Inflammation – or not
Over the last few years there has been a significant shift, from many researchers, towards the idea that atherosclerosis is an inflammatory process, to a greater or lesser extent. Below is a quote from a cardiac surgeon. A man who admits he was wrong about cholesterol being the main underlying cause CVD, so I can applaud him for that. He goes on to say:
‘Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped.
Inflammation is not complicated — it is quite simply your body’s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process, a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial.’1
And so on and so forth. More recently, a friend and fellow cholesterol sceptic, Aseem Malhotra, was lead author on an article in the British Journal of Sports Medicine entitled: ‘Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions.’
A major statin study called JUPITER, was designed to look at lowering C-reactive protein with rosuvastatin, to see if this would lower the risk of CVD – in those with low or normal cholesterol levels. C-reactive protein (CRP) is a non-specific marker of inflammation. To quote the lead investigator:
‘The recent JUPITER trial demonstrated that potent statin therapy reduces by 50 % the risk of heart attack and stroke among men and women with low levels of low-density lipoprotein (LDL)-cholesterol who are at increased vascular risk due to elevated levels of C-reactive protein (CRP), a biomarker of low-grade systemic inflammation. In JUPITER, both absolute risk and the absolute risk reduction with statin therapy were related to the level of CRP, whereas no such relationship was observed for LDL-C.’2
I could find another ten thousand papers all stating that CVD is caused by inflammation. Case proven? Well, the case is certainly proven, beyond doubt, that atherosclerosis is strongly associated with inflammation in the arterial wall. To which my response would be… and so what exactly?
If you twist your ankle, and tear ligaments, you will also find a great deal of inflammation in the surrounding area. You would, however, be stretching reality to suggest inflammation is the underlying cause of ankle ligament damage. I suppose you could try.
In my simple little world, inflammation is a result of underlying damage. It is not, and cannot be the underlying cause. Inflammation is a manifestation of the body attempting to heal itself. In fact, whenever I see the word inflammation, I mentally replace it with the word ‘healing.’ For many years I have smiled enigmatically at the widely accepted advice following a badly sprained ankle. RICE (Rest, Ice, Compression, Elevation). These are all ways of reducing inflammation, sorry, healing.
Just looking at the ‘I’ in RICE. Ice:
‘Ice works by decreasing the blood flow to an area, thus temporarily diminishing the swelling and inflammation that accompanies most injuries —- (when the tissue re-warms … the inflammatory process resumes). But in the 1970s we knew very little about the healing process. We did not understand that inflammation is actually a very important initiating event of the overall healing process.
When you are injured, the blood vessels to the area dilate. That causes the swelling and warmth you notice. The increase in blood flow brings with it very potent chemicals, proteins and cells. Those chemicals and cells set off a cascade of reactions that we refer to as inflammation. More importantly, this is also what initiates the HEALING process. Yes, inflammation is a necessary part of the healing process. The inflammation chemicals send a message to other cells to come to the injured area… they also wake up sleeping or dormant cells already residing in the area of the injury. Those cells in turn start to repair the ligament, muscle or skin at the site of injury.’3
‘Finally, conventional sports medicine catches up with Chinese traumatology. In Chinese medicine, we NEVER recommend ice for injuries. Simple physics will tell you that ice applications will constrict blood vessels which will reduce blood flow to the injury, meaning less waste products removed and less nutrition delivered therefore slower healing.’4
I say, reduce inflammation at your peril. You may reduce the swelling, and some of the bruising, and things will certainly look less ‘damaged’. But, again, so what. Two billion years of evolution have created some pretty effective healing processes, which we also call inflammation. Interfere with inflammation, and the results are predictable.
The most powerful anti-inflammatory agents known to man are corticosteroids, so called as they are all synthesized around the base compound, cortisol (a corticosteroid). Medically they are used in a number of auto-immune/inflammatory conditions, ranging from rheumatoid arthritis, ulcerative colitis, eczema, lupus, transplant organ rejection and suchlike [Asthma is a bit different].
In these conditions, there is a rationale for reducing inflammation. Here, we have the body ‘seeing’ various proteins as alien, and attacking them, through an ‘auto-immune’ response. Yes, there is inflammation. However, this is not the body trying to repair itself. This is the immune system causing damage, by attacking the body itself, with resulting inflammation. In short, do not confuse inflammation with inflammation.
However, if inflammation were the underlying cause of CVD, then corticosteroids should reduce the risk of CVD, as they are the most potent anti-inflammatories known to man. But they very much do not. A paper was published recently, called ‘Can machine-learning improve cardiovascular risk prediction using routine clinical data?’ A fascinating paper indeed. The purpose was, as follows:
‘Current approaches to predict cardiovascular risk fail to identify many people who would benefit from preventive treatment, while others receive unnecessary intervention. Machine-learning offers opportunity to improve accuracy by exploiting complex interactions between risk factors. We assessed whether machine-learning can improve cardiovascular risk prediction.’
I have not written about this paper before, although it identified LDL as completely irrelevant in predicting CVD risk, and the risks it did identify were almost completely different from those in the current risk calculators. In fact, the number one risk factor of cardiovascular risk was Chronic Obstructive Pulmonary Disease (COPD). I have never seen this on any risk calculator before, and I am trying to digest the implications.
However, getting back on track, the main point of interest here is looking at number three on the list of factors that can increase CVD risk:
Oral corticosteroid prescribed
At number eight:
Immunosuppressant prescribed
Immunosuppressants are also designed, effectively, to impair the inflammatory response. They are used in much the same sort of conditions as steroids. In fact, corticosteroids could also be termed immunosuppressants.
The highly damaging effect of corticosteroids, or other drugs designed to suppress the immune response, should not really come as any surprise. There is a medical condition called Cushing’s disease, in which too much cortisol is produced by the adrenal glands. The impact of Cushing’s disease on CVD is to increase the risk by, at least, 500%. 5
Other anti-inflammatory drugs have similar, if less spectacular effects, on CVD risk. The FDA recently increased the warning level on non-steroidal anti-inflammatory drugs (NSAIDs). Drugs such as ibuprofen, naproxen, diclofenac.
‘The FDA is strengthening an earlier warning about the cardiovascular safety of non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs), both prescription and non-prescription, the agency said Thursday. After a comprehensive review of new safety information, the FDA is requiring updates to the labels of all prescription NSAIDs to reflect recent information on risk of heart attack and stroke. Over-the-counter non-aspirin NSAIDs already contain some safety information, but the labels on these drugs will also require an update, said the FDA in its announcement posted online.
The new labels for prescription NSAIDs should contain the following information, according to the FDA:
- The risk of heart attack can occur within weeks of starting an NSAID, and that risk may increase with longer use.
- The risk seems to be higher at higher doses.
- It’s not clear if the risk of heart attack and stroke is the same for all NSAIDs.
- The drugs can raise the risk of heart attack or stroke in both patients with a risk of heart disease and patients without.
- Patients with heart disease or risk factors for it are at a greater risk of heart attack or stroke following the use of NSAIDs, because they have a higher risk at baseline.
- There is also an increased risk of heart failure for patients using NSAIDs.6
Of course, it can be argued, and it has, that steroids and non-steroidal anti-inflammatory agents have other potentially damaging effects on the CVD. Whilst this is undoubtedly true (to an extent), you would still not expect agents that are, primarily, anti-inflammatory, to vastly increase the risk of CVD. If CVD is an inflammatory disease.
Personally, think that the science here has been done. Agents designed to reduced inflammation all greatly increase the risk of CVD – from moderately to spectacularly*. Thus, whilst it is true that you can find inflammation within arteries where atherosclerosis is developing, this DOES NOT mean that the inflammation is causing the problem.
What you are seeing is the body trying to heal damage, and then getting cause and effect twisted through one hundred and eighty degrees. ‘That’s looks abnormal, let’s get rid of it’. A pretty good summary of a great deal of medical research over the last few hundred years, I suppose.
1: https://www.sott.net/article/242516-Heart-surgeon-speaks-out-on-what-really-causes-heart-disease
2: https://www.ncbi.nlm.nih.gov/pubmed/23225175
3: http://www.howardluksmd.com/orthopedic-social-media/ice-ice/
4: http://www.drmirkin.com/fitness/why-ice-delays-recovery.html
5: https://www.ncbi.nlm.nih.gov/pubmed/8187313
6: https://www.medpagetoday.com/publichealthpolicy/fdageneral/52530
*aspirin is the exception. However, aspirin has strong anti-coagulant effects. It stops platelets sticking together. In this way, the anti-coagulant effects of aspirin, outweigh the damaging anti-inflammatory effect.
Dr. Malcolm Kendrick 
As a retired primary care physician and follower of your work for years I couldn’t agree more. While not subscribing to the received ‘wisdom’ concerning the etiology of CVD (for a very long time) the ‘inflammation’ theory has never made sense to me for the very reasons you so clearly enumerate. Thank you for the courageous work you do and for sharing it via this blog. Always enjoy reading it.
This is a terrific article. It’s the kind of thing I’ve been waiting to learn for some time now. Thank you so much, Dr. Kendrick, for providing clear-cut information.
Very interesting, taking the average of regression, Random Forest, Gradient Boosting and NN’s rankings for individual features we get the following rankings of significance (note some are negative like women, no pun intended). LDL trails well behind HDL, Trig’s and HbA1c. Seems to me that if your Total cholesterol is considered high but your HDL is high, Trigs low and HbA1c low then although not guaranteed bullet proof you should not be in Statins (not that Statins do anything for HDL)
Age*
Ethnicitya: South Asian
Female*
SESb: 2nd Townsend quintile
Smoking*
Ethnicitya: Black/Afro-Caribbean
SESb: 3rd Townsend quintile
SESb: 4th Townsend quintile
HDL cholesterol*
Oral corticosteroid prescribed
HbA1c missing
Total cholesterol*
COPD
Systolic blood pressure*
Ethnicitya: Other/Mixed
SESb: 5th Townsend quintile (most deprived)
Atrial fibrillation
Triglycerides
Family history of CHD < 60 years
SESb: Unknown
HbA1c
AST/ALT ratio missing
Ethnicitya: Chinese/East Asian
BMI missing
Ethnicitya: Unknown
Serum creatinine
Immunosuppressant prescribed
gamma GT
Diabetes
Chronic kidney disease
BMI
Anti-psychotic drug prescribed
Severe mental illness
Rheumatoid arthritis
Blood pressure treatment*
Hypertension
LDL cholesterol
gamma GT missing
CRP
AST/ALT ratio
Serum creatinine missing
FEV1 missing
Serum fibrinogen
CRP missing
FEV1
Serum fibrinogen missing
LDL cholesterol missing
Triglycerides missing
regarding the “ice”. why do sportsmen , rugby players in particular, have ice baths?
To reduce inflammation. Hint… its a waste of time.
Or you could take a joint.
https://www.sciencedaily.com/releases/2017/06/170606090806.htm
I wondered if this subject might be mentioned. I’m not sure it’s as harmless as a waste of time. Although coverage of rugby injuries concentrates on concussion there seems to be a very real and growing problem with soft tissue injuries.
Professionalism is often blamed – bigger, fitter players, with more to play for – but perhaps the cause is treating inflammation? The players are now available all week to see the club’s medics and there is more pressure to get them back on the field. However, some injuries seem to be an almost permanent fixture, never really healing.
I suspect you may be right. The focus appears to be on reducing inflammation at all costs a.k.a. reducing healing at all costs. Humans hate seeing ‘abnormal’ things, and try to cover up/suppress at much as possible.
Dr K,
Regarding your previous post, isn’t it possible that people experienced more statin side effects in the non-blind portion because it followed the blind one, and therefore they were on the statins for a longer time?
It’s not only about inflammation. Per Wim Hof, the Iceman:
Don’t know about the science, but a cold shower in the morning makes me feel great indeed 🙂 .
There are also increases in both heat shock proteins and cold shock proteins from cold exposure.
I guess then, the ICE approach is the religeous response, supported by the analgesic effect, though not necessarily useful. With the same going for paracetamol etc. Though what about headaches?
So no wonder people can have heart attacks when under great stress – when cortisol is elevated. Who woulda thunk it?!?
Just wondering about long term steroid therapy. Perhaps the most common ones prescribed as steroid inhalers for asthma. Is there any evidence you know of that these can raise CHD risk?
They do not, but oral steroids do. I assume the absorbed dose of inhaled steroids is sufficiently small.
Thank you Dr Kendrick. Very, very interesting.
Admirably succinct, clear, and humourous, as usual. Trying to persuade those treating such things as a twisted ankle not to use ice will, however, be almost as difficult as trying to persuade them that salt is not the cause of hypertension, fat is not the cause of diabetes, and cholesterol is not the cause of CVD. We can keep plugging away, and in 30 years’ time, our grandchildren will wonder at our ignorance, and what took us so long to arrive at the truth…
Excellent points . . . Is the 30 years an estimate on how long entrenched leaders will move over/ retire/suffer untimely demise? I never see them experiencing a damascene enlightenment.
Sorry, *humorous*. !
Oh please! MEAT is the cause of diabetes, everyone knows that! The proof is that we were vegan for millennia, right up until a few decades ago. Oh wait . . .
. . . the scary thing is that in the ongoing war between science and dogma, dogma seems to be winning. 😦
The religion is more important to them than inconvenient science. They take a moral position and try to make everything else fit.
I agree with you Gay, but after a lifetime of putting ice packs on twisted joints and nasty bruises, etc, it will take a lot of persuading to stop me. After all, it takes away the immediate pain, doesn’t it?
I have always been skeptical of the advice to ice injuries, and generally do not do it as it is counterintuitive. The thought of putting ice on an injury just seems creepy and mean. Likewise, when I have a fever, I always take a hot bath.
Anna – in total agreement. Ice hurts, warmth soothes.
How does one differentiate between healing inflammation and autoimmune inflammation? …And then address the autoimmune process? Clearly not with the long-time standby NSAID.
Turmeric and its isolate curcumin are touted as useful in “normalizing” the inflammatory response. Hogwash??
The immune response is always ‘normal’. The triggers for the immune response, in auto-immune diseases, are the abnormal thing. You need to convince the body to stop attacking itself – or other proteins that do not pose any threat.
In short… hogwash.
I guess that’s the big question – how to go about the “convincing”.
Is heart disease definitely never an auto-immune condition, then?
So the mode for natural anti-inflammatories, curcumin etc, is just that, mode?
Can auto immunity be a cause of damage to the artery wall, then?
Now… there is a simple question. I do not think I can answer it with any degree of confidence.
Regarding curcumin, I think we have to distinguish between not seeing inflammation itself as a cause, and a substance with wide healing properties such as curcumin, which will heal up some of the causes of the inflammation, and thereby reduce inflammation. Not artificially like ibuprofen, for example.
For years I took a NSAID (Arthrexin/indomethacin 25 mg) to manage my ankylosing sponylitis. The sponydylitis had pretty much burned itself out, but the Arthrexin helped restless sleep and the odd case of sciatica. Then it went off the market. I tried Diclofenac briefly, but now take a 1/4 tsp of turmeric nightly instead. Subjectively, I estimate it is equivalent to about 15 mg of indomethacin.
