossible right now, as so many different factors come into play.
Familial hypercholesterolemia, CVD, and even sudden death are everywhere in my family. I’m having a terrible time trying to figure out how to treat it with only diet and natural methods. The “alternative” recommendations all contradict each other, and I’m already eating a very specific diet due to kidney stones and autoimmune conditions.
Hello Dee
Family hypercholesterol.
My father did both wars, was gassed in the first, my mother died when she was 50, and my father was brought up in the not good part of Glasgow. My ex lipids man, says I am at risk genetically, in spite of all the above.
Doctors, aren’tcha sick of them!
Hi Mr. Chris,
A little bit. 🙂 I’ve been sick a lot the last couple of years. Sometimes I kind of forget about the cholesterol issue, ’cause it’s not currently bothering me as much as everything else!
Interesting to hear from someone with a Scots background. I have a little in my family, and cherish a hope to visit someday.
Sorry to hear about your parents. Can’t imagine what those who were gassed went through. The first war especially was just so sad.
It’s hot here. 97 degrees F yesterday.
Ice cream!
I’m struggling to keep away from pre-diabetic status. So, naturally, I searched for low or no sugar chocolate ice cream. Yes, chocolate of course. I found three. But they were loaded with artificial sweeteners! Tried them anyway. Fell asleep for an hour or so about an hour and a half after having a dish. Happened with each on separate days. Crash. This cannot be good. I’ve read that the artificials can boost insulin output just as much as the real thing.
Does anyone know of a decently healthful ice cream product? Ice cream is generally far to sweet for a good flavor experience anyway.
And, think of the healthful fats we could be enjoying.
I don’t think you can make ice cream without sugar (other than making ersatz ice cream with various chemicals). The sugar stops it freezing into a solid block.
David,
Thanks, but. Years ago, when the kids were still here, we made a very nice peach ice cream using an old-fashioned dasher. No sugar – other than what the peaches brought with them. No peculiar ingredients.
What I’m after is a no-sweat (Dashing is HARD work!), no/low sugar chocolate cold confection.
I’m wondering if honey would work. We’ve gotten indications that honey might be OK for diabetic tendencies.
That makes me wonder about other naturals such as maple syrup. A nice maple walnut ice cream would be my second choice.
JDPatten
Unfortunately ice cream can’t be made without some sugar and freezing dulls the sweetness so that it tends to be sweeter than we believe it to be. But this is a delicious and easy compromise – healthier than shop versions anyway:
1 405g tin condensed milk
900 ml double cream
a drop or two of vanilla essence
Whip up together until thick and put into a freezer for a few hours. That’s it!
Very traditional taste. You can eat a bit of good dark chocolate with it.
(I always have some in our freezer.)
P.S. Whilst on the subject of simple recipes which never fail to impress:
Smoked mackerel pate:
Packet of the best smoked mackerel you can buy (not peppered. I use ‘Sainsbury’s British Smoked Mackerel, Boneless, Taste the Difference’ (approx. 130g))
Equal quantity of the best full fat cream cheese you can buy (I use half a tub of Sainsbury’s Soft Cheese, SO Organic 250g)
Wash your hands well. Mix the two ingredients together using a hand!
Mmmm. Mackerel Ripple ice cream!
(Kidding)
Thanks. Both recipes seem simple and good.
Here is a totally healthy recipe taken from Nourishing Traditions by Sally Fallon.
Ingredients:
3 egg yolks, preferably organic and local from pastured hens
1/2 cup maple syrup
1 tablespoon vanilla extract
1 tablespoon arrowroot powder
3 cups heavy cream, preferably raw, not ultrapasteurized
1/2 cup walnuts, finely chopped (optional)
Beat egg yolks and blend in remaining ingredients. Pour into an ice cream maker and process according to ice cream maker instructions. For ease of serving, transfer into shallow glass container, cover and store in the freezer.
re. mackerel pate:
Forgot to say peel away skin from the mackerel – comes off easily.
Love simple recipes, don’t wish to spend hours stuffing things. The mackerel dish sound lovely, healthy and tasty, not expensive. Thank you.That condensed milk recipe is making me drool.
Yes, the sugar prevents the ice cream from becoming an ice cube in the freezer. A low carb alternative is to substitute 1/2 cup polydextrose and 10 packets (8 tsp) of Truvia for the sugar in a basic 1 quart (US) recipe. I like to start with a custard of egg yolks and heavy whipping cream (36% milk fat) and “freeze” with an electric ice cream maker. I do add one tablespoon of real sugar.
Phil
What a weird medical world we are living in!
Approaching this world from the outside and trying to understand for some years now it was so strikingly evident already at the start for me that cholesterol is one of the most valuable molecules for building our cells and employed during the course of the many millions of years of evolution. How the h..l was it possible for the medical community to demonise this substance if this community was not totally corrupt already 50 years ago? I don’t believe in any ignorance on the part of Big Pharma.
