Heart disease and inflammation.
A few people have sent me links to a recent paper called ‘Inflammation and Atherosclerosis.’ This was published in Circulation, and the authors were: Peter Libby, MD; Paul M. Ridker, MD; Attilio Maseri, MD. Remember two of the names.
Here is a relatively long section of the abstract:
‘Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis.
Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors.
Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.’ http://circ.ahajournals.org/content/105/9/1135.full
This paper interested me for a number of reasons. I focused down for a few moments on the phrase ‘Atherosclerosis, formerly consider a bland lipid storage disease…’ Does this mean that the world is moving on… Atherosclerosis has nothing to do with lipids e.g. LDL a.k.a. ‘bad cholesterol’? Now that would be something. Especially as it was published in the mainstream CV journal ‘Circulation.’
It seems that these authors are trying to shift the thinking away from cholesterol to inflammation. However, before discussing anything else I wanted to point out something that most people may have missed – by looking at a bit of background on the authors. First, Paul Ridker, who ran the JUPITER study, and who is a hugely influential cardiologist.
It should be noted that Paul Ridker has a major interest in moving thinking about atherosclerosis from a lipid storage disorder to an inflammatory condition. Because he has patent on the high sensitivity CRP test (C-reactive protein).
‘Dr Ridker is named as a coinventor on patents filed by the Brigham and Women’s Hospital that relate to the use of inflammatory markers in cardiovascular disease.’ http://circ.ahajournals.org/content/108/12/e81.long
What this means is that every time someone uses a high sensitivity CRP test, Paul Ridker becomes a little bit richer. However, in this paper, this massive financial conflict of interest is not mentioned. Instead, we get Acknowledgements:
This work was supported in part by grants from the National Heart, Lung, and Blood Institute to Drs Libby (HL-34636, HL-48743, and HL-56985) and Ridker (HL-58755 and HL-63293), and by the Leducq Foundation (to Drs Libby and Ridker). Dr Ridker is also supported by a Distinguished Scientist Award from the Doris Duke Foundation. Dr Maseri is supported by a grant from Fondazione Internazionale di Ricerca Per il Cuore onlus
No conflicts Dr Ridker? Mind you, Paul Ridker does have considerable form in not disclosing his financial conflicts. Some years ago, the Journal of the American Medical Association JAMA, was forced to publish a statement on ‘Unreported Financial Disclosures’ that were spotted in paper ‘Associations of LDL, Cholesterol, Non-HDL Cholesterol, and Apolipoprotein B levels With Risk of Cardiovascular Events Among Patients Treated with Statins: A meta-analysis.’
This statement mentioned many, many conflicts that the authors had failed to mention at the time. The section on Dr Ridker reads thus:
‘…Dr Ridker reports board membership of Merck Sharp and Dohme and receipt of a grant or pending grant to his institution from Amgen.’ [Amgen, as you may know are pushing PCSK-9 inhibitors]. This is covered in my book Doctoring Data.
Just to spell this out in a little more detail, Paul Ridker was an author on a meta-analysis of statins, yet failed to report that he was a board member of a pharmaceutical company (Merck) that marketed statins.
In truth, the moment I saw a paper promoting the ‘new idea’ that atherosclerosis is all due to inflammation, my antennae started to twitch. Especially when I knew that Paul Ridker was involved. A man who holds patents on a test for the inflammatory marker that we should be using.
I then immediately wondered, Is Paul Ridker now running a clinical trial on behalf of a pharmaceutical company, looking at the use of an anti-inflammatory agent to treat CVD. So, I had a little look round the internet. And guess what. Paul Ridker is, indeed, running a trial on an ant inflammatory for the treatment of CVD. The CANTOS study http://www.thecantos.org/steering-committee.html If you look down the list those on the committee running this study, you will find that Peter Libby is also on the steering committee. A conflict that remained unmentioned in the Circulation paper either.
What is the drug, it is Canakinumab. Here, from Wiki:
Canakinumab (INN, trade name Ilaris, previously ACZ885) is a human monoclonal antibody targeted at interleukin-1 beta. It has no cross-reactivity with other members of the interleukin-1 family, including interleukin-1 alpha.
Canakinumab was approved for the treatment of cryopyrin-associated periodic syndromes (CAPS) by the U.S. Food and Drug Administration (FDA) on June 2009 and by the European Medicines Agency in October 2009.CAPS is a spectrum of autoinflammatory syndromes including familial cold autoinflammatory syndrome, Muckle–Wells syndrome, and neonatal-onset multisystem inflammatory disease.
Canakinumab was being developed by Novartis for the treatment of rheumatoid arthritis but this trial was completed in October 2009. Canakinumab is also in phase I clinical trials as a possible treatment for chronic obstructive pulmonary disease, gout and coronary artery disease. It is also in trials for Schizophrenia. In gout it may result in better outcomes than a low dose of a steroid but costs five thousand times more. https://en.wikipedia.org/wiki/Canakinumab
I thought I would highlight the final sentence, just to give you some idea of the potential cost of this drug, should it ever be marketed for the treatment of CVD.
I know that this may seem a diversion. However, I have been around the world of cardiovascular research for long enough to take nothing at face value. Here is a paper suggesting that atherosclerosis has little or nothing to do with lipids. It is primarily due to inflammation. Which is a reasonable hypothesis. But guess what, one of the authors has a patent for an inflammatory marker. He and another author are running a clinical study, funded by Novartis, on the use of an anti-inflammatory agent in CVD.
However, just because there is money in the background, it does not necessarily mean that everything written is wrong. Perhaps inflammation truly is the underlying cause of atherosclerosis. Many other people have been saying this for years. Some of them, I know, certainly believe it from a purely objective scientific perspective. For example, Duane Graveline – who writes a great deal about CVD on his blog www.spacedoc.com, and is also a friend. He fully believes that atherosclerosis is an inflammatory condition, and he has no horse in the race.
My own take on this matter is slightly different. Yes, if you have a high C-reactive protein (CRP) level, this means that there is inflammation going on within the artery, and this is a sign of increased CVD risk. This is true, but what does it mean? Is the inflammation causing the CVD?
Whenever I see anyone stating that inflammation is a cause of anything I simply change the word inflammation to the word ‘healing,’ to see how sensible it then sounds. Inflammation is, in most cases, the way the body heals itself after injury. If you twist your ankle, it will become swollen and inflamed. The injury comes first, then you get the inflammation/healing. You would be hard pressed to state that inflammation causes twisted ankles.
Of course, there are some conditions where the inflammation itself can become greater than the original problem. Just to name three: Asthma, Crohn’s disease and Rheumatoid arthritis. In these diseases the body’s inflammatory/healing system becomes revved up, and starts attacking itself. This out of control inflammation can then lead to further problems downstream e.g. joint destruction. Such conditions are often ‘treated’ or controlled by anti-inflammatory agents e.g. steroids.
Equally, if you have Systemic Lupus Erythematosus (SLE), this is an ‘inflammatory’ disease, and you also have a severe vasculitis (inflammation of vasculature). As mentioned before SLE can raise the risk of CVD, in young women, by up to five thousand per cent. Case proven? Inflammation causes atherosclerosis?
No, I don’t think so. The sequence in SLE is that the vasculature is damaged (the endothelium is damaged). This stimulates the body to try and heal the damage. The healing is what we call inflammation and the C-reactive protein level goes up.
Get rid of the inflammation, and you will not be treating anything. You will simply be interfering with the healing process, and the CVD will, most likely, accelerate. Even if C-reactive protein levels go down, along with any observable inflammatory action.
If I may return for a moment or two to twisted ankles. To quote Dr Mirkin:
‘When I wrote my best-selling Sports medicine Book in 1978, I coined the term RICE (Rest, Ice, Compression, Elevation) for the treatment of athletic injuries. Ice has been a standard treatment for injuries and sore muscles because it helps to relieve pain caused by injured tissue. Coaches have used my “RICE” guideline for decades, but now it appears that both Ice and complete Rest may delay healing, instead of helping.’
As he goes on to say:
‘Anything That Reduces Inflammation Also Delays Healing [I cannot resist stating that, this is because inflammation is healing]
Anything that reduces your immune response will also delay muscle healing. Thus, healing is delayed by:
- cortisone-type drugs,
- almost all pain-relieving medicines, such as non-steroidal anti-inflammatory drugs like ibuprofen
- immune suppressants that are often used to treat arthritis, cancer or psoriasis,
- applying cold packs or ice, and
- anything else that blocks the immune response to injury.’ http://www.drmirkin.com/fitness/why-ice-delays-recovery.html
At least Dr Mirkin has had the grace to admit that he was wrong. RICE reduces inflammation, but interferes with healing.
I am pretty certain that exactly the same thing will happen with ‘inflammation’ in CVD. I can state this with relative confidence, because the most powerful anti-inflammatory agent known to man are steroids/corticosteroids. Corticosteroids e.g. prednisolone, or hydrocortisone are potent anti-inflammatory agents, they are all based on the natural stress hormone cortisol – produced in the adrenal glands. Steroids = corticosteroids = cortisol (just about).
Cushing’s disease is a disease whereby too much cortisol is produce in the adrenal glands, usually due to a small tumour that overproduces the hormone. So, if you have Cushing’s disease, you have a powerful anti-inflammatory agent coursing through your blood vessels – at all times. And what is the effect of this on CVD?
‘In patients with Cushing’s syndrome (CS) cardiovascular complications determine a mortality rate four times higher than in an age- and gender-matched population.’ http://www.ncbi.nlm.nih.gov/pubmed/15579193
The same thing happens when you prescribe steroids, for various conditions:
‘Individuals who use glucocorticoids and exhibit iatrogenic (caused by the medicine) Cushing’s syndrome should be “aggressively” targeted for early screening of cardiovascular (CV) risk factors, say researchers.
Laurence Fardet (University College London, UK) and colleagues found that individuals with iatrogenic Cushing’s syndrome who were prescribed glucocorticoids had a significantly higher incidence of CV events (including coronary heart disease, heart failure, or ischemic cerebrovascular events) than individuals prescribed glucocorticoids without iatrogenic Cushing’s syndrome, or those not prescribed glucocorticoids.