…spondylitis, dammit. NSAIDs clearly affect one’s ability to spell ;o)
Martin, have you heard of the Low or No Starch Facebook page re AS. The postings and comments are quite informative.
how do you take the tumeric
Put some on your porridge, it may turn it yellow but does not impair the taste once you have your berris or kiwi fruit on it
If you need NSAIDs a better alternative with better side effects profile for pain, inflammation and CVD is boswellia serrata.
http://www.sciencedirect.com/science/article/pii/S2225411016301961
Frankincense (乳香 Rǔ Xiāng; Boswellia Species), the resinous extract from the trees of the genus Boswellia, has been used for centuries in cultural ceremonies, as a cosmetic agent, and as a traditional medicine to treat a variety of ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer, and some other illnesses. Boswellic acids are the active compounds of frankincense and AKBA (3-O-acetyl-11-keto-β-boswellic acid) is the most important and effective acid among them. Some studies have shown that the use of frankincense can also improve the learning and enhance the memory in animals and human beings. It seems that frankincense might have a potential ability to be used as an alternative natural medicine not only for chronic and inflammatory diseases but also for brain and memory disorders.
Hi Martin, curcumin is poorly absorbed by the body if you take just turmeric on its own. Try this for the best results: 9 parts turmeric + 1/4 part black pepper + 1/4 part ginger. The piperine in the black pepper is the key catalyst and the ginger assists and the bioavailability is boosted some 10000%. This has been known for centuries in India where they practice Ayurvedic medicine as well as allopathic medicine.
I have psoriatic arthritis and since using this ratio my symptoms have abated.
This is good advice, some data on increased uptake of Turmeric through black pepper was highlighted in a Nutritionfacts.org video presentation
Frances,
I know about the no-starch London Diet. Unfortunately, I was diagnosed in 1975, before the diet was invented and there was the internet to find out about it. My spine is totally fused, so there’s not much more the AS can do. I eat a low-ish carb diet, but make no effort to bring carbs to zero.
biddy,
Piperade and fat help the body absorb curcumin. Turmeric is slow to dissolve. So after supper I put a 1/4 teaspoon of turmeric with a grind of black pepper (for piperade) in a mug, add boiling water, and leave it for an hour or two to dissolve. When it is still warm I stir it up and drink it, leaving the dregs, while scooping coconut oil from the tub and eating the oil (which is solid at the moment) between mouthfuls. It’s not delicious, but if I don’t take the turmeric I feel the effects.
On the topic of turmeric . .
Inflammation in some of the joints of the left hand makes playing the guitar a bit of a pain (literally). I can play through it, and the more I play the more I can keep the inflammation at bay. Over the years it comes and goes, but over the past year or so it has been particularly persistent.
So I decided to give turmeric a whorl, starting at the beginning of the year. Teaspoon a day plus a couple of curcumin capsules (high availability variety). After a couple of months there was a noticeable improvement and now 5 months later there is no throbbing pain, no problem moving up and down the guitar frets playing those pesky bar chords.
Like others I have had to find a palatable way of taking it . . . so here is the recipe: 2-3 teaspoons of home made low carb tomato ketchup, 2 ts of homemade mayo, 2 table spoons of cider vinegar, 2 table spoons of unpasteurised high fat yoghurt (thought to give the gut bacteria a treat). I like to sprinkle with a dozen blueberries. I call it my turmeric mousse . . . . with the blueberries it is just about palatable.
Is improvement in the hand down to the turmeric mousse? Or did starting the turmeric coincide with a periodic improvement? Or could it be the homemade mayo??? I suppose I will see how things go for a couple of months more, then pack it in and see if the inflammation rises again.
Interesting! I put loads of turmeric in my curries, and grind black pepper onto them just before eating. I can’t say I notice any medical effects (apart from orange tuds if I overdo it) but it tastes damn good.
For what it’s worth,I stick half a teaspoon or so of turmeric in my morning coffee. Quite enjoy the flavor. And I ain’t dead. Yet.
Mary,
The Skeptical Cardiologist doesn’t do his own research; he links to an article on the Science-Based Medicine website. The latter is clearly a front for Big Pharma. They diss everything which isn’t made in a factory and sold at a profit.
Mary Taylor: This sounds like a pharma-shill website. It is a fact that the vast majority of pharmaceuticals are derived from plant compounds. Our forbears had plenty of time to experiment and discover which plants were healthful foods, and which were medicinal. Turmeric and ginger fall into both categories, as do cinnamon, cloves, cardamom, and many others used by south Asians in traditional medicine and cuisine. This cardiologist appears to have a mind of the closed variety, unfortunately, and what he has written is an insult to the wisdom of our ancestors. His way, traditional cardiology, certainly has little to boast about, other than a healthy bank account.
Very healthy
There’s very little science in these so called “science based medicine” blogs. Mostly pharma propaganda. I listened to Harriet Hall once for a few minutes. She sounds like she can’t take care of her own sinuses let alone comment on turmeric.
Thank you
When an insect bite gets swollen and red, and itches like crazy, I have been told by the “experts” that I need to use an ice pack. What i do is wring out a face cloth in water as hot as I can bear to put my hands in and wrap that around the spot. Instant relief and faster healing if repeated. Tummy aches were helped by hugging a hot water bottle (or the terrier, when she was alive).Warmth is very healing.
I’ll try to remember that next time I get bitten by mozzies – it’s going to be hard not to reach for some ice!
And what about bumps and bruises? Ice or hot water bottle?
Bumps and bruises get arnica ointment – yes I know it is made by the homeopathic people, but the ointment actually contains a therapeutic dose of the tincture – as used by Aunt Izzie in “What Katy Did” so it is nothing new!
fresh aloe leaf really works for me when the mosquitoes get me.
Arnica for bruises
I always put hot, hot as I can bear, on insect bites. The relief from the tching lasts approx 10 hours and then I do hot again (put very hot water in a cup and hold the cup against the bite). I read some years ago that doing that breaks up the proteins from the ‘poison’ the insect injects, but I’ve always felt that the increased blood flow to the area that hot engenders is what helps bring relief. Hot has always worked with me. Cold never works because as soon as the area warms up the itching returns.
The only other thing which goes towards helping me with insect bites is antihistamine such as fexofenadine.
Someone once told me that joint pain (e.g. small amounts of osteoarthritis) responds if you just think about the joint in question as you use it – e.g. think about your knee as you walk.
I know this sounds very “New Age”, but in my experience it works – and seems to fix the problem for some time. I used to use diclofenac for this, but this works instead, and doesn’t increase my risk of CVD (I presume).
As for bumps, insect bites, bruises – just ignore them!
We also use apple cider vinegar and dab on the bite.
Alcohol. Works wonders for mozzie bites.
Interesting, Jean. When I get a bullant bite, if I do nothing it gets red, swollen, itchy and throbs, lasting a few days. If I put ice on it, I get no after-reaction to the bite.
There are actually very few bugs in the part of the world where I live, considering it’s a forested region, but when we do occasionally get a mozzie bite or a bee sting, we use witch hazel.
Also, to those of you using turmeric, I hope you’re using a good quality, organic spice from somewhere like Mountain Rose Herbs or Frontier Co-op spices. Some herbs and spices are irradiated and have less than zero potency. Just FYI.
Thank you, Dr. K. Brilliantly thought provoking.
Jean, I so agree with you about warmth/heat. When I was younger and wearing silly shoes on uneven pavements, I was forever spraining my ankles (three on each one – ouch) I always applied heat or nursed the offending joint next to the gas fire. It was soothing in the extreme and I always healed quickly even though some of the sprains were quite bad. The same for pulled muscles and tendons and other sports injuries, belly ache – you name it. It was the advice of my mother and grandmother and long before the advent of the “ice” treatment.
I’ve just finished reading “The Case Against Sugar” by Gary Taubes. It seems to me that sugar is the bad boy in the room and should be sent outside forthwith – sugar and refined carbs. Naughty.
Excellent use of a terrier, by the way.
Soaking sprains in a basin of warmish/hottish water with epsom salts or magnesium chloride flakes is also very helpful for pain and healing.
Thanks for the advice. That sounds like good solid sense.
There’s even a little battery driven point heater to treat insect bites:
They also make a version for herpes bumps. Works wonders if used at the first itching, but a good hot cuppa will do the same if you dip your lip into it as long as you can bear and about two seconds more…
For a fire ant bite I use citric acid because the toxin is alkaline and will be neutralized with acid.
Since they don’t cure anyting, what is the rationale for giving anti-inflammatory drugs for auto immune disease other than masking symptoms?
I wish I knew the answer to that too!
Our 36 year old daughter has been very ill over the last 3 years with Pleuropericarditis, which initially started during pregnancy. After a ‘flare up’ last year she is now pretty stable but on a worrying amount of medication. Mostly antinflammatories.
She’s been told it’s an ‘Idiopathic’ illness, Auto immune or Auto Inflammatory, whatever! Nobody seems to know.
She’s been tested for almost everything from Lyme disease to goodness knows what.
I worry myself sick thinking about the cocktail of drugs she swallows every day to keep her ‘stable’ and the effect it’s having on her now and long term.
Shes having a small bowel biopsy shortly to test her for Celiac Disease. I’m actually hoping that’s what it is.
Dear Jennie
Even if she doesn’t have Celiac Disease it would be well worth going on a gluten free diet, and cutting out sugar. I’ve included a comment further down suggesting that an anti-inflammatory diet (SCD for example), as advised by Functional Medicine doctors, heals leaky gut, SIBO, Candidiasis, all of which cures auto-immune conditions. It’s all in the food one eats. I would chuck out the allopathic doctors for your daughter’s condition and visit a naturopath instead.
All the best.
ive tried a naturopath for high blood pressured. didn’t work for me.
@ Jenny: Not everything a naturopath (just like an MD) works for everyone the first time around. Maybe you need to go back and try something else. Naturopathy is surely preferrable to allopathic, no? There are hundreds of things people can try for blood pressure reduction and not all of them work for everyone the first time. I’ve tried several times to get off beta blockers but so far have found nothing that works, but I’m not giving up.
Ankylosing spondylitis causes the tendons of the spine (and elsewhere, if it spreads) to inflame. When the pain and inflammation die down, the tendons contract and calcify, leaving the characteristic rigid bent-forward “bamboo spine”, which I have.
The thinking is that by preventing the inflammation in the first place, you prevent the disfiguring posture from developing. I wouldn’t know, I stayed away from rheumatologists because I was afraid they would give me powerful drugs which were bad for me and which I couldn’t afford anyway. Did I make the right decision by staying away from medical specialists? I don’t know. But here I am, 69 and healthier than most my age, although permanently hunched over.
Fab! All exactly as I say it to my patients! For sprained ligaments and the like I always prescribe hot and cold and hot and cold therapy, as this induces a pumping effect in the local tissue. It is extremely effective. Thanks for this great essay. Afifah >
A good input as always in my CVD-eyes!
Without being specific and at the same time being a severe CVD-case I am getting more and more convinced that it was one of my “smartest” decision in life, now almost 20 years ago, not only to reject the CABAG offered but also all medication at the same time.
Therefor, I just now wonder about my present high doses of vitamin E, (2400 IU/day), which seems to keep my angina at bay.
Am I fooling myself?
However, I couldn’t imagine that unstable angina could be something beneficial or a healing effect. When I today climbed a steep hill without trouble I felt “cured” although when working one of my chain saws later there was evident “resistance” – effort angina – which I though think is just good “training effect” – larger collaterals?
Dr. K,
Do you have any opinion on Strophanthin for the treatment of CVD?
http://www.faim.org/g-strophanthin-a-new-approach-for-heart-disease
Goran, you’re an inspiration! It’s always good to read your input.
Goran,
I recommend Dr. Thomas Cowan’s book, “Human Heart Cosmic Heart.” It’s fascinating and contains information you might find helpful.
any good news? Sent using Hushma
What should be used to try to prevent chronic inflammation and it’s competences in orthopaedic issues, ?aspirin, turmeric, arcoxia if no kidney function gpptdp is set00 or something else? Obviously if can solve the reason for the chronic inflammation is best, probably dietary, stress.
Is aspirin good for inflammation process of the heart?
Is there any benefit to taking statins while trying to figure out how to address inflammation of the heart, or are they useless and only damaging
How much does CoQ10 help protect you from bad effects of statins?
Anne . . . from bitter personal experience statins are very damaging . . . besides muscle damage I also acquired diabetes. Females have an even greater chance of getting diabetes than men. Healthy diet, some exercise will do as much good as a statin for improving heart health.
A good diet, low in sugar or refined carbs, is at least three times more powerful than statins in reducing inflamation and has none of the adverse effects. Dr Mark Porter recently confirmed this in The Times.
So, why does Warfarin increase0heart attack risk when it’s an anticoagulant, like aspirin?
I would check your facts on that one.
(What is a fact – these days?)
Hasn’t it been shown that people short on vitamin K tend to lose calcium in bones and gain it in soft tissue, i.e. coronary arteries?
Or you could check yours. It is you who said warfarin increases heart attack risk.
Nope. I said warfarin increases calcium deposition in arteries. Which is not the same thing.
And do those deposits make me more likely to have a heart attack?
Doc,
Warfarin:
The people out here who declare things are almost unanimously declaring that CAC is a direct measure of plaque. (Placing me personally as having a “preexisting condition.”)
Not true?
Not necessarily true?
If calcification is a process that occurs in plaques, and warfarin speeds up this process. Does this mean that warfarin causes the plaque, or just causes it to calcify more rapidly? Calcified plaques are usually consider ‘stable’ i.e. unlikely to rupture. Normally calcification score would be a good measure of overall plaque development, thus probably a good measure of risk. But if the calcification is being accelerated by warfarin, this may paint a false picture. In reality no more plaques are developing, simply more calcification of existing plaque. Thus no more risk. That, anyway, is my current thinking on the matter.
@ JD Patten: Vitamin D3 and Vitamin K2 (used together) have been shown to move calcium into the tissues & bones where it’s needed instead of “storing” it in arteries, the way I understand it. I take both, and also drink raw milk which is rich in K2 (especially this time of year when the cows are on pasture). I try to get adequate sunshine for the slow increase of D3 too, but sometimes we don’t have sun every day, so I also supplement 5,000 IU of D3 and 100 mcg of K2 daily.
sun,
Right. I supplement exactly as you do. My point above is that warfarin is a powerful vitamin K antagonist. That’s how it interrupts the coagulation cascade, which is a pretty complex process.
But, reduce your K and you risk calcified arteries.
sundancer55
a question if I may? I supplement with D3 8000iu per day and can only raise my D3 level to 33. Age 73. I am told that with age supplementation has less effect. Have you found anything along this line – age reducing the D3 supplement effects?
Robert
Which units are you measuring in?
I
JD
Vitamin K1 and K2 are similar molecules, have different food sources, and very different bio actions.
My experience is:
K1 offsets the blood thinning effects of warfarin.
K2 (plus Vit D and magnesium) encourages calcium to move into bones from soft tissue. However, since taken K2 this has had a minimal effect on my warfarin dose to maintain INR readings between 2 – 3 as required by the Doc. My biggest problem is to assess if this is having a positive effect on me and after how many months?
Robert,
I’m wondering what you’re on warfarin for.
I had three ablations for atrial fibrillation. Still get enough very occasional arrhythmia to concern my electrophysiologist enough to prescribe anticoagulation. (Thinning is a misleading term.)
I could not keep my INRs within range on warfarin. Then, less than a week on dabigatran resulted in three months of gastrointestinal distress. Rivaroxaban was OK, but the risk of brain bleed is less with apixaban. Fortunately, I can afford the $25./ month for apixaban. ($400. or so retail without insurance.)
No worries about K or any other aspect of diet effecting treatment. I would never consider warfarin.
JD
thanks for your response
warfarin for AF – (which is well controlled) ablation not recommended for my specific condition.
no insurance for me for the newer anti-coagulants – full cost not affordable.
so stuck with warfarin, plus (K2, magnesium, vit D) to counteract.
I think warfarin is OK. The NOACs (Novel oral anti coagulation agents) are, to my mind, far from proven to be safe in the longer term. I think some things may well emerge.