But as long as people in general still has confidence in the health care system this complete madness of fighting “high cholesterol” will continue. The elephant in the room is today so big that it is almost impossible to be considered as “real” and if it will fall some day there is a risk that the medical community will lose most of it’s credibility.
And the nutritional part of medicine is so out of touch with our reality I just want to cry. And I firmly believe that LCHF constitute a fundamental threat to all insulin producers and perhaps this goes without saying – 500 million diabetics in the world is a “crazy” reality today!.
Well put and I agree.
Goran, one surgery in England saves £43,000 a year on its insulin bill by treating type 2 diabetics with a low carbohydrate diet. It’s Doctor Unwin in Southport. If this was done nationally, the NHS would save over £400 million. That’s just on one drug. We’d probably save a lot more by not having to carry out 130 diabetes related amputations a week. No wonder the drug industry is such a strong supporter of the current disastrous position.
Whenever I hear that the NHS is short of money I can’t help thinking about how much is wasted on making people ill.
Stephen,
How very encouraging to hear!
Is there a danger that a GP can loose his licence by advocating a low carb life style instead of medication.
Our famous Swedish LCHF-pioneer Dr. Annika Dahlqvist almost lost her licence when accused of misconduct relating to her diabetic patients on this basis. After three years of “thorough investigation” she was finally cleared since the LCHF diet was judged as “in agreement with science and with well known clinical practice” and thus approved by the Swedish authorities.
What about UK? Is low carb approved as a treatment of diabetics?
Absolutely not. However, you will not lose your license to practice. Sweden is about a decade ahead of the UK.
Goran, I think Dr Unwin’s success and the scientific support protects him. Dr Dahlqvist, who is a heroine, was a few years ago, so perhaps there’s been some progress. I think a NHS dietitian advocating a low carb diet to a patient who isn’t a diabetic would still face trouble. The sane dietitians seem to have to practice privately.
I saw a picture on Caryn Zinn’s Facebook page of a breakfast given by a diabetic patient. It was a dietitian approved meal for a diabetic and contained Weetabix, toast, some fruit, fruit juice and jam. Perhaps they bring the insulin as well. Mad!
The environment is changing, in popular press: Tour de France winner, Chris Froome is said to have achieved his phenomenal successes on Low Carb (Non Calorie Counting) http://www.businessinsider.com/chris-froome-weight-loss-tour-de-france-2016-7?r=US&IR=T&IR=T
The Science too is building up: The positive effects of exercise on the brain is via Ketone Body Beta-hydroxybutyrate https://elifesciences.org/content/5/e15092
The rug is being pulled from under the Carbo Pillars, gradually.
http://www.dailymail.co.uk/news/article-3706171/I-stopped-taking-statins-avoid-debilitating-effects-says-former-NHS-boss-Sir-David-Nicholson.html?login#readerCommentsCommand-message-field
Around 7million Britons take the drugs that save 7,000 lives a year – This equates to 1 in 1000; even worse than Collins’ 1 in 300 Unfortunately no reference.
Thank you, Mike. I’ve forwarded the article to a few interested people.
Further to your description of the diabetic breakfast: I have a friend (a consultant physician herself) who has a rare disease and a complication in her condition required her to have a high protein diet while in hospital. She was given great heaps of white rice and a wafer thin slice of processed turkey. When she complained to the NHS hospital dietician, in my friend’s words: “She came out with some rubbish about the body needing enough carbohydrates for energy, which would allow me to fully “utilise” the protein. Even the word “utilise” was a warning signal.Since I already had a high carbohydrate intake, her advice was a load of baloney.”
I hope you added a comment – I found this a while back, and added a comment, but now it is closed for comments.
I try to add a comment – describing my experience – every time I see an article for or against statins. I dread to think of the damage these drugs must have done – particularly when the problems start after a few years (as in my case) – there must be people who are just sliding into serious disablement just to make a profit for big pharma!
Is there a glitch here as unable to reply to a comment
Could Turmeric be the key to lowering Fibrigonen. One way that I use to get a constant input of this spice is to put about a third of a T spoon in my daily morning porridge. Yes it turns a bit yellow but does not impair the taste. Link here to Fibrinogen and Turmeric
Maybe it got something to do with salt intake:
http://www.medscape.com/viewarticle/830444
Not only have I seen warnings that too low sodium is a risk, I have always understood that the ratio of potassium to sodium is the critical factor.
So, if a person has high TC levels (325), high calculated LDL levels (233) & has been diagnosed with FH, but also has higher than average HDL levels (78) and low Triglyeride levels (69), wouldn’t aspirin do as an anticoagluant, with just the dosage in question?
Is the LDL or TC number the confirmation of heterozygotic or homozygotic FH or is there a genetic test done?