Indeed, Cushing’s syndrome patients prescribed glucocorticoids had a CV incidence rate per 100 person-years at risk of 15.1 compared with 6.4 and 4.1 in those without Cushing’s but who were prescribed glucocorticoids and those not prescribed glucocorticoids, respectively.
Multivariate analysis revealed that iatrogenic Cushing’s patients had a 2.27-fold increased risk for coronary heart disease, a 3.77-fold increased risk for heart failure, and a 2.23-fold increased risk for ischemic cerebrovascular events.’ http://www.news-medical.net/news/20120807/Cushinge28099s-patients-must-be-screened-for-heart-disease.aspx
Proving a medical hypothesis is never that simple. However, if you believe that CVD is due to inflammation, then the world’s most potent anti-inflammatory agents ought to decrease CVD risk. Instead, it increases it by at least 400%. [Far more in some studies]
Other anti-inflammatory agents, known as Non-steroidal anti-inflammatories (NSAIDs) also greatly increase the risk of CVD. Vioxx (a potent NSAID), launched then pulled off the market, was estimated to have killed over one hundred thousand people in the US alone, from increasing CV risk.
In short, if CVD is primarily a disease of inflammation, then potent anti-inflammatory agents ought to reduce the risk. Instead they increase it massively. There is no doubt that inflammation is associated with CVD. Equally, if you measure C-reactive protein (a marker of inflammation), a high level is associated with a higher risk of CVD. However, it is not a cause, and if you try to reduce inflammation you will almost certainly increase the risk of CVD, not decrease it.
Ergo. Inflammation is sign of active CVD. That is all.
These articles have been amazing, thank you
The paper is not recent, it is from 2002.
But Dr Kendrick’s point is still valid
See his latest non disclosure P.M. Ridker: None.
Association Between Markers of Inflammation and Total Stroke by Hypertensive Status Among Women
The fact “Dr. Ridker is a co-inventor on a series of patents filed by the Brigham and Women’s Hospital and Harvard Medical School that relate to the use of inflammatory biomarkers in cardiovascular disease”.
isn’t considered worthy of disclosure?
Thank you, as always, for cutting through the fog!
I would qualify this a bit. In the sense that inflammation within the vascular wall is part of a healing process and should not be interfered with is reasonable. However in the sense that inflammation in general (as occurs in RA or SLE) should not be interfered with sets up a problem. The evidence is clear that such inflammatory diseases vastly increase the risk of coronary artery disease. However there is also good evidence that successfully treating the underlying disease (and by implication reducing the level of inflammation) reduces the cardiac risk back to normal. Inflammation is not as simple as it looks! Many years ago I was impressed to find a website that listed all the interleukins, which numbered over 60 and for some of which no function had then been identified. Things have moved on, but even now, when IL-1 and IL-6 are both implicated in different autoimmune inflammatory diseases, other new ones such as IL-27 are being explored. And vasculitides such as Wegener’s, Takayasu disease and PAN etc are going to kill if the vasculitis is left untreated. Thus it’s important to specify exactly what type of inflammation is going on.
Wheels within wheels – as always. I would argue that, if you treat the underlying condition e.g. the vasuculitis, less damage is being done, less healing is happening, so the inflammation – and inflammatory markers – drop to normal. Along with risk… Does that sound reasonable?
So, if we treat the underlying cause of CVD, localized scurvy?, then we should see a drop in inflammatory markers.
1) Free Radic Biol Med. 2009 Jan 1;46(1):70-7. doi: 10.1016/j.freeradbiomed.2008.09.030. Epub 2008 Oct 10.
Vitamin C treatment reduces elevated C-reactive protein.
Block G1, Jensen CD, Dalvi TB, Norkus EP, Hudes M, Crawford PB, Holland N, Fung EB, Schumacher L, Harmatz P.
2) Rath M, Pauling L. Solution To the Puzzle of Human Cardiovascular Disease: Its Primary Cause Is Ascorbate Deficiency Leading to the Deposition of Lipoprotein(a) and Fibrinogen/Fibrin in the Vascular Wall. J Orthomolecular Med, Vol 6, 3&4th Quarters, 1991, p 125.
3) ASCORBIC ACID CONTENT OF HUMAN ARTERIAL TISSUE
G. C. Willis, MD; S. Fishman, PhD
Canad. M. A. J., April 1, 1955, Vol 72
I especially love #3.
Yes, Dr. Malcolm Kendrick it does indeed make much sense. You know…you are smart, possibly even superior in IQ. I’m with you, sir…so we better both be right. I chuckle here just a bit. Thanks again for a brilliant post. Rather a pity I had to look across the pond for answers. I am so glad I did. Thanks once again.
Who would have thought Dr. Kendrick would be one of the most talked about physicians in American politics?
Many thanks for the refs. Most useful
I find it remarkable that most doctors discount the value of Vit C both as an anti-oxidant and as an aid in the therapy of many conditions after Klenner’s findings.
Dr Fred Klenner
Click to access Klenner_1948_ch.pdf
Virus Pneumonia and Its Treatment With Vitamin C . Fred R. Klenner, M.D., Reidsville, North Carolina – Read by Title to the Tri-State Medical Association of the Carolinas and Virginia, meeting at Charleston, February 9th and 10th
South Med Surg. 1949 Jul;111(7):209-14.
The treatment of poliomyelitis and other virus diseases with vitamin C. KLENNER FR.
The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C
From Southern Medicine & Surgery, Volume 111, Number 7, July, 1949, pp. 209-214
Fred R. Klenner, M.D., Reidsville, North Carolina
HIDDEN IN PLAIN SIGHT: The Pioneering Work of FREDERICK ROBERT KLENNER, M.D.
by Andrew W. Saul Assistant Editor, Journal of Orthomolecular Medicine
J Orthomolecular Med, 2007. Vol 22, No 1, p 31-38.
Clinical Guide to the Use of Vitamin C The Clinical Experiences of Frederick R. Klenner, M.D.,
abbreviated, sumarized and annotated by Lendon H. Smith, M.D.
2233 SW Market Street, Portland, Oregon 97201
I take it this is because Vit C is not patentable and cheap and not an allopathic medicine.
any good for blood pressure.
OK, so inflammation is not the cause of CVD but instead is a symptom of an injury by some means or another to our arteries. If as you say, inflammation is actually healing (or trying to), then something is triggering the inflammation in the wall of the artery and clearly it ain’t cholesterol. In the athlete it’s a physical thing eg, twisting an ankle or damaging a hamstring.
What would be the equivalent in heart disease? Sugar perhaps, processed food, stress? Maybe a combination of all these things and more much in the same way as allergies happen as a result of the synergistic effect of multiple chemicals in our food, air and water (a brief piece in the New Scientist several years ago suggested this was the case. It explains why there are some many variables).
But what you say makes all kinds of sense to me.
Thank you Malcolm for this new great input.
I have been waiting for it
It is a twisted medical world we are living in!
Though, I thought this new twist was well established not least since my last (?) cardiologist, two years ago, was pointing his finger and saying: “I don’t prescribe these statins because of any high cholesterol on your part but because it reduces inflammation.” I knew that story and he knew that I would never go to the pharmacy get any of those drugs he prescribed.
He had measured the CRP-values but he actually didn’t mention any raised values. On the other hand he was not the least interested in talking this through with his “well read” patient. He was the guy who KNEW – period.
Goran, I wonder what a cardiac (CABG) surgeon would say to the NNT statistics you looked at? It might make for an interesting conversation, but I doubt it would change their determination to operate. I wonder how many of the 17,000 patients who had CABG last year in the UK had any sort of balanced information on the harms and benefits? Without such discussions, I believe operations are taking place without informed consent.
My first cardiologist I met 1999 was a reasonable man in contrast to my last (?) one and very much open for discussing my ailments. I pressed him about the benefits with the comprehensive CABG scheduled for me and he told me that the risk was 12 % for a patient like me to see a new but deadly cardiac event within year. That risk would be reduced to 8 % with the CABG. What I today know about Big Pharma I guess that this marginal difference still is a hype. Those numbers were anyway average for the age group 50 – 80 and he agreed that for me being 52 at that time the risk certainly was smaller for me than for a guy at 80. That helped me to take my decision to refuse.
I guess that it doesn’t hurt to be a researcher meeting this kind of ‘medicine men’. The last one was though completely entrenched – he was really not “interested”! Hostility from the first minute – he apparently didn’t like professors of metallurgy.
GOD knows best.
Behind that simple statement are ten thousand words of appreciation for a clearly stated explanation for all to understand.
You have inflammation, so what is the root cause? should always be the question.
I hear the cry, I am doing everything right! Therefore what else is wrong is the enigma wrapped in a conundrum of worry.
Dr Kendrick, In the realm of CVD, have you done any research on nanobacteria as the cause of arterial calcification and how this scenario plays out? I’ve been doing some research on this nanobacteria as I have aortic calcification which will sooner (or later) be a cause for heart valve replacement.
I have discussed nanobacteria with Paul Rosch on a few occasions
Dr Kendrick, are you familiar with nanobacteria and its role in CVD, specifically arterial calcification? I’ve been doing research on this nanobacteria because I have severe aorta calcification which will soon require aortic valve replacement.
Malcolm, how do you interpret the JUPITER-study where they enrolled peaople people with enhanced CRP and reported a marginal improvement by statin intervention?
Because statins (in my opinion), work by increasing NO synthesis and reducing thrombus formation – and protecting the endothelium
In my view the JUPITER trial is of no value since it is obvious that there was a strong preconceived idea that the results would favour statin intervention. They paid to get a Justification for their drug, the study name says it all.
JUPITER = Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin
True exploratory science would never use a study name like that.
Indeed. But they needed to make up the name of a planet. At the times all AZ studies were called something astronomical e.g Meteor, Jupiter, Asteroid etc.
With regard to c-reactive protein as a marker, uric acid levels (serum urate) are just as accurate and cost next to nothing by comparison. The thing is that nobody is bothered outside its link to gout. Maybe we should be looking at uric acid levels the same as cholesterol and prescribing Allopurinol as much for its anti oxidative stress properties as for lowering levels. Seems it has as much a theoritical base as any other theory.
Dear Dr K,
I wonder if you could elucidate something for me. Here in Belgium my hospital does a CRP test and mine comes out at 0.2 mg/DL. A doctor said I could get, for a fee, a CRP ultra-sensible. My reply was that with my levels what would it show me over and above what the bog standard test does. He started muttering about it being more accurate etc, and not the same thing. I told him there is only one protein, and the measurement I got strikes me as pretty sensitive already.