Recent research on Warfarin use and Vascular Calcification.
http://www.amjmed.com/article/S0002-9343(15)30031-0/fulltext
Dr Kendrick,
Is there reasoning behind your thought that something may emerge concerning NOACs? What??
Or does it fulfill your bias that profit making new drugs are likely problematic?
Robert,
Have you seen this guy’s stuff?
http://a-fib.com/steves-a-fib-blog/
Are you on Warfarin?
I think I have already seen the “If you have been damaged by _____, call us” lawsuit ads on TV about one of the newer anticoagulants.
Warfarin is a pain in the ass to monitor, but the others are not monitored.
JDPatten
thanks for the AF link
Use it or lose it—-
PMC full text:
Compr Physiol. Author manuscript; available in PMC 2014 Nov 23.
Published in final edited form as:
Compr Physiol. 2012 Apr; 2(2): 1143–1211.
doi: 10.1002/cphy.c110025
Copyright/License ►Request permission to reuse
Table 1
Estimated historical reductions in daily steps by humans.
Population Year Steps per day
Paleolithic (~20,000 BC) ~13,200–21,120 (men) ~10,560 (women) (385)
Amish (2002) 18,425 (men) 14,196 (women) (27)
Mean of 26 studies (1966–2007) 7,473 (mainly women) (63)
Colorado (2002) 6,733 (men) 6,384 (women) (573)
US adults (2010) 5,340 (men) 4,912 (women) (26)
Left out conversion—approximately 2000 steps in a mile
Blaming inflammation for CVD, then, is like blaming the fireman for causing the fire, or cholesterol for causing plaques. Thank you for reminding us of the importance of inflammation. As for RICE, more than 40 years ago I injured a lower back muscle in an accident. The following day my job was to run a front-end loader back and forth on a road under construction, hauling borrow material, bouncing up and down all the while in excruciating pain. I went to good ole’ Doc Hayden, the only physician in the small mountain town. The nurse put blazing hot. moist towels on the spot, replacing them periodically as they cooled. I walked out of there a new man, pain free. And the following day, still bouncing up and down, but pain free! Later I became a runner, and was taught RICE, but I knew better; I use one of those things you stick in the microwave. Works like a champ.
If I understand that article correctly, when inflammation is present, it would be a good idea to look for what is causing the inflammation. That could be a number of internal (autoimmune disease) or external (lifestyle or injury induced) factors. These can be addressed in different ways.
If inflammation is necessary for repair (rather than as a result of the body attacking itself), then it is best left to take it’s course. The body is trying to heal the damage. Excellent.
And once inflammation has completed the healing process, it is done.
There is also a mention in a quote by the cardiac surgeon of a chronic inflammation process caused by lifestyle. He states that without inflammation (if that is a possible state in the body) there would be no clogging of arteries. That seems a little too simplistic. What’s the real answer, and does medical science have any ideas?
Thank you Dr. Kendrick. You’ve put me off NSAIDS for life! I take methotrexate for rheumatoid arthritis. As I understand it, it is supposed to ‘dampen down’ the immune system. Any comments?
This boy takes his diclofenic wherever he goes. Sorry but until something else works when
a gout attack happens nsaids for me, don’t rely on a hot water bottle.
Unless you’re devout for allopathics, you could do some research into cherry juice and cherries (tart, black or Bing) for gout. I’ve known some it helped, and some it didn’t – but it’s certainly worth a try. A friend of ours ate a handful of frozen organic black cherries in the a.m. and another handful in the p.m. and in about 2 weeks could feel relief and in about 1 month he felt solid relief. He still eats the cherries!
@Goutboy
Have you tried reducing fructose and/or alcohol intake? Stay well hydrated as well.
But could it not be said that a heart attack is a response from chronic inflammation and what behaviours that cause the chronic inflammation is the problem. In taking on board some of the benefits of being cold, I have lost some belly fat without changing diet and exercise so I think there must be something in it.
Is it still a good idea to take Turmeric which is reckoned to reduce inflammation.
Thanks for the bulletins very interesting.
very good
good
Apologies if this has already been covered but below is an extract from the link show below on an interesting piece on Myogenic Therapy I came across while googling Lactic Acid and Heart attacks
Link – https://www.westonaprice.org/health-topics/what-causes-heart-attacks/
“It turns out that there are simple, inexpensive and very effective compounds that effectively prevent lactic acidosis in the heart tissues. These medicines have been known for centuries as cardiotonics and have been used for treating heart disease in every traditional medical system in the world. The two best known are digitalis (the common foxglove) and strophanthus, an African vine. These plants are the source of so-called cardiac glycosides: digoxin and digitoxin from digitalis, and ouabain from strophanthus. The function of these compounds is to regulate the rhythm and power of the cardiac contraction and to prevent or reverse lactic acid buildup in the cardiac tissue. This is why these plants have been used for centuries to treat congestive heart failure, rhythm disturbances and other disorders of heart function.
The amazing thing is that these compounds are exact chemical copies of hormones made by our adrenal glands. And our adrenal glands produce these cardiotonics out of . . . cholesterol! Now we know why all the draconian dietary and pharmaceutical measures to lower cholesterol have not resulted in a decrease in the rates of MI, and why numerous studies have shown that as we age, those with the highest levels of cholesterol live the longest. When we lower cholesterol, we are depriving our bodies of the very substance they need to manufacture cardiotonics.”
Dear MalcolmI’ve been following your blogs for a while, with admiration. You seem to me to cut through the egos and waffle to the key issues.I’m reluctant to ask this question as you are not setting out to be a universal doctor but I am left wondering in the light of this post whether I should continue to accept steroid treatment for swelling and raised pressure in my eye as a result of a blood clot. The idea was to reduce the swelling (the blood clot itself is not being treated)…but would it be better to let my body try to heal itself?Your thoughts would be welcome if you have time to consider this.Best wishesSue Gerhardt
sue,
I’m not a doctor, but I did get severe inflammation in an eye as a result of leaky blood vessels. I was put on steroid eye drops (Pred Forte) by the specialist and made a full recovery with no adverse effects. Took a couple of months.
The key question remains, what causes the lesions in the arteries, which in turn causes the inflammation. If I recall correctly Dr Kendrick summarises his view that it is stress – both psychological and physical. He also stated that it has something to do with the thrashing of the blood in the arteries, that’s why atherosclerosis is only found in arteries and not the veins.
As I recall, there is the source of damage to the arteries and the healing response. The sources of damage are legion and in some ways not important, it is going to happen. The healing response and when it is hindered seem to be the key to CVD.
Under “normal” circumstances there is damage that is healed. Even under more damage situations, my guess is that the healing process ramps up to accommodate.
It is when the healing process is hindered by other factors (stress, lack of vitamin C or D, etc.) that the arterial plaques grow until they burst, causing heart or brain infarctions. (Right?)
I just had a cardio evaluation since I have been on ritalin for over 20 years for ADD. (The office visit to get told everything was fine was silly, why not do it over a phone call?) I wondered why they didn’t look for arterial plaques to asses my CVD risk. Would seem to be a very direct indication of risk.
jgt10
may I suggest you research Dr David Perlmutter in respect of ADD – he seems to approach Brain problems with the same no nonsense attitude of Dr K. I think Perlmutter is very interesting.
The NSAID thing has me a bit worried. I have a disc that slips out every now and then and the pain when that happens is excruciating and prevents me from walking. I know the acute phase won’t last more than a few days, but to take the edge off the brutal pain, I take a combination of co-codamol and diclofenac (NSAID) at the highest dosages permitted. Is that kind of short term usage ok, or does even that put me at risk of CVD? What about those ibuprofen taken for flu symptoms, when paracetamol isn’t quite strong enough – are they risky too?
I guess I am asking for clarity on occasional use vs long-term use?
My understanding these days is that NSAIDS maybe ok for occasional short term pain relief (minimum effective dose) but not popped regularly. Not sure I’d ever take it for flu though.
I have also read that ibuprofen can raise blood pressure, even when taken occasionally, so I avoid it if at all possible as I have high bp anyway.
Don’t forget pain itself can cause a great deal of stress which is a major risk factor for CVD.
I pulled a back muscle a few months ago and ibuprofen was the only thing that allowed me to move/sleep but I only took it for a day or so really. My gp suggested I tried the high strength gel but that just brought me out in a rash!
All about the good old risk/benefit. You makes your choices …
I am convinced it was ibuprofen that has caused my bp. Suffered for years with period problems and the GP said to take ibuprofen. Took them like sweeties as the pain was so bad and nothing helped. Turned out when I got to 50 that I had all sorts going wrong for years which the doctor failed to find out or investigate. Too late then.
For a minute I thought that was me writing again Biddy!
Ditto – ibuprofen were the only thing that would work on crushing period pain and for years I popped them a bit like sweeties for 2 days every month.
But I also know I didn’t have high bp in those days as I used to measure it just out of curiosity. My bp started going up the instant I hit the menopause and has caused me grief ever since.
The only good thing about the diagnosis is it brought me to this site for which I am thankful.
Nigella,
We’re the only beast that stacks our vertebrae one on top of another in order to support all our body weight. Even our closest relatives are sometimes quadrupedal.
I discovered (having been in your situation!) that the only reasonable way to keep those building blocks in line is to strengthen the muscles that are in a position to hold them there.
I suggest you find someone who knows what’s what to advise you on a serious exercise routine to build up your rectus spinalis, abdominals and associated musculature. The fix is already within you.
About NSAIDS, for what it’s worth:
http://www.bmj.com/content/357/bmj.j1909
JDPatten, Good advice.
Nigella, I suggest giving Pilates a go, very conservative, but will gradually build your strength.
Nigella: In addition to JDPatten’s excellent advice, I highly recommend “8 Steps to a Pain-Free Back.” It’s an excellent course in posture-amazing how important posture is to back health. It is possible to get the book and teach yourself, but better to take the class. You can go to the website (Esther Gokhale is the author) and find a class. They do them in the U.S., Canada, and several European countries.
Another site to try is Sarah Key, an Australian physio, admired by Prince Charles. She has a series of exercises to loosen lower back muscles and thereby the spine.
It was suggested I should be operated for stenosis, I did her exercises and never looked back ( play on words)
Hi JDPatten, I do pilates and go to the gym after doing extensive work with a physio who specialises in spinal rehab and strengthening. My core is in a better state than it’s been since I was a teenager. Unfortunately, none of that prevents me from stumbling over my suitcase or twisting awkwardly to catch a small child, and it is those kind of things that make the disc pop out. I’ve seen the MRI of my spine and it was not good – a lot of horrible black areas indicative of degenerated discs, so I am keen to look after what’s left of it!
Nigella,
Sounds like you’re on the right track.
All I can contribute is what I know worked for me.
I can’t go into the mass of stuff that I tried and failed with. It of course included the usual from doctors and physical therapists. A couple of wasted years in my mid thirties.
I went my own way. I’m talking about heavy weight training to gain muscle mass . . . . very, VERY gradually. It took more than an additional year.
It seems that, with my wonky discs, it takes a column of heavy muscle to keep it all in place. Diving for the kiddies when that mass of muscle is always in good TONE served me well. (Stay-at-home-Dad!)
JDPatten: Absolutely right! Building the musculature is key. Also learning how to bend (hip-hinge) properly is crucial to protecting the discs. I used to get a flare-up of my long-ago injury whenever I tried to lift anything heavy. This no longer happens, and I can lift very heavy objects even from below ground level, as I recently had to do removing globs of concrete while replacing some fence posts. I did this by body-weight exercise (push-ups, pull-ups, and squats), and the posture course.
I also have dodgy disks. Plenty of walking seems to be the best exercise, although I do other exercises as well.
The big thing to avoid is twisting the trunk while carrying a load, such as picking up a heavy suitcase and turning to put it in the boot of a car.
Gary,
Body weight is good. (Self dumb-bell! 🙂 )
I got up to just short of 200 lbs doing sets of dead-lifts with a barbell. As I’ve said: I worked up to that VERY gradually. In my middle thirties. Half my life ago, I just now realize. I maintain conditioning with a bit less now. OK, quite a bit less.
I think that if your column is at all compromised, quite a bit more muscle in excellent tone is needed than “Normals” can get away with.
JDPatten: I didn’t start till I was 65, and also worked up very gradually, from barely 2/3 of a pull-up with both feet on a stool, to 4 sets of 5 free hanging after three years, and from ten pushups to a hundred in a year. I couldn’t do a squat, but now do 4 sets of 15. Equally important to muscle strength, though is proper spinal alignment, and decompression. I begin my warmup with a spinal decompression exercise. Easy to do, and it feels wonderful.
Our closest relatives are almost entirely quadripedal.
I have an inherited propensity to develop autoimmune disease, and I’ve collected four such conditions to date. About four years ago, early rheumatoid arthritis emerged, causing severe inflammation in my wrists and hands. Since 2015, I’ve been taking Low Dose Naltrexone on private prescription. It cleared the inflammation completely over the course of a month.
Uncertainty surrounds the specific immune modulation process by which the LDN protocol works, so I’m unable to reach an informed opinion about whether or not its anti-inflammatory effect will raise my risk of developing CVD. My familial risk is high anyway. Other, more exacting, protocols exist which may successfully address the triggers of autoimmunity. The Paleo Autoimmune Protocol (AIP) is one such approach, but I found it impossible to follow in my current state of ill-health. It’s hard to know what to do for the best – I need my hands!
I’ve been following your “What causes heart disease” column with interest for some time and as far as I can remember I don’t think you have discussed the effects of high blood pressure as being a possible cause. It’s mentioned all the time in the usual medical sources as being one of the main causes of CVD, I’m interested to know your view – just generally at this stage.
Hi John, another Malcolm here,
I think blood pressure is a symptom rather than a cause, so the key question is what is causing the high blood pressure? Of course, the high blood pressure might then have an effect on CVD as a knock-on effect, e.g. by increasing the damage caused by the surge of each beat.
But stiffened arteries due to atherosclerosis probably causes higher blood pressure – so the causation can be in the other direction.
Either way, reducing high blood pressure has to be a good idea if you have it, so people who are overweight should consider eating fewer carbs to lose weight, and people with stiff arteries should consider eating more fat (and therefore fewer carbs!) to improve the condition of their arteries (I think Peter at hyperlipid has talked about measuring this but I can’t find the link just now).
http://high-fat-nutrition.blogspot.co.uk/2010/01/who-pays-piper-for-arterial-stiffness.html
About 14 years ago, I had my left knee replaced. A year later, my right knee suffered the same fate. Two years ago, I got my left shoulder replaced. Osteoarthritis sucks.
For the knee replacements, I was told to use ice packs. But I didn’t because I found them difficult to manage (my then partner was working full-time so I was home alone during the day) and just plain uncomfortable. For the shoulder replacement, they gave me an ice machine. Again, didn’t use it because it was just too much bother. In all 3 cases, my surgeons were surprised by how quickly I healed.
I’ve never been a fan of icing injuries, or (like Jean) insect bites. I had no “scientific” training to back up my belief that heat worked better on inflammation, so I just kept quiet about it and carried on doing my own thing.
Before my shoulder surgery, my PCP told me my C-reactive protein was high and I should take statins. When I told him that it’s a marker for general inflammation rather than cardiac risk, that I was about to have surgery for osteoarthritis and showed him my arthritic hands, he reluctantly agreed that there might be a non-cardiac cause.
How little we know about MI!
Stress seems to be crucial!
smartersig – about digitalis
The vagus connection is important for how the internal nervous system of our hearts work or rather not work properly. For whatever reason heart rate variability is an issue at acute MI. How extremely little we know about this nerve connections and what beta-blockers do in the long run.
This is so interesting! I do agree with Chinese medicine not using ice. Instead cooling down is the key to keep working.
Any questions in this post are purely rhetorical…
As someone who takes Naproxen and Tramadol for chronic pain for which no cause has ever been identified I find this whole subject worrying.
The only thing that actually makes a difference to my pain is antibiotics (erythromycin is the only one that has worked so far, but many more have never been tried) and these reduce my need for the painkillers for as long as they last, leading me to believe the problem is a chronic infection. But as soon as the antibiotics run out I’m back to square one.
Giving up my painkillers is not an option. When the NHS collapses completely in the next year or two, and no insurance company will cover me for anything, what am I supposed to do? Go bankrupt, become homeless in my old age, or kill myself?
Whinge, whinge, whinge…
…then you could look up NOI and David Butler as a solution for pain, chronic or otherwise. No meds, just excercises that heal nerves, from a brilliant Ozzie. Cleared my fibromyalgia in three months. Pain gone. I’m a happy bunny.
When the NHS is made to collapse!!!
In 2012 the govt sneakily passed the appalling Health and Social Care Act, which removed the duty of the state to provide the legally enshrined free cradle to grave health care which we have considered a human right since 1945. Almost no-one in the country knew of this, (I never met anyone anywhere socially or while campaigning who did) so much for “democracy” This was in preparation for the dismantling and sell-off of the lucrative parts as well as the deliberate underfunding and the press propaganda highlighting only what goes wrong ( despite the dedication of the underpaid overworked staff). What is happening is an ongoing and irreversible tragedy. A crime on a par with bombing far-off countries no threat to ours. . We are being forced into a US style insurance -based system which will be twice as expensive, unaffordable for most,, and will deliver third world levels of general health care.
We are allowing, with no public debate, our government to destroy the most cost effective system in the world which up to a few years ago was delivering results comparable to systems costing much much more pro capita.
Really sorry to be a bit off topic on this wonderful blog. Dr K`s latest is just fantastic. I went into science for this kind off approach – thinking hard, asking fundamental questions, being excited at finding holes in reasoning, correcting wrong assumptions. I naively thought that that was what science was supposed to be about! Now we seem to be in a looking- glass world where millions are spent world propping up clearly terrible science – hypotheses that solidify into pure dogma. It`s mind-boggling!!!
This space gives me hope, plenty of enquiring caring minds!!!!!
Very informative blog about inflammation. It’s good to see there’s some establishment agreement about the need for new revised warnings about NSAID’s. Encouraging to see the FDA doing the right thing for a change.
A close friend took ibuprofen for seven years to try and relieve the agonising pain of an undiagnosed dislocated shoulder, which was then correctly diagnosed by an observant physio she was seeing for an entirely different problem. We later realised that the ibuprofen, along with ten years worth of alendronic acid, were the most likely causes of her stomach problems – for which she has been prescribed omeprazole, which only seemed to make things worse. She was also on the dreadful statins. After doing some research two years ago, including finding information on here, she decided to ditch all her medications entirely. She now takes apple cider vinegar and only occasionally experiences heartburn, although her lower jaw has been irreparably damaged due to the alendronic acid and she still experiences some occasional discomfort from the seven year dislocation. However, overall she feels much better and livelier than she has for many years. I will now show her this blog and we’ll try and work out how much she has reduced her risk of heart problems.
On a different note – another great maverick committed to making a difference, Prof Fred Kummerow, has passed away at the age of 102. He did very good work on trans fats and heart disease, discussed in earlier blogs here, including suing the FDA which resulted in them changing their guidelines about trans fats.
https://www.washingtonpost.com/local/obituaries/fred-a-kummerow-scientist-who-raised-early-warnings-about-trans-fats-dies-at-102/2017/06/03/5d33a946-47d6-11e7-bcde-624ad94170ab_story.html?utm_term=.655c3dad85e3
Interestingly, ice or a cold bath to bring down a fever has the same effect as putting ice on a sprain; it slows down the body’s ability to heal itself.
I see a world of difference between acute inflammation, a beneficial healing response to something, and chronic inflammation. Rather than treat the inflammation – or blame it – drill down and look for the cause. I have personal/familial reasons to blame hyperglycemia and possibly more importantly hyperinsulinemia so that’s what I address. Of course plenty of other causes exist. That’s where one size does not fit all.
Thus, the question becomes – which factors increase inflammation in the arteries?Increased BP, higher concentration of glucose in the blood, presence of various bacteria in the blood (as in chronic gum disease that leaks bacteria into the blood stream). It’s possible that agents which “cleanse” the blood would decrease CVD risk.
Talking causes of CVD they strongly points towards high insulin levels/the metabolic syndrome/diabetes as being the main culprit.
As the famous clinician Dr. Kraft, who measured blood glucose and serum insulin levels at the same time on his 14 000 (?) patients during 40 years, pointed out: “Those with CVD who have not been diagnosed as diabetic are just clearly UNDIAGNOSED!”
So, now this very early morning in the land of the midnight sun, I read about the same thing in the following input from another outspoken clinician “star” on diabetic treatments, Dr. Jason Fung.
https://intensivedietarymanagement.com/glucotoxicity-double-diabetes-t2d-36/
I find what he here writes almost of the same lucid style as the content of the present blog input by Malcolm.
Yes I agree with you, Goran. Dr. Fung’s writing content and style are similar to Dr. K’s. Also when Dr. F states that when we treat diabetics with meds to lower blood glucose, it is treating the symptom and not the problem. How clear that is. Somewhat similar to what the establishment protocols offer for heart disease. How about how we treat chronic inflammation? Is that not similar? We need to treat the cause and not the symptom, although I admit that in some cases this is not an option when the cause is not well established and the inflammation is debilitating.
Ok let’s see…
Statins reduce LDL – irrelevant
Statins have anti-inflammatory effects
CAUSE?
Why take aspirin? From NHS – in this study “the administration of aspirin compared with placebo did not result in a significant reduction in vascular events.” Fourteen patients in the aspirin group required admission to control bleeding (reasons not given) compared to five in the placebo group. http://www.nhs.uk/news/2010/03march/pages/daily-aspirin.aspx Also – those taking aspirin had a 70% higher chance of having microscopic bleeding in their brains. http://www.nhs.uk/news/2009/04April/Pages/AspirinBrainBleeding.aspx
Randall: According to the aspirin chapter in Joel M. Kauffman’s “Malignant Medical Myths,” all the trials which showed a benefit in primary prevention used bufferin, not plain aspirin, meaning it’s likely the magnesium which gave the benefit. The benefit in secondary prevention was very small. I avoid all OTC and prescription drugs like the plague.
I only took painkillers occasionally, but when I did something unspeakably painful to the complex of muscles/tendons between shoulder and neck I was popping aspirin for a while along with paracetamol.
Then I started getting attacks of tinnitus so stopped the aspirin.
I was persuaded to start LOW DOSE aspirin again for cardiovascular reasons. Now the tinnitus is permanent. One theory is ,microbleeds in the ear/nerves.
Thanks for nothing, and I mean that most sincerely.
More than than a million people with a common heart condition have been told not to take aspirin to guard against stroke, in a reversal of previous NHS advice. http://www.telegraph.co.uk/news/health/news/10907673/Aspirin-cant-help-1-million-heart-patients.html
Turmeric: “hogwash”. See the good doctor, above.
So..followng an MI should patients refuse statins and let inflammation heal their damaged arteries? I’m confused!
An MI is caused by a blood clot (usually). This happens once the arteries have become seriously damaged. It has nothing to do with inflammation/healing per se. Ways to remove blood clots are clotbusters, stents, and suchlike.
So…what’s a guy to do for his lower back pain a couple times of week? Tylenol supposedly beats your liver up, on the other hand ibuprofen may lead CVD and ? MI. I sure feel it the next day after squash B league play.
ricksanchez: Two things you can do: Correct your posture, and build your core muscles. Then you will be making all the movements in whatever you do correctly. At 68 I can do nearly anything I could do at 30, but in my 40’s and 50’s, though fit, I had recurring back problems. Back pain is not normal, and it is not the result of sports activities or normal, everyday activities, except in the case of injury. It is a result of poor posture and weak core muscles.
What has helped me is the following exercise (from https://www.amazon.com/Body-Science-Question-Answer-Book/dp/145057341X). Use a pull-down machine (https://en.wikipedia.org/wiki/Pulldown_exercise) with your legs tight to the ground and under the pads. Instead of doing a pull down, keep your arms straight. Use your back to lower your head toward the floor (maybe such that your body is perpendicular to the floor). Do this slowly, with no rest at the top for 1-2 minutes.
They recommend another exercise in the book for your back, which I also use. However, that is too hard for me to describe. I’m not sure even reading the book I’m doing it correctly, so I don’t want to mislead anyone.
Another exercise that helps is crunches or oblique work. I just recently started using the Body by Science program, and I only do abs each time I workout, which was once per week, though I’m thinking of going to every 5 days. Note that I have two workouts, Back and Chest/legs, so I would workout the back only every 10 days (currently every 2 weeks, but I lost strength at my last workout, which means there’s too much time between workouts). I do crunches, rotations, or oblique work on machines, using the same slow technique for 1-2 minutes. I keep track of time and weight. If my weight stayed the same, but time goes up, then I know I got stronger. They recommend only doing abs once a week or less, so since I’m going to be working out every 5 days on my abs, I’m going to try different parts of the abs each 5 days, to make an “effective” 10 day difference.
BobM
Sarah Key australian physio has a series of exercises for lower back pain. This worked for me, especially since the hospital was talking about operating.
By the way, she is highly recommended by Prince Charles.
CVD INFLAMMATION CONNECTION
Endothelial dysfunction initiated by high steady and high postprandial blood glucose levels
1) glycocalyx shedding, protective coating of endothelial surface layer is lost
2) injury to endothelium from hyperglycaemia: dead and dying cells initiate immune response
3) inflammatory response initiated to repair damaged cells
4) Macrophages and T-cells secrete IL-6 , IL-6 activation induces monocyte and leukocyte adhesion to endothelial cells
5) hepatic tissue reacts to IL-6 by secreting CRP
6) CRP binds to dead and dying cells to mark them for phagocytosis by macrophages
7) new endothelial cells form, inflammation returns to normal
8) chronic carb loading will result in progressive endothelial damage
Glycocalyx endothelial surface layer takes several days to return to normal when hyperglycaemia stopped.
Effect of loss of glycocalyx endothelial surface layer
– capillary leak, vascular permeability increased
– coagulation activation, hypercoagability
– edema
– platelet aggregation
– Inflammation
Conclusion: CVD is caused mainly by low fat/high carb diet
Pharmacological remedies will probably be developed to cure inflammation.
Andy. I think that is an excellent summary. I think that there are other factors that can also damage the endothelium e.g. smoking, air pollution, stress/increased stress hormones.
Thank you Dr. Malcolm Kendrick for encouraging us to ask questions and apply any lessons learned into our daily lives. This blog number XXX raises the question “does inflammation cause CVD?”. Your answer is that anything that affects the endothelium could contribute to heart disease.
How big is the endothelium?
“But if you took all the blood vessels out of an average child and laid them out in one line, the line would stretch over 60,000 miles. An adult’s would be closer to 100,000 miles long. There are three kinds of blood vessels: arteries, veins, and capillaries.”
Take away lesson: Endothelial dysfunction can affect every tissue, heart, brain, eyes, nerves, etc.. What ends up in the blood after every meal can impact your health in many ways.
Malcolm,
Can you explain how smoking and air pollution (are we talking about SO2, NO2, CO, particulates…) damage the endothelium? I am not questioning this, but what exactly is the mechanism?
Still pondering the connection with COPD in the machine-learning study. Could it be an indicator of previous smoking or something more direct like reduced oxygen levels, or an effect on the NO?
Also in the Machine Learning analysis Fibrinogen came pretty low on the list ….confusing
Indeed. The problem with that list is that it is ‘blind’ to combination causality. In the end someone has to established that x causes y which then causes z. Ergo without x, y would not exist.
Mmm true but it would still show up that x and y are quite high risk, what it simply would not do is show that x and y together outtrump both as a cause
So how does this fit in with the fact that CVD doesn’t develop in veins? Would hyperglycaemia that injures the endothelium of arteries also damage veins?
Craig,
Thinking as an engineer, pressure must enter into the picture. A higher blood pressure clearly requires a stronger endothelium to withstand it.
By the time blood enters the capillaries and veins, the high arterial pressure pulse has dissipated, but at some points in the arteries like bifurcations, the momentary pulse pressure is magnified by reflected pressure waves. Blood would have a better chance of forcing itself through a weakened endothelium at these places, and it is at these locations that the worst plaques are seen, apparently.
Plus the shear force of the blood rushing in the arteries would also tend to make endothelial repair more difficult, rather like trying to fix the roof in a high wind.
Perhaps this is why some exercise is beneficial but excess can be damaging and certainly does not result in extended life
Thanks Martin I think the pressure side of things is key but still can’t see how the glucose/carbs would cause damage as per point 8) in Andy’s post. Is there a proposed mechanism? Surely the pressure is independent of blood glucose level?
Probably because increased glucose concentration in the blood changes its viscosity.
Good point Sasha, plenty of research shows increased blood glucose results in increased blood viscocity and stickiness
So I suppose the fact that I bleed like a stuck pig after every BG test is a good thing?
I don’t think it works like that. I may be wrong, though.
Craig,
I haven’t followed the detail discussion, but I think that the endothelial cells are held in place by a sort of intercellular glue or grout, and it is the glue which is weakened by blood sugar, allowing endothelial cells to be more easily stripped away. The glue is related to collagen, which requires vitamin C for maintenance, and if vit C levels drop, e.g. with scurvy, blood vessels start leaking. Because vit C and glucose are physically similar molecules, glucose can displace vit C, weaken the glue, and hence damage the endothelium.
Will someone who knows more than I please correct this explanation?
Yes it my understanding that Vit C and Glucose compete for uptake and when Glucose is high it trumps Vit C which is probably one reason why sugar is so damaging to arteries if Vit C is vital to artery health
I tried posting this response earlier, but something seems to have gone wrong, try again (this is my last saved version of the post):
Andy S, that’s a great summary that points to many interesting avenues, a couple of which I follow for a step or two:
There is a nice open access review paper here: https://www.hindawi.com/journals/mi/2014/694312/ (Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions
Hana Kolářová et al). It covers a lot of ground with many references.
As Kolářová et al point out, measuring the glycocalyx is a delicate matter and there may be a lot to learn still by studying its physical properties in different tissues. Note the links with NO synthase, NO and vascular tone; any aspects of coagulation; and its function as a place for cytokines and cells to bind.
When it comes to inflammation, it is always a bit of a nightmare to sort out causes and effects, as there are so many positive feedback loops (required to boost healing, but undesirable when they go too far).
Section 5.1. Mediators Released during In ammation Contributing to Glycocalyx Destruction contains a lot of fascinating material, and bears close reading (every word tells a message here).
In Section 6, note too the significance of capiliary leakage as well as coagulopathy.
Where the review is a bit weak is in consideration of causes of long-term damage.
In that regard, I see mention expected links with ROS (among many other factors). That leads me to expect that physical or chemical stress on the endothelium that leads in turn to mitochondrial complex I stress (for example), will cause trouble in the long term.
So I’ll add a zeroth item in Andy S’s list. (I’m not sure exactly how to write it, but here is the gist):
0) Endothelial stress resulting in weakening of the glycocalyx (mediated by O2-, ONOO-, and/or other free radicals)
I’m not taking anything away from point 1) in the list: i.e. sugar causes both short and long term damage, but some toxins (dose makes poison) have clearer effects on the longer term by damaging the endothelium directly.