Has Dr Ridker, come up with different money spinner?
There may be a difference between using artificial (pharmaceutical) methods of resolving inflammation and natural, dietary/lifestyle interventions to do the same.
We know naturally indigenous peoples living near naked under the sun have 25(OH)D levels around 115nmol/l 46ng/ml (Luxwolda) and around that level vitamin D is best able to resolve inflammation
Vitamin D Inhibits Monocyte/macrophage Pro-inflammatory Cytokine Production by Targeting Mitogen-Activated Protein Kinase Phosphatase 1
We also know that at that level free bioavailable cholecalciferol is measurable in tissue.
Circulating Vitamin D3 and 25-hydroxyvitamin D in Humans: An Important Tool to Define Adequate Nutritional Vitamin D Status
This is important because we now know cholecalciferol (half life 19-25hrs) stabilizes the endothelium.
Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium
Apart from Vitamin D deficiency it’s also the case that more than 50% of the population consume less than half the Magnesium RDA.
Magnesium deficiency not only has an impact of vitamin D status but it also plays a role in preventing damage in diabetes.
Oral magnesium reduces gastric mucosa susceptibility to injury in experimental diabetes mellitus.
Low magnesium promotes endothelial cell dysfunction.
Many people are exposed to artificial light at night and have disrupted circadian rhythm and melatonin production.
Melatonin ameliorates endothelial dysfunction, vascular inflammation, and systemic hypertension
There may be a difference between maintaining a natural anti-inflammatory status by ensuring diet/lifestyle/circadian rhythm to enable natural levels of cholecalciferol, melatonin, magnesium and using pharmaceutical drugs to treat inflammatory markers.
Many thanks for the links. I sincerely believe that Vit D3 is of general value in maintaining health; unfortunately while the UK CMO has supported its clinical use, the NHS in its dermatology clinics have a huge display of sunscreen advice – at least in my local Trust hospital this is the case. The importance of Vit D is totally ignored.
Sunscreen screens out UVB. UVB is what is needed to synthesize D in your skin. Imagine the damage that UVA does. Sunscreen does nothing for that.
I think newer sunscreens do filter out both?
According to my dermo man, the fancy priced sunscreens are more technical and filter out both.
That’s excellent for you fortunate folks who don’t have to contend with the FDA.
Vit D may have an optimum level that is lower than many think:
Masterjohn has not taken into account the active role of cholecalciferol in that form
Try reading the links I provide.
At what level do indigenous peoples living naked under the sun achieve 25(OH)D equilbrium.
At what 25(OH)D is human milk vitamin d replete?
What 25(OH)D level ensures bioavailable unbound unhydroxylated is present in measurable amounts in tissue?
As some who has no bladder function I experienced year of UTI until I raised my 25(OH)D to 50ng/ml 125nmol/l and since then I haven’t used an antibiotic.
Because of the late effects of polio I also experienced years of Neurogenicjoint pain.Since improving 25(OH)D I haven’t used any pain medication.
Obviously quality of life with repeat UTI and constant pain also affects mood so eliminating those problems means I haven’t needed anti-depressants either.(although it’s probably vitamin d levels also improve mood and cognitive function.
Thank you for bringing up the level of vitamin D on a regular basis. My broken foot healed in record time with 5000 I U a day supplementation. For the rest I feel fine so probably am. Why are people so wary of having a decent vit D level?
Dr Holick, a leading researcher on Vitamin D lost his job because he dared to suggest that a short time in sun without a sunscreen annoyed the sunscreen manufacturers that they complained to the ADermatologyA who they sponsored and he worked for. May be the same situation applies to the FDA through their revolving door system
mikecawdery, Thanks for that. I enjoyed the video. Hadn’t seen it before. The man practices an hour from me in the Big City.
You had me alarmed for a moment that they fired him again. But that was in 2004 I believe. They can’t be that stupid twice. . . . can they??
sorry, copy malfunction, this is the link (Chris Masterjohn on too much Vit D):https://www.youtube.com/watch?v=9H7tbWVNrXQ
Thanks Edward Hutchinson, that is the last thing I must get under control…that circadian rhythm. I took all yours and the advice of Dr. Kendrick and company. I have the vitamin D levels normalized, the magnesium, but that sleep thing is the worst for me at this time. That is the last one…safe to say, I am working on it.
One of the best in this series. Thank you.
The body will try to heal itself from injury resulting from exposure to environmental toxins, pharmaceuticals, poor diet and stress. Unfortunately there is not a lot of profit to be made from life style changes.
I worked for GSK and they tried 2 extremely large studies (because the effect would be so little) to try and show Advair and the new Breo lowered the mortality risk in COPD. They thought it would work because it would lower CV disease since both drugs had a corticosteroid in it. Both flopped!! Neither worked! To your point!
Sent from my iPad
“I know that this may seem a diversion”, No Malcolm I disagree. this is not a diversion. Again it is what it is all about
I am so grateful for your ability to cut the twaddle and clarify the real issue. Thank you for all the research and work you put into your blogs.
Are you familiar with Uffe Ravnskov and his hypothesis that LDL as part of the innate immnune system is involved in atherosclerosis?. It seems that we all form plaques in response to infedtion. Isn’t it the vulnerable plaques we need to worry about? These are plaques that don’t heal and their rupture can be deadly. Can you comment on the new LpPLA2 test that measures these? Shouldn’t we be working on building up our immune system so that these plaques heal over quickly? I would appreciate your input on this. Thanks
Regarding inflammation: I was told to put an ice pack on an acutely inflamed insect bite. Didn’t help, and anyway, we needed the frozen peas for dinner. On an instinct, I applied a face cloth wrung out from water that was nearly too hot to put my hands into. Instant relief from the pain, itching and redness, and the whole thing recovered in double quick time.
Fighting fire with fire? Just doubling my body’s response? Whatever, I still take the same measure in similar situations.
Heat stimulates mast cells to overproduce histamine to the point of exhaustion. The itch is in the histamine.
Question is: Are you setting yourself back by doing this?
I would not think so. Only certain insects do this to me and I know that heat will cause much quicker healing. Like a thick bandage will stop a cut from hurting, and help the healing process – by keeping it warm.
Thanks for the link. So if the water is not hot enough, I shall reach for my hairdryer!
It’s all a bit off topic, but is just another example of “see a reading, adjust it with a pill” being a very simplistic way of looking at disease.
Doesn’t surprise me, as raising the body temperature, i.e. fever, is one of the body’s innate healing methods!
Maybe the heat affected the venom, not the inflammation. Apparently all venoms are proteins and coagulate with heat like egg white does, rendering them ineffective. So if far from help and bitten by a snake, put the body part in boiling water or the campfire, as hot as you can stand. (Never tried it myself.)
As kids when we got very sunburned we were told to take an extremely hot shower. It’s very painful. I always thought the advice was given by sadists who had a good laugh at our expense.
Seems to me that if you’ve heated the venom enough to cook it, then you’ve cooked yourself.
The trick is, your skin’s mast cells secrete histamine in response to a bug bite. Heating you skin to discomfort level will catalyze that secretion. (No cooking!) The heating produces a surge of histamine and a brief surge of amazing itch. Then the mast cells are exhausted. No more itch. Not for ten minutes or so, anyway.
On the topic of insect bites: Good quality tea tree oil — undiluted — works well for me.
Jean Humphries: Many years ago I had a very painful back injury. A rural area served by a country doctor, the only one is town. He had the nurse put a series of ever hotter, moist towels on, and I walked out of there a new man, painless, and with a big smile on my face. I get occasional exercise injuries, and this is still how I treat them, with excellent results. I may be wrong, but I believe the heat increases circulation to speed healing.
I’m reminded of my Father’s descriptions of being treated for a chest infection by having a hot poultice put on his chest “to draw out the poisons” . A tin of something – maybe kaolin and something aromatic – boiled until very hot then slathered onto a sheet of strong brown paper and slapped on the infant chest. Since there was no penicilin, it helped to have a robust constitution
Every child in Russia even today gets mustard patches put on their chest when they get a respiratory infection. Rather than “draw out toxins”, this treatment warms up the area and expands the capillary network to help the body bring oxygen and nutrients to the tissues and clear the pathogen. Cupping, another therapy used throughout China, Middle East, and Eastern Europe, employs a similar principle. In the US today most kids will get an antibiotic which will damage their gut biome setting them up for more immunity issues in the future…
Sasha: What about the CVD rate today in Russia. How has it changed in recent decades? What sorts of treatments do they use?
Gary: I have no idea. It’s probably higher than in many developed countries, just like Dr. Kendrick mentions. There’s lots of smoking, drinking, and other risky behavior, especially for Russian men. And unbelievable amounts of stress from all directions. Of course, it doesn’t apply to everybody, most of my relatives lived into late 80s and early 90s without taking even a fraction of drugs that people in the West take. I believe it was due to their strong constitution, sensible behavior and unadulterated food.
Also, I think that the rates of CVD have been coming down in Russia. They really shot up in the 1990s when times were really tough.
What people use to treat CVD there I am also not sure. I would assume that they do use lots of herbal medicine and folk remedies because the tradition of folk medicine is quite strong in Russia. I can do some research for you, if you like… Just narrow it down for me, there’s tons of info out there on Russian sites.
Sasha: I would be very interested to know what Russian physicians think about the rise in blood pressure as we age. That is, what is considered a reasonably healthful range of BP in different age groups. Also, what are the protocols for taking an accurate measurement? Hope this makes sense. Haven’t yet had my coffee.