In the review paper the emphasis is on the ROS coming from immune cells (short term damage from the process of inflammation), but endothelial cells with stressed or damaged mitochondria, whether from glucose or smoking [1].
Ken
ps. the immune system and therefore the process of inflammation can be disregulated, e.g. due to mast cell hyperplasia, vitamin B6/Zn deficiencies, or Th1/Th2 imbalance due to lack of methlyation for epigenetic programming (to give three very different example root causes).
.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212590/ THE ROLE OF TOBACCO SMOKE INDUCED MITOCHONDRIAL DAMAGE IN VASCULAR DYSFUNCTION AND ATHEROSCLEROSIS Zhen Yang et al.
Anyone watch the Michael Mosley programme last night about blood?
He showed us his cloudy (fatty) separated blood serum post traditional fried breakfast (containing bacon eggs, but also potatoes) and then he had a blood test done that showed rise in inflammatory markers after said breakfast, but not after the one which was blackberries and yoghurt? It seemed like the implication was that fat ingested turned to fat in the blood, which was seen as a bad thing of course! Naturally, it skated over the top and didn’t delve down into proper detail, as we are all far too stupid to understand any real science on popular TV.
Anyone with a more scientific mind care to comment?
Is this a programme he did some years ago, I think he’ s change his stance on the fat thing. Anyway the programmes he and his like do are children’ programmes designed for adults, it’s the BBC’s way. I have complained a couple of times suggesting what people might actually be interested in, the replies are written by establishment automatons. The blogosphere rules.
Hi Nigella, as a consumer of bacon, eggs, saturated fat (butter) Moseley’s experiment needed to be investigated. Firstly the gut can be a large source of inflammation via leaky gut. Lectins and gluten in wheat are a problem (autoimmune diseases). The reaction to inflammatory foods can be quite rapid.
The inflammation of blood vessels by high glucose is a separate problem.
After digestion fat is transported via chylomicrons to various tissues. Yes this is equated to fat in the blood but is normal and harmless. Adding glucose seems to be the problem.
Yes, I clocked this too and would love an explanation for the increased inflammatory markers.
Nigella
I saw the programme and like you I was taken aback by the apparent fats in the blood. What I think you are seeing are chylomicrons – these are relatively big lipoprotein particles filled with fats (triglycerides) from the breakfast. The fat filled chylomicrons are constructed in the intestinal cells from the fats you eat. The chylomicrons enter the blood stream and head around the body where they transfer their triglycerides (one fatty acid at a time) into cells as fuel or substrates for the synthesis of new chemicals. As I understand it, they deliver much of their load within a couple of hours. Because the liver is not involved directly in the delivery of this source of fats, it can get on with dealing with other things like creating triglycerides from glucose and packing them in to VLDL particles for delivery.
So it is good to know that if you eat your olive oil, coconut oil, beef dripping etc that you should not be troubling the overworked liver. Also, I have yet to read that these huge soggy chylomicrons which are big enough to make the blood cloudy, are associated with atherosclerosis.
Thanks for replying Antony. I was really dismayed to see this stuff on national TV, without a proper explanation.
When you eat a lot of fat WITH a lot of carbs, the body prioritises the clearance of the glucose before it goes round glycating everything in sight. It leaves the less damgerous fat in the blood until it can deal with it later. Of course if you then eat more of your dietician-approved carbs, later never comes I suspect this is another factor.
What did they fry the potatoes and eggs in? Omega 6 oils? Those raise inflammation, esp when fried.
Very strange:
Reduce plaque burden (in mice) by boosting macrophage activity with a particular . . . sugar.
Eating it doesn’t work. You have to inject.
Up for it?
Explained:
http://www.medicalnewstoday.com/articles/317823.php
Official medicine operates on a consensus given by the “elites”. They think about what is the best drugs to give to their victims, oops i mean patients, and spread the word to the whole medical community. This is not science based at all. It is largely subjective, and largely financed by pharmaceutical companies.
What astonishes me about inflammation is, that it is not recognized for what it is by every single doctor out there; the starting process of healing. What is worse, the ability of the human body to heal itself, use millennia old mechanisms to repair ( via cholesterol ) is sent into oblivion.
Is this the rhetoric that has to be used in order to sell (dangerous) drugs to the population ?
________________________
What would be a good idea i think doctor on your blog is, what is everyone thoughts here, about what causes heart problems.
Malcolm
Super article.
I am a very simple GP.
Inflammation is a necessary part of the healing process, as you say, and I say that to my patients too.
When I broke my tib and fib, my surgeon told me under no circumstances to use a NSAID, and to exercise my leg 20 minutes twice a day on an exercise bike from week 1( I had internal fixation). I do not see the point of NSAIDS for injury, but they are a bad habit most people have when an injury occurs.
I have long thought of atherosclerosis as the result of an aberrant healing process, or perhaps a repeated abnormal healing response to frequently repeated injuries. A skin equivalent would be a non healing leg ulcer, or unremitting psoriasis. What I want to know is the list- the range of causes- for the the injury in the first place, that leads to the need for healing.
Joanne
________________________________
Boswellia is far superior than tumeric. It can substitute NSAIDS without many of the side effects; They can also be taken together tumeric and boswellis and are the most effective for osteoarthritis.
https://www.ncbi.nlm.nih.gov/pubmed/27671822
Boswellic Acids and Their Role in Chronic Inflammatory Diseases.
Abstract
Boswellic acids, which are pentacyclic triterpenes belong to the active pharmacological compounds of the oleogum resin of different Boswellia species. In the resin, more than 12 different boswellic acids have been identified but only KBA and AKBA received significant pharmacological interest. Biological Activity: In an extract of the resin of Boswellia species multiple factors are responsible for the final outcome of a therapeutic effect, be it synergistic or antagonistic. Moreover, the anti-inflammatory actions of BAs are caused by different mechanisms of action. They include inhibition of leukotriene synthesis and to a less extend prostaglandin synthesis. Furthermore inhibition of the complement system at the level of conversion of C3 into C3a and C3b. A major target of BAs is the immune system. Here, BEs as well as BAs including KBA and AKBA, have been shown to decrease production of proinflammatory cytokines including IL-1, IL-2, IL-6, IFN-γ and TNF-α which finally are directed to destroy tissues such as cartilage, insulin producing cells, bronchial, intestinal and other tissues. NFĸB is considered to be the target of AKBA. The complex actions of BEs and BAs in inflamed areas may be completed by some effects that are localized behind the inflammatory process as such tissue destruction. In this case, in vitro- and animal studies have shown that BAs and BEs suppress proteolytic activity of cathepsin G, human leucocyte elastase, formation of oxygen radicals and lysosomal enzymes.
PHARMACOKINETICS:
Whereas KBA is absorbed reaching blood levels being close to in vitro IC50, AKBA which is more active in in vitro studies than KBA, but undergoes much less absorption than KBA. However, absorption of both is increased more than twice when taken together with a high-fat meal.Clinical Studies There are a variety of chronic inflammatory diseases which respond to treatment with extracts from the resin of Boswellia species. Though, the number of cases is small in related clinical studies, their results are convincing and supported by the preclinical data. These studies include rheumatoid arthritis, osteoarthritis, chronic colitis, ulcerative colitis, collagenous colitis, Crohn’s disease and bronchial asthma. It can not be expected that there is cure from these diseases but at least improvement of symptoms in about 60-70 % of the cases. Side Effects The number and severity of side effects is extremely low. The most reported complaints are gastrointestinal symptoms. Allergic reactions are rare. And most authors report, that treatment with BEs is well tolerated and the registered side effects in BE- and placebo groups are similar.
Two articles that may be of interest to some of your readers;
A Natural Anticoagulant Regimen
by Philip Lee Miller, MD
http://www.townsendletter.com/May2017/anticoag0517.html
Stop Fixing the Adaptive Response:
Why Cardiovascular Disease Should Be Named Chronic Scurvy
by Daniel Cobb, OMD
http://www.townsendletter.com/May2017/stopfix0517.html
Is it possible to measure the health of the endothelium directly? It might change the focus of therapy for CVD if endothelial damage could be correlated with CVD.
I’m thinking if the endothelium is fragile as e.g. with vit C deficiency, there must be more endothelial cells than usual torn off the artery walls and floating loose in the bloodstream. Perhaps there is a simple method of identifying and counting them, and comparing with baseline measurements.
Indeed! People need to wake up. Something to add to the point made here: https://healthfully.wordpress.com/2013/05/05/at-the-heart-of-heart-disease/
Thank you for the link, it seems to be useful guide lines which should be easy to follow.
And here’s a prescription that I think most of us could approve of – http://www.lincolnshirelive.co.uk/pensioners-should-be-prescribed-dogs-to-keep-fit-according-to-latest-study/story-30383523-detail/story.html
That might be a personal benefit to some pensioners, but to others it will be a large outgoing for the dog’s upkeep, and for the rest of the community it will be an ecological load. The study is possibly as scientific as the studies which recommend such things as, er statins. As a general policy it’s not one that I would support.
Interesting new method—to map composition of arterial plaques
A new study shows that a hybrid molecular imaging system unites three imaging modalities to map the composition of dangerous arterial plaques before they rupture and induce a major cardiac event. The research was presented at the 2017 Annual Meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI).
Certain types of plaques associated with atherosclerosis are prone to instability and tend to break apart, which can lead to embolism and sudden death, if left untreated. Lesions called thin-cap fibro atheroma (TCFA) are especially prone to rupture. Stanford University researchers have developed a scanner that unites optical, radioluminescence, and photoacoustic imaging to evaluate for TCFA.
“This is the first clinical imaging system able to detect vulnerable plaque in their earliest stages,” said Raiyan T. Zaman, PhD, instructor of cardiovascular medicine at Stanford University School of Medicine in Stanford, Calif. “Our novel imaging system can detect these vulnerable plaques despite their small size, complex biochemistry and morphology. This could lead to a paradigm shift in the way coronary artery disease is diagnosed and assessed.”
Early diagnosis and treatment could save lives by preventing the progression, and subsequent rupture, of these plaques. That is precisely why researchers designed the Circumferential-Intravascular-Radioluminescence-Photoacoustic-Imaging (CIRPI) system, which allows not just high-acuity optical imaging via beta-sensitive probe, but also radioluminescent marking inside the artery to determine the extent of inflammation. Photoacoustic imaging also provides information about the often-complex biological makeup of the plaques (how much is calcified or comprised of cholesterol or triglycerides).
“This is an important and potentially life-saving tool that could one day be used by interventional cardiologists to identify the appropriate treatment plan for patients at risk of future TCFA rupture,” explained Zaman.
For this study, researchers focused on atherosclerotic samples of both human and mouse carotid arteries and performed CIRPI following injection of fluorine-18 fluorodeoxyglucose (18F-FDG). Photoacoustic lasers were used at different wavelengths to delineate plaque composition. The result was a never-before-seen 360-degree perspective of arterial plaque burden, confirmed effective by follow-up radiography, ultrasound and histology.
According to 2017 statistics from the American Heart Association, cardiovascular disease, including but not limited to coronary artery disease, accounted for more than 17.3 million deaths worldwide in 2013 — making it the leading global cause of death. The toll is expected to rise to 23.6 million by 2030. Coronary heart disease is estimated to cost an average of $10.4 billion annually. This amount is expected to increase by 100 percent from 2013 to 2030.
Story Source:
Materials provided by Society of Nuclear Medicine. Note: Content may be edited for style and length.
Sounds like someone is planning to make lots and lots of money. Be interesting to look at funding sources.
eat real food and move—-exercise
http://www.huffingtonpost.com/entry/japan-healthiest-people-in-the-world-carbs-high-grain-diet_us_56f08cc4e4b084c6722139ca
Interesting. Here I must keep a lid on my confirmation bias, BUT, a couple of points – the Japanese people, I believe, consume very little sugar whereas we in the West consume mountains of the stuff and the Japanese culture for the most part is very cohesive and stable with a pure bloodline, unlike ours which is a total mishmash dating back centuries and becoming ever more diffused. The Japanese man or woman fundamentally knows what it is to be Japanese whereas I who am English live in an extremely multicultural society and that very basic psychological certainty is not available to me. And of course the same applies to those who are not ‘English’ or Scots or Welsh by birth and find themselves uprooted for whatever reason and living in a foreign, to them, culture.
And please, for anyone inclined to interpret this as a racist rant, that is ABSOLUTELY NOT my intention but just to point out that multiculturalism has its cost for all concerned, whatever the benefits (many) accrued. And I speak from experience since almost fifty years ago I moved from the Midlands to Cornwall and it was like moving to a foreign country – very stressful but ultimately with wonderful benefits.
What about the fact that Jap’s who migrate to say the USA for a ‘better life’ come down with the same rates of HD as the Americans within a few years. This suggests that any genetic factors associated with race is not really offering any protection.
I wasn’t exactly suggesting that there was a genetic component. Rather that Japanese society being more cohesive than ours might lead to a less stressful way of life, more of a feeling of belonging. Dr. K has pointed out that those who migrate suffer inordinate amounts of stress which may contribute to an increase in CVD. It’s all very worrying as the world seems to be on the move and there are countless unhappy and displaced people out there.
smartersig: Her point was that social factors, not genetic factors, play a positive role in the Japanese population.
smartersig, it’s supposedly the Japanese who continue to follow their old way of life while in the US who do not get high rates of HD. This suggests it’s the way of life and not food.
I personally think it’s both. Stress of the kind we put on ourselves in the US is very, very bad. I’m going to get about 2 weeks of vacation this year, which will be split into two time periods about or less than a week long. We have a friend in Sweden. His vacation? 9 weeks. Continuous. Who will be more stress this year, me or him? (I’ll give you hint — it’s me.) And how does that affect heart disease? Considering I developed idiopathic dilated cardiomyopthy due to an incredibly stressful period in my life, I’d say stress kills.
On the other hand, sugar and carbs are bad unless you’re genetically predisposed to do well with them. If you do research on idiopathic dilated cardiomyopthy, what’s one possible cause (or exacerbation)? Insulin resistance.
Combine high insulin resistance with stress of the kind we force on ourselves in the US, and it’s a bad situation.
I would imagine that ‘way of life’ also incorporates food
JanB: Very good sociological point. The upside of the social cohesion is good health and longevity, the downside being excessive conformity.
An interesting study on the issue of culture on health . . .
ACCULTURATION AND CORONARY HEART DISEASE IN JAPANESE-AMERICANS
Michael Marmot et all Journal of Epidemiology 1976
Notes made on reading the paper
They studied Japanese in Japan, Hawaii and California.
Wanted to see if Japanese moving to the US had any changes in the notoriously low CHD rates.
Any changes might be put down to the US diet – in particular they looked at the amount of fat – Again very low in Japan.
They measure how Americanised they had become, or felt they had become – This did not necessarily mean they Americanised = US diet
However, among men eating equivalent diets in Japan, Hawaii and California, it was the Californian-Japanese that had higher serum cholesterol.
Those who adhered to Japanese traditions after migration kept their low risk of CHD independently of what they ate. In fact, migrants, who were brought up in a non-traditional fashion but preferred the lean Japanese food had almost twice as much CHD than those who were brought up traditionally but preferred American food.
Yes, a very interesting study that fell upon deaf ears.
I have difficulty believing that study. I live in Hawaii and the Hawaiian Japanese I see who eat standard American diet are usually quite unhealthy. Besides, what’s “traditional culture” if not food? Participating in Bon dances? Food has always been a huge part of any culture.
Antony,
Similar to the Roseto Effect, as reported on by Malcolm Gladwell. Citizens of Roseto in Italy moved to America and built a town they also called Roseto.
After eliminating diet, exercise, and genetics as causative factors, Wolf was forced to conclude it was the close social relationships that the Rosetans had replicated in America that led to their good health.
Hi Sasha
I was married to a Japanese women for 5 years. If I compared my Japanese friends with Western friends the fact that there were cultural differences was clear, although it is difficult to characterise exactly what these differences were. So, giving it a try: there was something chaotic about the lives and relationships of my western friends when compared to my Japanese friends. Even the Japanese friends who were rebelling against the conventional Japanese expectations (women knowing their place – next stop was marriage – hide your mouth when smiling/laughing. . . young men who wanted to belong to the rock culture and did not relish the idea of joining the business treadmill) . . . yet when they got together they all seem to be singing from the same Japanese song sheet (They all got very edgy if you criticised Japan) The food they ate was traditional and eaten together . . . their expectations in what they would be presented with on these occasions seemed to be met. Yes, food is part of the culture, but that includes the way food is taken – taken together – It was like an extended family. We even had the calm of tea ceremonies (in Somerset!).
I knew what to expect, I knew how to behave and I knew how they would behave. With my dealings with English people there was never the same clarity.
As pointed out, the social cohesion – including the strength of family ties – with people knowing where they stand – has a significantly positive health benefit in general, but as Gary points out it demand a level of conformity that is uncomfortable for most of us.
All the above was happening in the mid-1970s . . . so the Marmot paper was smack bang in the middle of my experience. What was surprising in the paper was the conclusion that, even among those Japanese (Hawaiian or Californian) who adopted the US diet, those that said they maintained a Japanese way of life within the home and in their outlook had lower CVD rates.
Antony, I agree with you completely that social interactions are a big part of culture and that they have a huge effect on peoples health. But that’s quite a different statement from the claim made by the study you linked. Your original post said that the study showed that men who were brought up traditionally and ate American food had half the rates of CHD than those who preferred Japanese food but were brought up non traditionally. It’s that claim that I very much doubt.
To begin with – what is that “American food” they were eating? Unlike traditional societies which have limited food choices that don’t change much over decades or even centuries, Western societies have virtually unlimited selection of things one can eat. So I would think that there was quite a number of things people on American diet were eating. How can they all be lumped together to extrapolate results?
Also, as anyone who had a traditional grandmother can attest, it’s impossible to separate being “brought up” from what you eat. So where did they find these study participants who were brought up traditionally while consistently eating non traditional things? I would think they all had regular exposure to traditional diet if they were brought up traditionally.
The study basically makes this yogic claim that mind is primary and it takes precedence over what you eat. I would think that the study you mention has too many variables to make a claim that strong.
“Although the prevalence of obesity [body mass index (BMI; in kg/m2) .30] in the Japanese is lower than in Westerners (Japan: 3% in both men and women; United States: 31% in men and 33% in women) (3), the prev- alence of type 2 diabetes in Japanese populations is not dra- matically lower than that in Western populations (Japan: 7.3%; United Kingdom: 4.9%; United States: 12.3%)”
Conclusion: Eating a low fat and high carb diet combined with exercise will result in skinny type 2 diabetics.
And what about a skinny type 2 of 60 years duration following a HFLC eating pattern – namely me. I’m confused. I’m from a thin family where diabetes, both insulin dependant and not, runs like a river through and across the generations. When I was diagnosed at 15, the same age as my brother though 7 years later, I was as my mother would say, “thin as a match with the wood scraped off.” My brother was the same though he also had the added complication of TB. I just don’t understand anymore. Insulin resistant, as my DN insists or not? I have a waist measurement of 25 inches so I’m hardly storing visceral fat.
P.s. I’m very active – 15 to 25 steps most days.
P.p.s I eat a lot of fat and have a fantastic immune system.
Anyone?????
Click to access DiabetesUK_Facts_Stats_Oct16.pdf
2015 pop. of the UK 65.14 million
diagnosed type II—3,453,034
estimated undiagnosed 1,100,000
total 4,553,034
% of total pop. .06989—-7%
In my post the other day, I said that I’m very active – up to 25 steps a day. What an idiot! I should of course said 25 THOUSAND steps. That’s what comes of replying whilst eating breakfast.
JanB, this article by Chris Kresser might throw some light on your condiition “What causes high blood sugar and T2DM in lean people?
Not surprisingly, the causes of T2DM in lean people are similar to the causes of T2DM in the obese. They can be loosely grouped into the following categories:
Genetics
Fatty liver
Inflammation
Autoimmunity
Stress”
Thank you, Andy – I’ll see if I can find him on YouTube or Google. I think that genetics play a major role in my case. I certainly don’t have a fatty liver though I do have some psoriasis and wonder if that would count as “inflammation.” I was told by a couple of endocrinologists some years ago that I was “mody” but that theory has been thrown out by my DN who insists that I am insulin resistant, even though the only possible symptom I have is increased blood glucose levels – all kept VERY firmly under control by HFLC which works very well for me…though I am “as fat as a stick with the wood scraped off.”
Just wondering if anyone else here has similar problems….also wondering if it would be worthwhile to pay for an insulin assay.
One thing I’m starting to get interested in with DM Type 11 is that there seem to be two subgroups with, apparently, little or nothing in common: those deficient in insulin (seems more like Type 1 to me), and those with a surfeil of insulin but with insulin resistance. All are diagnosed by high fasting glucose levels/failing glucose tolerance test, or just by elevated HbA1C these days. All are (allopathically) treated with drugs to increase insulin secretion, and then if that doesn’t work insulin itself injected. There seem to be many questions one could usefully ask, such as what the hell sort of disease encompasses such diametrical diversity? Or why would you treat someone with insulin resistance and (presumably) consequent elevated insulin levels by… increasing their insulin levels? Is it actually the elevated sugar levels that cause damage to epithelium and thus organs? Or is it elevated insulin levels? Or something else entirely? And why don’t we routinely measure insulin levels, rather than just glucose? Does someone rail thin with elevated glucose levels actually have the same disease as someone morbidly obese with the same levels?
I have the nagging suspicion that answering questions like these will open the way to understanding a whole lot of things we don’t understand now, big things, like heart disease genesis and maybe cancer genesis and treatment.
You may find some interesting stuff if you dig around here
http://www.diabetesgenes.org/
There are actually a whole bunch of different conditions grouped under the title of “Type 2” diabetes. What I have is shared by a small but significant number of others all over the world. It is characterised by symptoms of diabetes beginning in early childhood and including symptoms of reactive hypoglycemia, followed by a slow progression and normal or even low body weight. Only about half the people I know have gone on to be DIAGNOSED diabetic – which is supposedly set where at least 50% of the beta cells are deceased. The others, like me, remain “prediabetic”. It’s similar to one of the MODYs but not monogenic, the familial distribution is wrong.
In my family it predominantly affects males, someone else has it mostly in females and in others it is more equally divided between the sexes, or I should say among the genders. One believed as a child that old people shed limbs in the same way that trees lose their leaves in autumn, that’s how common it was in her family.
The mechanism appears to be a failure to produce, or store, or release, Phase 1 insulin, but Phase 2 insulin remains intact for a long time. Or if you believe Roger Unger the insulin fails to shut down postprandial glucagon. Either way, glucose spikes after eating too many carbs – where too many is a fraction of what dieticians claim is essential – then the insulin turns up late to the party and stays after all the glucose has gone home, driving BG low and causing a panic reaction where the alpha cells dump a load of glucagon and the rest of the endocrine system joins in, producing cortisol, epinephrine, norepinephrine, neuropeptide Y etc. to get the BG back up, and induce carb cravings. Rinse and repeat.
Unlike “genuine” MODY insulin resistance is also a major factor. Sound familiar? The usually suggested treatment is to eat carbs every couple of hours, The treatment that actually works is to reduce carbs until the BG no longer spikes, then the insulin no longer spikes, then the IR comes down, and let your body run predominantly on fats and ketones.
Does any of this sound familiar at all?
If not, don’t worry, there are a whole bunch of other variants, none of them fitting the usual explanation that diabetes is caused by being fat and lazy and being fat is caused by eating fat and meat.
TYPE 1 AND TYPE 2
For all adults and children, we estimate that:
• 10 per cent of people with diabetes have
Type 1 diabetes.
• 90 per cent of people with diabetes have
Type 2 diabetes8,9.
Slightly more men than women have been
diagnosed with diabetes. Audits suggest that about
56 per cent of all adults with diabetes in the UK are
men and 44 per cent are women8,9.
Distribution of diabetes by age group in England
and Wales8
and Scotland9
.
Age, E&W, Scotland
0 – 9 0.21% 0.25%
10 – 19 0.94% 1.18%
20 – 29 1.69% 2.06%
30 – 39 3.76% 3.53%
40 – 49 10.67% 9.5%
50 – 59 19.3% 19.09%
60 – 69 26.2% 26.46%
70 – 79 23.92% 24.55%
80+ 13.3% 13.38%
http://www.telegraph.co.uk/news/2017/06/13/daily-aspirin-behind-3000-deaths-year-study-suggests/
Aspirin was just one of the drugs I was subscribed almost 20 years ago but refused to take among the others.
Instead I am now I am sipping my 15 grams of vitamin C every day together with 2400 IU vitamin E and some other vitamins. May be a waste of money but I feel nevertheless swell.
I too take plenty of Vit C, though not 15g a day. I started about 50 years ago when one of my students asked if I had read the Linus Pauling book – I had a ‘cold’ at the time. He lent me a copy. I did not find it cured the ‘cold’ but it has been spectacular in healing injury. After a burn (as one gets sometimes cooking) I take 2g Vit C, the pain goes in minutes and at worst there is damaged but tough skin and no soreness. The only analgesic I have used, and that very rarely is aspirin. There is an article on stress & inflammation in the New Scientist this week (17/6/17) in which it suggests that stress does not merely fade away when the stressor is removed, but that there is an off-switch, and aspirin can stimulate the chemicals that do the off.
I have been taking Vit C for 4 years in the form of a Pink Grapfuit in the morning along with Kiwi Fruit in my porridge and 500mg of Vit C supp’. One thing I have noticed is that before adopting this ritual I used to get occasional gum bleed when tooth brushing. Nothing major but enough to notice. I now never get any bleed at all, I cannot remember that last time I spat in the sink after brushing and witnessed blood
Alas, the comment in The Times article today was to keep on taking the aspirin, and to add a Proton Pump Inhibitor. Talk about poly pharmacy, the lessening of stomach acid affects the ability of the microbiome to fully digest food, and there are serious questions about the effect of long term PPIs on osteoporosis.
On taking aspirin . . . I groan when it is suggested in the study that you can keep on taking aspirin provided you have something to reduce the likelihood of bleeding (proton pump inhibitor – not without its own problems) . . . Do you have to take something to reduce adverse effects of proton pump inhibitors? . . . and then do I have to take something else . . . etc. It is a bit like the song about an old woman who swallowed a dog. . . “she swallowed a dog to catch the cat .. . she swallowed that cat to catch the bird . . . she swallowed the bird to catch . . . etc. (Just reread this section and realised I had forgotten about the end . . . “I don’t know why she swallowed a fly; I guess she died”.
I would like to ask the doctor . . . what is it that I am doing wrong that I need to take an aspirin?
(Is there a fantasy land somewhere where realistic answers might be given?)
Manipulating your surrogate biomarkers won’t necessarily improve your clinical endpoints.
HDL, greatly increased with experimental drugs improves . . . nothing whatsoever.
pdf link:
https://t.co/3PwWd5YDnL
Just ran across an interesting article about inflammation. It agrees with Dr K that inflammation is good at first but the problem is it doesn’t get turned off when it should. From the article:
“One clue came in 2000 when [Charles] Serhan and his team revealed that inflammation has an off switch. Until then, the reaction was thought to peter out as the immune cells that secrete cytokines gradually reduced in number and their effects became diluted. In fact, Serhan found that neutrophils and macrophages, the types of white blood cell that kick off the process, actively change tack once it has got going, releasing a second set of chemicals – called resolvins – that help mop up any remaining cytokines and sweep away any debris.
This made Serhan and others wonder whether chronic inflammation might be caused not by the on signals being turned up too high, but by a problem with the off switch. In the years since, he has been studying resolvins and related chemicals to see if there is a way to harness or mimic their actions.”
The article is called “How to extinguish the inflammation epidemic” but unfortunately I can’t find a version that doesn’t require a paid subscription.
Eliot: A very interesting pilot study was just completed at UC San Diego using suramin, an African sleeping sickness drug, to turn off the cell danger signal in autistic children. Only 5 were enrolled, but the results were very promising. It is a form of neuro-inflammation which results in autism. Two of the children (a five- and an eight-year-old) spoke for the first time.
Are Danes and Koreans really THIS different from each other??
https://www.ncbi.nlm.nih.gov/pubmed/28521886?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/28588091?dopt=Abstract
Who’s right?
Who’s wrong?
Ditching butter and other saturated fat and eating margarine and vegetable oil instead cuts the risk of heart disease as much as statins, health officials said.
An official advisory by the American Heart Association, issued to cardiologists around the world, said consuming the polyunsaturated fat in ‘healthy’ spreads and oils could cut the risk of cardiovascular disease by 30 per cent – the same benefit as seen from taking cholesterol pills.
Read more: http://www.dailymail.co.uk/health/article-4607854/Why-switch-butter-margarine.html
I think you’ll love this :))
I wouldn’t waste effort posting anything about reports from the AHA or any other US body for that matter. Or any report from the Daily Mail. In 2015 the US dietary guidance committee said cholesterol was no longer a nutrient of concern. This was followed quite soon by a statement from the chairman of the committee saying the scientists had made an error, and cholesterol was still a demon. I wonder who paid him off.
From the article:
“His team wrote: ‘Randomized controlled trials that lowered intake of dietary saturated fat and replaced it with polyunsaturated vegetable oil reduced cardiovascular disease by approximately 30 per cent –similar to that achieved by cholesterol-lowering drugs, known as statins.'”
So they are talking about relative risk if it is the same as statins.
An update: Went to the sawbones yesterday. BP was 142/86 (without any drugs). It was taken, as usual, with my legs and arms dangling, and immediately following a perfectly amiable chat with the nurse. I mention these because they are all said to raise BP. My doctor said I was at the upper range of normal and wasn’t the least bit alarmed (nor am I). We talked about the K supplement I’m now taking, and she had some concern, but no alarm (she says kidney problems are common). She wants a kidney function test in December (these have always been normal, the most recent two years ago). I am lucky and blessed to have a real doctor (27 years now).
Does K supplements cause kidney problems?
This was just published by the AHA June 15, 2017
Comments??
http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510
It appears that the AHA is a propaganda tool for for the drug companies and the food industry.
“The financial ties between large pharmaceutical companies and the AHA are numerous and very remunerative for the AHA, including huge donations from Abbott, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb (BMS), Eli Lilly, Merck and Pfizer.
The AHA also rakes in millions from food companies which are also million dollar donors and which pay from $5,490 to $7,500 per product to gain the “heart-check mark” imprimatur from the AHA, renewable, at a price, every year.”
http://www.medscape.com/viewarticle/881689
some of the responses are very incisive, and entertaining as hell.
One word suffices: Rubbish.
David Tepper,
Here is a comment: https://theskepticalcardiologist.com/2017/06/18/beware-of-more-misinformation-from-the-american-heart-association-on-coconut-oil-and-saturated-fats/
Phil
Nutrigenomics:
A recently published Cornell University study describes how shifts in the diets of Europeans after the introduction of farming 10,000 years ago led to genetic adaptations that favored the dietary trends of the time.