Gary: I’ll look around the Russian web and ask some members of my family who are MDs and my acupuncture teacher who was trained as a surgeon. I’ll let you know what I find out…
Gary: I haven’t yet been able to find much information on your questions from the Russian docs I asked except one recommendation to use BP cuff when checking BP and not to use digital machines because they give artificially higher readings. (A long technical explanation followed on why this is so of which I understood little…)
However, I recently came across Malignant Medical Myths by Joel M Kauffman, PhD and Chapter 4 in his book seems to answer a lot of your questions. I don’t know if you’ve read it, but if you didn’t, Dr. Kauffman has a PhD in Organic Chemistry from MIT, spent 14 years in drug development and holds 11 patents, including 2 on anti-TB drugs, so this is not his first rodeo…
The books is excellent and the chapter on BP is very informative. The book also seems to have been developed in collaboration with some of the authors recommended here and elsewhere: Ravnskov, Ottobanis, Graveline, etc. You may want to take a look at it or, if you want, I can summarize what he says about treating HBP in another post..
sasha: Thanks! I read Dr. Kauffman’s book five or six years ago, and refer to it frequently. A fine piece of work. Good advice, too about the reliability of the cuff over digital. This means that the year I did marathon training at age 55, and took my BP with the digital device frequently and got a mean of about 108/68, my BP was actually lower than that. It is mainly Dr. Kauffman’s chapter on BP and Dr. Graveline’s blog posts about it which have given me the confidence to go off Lisinopril, and stop being concerned about my BP. We do too damn much measuring, testing, and worrying and not enough living. The last time, in winter when it is normally higher, it was 131/78, and not even taken properly (according to Dr. Graveline’s protocol). Not bad for 66. It has been trending downward over the past two or three years as I’ve made dietary tweaks and added HIIT and strength training to my exercise program. The Obamacare computer in the examining room makes it difficult to take properly anyway. But Dr. Kendrick’s blog has been a powerful tool for me to begin to put all the pieces together. Rich and absorbing.
Yes, in Traditional Chinese Medicine ice is never used even for acute injuries and definitely not for chronic pain. Seems your country doctor was of the old kind, there aren’t many of them left, unfortunately.
Sasha: You’re right, I think. This one practiced medicine for a very long time, and just passed away last year.
Sasha I would be interested to see what he says on blood pressure. I’m on bp medication but trying my best to get off them without success
Tom: he says that RCTs not sponsored by Pharma do not show benefits of antihypertensive drugs unless BP treated is extremely high. People with systolic BP higher than the 90th percentile for their age and sex might benefit from treatment. Here are the numbers for 90th percentile:
45-54 (age) 165 (F) 159 (M)
55-64 183 173
65-74 190 184
He also recommends low-carb diet and supplements: magnesium, L-arginine, and fish oils high in omega-3s.
In reducing salt intake only 20% of patients showed benefit while about the same number had increased mortality.
Tom: What convinced me that my BP didn’t need to be treated by pharmaceuticals was three things: 1. All that I’ve learned from Dr. Kendrick’s blog. 2. Dr. Kauffman’s book (which sasha describes very well in a recent comment), chapter 4. 3. Especially what Dr. Graveline writes about BP on his blog-spacedoc. I have great confidence that I’ve made the right decision, and it pleases me no end not to have to go back to the pharmacy again. But you have to make your own decision. The vaccine controversy here in the U.S. has given me great clarity about all things pharmaceutical. Curiously, the presidential race, which has empowered and energized so many angry people here, has added to my resolve.
Had the same experience, Jean. I get bitten regularly by ants in the garden (one particular species). Ice always helps reduce inflammation, stops itching and promotes quicker recovery. Recently, I was bitten by a different species. Ice made my finger swell to double size very quickly and the pain and throbbing was intense. I put the finger under the hot tap and I wouldn’t have believed the difference. I concluded…different species…different poison…different reaction.
Standard treatment for weaver fish stings is to immerse foot (nearly always feet) in hottest water you can bear…
Interesting. Last year my husband had a bad wasp sting on his left side and he’d heard that cold milk would help. We put some on and it dampened the inflammation instantly. However, not many days later, he developed cellulitis with sepsis in the left leg (we knew this could be a risk for him due to lymphoedema following inguinal lymph node removal) and was hospitalised for a week. This sting may have had nothing to do with the subsequent infection but when you consider that one aim of swelling is to isolate the toxin from the rest of the body, I don’t think I would rush to stop this natural response in the future.
I’ve also been looking for the cause(s) of metabolic diseases for years. I think that in this case both you and them are correct. How comes?
Usually the cause of CVD is inflammation, but the mediator is blood clotting. Other, less frequent causes converge at the same mechanism of increasing blood clotting.
Here is the connection:
Mechanisms of thrombosis in obesity
(Figure 2 is telling)
And the start with chronic activation of an otherwise benign signaling system involving IL-1β:
The Inflammasome Puts Obesity in the Danger Zone
+ how hyperinsulinemia connects to increased thrombogenesis:
Insulin resistance in the vasculature
It all starts with chronic stress in white adipose tissue.
Many thanks for the links
Try this http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781481/ sorry can’t seem to link it for you.
We have ignored uric acid as a major issue, probably because it’s all about gout. At least the true wonder drug Allopurinol comes to the rescue.
Of course I know what Prof. Johnson proposes. However, he seems to focus on the liver while the main regulator of metabolism is white adipose tissue. It is chronic adipose oxidative stress that sends us down the metabolic disease route. Uric acid (nowadays mostly from fructose) is a prime stressor, but high insulin and glucose excursions, even antibiotics and other drugs (statins?) can do the same. When acute immunomodulation of the metabolic response becomes chronic (IL-1β, IL-6, TNF-α, etc.) the metabolic mayhem begins. Suppressed adipocyte differentiation, hypertrophy of existing fat cells, exacerbated local inflammation, and finally insulin resistance, as an antioxidant defense mechanism. Then ectopic fat accumulation starts, usually in visceral fat first, next in the liver, muscles, etc. The spiral continues until the underlying cause, the metabolic stress is removed. Lower insulin, reduce inflammation. Eat high fat, low carb natural foods, fast regularly.
Not so sure how ‘wonderful’ allopurinol is. One side effect is gynecomastia – I know, altough I don’t know how much blame to apportion to allopurinol, how much to rosuvastatin and how much to amiodarone – they are all implicated. Fortunately, I dumped them all nearly 5 years ago, to good effect, although I remain less flat-chested than I would wish. In my own case, changing from HCLF (60%+ gluose/fructose, 15% fats) to LCHF (15%- glucose/fructose, 60% fats, mostly SFA) solved the gout problem (and a bunch of others).
That you were on amiodarone suggests to me that you had a rhythm problem. I wonder if you could say how that is now. Fixed? How’d you do it?
I too would like information on stopping Amiodarone. I’m starting to drop all my medications and started by halving the dosage. The local pharmacy actually ran out a couple weeks ago so I have been able to enjoy the sunshine again!
Good day. I think you are a brilliant and clear thinker. I am grateful to you for your clean and simple approach to data analytics. I appreciate your dissonant thinking. I wish you a long and healthy life. Thank you for all your work. David Tepper Deerfield,IL USA.
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Email to Text: email@example.com Cell:847-431-7721 Text or call Sideline: 224-300-0838 Text or call
“These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.”
“. . . scourge of growing worldwide importance.” I guess they want us to take their infomercial seriously.
Thank you, once again, Dr. Kendrick, for another look at things-as-they-really-are. I’m so grateful for your work.
Dr. Paul Ridker: “…this scourge of growing worldwide importance.”
Dr. David Grimes: “It is clear from this study that there has been a major decline of age-related CHD deaths internationally, by up to 80% between 1980 and 2007.” — http://www.drdavidgrimes.com/2016/01/the-decline-of-deaths-from-coronary.html
So are things getting worse or are they getting better? I’m going with Dr. Grimes. Things are getting better. The mortality statistics he quotes bear him out. The implication being that cardiac medicine is a dying (heh) field. They are desperately trying to maximise revenue from a shrinking pool of patients.
Thanks for the Grimes article, Martin! In truth, the real “scourge” of CVD is probably all the heavy-handed treatment.
Besides, when I saw the word “scourge,” I could only think of my two grandparents who died suddenly of heart attacks, at a reasonable age. They were the lucky ones. There are many other causes of death that might better be called “scourge.”
Interesting point. Grimes makes a case for a substantial rise* and later fall of CHD mortality peaking some decades ago. After reading his book, I tried to find good mortality data for the last three decades, but could not convince myself I had enough data to see the trends fairly. There seems to be more than a hint of flattening off of the decrease, or even a slight rise (UK).
Some thoughts and questions:
The “causes” are multi-factorial. E.g. Dr Kendrick mentions stress (e.g. of migration) in tGCC. Smoking, as a severe cause of mitochondrial damage (and NO suppression), would be expected to cause CHD, and it did peak in (UK) men around the CHD peak, but it does not look like the only cause, just one of several. Even so, having grown up in the 60s and 70s in SW Scotland, the drop in mortality in middle-aged men is evident and profound, and the timing and trend indicates it is little to do with medical advances.
Joseph Kraft tells us that CHD = IR (diabetes in situ, according to his diagnostic and terminology). IR = damaged mitochondria (almost by definition). There is a strong increase in T2DM diagnoses (and pre-diabetes too). These, however, are diagnosed by techniques (FBG, GTT) that Kraft shows to be unreliable. Given expanding waistlines (etc.), it seems plausible that IR is on the increase and so increasing CHD should follow. Is it? Is T2DM-related mortality recorded in a way that masks CHD mortality to some extent (e.g. death following amputation, renal failure – does T2DM/IR kill more quickly by other means, given modern treatments)?
* I accept doubts raised in earlier comments in this series of posts regarding reliability of data during the rise in the early 20th C. The fall in the closing decades seems clear enough.
A dozen years ago I took large doses of ibuprofen to prevent sore muscles before I went into the deep woods to haul out firewood – wheelbarrow after wheelbarrow. (You listening, Goran?)
The plan worked. No sore muscles.
However, the case of diarrhea I got was so severe that I was (mis)diagnosed as having Crohn’s disease. Extremely scary. It resolved after six months, an unhealthy weight loss, and more anti-inflammatory as Asacol. (What did all that do to my heart??)
A few years later I took a couple of naproxen for short-term relief of a sore throat. This time the diarrhea lasted five weeks and was diagnosed as the lymphocytic version of microscopic colitis.
JDPatten, many thanks for the cautionary tale. Points noted and taken.
“You listening Goran?” made me chuckle too.
“I hear you clear and loud”! 🙂
I was brought up cutting trunks (no chain saw at that time) and chopping firewood.
Living in the states some years ago I had a truckload of firewood delivered by my mail box. I had to clear that area and in a short period of time and I used my wheelbarrow but finished with a very inflamed elbow. Though at that time I was a “traditional” carb-eater prone to inflammations I guess.