Before the Neolithic revolution that began around 10,000 years ago, European populations were hunter-gatherers that ate animal-based diets and some seafood. But after the advent of farming in southern Europe around 8,000 years ago, European farmers switched to primarily plant-heavy diets.
The study — the first to separate and compare adaptations that occurred before and after the Neolithic Revolution — reveals that these dietary practices are reflected in the genes of Europeans.
“The study shows what a striking role diet has played in the evolution of human populations,” said Alon Keinan, associate professor of computational and population genomics and the paper’s senior author. Kaixiong Ye, a postdoctoral researcher in Keinan’s lab, is the paper’s lead author.
The study has implications for the growing field of nutritional genomics, called nutrigenomics. Based on one’s ancestry, clinicians may one day tailor each person’s diet to her or his genome to improve health and prevent disease.
The study shows that vegetarian diets of European farmers led to an increased frequency of an allele that encodes cells to produce enzymes that helped farmers metabolize plants. Frequency increased as a result of natural selection, where vegetarian farmers with this allele had health advantages that allowed them to have more children, passing down this genetic variant to their offspring.
The FADS1 gene found in these vegetarian farmers produces enzymes that play a vital role in the biosynthesis of omega-3 and omega-6 long-chain polyunsaturated fatty acids (LCPUFA). These LCPUFAs are crucial for proper human brain development, controlling inflammation and immune response. While omega-3 and omega-6 LCPUFA can be obtained directly from animal-based diets, they are absent from plant-based diets. Vegetarians require FADS1 enzymes to biosynthesize LCPUFA from short-chain fatty acids found in plants (roots, vegetables and seeds).
Analysis of ancient DNA revealed that prior to humans’ farming, the animal-based diets of European hunter-gatherers predominantly favored the opposite version of the same gene, which limits the activity of FADS1 enzymes and is better suited for people with meat and seafood-based diets.
Analysis of the frequencies of these alleles in Europeans showed that the prevalence of the allele for plant-based diets decreased in Europeans until the Neolithic revolution, after which it rose sharply. Concurrently, the opposite version of the same gene found in hunter-gatherers increased until the advent of farming, after which it declined sharply.
The researchers also found a gradient in the frequencies of these alleles from north to south since the Neolithic Era, including modern-day populations. All farmers relied heavily on plant-based diets, but that reliance was stronger in the south, as compared to northern Europeans — whose farmer ancestors drank more milk and included seafood in their diet.
Plant-based alleles regulate cholesterol levels and have been associated with risk of many diseases, including inflammatory bowel disease, cardiovascular disease, arthritis and bipolar disorder.
“I want to know how different individuals respond differently to the same diet,” Ye said. Future studies will investigate additional links between genetic variation, diets and health, so that “in the future, we can provide dietary recommendations that are personalized to one’s genetic background,” he added.
Story Source:
Materials provided by Cornell University. Original written by Joe Schwartz. Note: Content may be edited for style and length.
Journal Reference:
Kaixiong Ye, Feng Gao, David Wang, Ofer Bar-Yosef, Alon Keinan. Dietary adaptation of FADS genes in Europe varied across time and geography. Nature Ecology & Evolution, 2017; 1: 0167 DOI: 10.1038/s41559-017-0167
If you are adapted to eat something, should you eat more of it or less of it? For instance, modern Americans are clearly adapted to consume fast foods, but maybe they should cut the quantity thereof.
In the past our foraging ancestors consumed a wide variety of foods. “In Australia, Aborigines are known to have eaten some 300 different species of fruit, 150 varieties of roots and tubers and a dizzying number of nuts, seeds and vegetables” — http://www.nature.com/ejcn/journal/v61/n1/full/1602486a.html What is seldom mentioned is that the food was probably none to clean when consumed.
The most likely place to find a microbe that eats a particular food is on the food. So by eating unwashed fruits and vegetables, our ancestors were at the same time ingesting the beneficial bacteria that helped to digest said food. Our gut bacterial population can evolve far quicker than our genes, but no studies have been done on ancestral gut bacteria, AFAIK. What we can be certain of is that modern processed foods have far fewer of the specialist food-eating bacteria. So our colons are not renewing their bacterial populations to evolve along with our foods.
Which is probably why sweet and carb-y foods have become popular. The simple sugars are absorbed in the small intestine, while the more difficult fibrous material which needs specialist gut bacteria in the colon to digest is avoided.
There’s a nice, if somewhat veg-centric, discussion of human gut evolution here: https://blogs.scientificamerican.com/guest-blog/human-ancestors-were-nearly-all-vegetarians/
I doubt modern Americans are adapted to eat fast foods. I don’t think human body is capable of such an adaptation. As the satirical weekly The Onion once put it: “McDonald’s stock plunges as more Americans turn to food.”
It’s also unclear whether bacteria that lives on unclean food can survive the acidity of the human stomach or the chewing and salivary processes and just migrate to our small intestine…
Sasha: I don’t have a reference, but as I understand it, some microbes indeed do make it through the stomach to the intestines. Otherwise, how could a newborn be inoculated with the microbes from the birth canal and mother’s skin at nursing?
Gary: good point, I didn’t think about that. Even though I thought that birth canal bacteria innoculates primarily the nasopharyngeal passages of a newborn but I may be wrong.
Here we go again http://www.bbc.co.uk/news/health-40300145
All these studies link saturated fat to increased LDL and in turn cite LDL as the main indpendant risk factor for HD but we know this is not true. LDL is not, by a long way, the most relevant risk factor for HD
They must have ignored the Minnesota Coronary Experiment (MCE), that was done by a colleague of Ancel Keys. It showed that unsaturated fat did indeed lower cholesterol. It also increased risk of death. The results were not published at the time (I wonder why).
http://www.bmj.com/content/353/bmj.i1246
“Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol …”
Thank goodness for that, as long as the the sat fats are all as bad as each other, I can eat any of them.
Martin K: More rubbish.
Gary Ogden: Isn’t it just
Cholestrophobes vs. Cholestrophiles: the battle continues.
CBC Canada documentary – on why Okinawa Japan people live so long concluded it’s Anthocyanin from the large amount of purple sweet potatoes they eat. Just so happens it is in my Bilberry extract.
I thought I was acquainted with most ideas and medical treatments associated with MI but the one I now read about in a new paper in Science Advances is revolutionary to say the least.
http://advances.sciencemag.org/content/3/6/e1603078.full
The new to me is about using cyanobacteria and photon therapy to enhance oxidation ot the ischemic parts of the heart.
Again – how little we know!
This is for the case where the heart muscle isn’t getting enough blood delivering oxygen and glucose. So how will they deliver the bacteria? If they can simply inject bacteria, why not just inject blood instead? They say this is only envisioned for the acute phase i.e. the first few hours of an MI, not long-term therapy, and anyway the bacteria are cleared by the body after 24 hours.
It’s interesting, and who knows where the research will lead, but if you have a heart attack, I don’t think they’ll reach for the laser for a while yet.
Just discovered why eating greens and exposure to sunlight are beneficial.
“The researchers, working out of Columbia University Medical Center, conducted a number of experiments in order to ascertain whether animals as well as plants can use light-absorbing chlorophyll molecules to capture light energy for ATP synthesis.
While it has been prevailing wisdom that only plants can use sunlight directly for producing energy (photosynthesis), it can not be denied that not only do many animals consume chlorophyll through their diet but that research has been performed showing chlorophyll metabolites “retain the ability to absorb light in the visible spectrum at wavelengths that can penetrate into animal tissues.” (Ferruzzi and Blakeslee, 2007; Ma and Dolphin, 1999). Given these facts, the authors of the new study “sought to elucidate the consequences of light absorption by these potential dietary metabolites.” What they discovered was simply remarkable:
We show that dietary metabolites of chlorophyll can enter the circulation, are present in tissues, and can be enriched in the mitochondria. When incubated with a light-capturing metabolite of chlorophyll, isolated mammalian mitochondria and animal-derived tissues, have higher concentrations of ATP when exposed to light, compared with animal tissues not mixed with the metabolite. We demonstrate that the same metabolite increases ATP concentrations, and extends the median life span of Caenorhabditis elegans [worm], upon light exposure; supporting the hypothesis that photonic energy capture through dietary-derived metabolites may be an important means of energy regulation in animals. The presented data are consistent with the hypothesis that metabolites of dietary chlorophyll modulate mitochondrial ATP stores by catalyzing the reduction of coenzyme Q. These findings have implications for our understanding of aging, normal cell function and life on earth.”
Andy S: Wow. Fascinating work. We are plants, after all (with the advantage of mobility), and eating them is probably a good idea.
Andy S. Thanks for your contribution, although I found the explanation a little hard going. BUT..it seems to back up my current dietary theme. These days I ensure I have a continuous supply of organic sprouted micro greens in my kitchen, and eaten raw, or lightly steamed, on a daily basis. I have dabbled in sprouting seeds over many years, however, after having read round the subject in more depth, I believe it is essential to eat greens ( chlorophyll) regularly, and also to get out into the sunshine as much as possible.
Please continue contributing your ‘scientific-type’ reports, because the “need to know why” population can certainly glean a lot of good stuff, thus reinforcing the message …..”eat your greens, and enjoy the sunshine”, …..just like our great-grannies taught us.
Meat and greens, my favourite! Yum!
Dr Goran,
Just for clarity, I believe you meant “oxygenation”, yes?
Official medicine operates on a consensus given by the “elites”. They think about what is the best drugs to give to their victims, oops i mean patients, and spread the word to the whole medical community. This is not science based at all. It is largely subjective, and largely financed by pharmaceutical companies.
What astonishes me about inflammation is, that it is not recognized for what it is by every single doctor out there; the starting process of healing. What is worse, the ability of the human body to heal itself, use millennia old mechanisms to repair ( via cholesterol ) is sent into oblivion.
Is this the rhetoric that has to be used in order to sell (dangerous) drugs to the population ?
________________________
What would be a good idea, i think, doctor on your blog is, what is everyone thoughts here, about what causes heart problems. -Part XYZ-
Gaetan: I cringe whenever I hear the word “consensus,” a political term, used in the context of any scientific endeavor. Here is Micheal Crichton’s view, without equivocation:
https://www.ncbi.nih.gov/pmc/articles/PMC2719747/
Pharma has gotten its filthy little fingers into every aspect of medicine. Academia shares some of the blame for the mess we’re in, with its warped incentive systems, and funding sources (such as NIH), with their own set of biases and vast resources taken out of the pockets of working folks, even greater blame.
I read Michael Crichton’s Jurassic Park a long time ago 🙂 The movie was great but the book even better!
When we see the vast amount of cash at Big Pharma’s disposal, and when we consider how short our lifespan is, many human beings unfortunately, are tempted to accept their bribes and abide by the consensus. Yeah consensus should never be part of science or medicine but a big problem medicine face is; They don’t know often how to heal people. For example, what is the best thing to do versus cancer? they don’t know, so they go with the consensus, chemotherapy…
Why is it the consensus, my guess is, follow the money as usual…
AHA??
Gary Taubes speaks out:
http://www.cardiobrief.org/2017/06/16/guest-post-vegetable-oils-francis-bacon-bing-crosby-and-the-american-heart-association/
JD
Thanks for the link!
Gary Taubes is to me always great reading and this late one I find one of the better when he is now using his broad science methodological brush.
http://www.thefatemperor.com/blog/2017/6/14/denvers-diet-doctor-gets-published-insulin-and-crp-revelations-
Well lookie here, what have we got? Looks like the inflammatory marker of CRP is intimately related to elevated Insulin. Can’t say I’m surprised – but super job to Dr. June S Yang and Dr. Jeffry Gerber to extract the reality from the data. But what about the amazing LDL? Surely it too correlated with CRP? Given the enormous focus on LDL for several decades?
Eh, no. As usual when you look closely…LDL sneaks away in shame.
This is a very well-written and accessible paper, with very significant implications indeed. Please share it far and wide ! Link to full paper below:
http://BMJOPENSEM.BMJ.COM/CONTENT/3/1/E000236
Concentrated broccoli sprout extract may help type 2 diabetes patients manage their blood sugar, according to a new study.
The findings could offer a much needed alternative to address the condition, which has become a worldwide epidemic.
Type 2 diabetes afflicts more than 300 million people globally, and as many as 15% of those patients cannot take the first-line therapy metformin because of kidney damage risks. Seeking a more viable path forward, Annika Axelsson and colleagues used a computational approach to identify compounds that might counter the disease-associated gene expression changes associated with type 2 diabetes.
The researchers constructed a signature for type 2 diabetes based on 50 genes, then used publically available expression datasets to screen 3,852 compounds for drugs that potentially reverse disease. The most promising chemical — sulforaphane, a naturally occurring compound found in cruciferous vegetables — tamped down glucose production by liver cells growing in culture, and shifted liver gene expression away from a diseased state in diabetic rats.
When the researchers gave concentrated broccoli sprout extracts to 97 human type 2 diabetes patients in a 12-week randomized placebo-controlled trial, obese participants who entered the study with dysregulated disease demonstrated significantly decreased fasting blood glucose levels compared to controls.
The authors say developing gene signatures to investigate large public repositories of gene expression data could be a valuable strategy to rapidly identify clinically relevant compounds.
Story Source:
Materials provided by American Association for the Advancement of Science. Note: Content may be edited for style and length.
Journal Reference:
Annika S. Axelsson et al. Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. Science Translational Medicine, 2017 DOI: 10.1126/scitranslmed.aah4477
Thank you Dr Kendrick for unravelling all these things for us I also find many of the comments quite thought provoking. I am interested also on the number of us who are looking for alternatives to drugs to heal what’s wrong with us, I had wonderful results using curcurmin I injured myself (manual handling injury) while weeding thought I could pull the big weed out to my left without addressing it and felt immediate agony. This continued for over 15ths as I have significant scoliosis I have a short leg nearly 1 inch so it played up as well my Dr. sent me for an ultrasound and steroid injection which brought it down to about 8out of 10 and the next step would have been surgery. In the interim I read an article on turmeric used as a natural anti-inflammatory I cannot take the others make me sick and I used ibuprofen which being over 68 is not recommended. I hobbled to the vitamin store where they have a naturopath and she recommended a high dose of cumerone in tablet form and to take two per day amazingly within 2 weeks the pain had subsided down to about 2-3 and at that point I was able to go back to walking every day and joined the gym and regularly applying weight training under supervision the problem has all but disappeared. I thought my Dr. would be happy for me but, not so I walked in not limping or hobbling and showed him the bottle well he looked at me as if the only thing missing was the broomstick, hat & black cat & said nothing took his forefinger and pushed it back to me I was so disappointed this was the man who had been so helpful to me with other things and had once been heard to use the word science when explaining something to me in the past. I guess this comes down to the rigid training for allopathic doctors and for them here in Australia no deviation is tolerated at all a dim view is taken of any natural therapies, changes of thought regarding diet etc. is very much discouraged even people reading blogs, or consulting health web sites have been covered by the AMA with public announcements in the Media stating that nothing good can be found there apparently we are a stupid lot who are unable to make out own decisions.
Well I am in my 71st year and as a human being with the ability to think and the gift of free will I have the responsibility to myself to stay as fit & healthy as possible I still have 20hours paid work per week and currently take no medication apart from vitamins etc.
Today Joe Mercola placed a tribute for Dr Fred Kummerow who won a case in 2015 against the FDA when he was 99years old to have trans fats banned. He died on 2/6/2017 at the age of 102yrs and interestingly he stated when asked what he ate he included meat and liked scrambled eggs fried in butter he discovered the trans fat in arteries of both humans and pigs during his work in the 1950’s he disagreed with all the cholesterol theory’s and was considered to have suffered with a problem of contraryism he was much maligned and I guess had he been an MD he would have possibly been de-registered,
http://articles.mercola.com/sites/articles/archive/2017/06/19/trans-fat-toxicity-scientist-fred-kummerow-dies.aspx?