Today I am amazed by myself with having no problems at all lifting and hauling. The heart is though a limit in the chopping business.
I love to tell your story to those people I meet who run around wondering how long they have to live if they ditch statins. They look a little glazed over. It takes while to explain…but you know I am so patient most of the time. What is sad are those who have been statinated for years on end. They act like the Pod people got them. Chronic pain and that “its all over for me” look. I can spot them a mile away. Oh well, some of us just don’t make it this time around.
Like your story.
Was contacted concerning one of my pensions by a finaincial advisor. He asked how many medicines I take regularly. I replied “none”
I asked how many people of my age gave him that answer. “Not many, they all seem to be on statins”
Tells its own story.
It’s great to see that you’re doing so well.
I’ve been wondering: On your LCHF diet, do you ever allow yourself a small portion of a truly WHOLE grail confection – on the theory that the carb gets absorbed so slowly that it makes no negative difference?
Um… That should be whole GRAIN. No one has found the grail yet. 🙂
JDPatten: I think it’s in those caves in Lower Silesia. They’re still looking
Brilliant, Dr. Kendrick, thank you once again for your expertise.
Isn’t it the same Dr Ridker who ran a study on giving Crestor to healthy people with elevated CRP? They then trumpeted the results as Crestor reducing CVD risk by 50%. Then somebody actually looked at the study: out of 500 people on Crestor 1 had a CV event and out of 500 on placebo -2. ARR of 0.2%.
Once again you have produce an interesting and stimulating article which takes time to thoroughly digest the contents. It amazes me that you have the time in your busy practice with hazards like QoF et al to contend with. Congratulations.
I too spotted the name Ridker and JUPITER but I preferred Dr de Lorgeril’s demolition of it. I am not surprised at this attempt to flog drugs and tests.
It seems to me that medical research these days is solely concerned with showing trivial “significant” differences and then inflating the result by using Odds ratios or Hazard Ratios with a clear advertising intent.
After a full examination I hope to come back with further comments
If the standards of getting a drug on the market are #1 efficacy- which means the drug has to outperform a placebo, which essentially it doesn’t have to show much, right? Kind of just better than nothing and #2 safety- where the standard is the benefits outweight the harm, I guess if a drug helps 51 people but harms 49, then following this logic, the drug meets the FDA’s standard. From what I’ve read recently the FDA is approving approx. 93% of drugs sent their way.
You may have noticed that these studies on statins usually involve 1000s of patients. This practice allows tiny differences in real terms to be identified and statistically significant. The HPS study ( involving patients with a prior MI or very seriously at risk) is the classic example of this. You may remember after the differences between Collins and the BMJ that Collins trumpeted the following on the BBC and wherever else he could: “Treat 3 million and save 10 thousand lives a year. In more understandable terms that is one in 300 or an efficacy rate 0.3%, In short 299 out of 300 would not benefit but some 60 are likely to have adverse reactions to a greater or lesser extent. Even taking for 10 years only 1 in 30 can expect benefit while 29/30 will not benefit. This comes out with the numbers published in the paper. I personally am loathe to take such a drug given those odds
What I you have a CRP of 1 (on a scale of 0-10) and have developped severe stenosis (like I do). Ok I only know my CRP as measured in september 2015 which was 1 (on a scale of 0-10) and june 2015 (0,4 scale unknown). One might argue I don’t know the CRP values of the first 49 years om my live and meanwhile been taken extra Vit C.
Exactly. My hsCRP from a year ago was .5 (point five). Good, right? But my Agatston coronary artery score from the same time was 1,6040. (Above 400 is very bad.)
But, as Dr Kendrick pointed out, calcium score indicates only your history.
I’d like to think that we’ve both been doing some right living for ourselves more recently.
Surely CRP doesn’t always correlate with coronary disease/atherosclerosis ? Last year, following a wisdom tooth extraction, I developed ‘dry socket’, very painful and inflamed – my CRP, which hapened to be measured, was 87 ! The following week it had reduced to 5, a few weeks later it was <1.0. Surely my CRP at that time was due soley to the dry socket inflammation ? Did it mean I also had a higher risk of atherosclerosis at that point ?
Of course. CRP is just a general inflammatory marker. It will go up with infections, trauma, etc. etc. It is not specific to atherosclerosis.
Dr. Kendrick, thank you for your dedication to getting all of this information disseminated. I find it endlessly fascinating. This might sound rather dim, but if a drug that targeted inflammation broadly might increase CVD, why would diet, exercise and other modes of reducing general inflammation reduce one’s likelihood of CVD?
Because you are not reducing inflammation directly. You are removing underlying causes of inflammation, so the inflammation goes away. To me this all seems simple. Inflammation is always caused by something else. I does not arise spontaneously. Your body does not wake up one day and think to itself. Today I shall start inflammation in my joints, or arteries. It may be that the underlying cause is an auto-immune problem, whereby the body fails to recognize parts of itself as…itself. When this happens, your immune system can attack joints, the GI system, the beta-cells in the pancreas, the thyroid gland etc. etc. At which point there will be a lot of inflammation going on as the body attacks itself. However, even in this situation the inflammatory response that occurs is a result of a dysfunctional immune system. The inflammatory response never starts first. Is that clear? Or is there something that I am incapable of understanding… or explaining?
Interesting. I have been taking medication for cardiomyopathy. Some of the medication effects (I’d say “causes”) asthma. I started to have bad asthma to the point where I was put on some inhalers and steroids. This lessened my asthma, and I finally was taken off these. However, what seems to help the most (and also helps seasonal allergies tremendously) is intermittent fasting. I also primarily follow a low carbohydrate diet too, so this factors in also, but I think the primary effect is through IF (intermittent fasting). If I perform IF (not eating breakfast and/or lunch and/or dinner, sometimes not eating for days), I basically cure my asthma and allergies. If i eat carbohydrates (normal wheat in particular), asthma and/or allergies come back. I always thought IF reduced inflammation, but under your theory — which makes sense to me — I’m actually doing something else, which effects reduced inflammation. Certainly, not eating wheat helps, but I only eat wheat periodically on low carb, and low carb seems to help with asthma and allergies, but not to the extent IF does.
Since I am uniquely living on my collaterals with all the main coronary arteries blocked according to the angiographic report I have a special interest in this subject for 17 years now. On Malcolm’s last blog I entered a link to a five minutes video illustrating this phenomena.
With all the competent participants on this blog I would really appreciate any informed comment on this video which to me is devastating for the present consensus view on heart attacks. Anyway it supports my own decision to refuse the CABG.
Related to this is perhaps what I read a few years ago about the earliest “evidence” for diabetes in the standard textbook “Diabetes Mellitus” by Joslin in a 1970 edition. It was found in the capillaries (those on which my heart an myself now are surviving) where it was possible to measure by the electron microscope that the basal lamina, backing up the epithelia, was significantly narrowed.
A sign of inflammation?
Maybe but for sure not a cause – sugar, PUFA’s and why not stress?
Dr. Göran: Very interesting that all of your coronary arteries are blocked. You are living proof of the wisdom of nature in giving us collaterals, and the short film is graphic proof of this. May you continue to live long and well.
This is why a love this site. A random link leads to a whole website that opens yet another take on something.
In this case, hidden under “FAQ” and “print version”,
there is another attempt to develop an alternative narrative of what causes heart disease. In many respects, it is similar to Malcolm’s take. In others, it is markedly different. For example, blood clots are not seen as the culprit but rather a witness. There is also a lot about the almost forgotten miracle drug oubain.
I have recently fallen in love with a series of studies carried out on Finnish monozygotic twin pairs discordant for BMI. I would like to draw your attention to two of these. The order is not chronological, but rather reflects my impression on the etiology of metabolic diseases (metabolic stress, inflammation, insulin resistance, and impaired coagulation):
Impaired mitochondrial biogenesis in adipose tissue in acquired obesity
Acquired Obesity Increases CD68 and Tumor Necrosis Factor-α and Decreases Adiponectin Gene Expression in Adipose Tissue: A Study in Monozygotic Twins
Obesity-Related Derangements of Coagulation and Fibrinolysis: a Study of Obesity-Discordant Monozygotic Twin Pairs
I wish they studied IL-1β next. By the way, the effect of IL-1β blockade is quite dramatic in clinical practice, not in the same league with cholesterol lowering:
“the primary outcome occurred in 4.5% versus 16.0% (hazard ratio: 0.29; 95% CI: 0.15 to 0.56; p ! 0.001).”
Low-Dose Colchicine for Secondary Prevention of Cardiovascular Disease
If inflammation is looked at as THE primary process for healing, and it is reasonable to consider that it is, then one must consider that the in the natural uncontaminated environment, the cause of the inflammation is always temporary and that the inflammatory pathways, mostly the cytokine response, is also meant to be temporary. Normally, once the instigator of the inflammation is removed, full healing can take place. It is the unrelenting onslaught of toxic substances leading to chronic inflammation that leads to an unnatural state of non-resolution of the inflamation and that sets up a diseased state. Within our diet there are so many factors that can lead to this, probably most of them unrecognized but I’d place a bet on grains, preservatives, toxic pesticides and herbicides, sugar, glucose AND fructose, and insulin, and oxidised unsaturated fats as a good starting base.
If there is a chemotactic response from an inflammed artery that signals for an increase in cholesterol production, as has been postulated, it is easy to see why cholesterol has been blamed, incorrectly it turns out, for CVD. We are just blaming the firefighters that we see at all fires for starting the fires!
Is it true that increased serum ferritin -> increased myeloperoxidase -> increased endothelial damage/healing? If so, is there any evidence that reducing serum ferritin by any means leads to a reduction of damage/healing?
Generalized pruritus in dysmetabolic hyperferritinemia treated by phlebotomy.
Regular phlebotomy (blood donation?) reduces iron overload.
The relation between body iron store and ferritin, and coronary artery disease
The Association of Serum Vascular Endothelial Growth Factor and Ferritin in Diabetic Microvascular Disease
“Most diabetes patients have higher serum levels of ferritin that may participate in diabetic vascular complications through high oxidative stress induced by iron. ”
Irrespective of whether you are diabetic or not, it makes sense to reduce iron overload by regular blood donation.
If you are aged between 17 and 66 (or 70 if you have given blood before) are over 70 and have given blood in the last two years you can donate blood regularly.
You won’t be allowed to donate if they think iron levels are too low.
If you haven’t donated before and are approaching age 65 it would be worth starting now as that way you can continue to have excess iron reduced regularly for free (and get a free tea/coffee you are not forced to eat the biscuits/crisps)
Know to whom you are giving advice. It seems the world is bigger than you know
I understand the application of the precautionary principle in the case but that is insufficient because:
a) I was a regular blood donor
b) I had an NSTEMI 7 years ago
c) I have steadily elevating serum ferritin
d) The Red Cross, which runs blood donation services in Australia, will not take blood donations from one who has had MI and will not venesect anyone who doesn’t have a very narrow set of conditions
I need to know the risk associated with increasing serum ferritin and what value there might be in taking direct action, such as venesection or chelation, to address the levels rather than identify root cause
This advice (regular blood donation) can also be found in one of Drs Eades’ books. If however you are a former UK resident living in the USA, you will probably find the American Red Cross does not accept your blood donation (it depends on the range of years of residency), because of risk associated with the 1990s UK outbreak of jacob-creutzfeld (“Mad Cow”) disease.
I’ve not found an alternative source for UK ex-pat blood donation in the USA.
If anyone has any suggestions. . . .
“If anyone has any suggestions. . . .”
Leeches. You can kill more birds with one worm.
An extract from medical leech improve the function of endothelial cells in vitro and attenuates atherosclerosis in ApoE null mice by reducing macrophages in the lesions. (Zhao, 2014)
Leech Therapeutic Applications (2013)
Ferritin accumulation is a pretty rare genetic disorder. Does the advice to get rid of Exzess iron apply to the general population?
Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases
Cardiovascular benefits of phlebotomy: relationship to changes in hemorheological variables
Iron accelerates aging P. D. Mangan
Iron the primary driver of aging?
I think it makes sense for post menopausal women and all men to be blood donors.
Plasma ferritin is not necessarily a good marker for iron status. Ferritin is an intracellular storage protein for iron, and increased extracellular level can be a sign of increased cellular turnover/cell death in general. For instance, in many types of cancer ferritin is elevated, even though iron status is normal by other measurements, such as transferrin bound, etc.
It’s just as bad a marker for generic inflammation. I know folks with a CRP of 2 and a ferritin of 5-600.
Dave Liddy asked
” is there any evidence that reducing serum ferritin by any means leads to a reduction of damage/healing?”
The links I’ve provided (if you actually bothered to read them) show there is risk reduction resulting from lowering ferritin (along with other benefits.) from regular blood donation,
” reducing vascular iron stores would reverse endothelial dysfunction, Duffy et al. examined the effects of the iron chelator, deferoxamine (500 mg intra-arterially over 1 hour), on vasomotor function in forearm resistance vessels of patients with coronary artery disease. They found that deferoxamine improved nitric oxide–mediated, endothelium-dependent vasodilation in patients with coronary artery disease, suggesting that iron availability contributed to impaired nitric oxide action in atherosclerosis.”
“Serum ferritin concentrations in normal, healthy, menstruating women are approximately half those of men (34-50 vs. 54-128 ng/ml) and rise substantially, nearly doubling after the menopause. With blood donation, ferritin concentrations of men approach those of premenopausal women which can be a target of therapeutic phlebotomy.”
“The evidence that phlebotomy has a marked influence on the rheological properties of blood by significantly lowering Whole Blood Viscosity (WBV,) plasma viscosity, hematocrit (Hct) and fibrinogen and that there is a relationship between elevated WBV and the occurrence of major cardiovascular events, strongly suggests its therapeutic potential in lowering the risk of cardiovascular disease. ”
Iron Stores and Vascular Function in Voluntary Blood Donors
“High-frequency blood donors had evidence of decreased body iron stores, decreased oxidative stress, and enhanced vascular function when compared with low-frequency donors. These findings support a potential link between blood donation and reduced cardiovascular risk that warrants further investigation in prospective outcome studies.”
Dr. Kendrick, again thank you so much for this. You make me think. As usual, the medical industry continues to ignore the obvious-whence cometh the inflammation? Food for much pondering.
Hi Dr Kendrick,
Awesome series, cannot wait for the final conclusions. I certainly credit your book “The Great Cholesterol Con” to my personal salvation.
On a more holistic level; I would be interested in your take on Ron Rosedale, M.D.’s hypothesis regarding the body’s growth vs repair hypothesis? In a nutshell he is arguing that excess consumption of carbohydrates and (in particular) proteins stimulate the body towards growth at the expense of repair, and thus leave the body susceptible to the diseases of aging including cancer & CVD etc.
Web reference below,
Dr. K – this just gets better and better. A huge THANK YOU.
Regarding sports injury and the like, I have always instinctively reached for the hot water bottle to apply heat to the hurt, much to the chagrin of my friends, and tried to ‘tweak’ the injury, little by little. It seems to work.
I enjoyed this talk more than some recent ones that just contained so much medical jargon that they went right over my head!
After some previous discussion about NSAID’s, whenever I hear how this or that disease is caused by inflammation I realise how idiotic this usually is because the inflammation is obviously there for a purpose!
Maybe it would help if medical researchers tried to think of an ailing body as an entity that is actively trying to heal itself rather than a machine with a broken component!
Can I just say that if little ones fall, as they often do,producing a large lump on the head, I always run a cloth under cold water tap, apply, soon after injury for a short time, because head injury can be serious,no room for the swelling to dissipate. Same for scalds, not very cold water, cool. other injuries may benefit from warmth . Do reach for my homoeopathic remedies.
Damning evidence Dr Kendrick, transparency lacking, as in politics. To highlight as you do informs and arms us. I do stand to be corrected, I have a terrible fault, as my husband says, I think I am always right.
Rule number one in my life:
“Never argue with your wife!”
I have though been married with my woman for about 40 years now.
A few crises emerged when I broke the rule.
Dr. Göran: That’s the first rule every guy learns the minute he says, “I do,” if he doesn’t want to get hit over the head with a cast-iron skillet.
Sylvia, the type of injury you describe is subdermal and will have all the room to dissipate. A head injury where swelling has nowhere to go ( ie subcranial) will not be helped by a.cold compress…
Just two quick questions:
1. Why would one use immunosuppressants to treat cancer, as mentioned in one of the quotes?
2. Hasn’t low dose aspirin been shown to decrease CVD risk? How does this tie in?
The immunosuppression is an unwanted side-effect. Aspirin is an anti-coagulant – it stops platelets sticking together so it is more difficult for clots to form.
Eric: Sorry to butt in, but according to Joel M. Kauffman, PhD.’s “Malignant Medical Myths,” (he quotes spacedoc on this, too), there is no mortality benefit from taking low-dose aspirin, but only with bufferin. Bufferin contains magnesium.
Surely the benefits of aspirin and magnesium should be considered separately. If people need to buffer their aspirin by taking a preparation that contains calcium carbonate, or magnesium carbonate, fine, but it would be crazy to take aspirin just for the sake of the buffer that was added!
I am confused about something regarding aspirin. Acetylsalicylic acid is only a weak acid compared with the hydrochloric acid to be found in the stomach, and I always understood that the action of aspirin on the lining of the stomach was the result of its inhibition of COX-1 enzymes – not its sheer acidity – so why is it beneficial to buffer it in the first place?
David Bailey: I don’t know. My point was simply that there appears to be no benefit in CVD on a population level from taking aspirin. It is clear that magnesium is an essential mineral. Thus the small benefit seen in trials likely comes from the magnesium. I haven’t taken any over-the-counter drugs in decades, and never have taken them much. I stick with high-quality, nutrient-dense food. I must say that I feel better as I’m weaning from my only pharmaceutical (Lisinopril, from 20 mg to 10), but then it is Spring, and I’m replenishing my Vitamin D stores.
Hi Gary, how are you weaning yourself of the meds. I am trying to do the same. Am on 2 meds. Trying to take them every other day but find my blood pressure does spike. Any tips.
bob: I just decided to do it, by cutting the 20 mg pills in half (with a pill cutter). I’ll see the sawbones in June to let her know (she’s fully on board that I am in charge of my health, and she is one reason I have a high opinion of GP’s in general). I’ve done a great deal of research, and am near-certain that this is the right approach. Since I retired, I no longer have any of the stressors which gave me high blood pressure in the first place. I don’t bother checking it at home, and won’t be getting any more metabolic tests, unless something is wrong. I enjoy excellent health. If you’re not sick, why take medicine? Why even see the doctor? I go twice a year because it is always a good experience, and I trust my doctor’s judgement that this is prudent. At one time I was taking, in addition to the ACE inhibitor, a beta blocker and a diuretic. This combo gave me positional hypotension (which is dangerous), so, at my direction and over time, I stopped the other two. My last BP was 131/78, (at age 66) and not even taken properly (according to spacedoc). Now, with the Obamacare computer clogging up the room, there is no way to take it properly.
I also still take lisinopril hydrochloride combined with a diuretic (in one tablet) to control my BP. I am aware that Dr Kendrick has said there is no evidence that lowering BP that way is actually beneficial, but (unlike the statin!), there don’t seem to be any side effects for me. Since I suppose BP must spike in certain situations, and the spikes would be higher without the medicine I assume, I like to play safe. I must admit, I have wondered about dropping this medicine as well.
David Bailey: The only side effect I have is tinnitus, but that may just as well come from my years as a heavy-equipment operator (from the turbocharger on all equipment used at altitude). Read spacedoc’s posts about BP. It seems that wide variation in BP throughout the day is normal, depending on the activity. The diuretic concerned me because it can deplete minerals, so I stopped it some years ago. I know mine really spikes when I’m doing sprints or a long set of pushups or pull-ups, and these activities are supposed to be good for us. I’ve simply stopped being concerned about my BP. It is what it is. I’ll croak when I croak.
This is the most insightful article I have read for a long time. I confess it suits my own bias on thinking about injury confirming that one’s body usually knows what it is doing, don’t rush to medicate except in emergency situations. I have always used this policy on issues of pain, like headache, and not usually taken analgesics because the pain is a warning to stop or slow down.