SUN EXPOSURE AND INFLAMMATION CONNECTION:
“Mucosal Inflammation Research Group, Department of Pharmacology and Therapeutics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada
abstract
Nitric oxide (NO) plays an important role in mediating many aspects of inflammatory responses. NO is an effector molecule of cellular injury, and can act as an anti-oxidant. It can modulate the release of various inflammatory mediators from a wide range of cells participating in inflammatory responses (e.g., leukocytes, macrophages, mast cells, endothelial cells, and platelets). It can modulate blood flow, adhesion of leukocytes to the vascular endothelium and the activity of numerous enzymes, all of which can have an impact on inflammatory responses. In recent years, NO-releasing drugs have been developed, usually as derivatives of other drugs, which exhibit very powerful anti-inflammatory effects.”
ALSO FOUND THIS:
“The most recent discoveries on sunlight point to its ability to improve the human cardiovascular system. Sunlight tells our bodies to produce more nitric oxide, prompting increased relaxation of blood vessels, promising protection throughout the entire cardiovascular system. This also translates to increased production of serotonin, leading to better mental health.
In his studies, Dr. Richard Weller from Edinburgh University found that with increased sun exposure, the elderly enjoy lower risk of heart attack, high blood pressure and stroke. Remarkably, the positive cardiovascular effect had nothing to do with vitamin D. Another component within sunlight communicates directly with the body’s nitric oxide production, allowing the blood vessels to widen, improving cardiovascular health.”
But do not go into the sun, for goodness sake. Current medical advice.
I am the living proof, every time i go under the sun torso naked, i undergo an interesting transformation. All my veins seems to double in size and want to pop out of my body and i feel immediately more relaxed, a bit like when i am training intensely.
Gaetan: Very interesting comment! My veins stick way out, but I never connected it with sun exposure. I just conducted a brief experiment: Went outside, and they popped way up; came back in, and they settled down. Did that twice, with the same result. During my workouts, since my pull-up bar is two steps from the outside world, I always step into the sun between sets, even in winter, and it does have a calming effect, and I think aids recovery.
Thank God for that! I’ve just had a week in Sorrento while it poured in the North East of England, now I’m back to wall to wall sunshine in the garden! 😎 Must have the WIDEST blood vessels in Britain, not to mention a lovely tan!
Why I chose not to take warfarin and instead rely on fish oil and garlic to “thin” my blood. No sign of leaky valves.Garlic adverse effect at one bulb per day is a challenge. Looking into ways to “age” garlic before new crop arrives, 200 bulbs planted.
“J Thromb Haemost. 2009 Dec;7(12):2023-7. doi: 10.1111/j.1538-7836.2009.03630.x. Epub 2009 Sep 28.
OBJECTIVES: To investigate the incidence of mitral valve calcium (MVC), mitral annular calcium (MAC) and aortic valve calcium (AVC) in patients with non-valvular atrial fibrillation (AF) treated with warfarin vs. no warfarin.
CONCLUSIONS: Use of warfarin in patients with AF is associated with an increased prevalence of MVC, MAC or AVC.”
Hi Andy, Interested in your post given that my Mum is on Warfarin and I would love to get her off it. How does your regime affect your INR readings, do you still have checks on this and does your Garlic/fish oil keep them in acceptable range.
Hi smartersig, my GP and nutritionist did not know what vitamin K2 was, pharmacist said not to take K2 supplement (increases coagulation?). Mayo clicic advises not to eat too many greens containing K (increases coagulation, easy with fish oil (decreases coagulation). No INR readings were ever done. Protocol was to take warfarin and aspirin which I refused.
What I did: for breakfast eat lots of swiss chard and garlic from garden, with coconut oil and butter plus 2 or 3 eggs on top + cheese, supplements (K2, D3, C, fish oil, Mg). Followed low carb more fat, avoided seed oils.Sardines several times per week. Lost 10 lb in process. AFIB slowly diminished and is now non-existant. Kept a diary on foods consumed each day for reference and weight maintenance Also experimented with periodic fasting to promote autophagy in hope of re-juvinating heart cells.
Rationale: K2 REGULATES (not promotes) coagulation and prevents soft tissue calcification. There is still lots to be discovered about benefits of garlic and sulphur containing foods.
Word of caution, this works for me but we are all different.
Andy S
You and I are on almost the same supplements, I take L Carnitine and potassium in addition.
We shall see
Andy S: Me, too. I’m nearing the end of this year’s harvest, and usually try to plant at least 200, so the crop lasts a full year. I hold back about 25% (the fattest bulbs) for seed garlic to plant in October. My tenth year of growing garlic.
Gary Ogden: ditto. Hope you are making use of the scapes. Had 10 chopped up and sauteed with butter this morning topped with 2 eggs from my chickens. Not zoned for chickens but took a chance. Concerned about quality of commercial eggs from hens fed GMO corn and soybeans plus poor environment. Chicken poop back to garden, extra veggies to chickens, a win/win arrangement.
…And scape pesto!
I get a big bundle of scapes from my daughter every year and use much of them with olive oil, grana padana cheese, and walnuts or pecans to make a year’s supply.
Yummy.
Should we really be using Olive oil, there are plenty of studies that show that Olive oil produces endothelial dysfunction and that perhaps the Med’ diet is heart healthy despite the Oil and not because of it
Smartersig, Andy S,
I can’t speak to Andy S’s use of garlic and fish oil and their effect on INR but here is some information relative to warfarin, vitamin K and calcium.
Warfarin through its effect on vitamin K (it lowers K levels) can cause calcium to be misdirected to the vascular system per Andy S’s link above. Also, Google “vitamin k and the calcium paradox” and see the book by Kate Rheaume-Bleue. So K is very important and some have suggested adding K to a warfarin regimen see: http://www.lifeextension.com/magazine/2007/6/report_vitamink/page-01
Phil
Pittsburgh, PA USA
I would presume that if one took Garlic and fish oil then if nothing else it would mean that a lower dose of Warfarin would be needed to ceate effective INR readings. Its a win win situation ?
Fish oil plus warfarin: what is known…
A report from a few years ago suggests that not much is known.
afibbers.org/resources/fishoils.pdf
A more recent paper suggests the combo is safe.
https://www.ncbi.nlm.nih.gov/pubmed/27657121
This scary paper wants you to know it could be deadly.
https://www.ncbi.nlm.nih.gov/pubmed/28033135
Welcome to the coagulability casino!
Smartersig,
https://www.ncbi.nlm.nih.gov/pubmed/14742793
I would note that 1.5 mg/day of warfarin is a very low dose. In this study, the woman was on 1000 mg/day of fish oil during her initial warfarin regime.
Here is an opposite result: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037562/
Phil
Pittsburgh, PA USA
What am I missing here in my thinking. The patient is on Warfarin and then increases her fish oil and her INR go’s up. Well reduce her Warfarin for gods sake not take her off the fish oil
Since I refused all heart medication after my serious MI 1999 and went “natural” I replaced the asperin with garlic and fish oil. I brought this up with my cardiologist att that time and since he was a reasonable man he admitted that garlic worked in a blood thinning way. The latest cardiologist though considered my refutations of all the official medical dogmas about heart disease just as nonsens and didn’t want to listen to any of my “opinions”.
There are different ways to thin the blood and they do not all result in an INR change. So thinning the blood with garlic and fish oil will not necessarily raise your INR. Aspirin does not raise it and I don’t think that Plavix does either.
Absolutely. The INR is a specific test of certain clotting factors. You could affect several different factors and the INR test would not measure this at all.
Thanks for this but it still begs the question that if adding garlic etc to the cited ladies diet resulted in a raising of INR above the required range why not then lower the Warfarrin rather than ban the garlic ?.
If you did improve other clotting factors but not those covered by INR, would you still be at as much risk of DVT or further DVT?
So this fell into my inbox a couple of days ago… Now I’ve recovered from the concussion I gave myself by *headdesk*ing too hard, I thought I’d share it.
http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510
Thanks. Gary Taubes has done a pretty good demolition job on it. They decided only to look at four trials, most recent of which published in 1972. No other studies met their stringent inclusion criteria. Were it not so influential it would be beyond mockery. http://www.cardiobrief.org/2017/06/16/guest-post-vegetable-oils-francis-bacon-bing-crosby-and-the-american-heart-association/
It makes you want to weep, doesn’t it. I must sit down and have a spoonful of clotted cream to calm myself. What I don’t understand is how humankind managed to survive for so long before seed oils were invented. It’s a miracle.
According to the health “bible”…(Today’s Daily Mail!) A miracle is about to be bestowed upon us! A once a year vaccination to protect against High Cholesterol, which will “do away with the need for statins”. Early tests on MICE show the vaccine AT04A will cut cholesterol by 53%, and reduce damage to blood vessels by 64%(so it must be good!). It’s so promising, they are actually testing the drug on …..72…(yes 72) human patients in Vienna. Of course they are very optimistic, and who wouldn’t be at a proposed cost of between £1,000 and £2,000 for each shot, when there are currently 6Million people taking statins in Britain alone today. What a jackpot that would be 6,000,000 x £1000(Could be £2,000) = A MASSIVE PROFIT FOR SOMEONE! Where do I buy shares?
Has anyone noticed that “cholesterol” LDL and HDL is part of our bodies immune system?
Yes, this is well documented, Uffe Ravnskov and McCully wrote a controversial paper about that 2009.
http://www.thincs.org/unpublic.UR,KMcCully%2009.htm
Dr. Goran S, thanks for the reference. The question was meant to be addressed to people (GP’s and cardiologists) who promote the lowering of LDL as being a good thing. Need to know what is good about LDL.
Joyce,
My guess is that we will never hear about the final outcome (endpoints) from this “testing”.
Irreducible complexity——thousands of genes networked together
A core assumption in the study of disease-causing genes has been that they are clustered in molecular pathways directly connected to the disease. But work by a group of researchers at the Stanford University School of Medicine suggests otherwise.
The gene activity of cells is so broadly networked that virtually any gene can influence disease, the researchers found. As a result, most of the heritability of diseases is due not to a handful of core genes, but to tiny contributions from vast numbers of peripheral genes that function outside disease pathways.
Any given trait, it seems, is not controlled by a small set of genes. Instead, nearly every gene in the genome influences everything about us. The effects may be tiny, but they add up.
The work is described in a paper published June 15 in Cell. Jonathan Pritchard, PhD, professor of genetics and of biology, is the senior author. Graduate student Evan Boyle and postdoctoral scholar Yang Li, PhD, share lead authorship.
The researchers call their provocative new understanding of disease genes an “omnigenic model” to indicate that almost any gene can influence diseases and other complex traits. In any cell, there might be 50 to 100 core genes with direct effects on a given trait, as well as easily another 10,000 peripheral genes that are expressed in the same cell with indirect effects on that trait, said Pritchard, who is also a Howard Hughes Medical Institute investigator.
Each of the peripheral genes has a small effect on the trait. But because those thousands of genes outnumber the core genes by orders of magnitude, most of the genetic variation related to diseases and other traits comes from the thousands of peripheral genes. So, ironically, the genes whose impact on disease is most indirect and small end up being responsible for most of the inheritance patterns of the disease.
“This is a compelling paper that presents a plausible and fascinating model to explain a number of confusing observations from genomewide studies of disease,” said Joe Pickrell, PhD, an investigator at the New York Genome Center, who was not involved in the work.
From a polygenic to omnigenic model
Until recently, said Pritchard, he thought of genetically complex traits as conforming to a polygenic model, in which each gene has a direct effect on a trait, whether that trait is something like height or a disease, such as autism.
But last year, while putting together a paper on the recent evolution of height in northern Europeans, Pritchard was forced to rethink that idea.
In the earlier work on the genetics of height, Pritchard and his colleagues were surprised to find that essentially the entire genome influenced height. “It was really unintuitive to me,” he said. “To be honest, I thought that it was probably wrong.” His team spent a long time trying to understand the surprising result.
Instead, he said, “I gradually started to realize that the data don’t really fit the polygenic model.” That work led directly to the current Cell paper, he said. “We started to think, ‘If the whole genome is involved in a complex trait like height, then how does that work?'”
Therapeutic implications
The polygenic model leads researchers to focus on the short list of core genes that function in molecular pathways known to impact diseases. So, therapeutic research typically means addressing those core genes. A common approach to gene discovery is to do larger and larger genomewide association studies, the paper notes, but Pritchard’s team argues against this approach because the sample sizes are expensive and the thousands of peripheral genes uncovered are likely to have tiny, indirect effects. “After you get the first 100 hits,” said Pritchard, “you’ve probably found most of the core genes you’re going to get through genomewide association studies.”
Instead, he recommends switching to deep sequencing the core genes to hunt down rare variants that might have bigger effects. For clinical use, Pritchard said, there’s still a rationale for genomewide association studies: to predict the peripheral gene-based risk factors in individual patients in order to personalize medicine.
Implications for basic science
Pritchard’s omnigenic model promises to take basic biology in new directions and means biologists need to think a lot more about the structure of networks that link together those thousands of peripheral disease genes.
“If this model is right,” said Pritchard, “it’s telling us something profound about how cells work that we don’t really understand very well. And so maybe that puts us a little bit further away from using genomewide association studies for therapeutics. But in terms of understanding how genetics encodes disease risk, it’s really important to understand.”
Story Source:
Materials provided by Stanford University Medical Center. Note: Content may be edited for style and length.
Journal Reference:
Evan A. Boyle, Yang I. Li, Jonathan K. Pritchard. An Expanded View of Complex Traits: From Polygenic to Omnigenic. Cell, 2017; 169 (7): 1177 DOI: 10.1016/j.cell.2017.05.038
Cite This Page:
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Stanford University Medical Center. “Thousands of genes influence most diseases, researchers report.” ScienceDaily. ScienceDaily, 20 June 2017. .
For those of you who have missed that Dr. Kummerov, the persistent fighter against vegetable oils and especially the partially saturated ones with their trans fat content, has recently, on June 2, passed away at the age of 102 may read the tribute interview by Dr. Mercola. At 99 (!) he successfully sued FDA to yield to science and ban trans fats – will happen next year.
http://articles.mercola.com/sites/articles/archive/2017/06/19/trans-fat-toxicity-scientist-fred-kummerow-dies.aspx
You may here read the following excerpt:
“Kummerow was the first scientist to identify trans fat as the true culprit behind clogged arteries, which for years were blamed on saturated fats (and still are, in some circles). The opposition was tremendous. Part of the problem, the News-Gazette reported, was that politics were in play, overpowering a desire for the public to be healthier as a result of governmental food policies. He was quoted in an interview:
“Professor Kummerow said that in the 1960s and 1970s the processed food industry, enjoying a cozy relationship with scientists, played a large role in keeping trans fats in people’s diets.”6
Kummerow told The New York Times, rather tongue in cheek, that “other scientists were more interested in what the industry was thinking than what I was thinking.” Although Kummerow found a direct correlation between heart disease and trans fat consumption in women, which he called the “tip of the iceberg” after finding another disturbing link between trans fat and type 2 diabetes in women, it took another 20 years for the scientific community to acknowledge there might be something to his research.”
But what is inflammation, and how does it cause healing? When a fetus is injured in utero, does it use inflammatory processes to heal?
Inflammation = healing
That statement has zero informational content. Can healing occur (as in the fetus) without inflammatory molecular markers, or not?