Oddly, I used to use a tree paint when I cut branches from my trees (a lot of) decades ago, but then (mere) decades ago could not get hold of a tin of the stuff and found that it was regarded as worse than leaving the cut ‘natural’.
Recently I went to an alternative-type nurse practitioner and she concluded that I am full of inflammation. I have Heberden nodes on my fingers (a form of arthritis), had arthritis in a big toe and I have seen evidence of arthritis on X-rays. I also have partial frozen shoulder. How does a person begin to figure out WHY they have that inflammation??
I’m not sure Elaine but I find that my frozen shoulder (what a truly hateful condition), arthritis in my foot (due to badly healed breaks), spotty skin, eczema etc all benefit greatly when I lower my sugar intake. I can’t go too low carb because I’m hypothyroid & it messes with that if I go too low, but fairly low carb (no biscuits, cakes, bread, pasta, spuds, white rice & only berries for fruit) really helps. Sugar is inflammatory, so I wonder if our high carb diets these days have a lot to answer for. I’m not in any way medically qualified, so I wouldn’t dream of recommending anything, but there is growing research to suggest that lowering carbs can help with inflammatory type conditions. Here is one small piece that may be of interest. https://www.sciencedaily.com/releases/2014/05/140508095415.htm
I had frozen shoulder. Had a new treatment for it hydrodilatation. went private for it but the NHS do it but not many GPs have heard about. Worked a treat.
I believe Prolotherapy is a little-known but effective use of this principle which involves injecting a pro-inflammatory agent into an injured joint or muscle which then actually aids the inflammation and speeds healing
To goutboy’s comment above (May 9, 2016 at 10:37 am)
“With regard to c-reactive protein as a marker, uric acid levels (serum urate) are just as accurate and cost next to nothing by comparison.”
Uric acid is one step closer for sure, but neither uric acid nor CRP are primary inflammatory compounds. Please refer to Figure 2 in this paper:
Uric acid is most commonly a marker for fructose overload and hepatic de-novo lipogensesis. In fact inflammation develops from adipose tissue stress (as in Figure 2), first with IL-1beta signaling then with IL-6 response. IL-6 later provokes the acute pahse response in the liver, including CRP.
With over 2,000 patients now on (or trying hard to be) on a Low Carb High Fat (LCHF) diet, watching their biochemical changes has been illuminating. TC rises in most cases, falls in others, TGs plummet and HDL rises. LDL usually goes up. Oxidised LDL particles fall universally.
Liver enzymes fall. Frustratingly the standard response to finding that a patient has Metabolic Syndrome or simply fatty liver is for the GPs to recommend fat restriction and to increase grains and fruits. This instantly makes it worse. But then there is metformin, rosuvastatin and ezetimibe to ‘fix’ everything. We are not on a learrning curve here, we are in free-fall.
Have not heard this one, missed it completely. Just been for a pub lunch with family, one member on statins, had a TIA 2 years ago. He tells me he will be protected from dementia substantially because of this therapy. Beautiful day, collected my vit D in the garden, near to mid day. Have received my D tablets today, will purchase some Gouda and Brie to help K2 absorption. Blackbirds happily eating apples and pears, Blossom on apples and plum tree, not so many bees, sad.
Sylvia: Yes, pollinators are clearly on the ropes. Until a few years ago, our navel orange was so loud with the buzzing of wild honeybees that I could hear it across the yard. It no longer happens. The bloom is coming much earlier now, and I only saw a few this year, and couldn’t hear them at all. Same with all the other bee-friendly plants I have. Even the wild native bees and bumblebees have diminished. Bodes ill for the web of life, for the food supply.
Your post about uric acid levels does not have a “reply” tag, so I trust you will see this. In what way is uric acid a marker, except for gout?
Many of Dr Kendrick’s blogs in this series mention the role of Endothelial dysfunction.
High Uric acid levels have been shown to lead to endothelial dysfunction.
Here is an example
Uric acid enhances PKC-dependent eNOS phosphorylation and mediates cellular ER stress: A mechanism for uric acid-induced endothelial dysfunction
“In conclusion, the present study confirmed previous reports that high levels of UA trigger endothelial dysfunction, inducing apoptosis and reducing eNOS activity and NO production”
High fructose corn syrup has been linked to high uric acid levels.
thank you for this. I am a numbers man, I am at the limit, 7.3 mg/dl. Is this high, or top of the normal? Incidentally I see on the Mayo clinic website, that 42% of sufferers of gout have “normal” uric acid.
There’s more to it than gout:
Seems I was wrong in my previous reply, great:
With all that I read on this site, I tend to be very wary of medicines, especially miracle ones. So here is what I find on Allopurinol on Wikipedia:
Because allopurinol is not a uricosuric, it can be used in patients with poor kidney function. However, allopurinol has two important disadvantages.
First, its dosing is complex. Second, some patients are hypersensitive to the drug, therefore its use requires careful monitoring. Allopurinol has rare but potentially fatal adverse effects involving the skin. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophilia, hepatitis, and worsened renal function. Allopurinol is one of the drugs commonly known to cause Stevens–Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions. More common is a less-serious rash that leads to discontinuing this drug.
More rarely, allopurinol can also result in the depression of bone marrow elements, leading to cytopenias, as well as aplastic anemia. Moreover, allopurinol can also cause peripheral neuritis in some patients, although this is a rare side effect. Another side effect of allopurinol is interstitial nephritis.”
Have a read a lot on the uric acid stuff obviously as I have high levels plus if you believe in the influence of diet on one’s health there is not a lot us gouties can eat, maybe orgnanic grass. I guess my original point was that Hyperuricemia not just gout and indeed uric acid levels in general have as much accuracy in acting as a marker as total cholesterol, with the added bonus that Allipurinol does a first class job of lowering levels and reduces oxiditative stress through reducing xanthine oxidase. But I think I am on firm ground if I said I don’t think it would be prescribed outside gouty circles.
Thanks for the links here’s a goody I have just come across posted it earlier
I am just now reading a book from 2008 which I reluctantly and surprisingly have missed until now. It is the “Trick and Treat” by Barry Groves. It is a book in the true Hippocratic sense of “Let medicine be your food and your food your medicine!”
He is very convincingly advocating a strict LCHF way of living as well as stressing that the current high carb “healthy diet” may actually be the cause for many of our “modern” diseases which he, one after the other, scrutinises against the dietary background with more than 1000 references – impressive work!
Reading your post I couldn’t refrain from looking how he is arguing around gout and here he is spending one page on gout out of the 500, comprising the book. Evidently there are studies, especially one South African interventions study, which indicate that the the dietary advice to go for “low-purin, high-carbohydrate” eating is actually a miss concept. And the advice to eat fruit is also indicated as being a culprit rather than of a remedy for gout.
Robert Lustig has the whole chemestriy of carbohydrate metabolism in one of his two fructose talks that are available on youtube. It is quite clear from the citrate cycle that uric acid is formed from metabolizing fructose and ethanol.
Interestingly, gout seems to have been common in Tyrannosaurus Rex (the German wikipedia article on gout goes into a little more detail regarding dinausaurs than does the English article), even if they were probably the poster childs for an Atkins diet 🙂
I am so pleased that you have found Barry Groves’s very readable book. I would recommend it to anyone who needs to get to grips with the consequences of our dire modern diet, and the silly indoctrinations we have endured over the last half century, namely:-
1) the “5 a day” poppy-cock notion.
2) unsafe insistance on lowering cholesterol.
3) barmy advice to keep out of lovely sunlight.
4) unhealthy encouragement to consume all types of carbohydrates.
5) disastrous pressure to consume processed oils rather than animal fats.
and other gems…..
Although first published in 2008, I would say it is as relevant today as then.
You’ve all seen the headlines about medical error being the 3rd leading cause of death, right?
This fellow’s take has some thought and emotion provoking angles. The comments as well. Whatever side you come down on, it’s a lesson in writing. Enjoy.
JDPatten: Thank you for the link. It is indeed a fine piece of writing. I already know better than to trust what is presented in the media, but (confirmation bias alert!) I had more or less bought this one. Gives much-needed perspective to the issue. As if mortality was optional!
Thank you, JDPatten. Yes, both the original blog and the comments are valuable reading. Having recently spent two weeks at the bedside of someone in intensive care, followed by a week in hospice, my question is: How on God’s green earth would anybody know what actually went on? With all the coming and going of staff, and the countless wires, tubes, and monitors, how would anyone know for sure if there was a non-fatal mistake, a fatal mistake, a cover-up, a death of something other than the mistake. . . .?
And how close can someone from the outside come to reality, writing a report using only available after-the-fact reports?
And this is just about the issues that are universally recognized as medical mistakes. How about things that the officialdom thinks are good for you but which just ain’t so: statins, antidepressants, universal mammograms, psychotropic meds, aggressive BP lowering in the elderly leading to falls, broken hips and (possibly) increased mortality, polypharmacy… Once you factor all of those in, it’s almost possible to say that modern healthcare is one of the leading causes of morbidity and mortality in the developed world. Dr Kendrick touches on some of these issues in “Doctoring Data” as does Dr Goetzche in his excellent “Deadly Medicines and Organized Crime” and “Deadly Psychiatry and Organized Denial”.
Sasha, David, yes. I’ve often thought of how some of the things that are considered good medical practice might actually contribute to not-so-good outcomes. These are probably not the things that get tallied up as “medical mistakes.”
I agree that, though with English not being my mother tongue, I am truly impressed by the “high level” and not least the “hyperbolas”.
Anyway my profound feeling, reading this, is that he believes in the “system” while I don’t. Big Pharma is hovering friendly in his mind while it is a foe in mine.
I liked your article because it illustrates the way in which issues can be distorted by starting with data generated by a computer model, and then applying a ‘spin’ to the results so as to make headlines.
I mean, if your job is to patch up severely ill patients, you will make some mistakes – just as everyone else does in other walks of life. In software development, these are called ‘bugs’ and there are plenty of them – but the world is (at least arguably!) a better place because of all that software, even though it is imperfect!
Some years ago, there was a fad for proving computer programs correct. If you could prove your program was correct, it just couldn’t have any errors, could it? This did not remove bugs from software, because it was hugely hard to apply to decent sized programs, and it was conceptually flawed because it required a specification that was so detailed, that it itself was filled with errors – so the specification would have required a proof of correctness using a meta-specification…… Despite this, a lot of people made a name for themselves by promoting this fad.
It seems obvious to me that the number of people who die ‘needlessly’ in hospitals is a totally arbitrary construct, because it implicitly assumes either that doctors should reach some arbitrary standard (which could be adjusted up or down to obtain any desired number), or (unrealistically) that they all perform as well as the very best!
Furthermore, as Dr Kendrick often points out, people are never ever saved – they all die – and any statistic that refers to lives saved or lost is fundamentally meaningless.
I think it makes far more sense to focus on the errors that are deliberately perpetuated – low fat, high carb diets for diabetics, statins, types of operation that don’t seem to confer advantage, etc etc.
I just received “The Truth About the Drug Companies” (2005) by Marcia Angell the former “New England Journal of Medicine” editor for 20 years.
Having now read the introduction i realise that she believes in reforming the Big Pharma system while I myself firmly believes that a radical (root) change is necessary on a systemic level. However I don’t know how such a radical change is to take place although believing that it is absolutely necessary.
Perhaps it is only through a world wide grass root movement, as during the 70-th, enough pressure can be established.
I notice an understatement here:
Does anyone have any comments on the following article? It seems to me that the world is slowly waking up and seeing a little more clearly.
Click to access paradox.pdf
Lorraine: One minor error in the article: Ancel Keys was not an M.D. He had degrees in political science, biology, and oceanography, and his PhD. was in physiology.
Makes the whole thing a little more crazy then!
Some new interesting news on the new cholesterol lowering drug PCSK9.
“Another Major Insurer Is Tying Drug Prices to Health Outcomes”
Nitric oxide compromised by exercise?!
Do you trust this bit of research?
Is it probable, possible, or unlikely?
Intense exercise does the harm. Intense interval training is the go-to for “healthy” exercise now. Not?
Be careful not to overdo when chopping wood!
JDPatten: Interesting read. Note the effect was transient, and that no heart abnormalities were found in the control group, only a spike in ADMA and SDMA. I do my high-intensity interval training in sunlight, so perhaps the increased NO production mitigates this? Our ancestors would have been chasing down those wooly mammoths in sunlight.
I think you have to be very careful when you spot an ‘abnormality’ that you are not mistaking part of a healing process for part of a ‘disease.’ If you exercise there will be, short-term, damage to your muscles. This short term damage stimulates muscle growth and strength.
I get the damage to your muscles part – no pain, no gain – but I worry about the set-back in nitric oxide and consequences to the endothelium.
There is some evidence that very intensive exercise may be damaging. However, to suggest that exercise may cause atherosclerosis flies in the face of most of the evidence that I have seen.
Malcolm, very interesting series of posts on causes of HD.
Have you come across Dr Knut Sroka? He uploaded the following short video on how the heart can naturally ‘by-pass’ arterial narrowing. How does this fit in to your understanding of heart disease?
Heart Attack New Approaches, Dr Knut Sroka, 22 December 2012 (4:54 mins)
Dr Knut Sroka’s website – http://heartattacknew.com/faq
Showing new aspects in diagnostic and therapy of heart attacks, questioning the established and classical way. Why Stents and Bypass surgery are most often useless and new approaches are urgent!
Many times during the last ten years I have been convinced that the different dogmas within medicine are resting on very little scientific foundation. The statin business is just the tip of the iceberg.
Dr. Sroka has certainly added to my disbelief in these dogmas about heart disease and his video is a “killer”.
The collaterals can certainly carry blood around the blockage; the video shows that. But how much blood? A large-diameter pipe can carry a LOT more liquid than a smaller pipe. I would worry that the collateral flow was inadequate to cope with heavy exertion.
You seem pretty active without stents, Dr. Goran, but do you have to pace yourself, or do you not worry about the blood flow in your coronary arteries?
For sure I am limited in my physical activities since 1999. My blocked arteries will not open up so, with at typical English understatment, I am not much of a runner today and I have to rest now and then during my chain saw and wood chopping activities.
My own guess, as well as that of the cardiologist of 1999, is that prolonged exercise builds new collaterals all along, and according to that cardiologist the probably saved my life at that time, a view that seems to coincide with that of Dr. Sroka.
Still this surprises me as e.g. today when I was on a forest excursion and didn’t have any problems keeping the pace with all the other participants.
Actually, the diameter of a particular pipe is rather academic, so long as there are a LOT of pipes. And there are a LOT of collaterals. And exercise makes them bigger.
Thanks for those replies. So your heart can remain healthy without medical intervention provided you make lifestyle changes and adjust to its reduced capacity.
I found this quote in Natural Bypasses Can Save Lives:
“When blood flow is increased, the inner layer of vessel cells (endothelial cells) sense this necessity and start the process of enlarging from capillaries into genuine collateral vessels. In response to endurance exercise training (such as running, bicycling, swimming, and hiking), blood flow is increased, which leads to a conversion from capillaries into collaterals. This is a very elegant treatment everybody can accomplish.”
Incidentally, my very first job as a civil engineering technician was to calculate how the flows and pressures in two municipal water supply networks would be affected if they joined them together to share costs. Effectively, it was a network of main arteries, collaterals, and capillaries bleeding off (i.e. house connections). This was before computers. It’s an iterative process where you first guess the answer then calculate a correction factor to each little loop to improve your guess. Rinse and repeat. Each iteration took me a week, and I did three iterations before the boss said that’s close enough. These days a computer would take a couple of seconds and be far more precise..
Engineers are special 🙂
Our job, contrary to that of almost all ‘medicine men’ is to look for solutions to technical problems. I think that is why I arrived at refusing by-pass and heart medicines an finally skipping all carbs.
Someone here on this blog gave a link where I ended up with watching an appealing great talk by of another engineer, Ivar Cumming, apparently with the same attitude as mine. I guess that is why I almost completely agree with what he is saying (except about the mammography as a reference point).
I think it is a well spent hour listening to this pedagogical lecture about causes for most modern diseases – “Insulin resistance syndrome” driven by excess carbs.
@ Dr. Göran Sjöberg
re: Many times during the last ten years I have been convinced that the different dogmas within medicine are resting on very little scientific foundation.
CVD prevention/treatment, dietary advice, diabetes prevention/treatment, thyroid testing/diagnosis/treatment are all festering scandals, not to mention all the other utterly optional chronic ailments that result from the defective dietary advice.
re: My blocked arteries will not open up so…
What led you to that conclusion? Have you had a CAC scan? Here in the US, Dr. William Davis used to be primarily focused on slowing, arresting, and reversing calcium scores. His 2011 book on it is available as a free download at:
Click to access TrackYourPlaque_2ndEdition.pdf
See Chapter 6: Can I reduce my heart scan score?
The TYP book was replaced by the web site that now hosts it, and the dietary advice saw further refinement in his 2014 book “Wheat Belly Total Health”. Click my user name for disclosures relating to all this.
Thank you for your advice.
I have not have had any CAC scans although I now understand that this is probably the best way to “measure” the state of the heart affair. Angiography might be the second best but here I keep away as well. I believe the my body is the best measuring instrument. When it tells me that I am OK I am probably OK and just now it is telling me that I am fine.
The message is clear. Go for the cause, as Ivor Cummings suggests, read all carbs plus PUFA’s, and chop your fire wood with all your might and relax in front of your fireplace with a glass of wine (as I do just now); evidently it doesn’t hurt.
And of course keep away from the health care system if you don’t break your leg. They would be more than happy to perform all sorts of scanning on me and throw a number of diseases on me. “High cholesterol”, “High BP” etc. They are creating a lucrative market for their business.
Let’s feed statins to mice instead.
Statin treated mice are able to more efficiently clear themselves of Lyme disease. They are an essential reservoir of this disease that effects so many of us people. Better they should get the statin. Each little wildling should have his own little prescription for tiny statin pills. Or we could spread statinated bait by crop-duster? How probable is that?
Interesting but useless research that’s not likely to go anywhere.
Another useless drug? JAMA on β-blockers. Among patients enrolled in the international REACH registry, β-blocker use was not associated with a lower event rate of cardiovascular events at 44-month follow-up, even among patients with prior history of MI. http://jama.jamanetwork.com/article.aspx?articleid=1367524
I dropped the betablocker half a year after my serious heart attack 1999. I had read enough about the “side effects” as well as they having turned myself into a zombie to take that decision.
My posiiton today, practically, is that all heart drugs are useless together with the CABG.
Go for the cause instead – carbs an PUFA’s.
Off topic but important
Known nearly 20 years ago but only published on line in 2012
Lovastatin A New Cholesterol-Lowering Agent
Julie J. Krukemyer Pharm.D. andRobert L. Talbert Pharm.D.*
Article first published online: 24 JAN 2012 DOI: 10.1002/j.1875-9114.1987.tb03524.x
Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy Volume 7, Issue 6, pages 198–209, November-December 1987
The most common adverse effects are gastrointestinal, while the most serious are elevated transaminase levels and the potential for lens opacities. ie cataracts.
Who is responsible for hiding this data and for the millions who subsequently suffered from cataracts?
Dr Malcolm – I have been following this series of blogs with enhanced interest. My husband suffered a massive heart attack on 22 March, and now has three stents, and is taking a massive concoction of drugs to control heart rhythm, thin his blood, make him pee, control his blood pressure – you name it, he’s probably taking it! We were both astounded when the consultant said that it was “more than likely” that the radiotherapy he received in October for male breast cancer had brought this attack on. He talked about inflammation, of course, and this is why your latest post has caught my attention. To see it as “healing” rather than an “injury” (is that the word I want??) is a bit of an eye-opener to me. I’ve always seen “inflammation” as something that needs to be quelled in some way. Just to add to his catalogue of woes, my poor husband also developed discoid lupus erythamatosis (again, is that correct?) following the radiotherapy. We were told categorically that the radiotherapy had not caused the latter, but when I delved a little, it seems it comes about when the body’s immune system is interfered with in some way, and I would say that radiotherapy is quite an interference! Thank you so much for your enlightening articles.
Just in: Dietary fat causes heart disease – from Ornish himself, at length.
I saw this today, a way to explain how statins cause muscle damage.
My thanks to JD, Cindy and David for the interesting links and of course to Dr Kendrick to providing the basic blog and supporting the contributions of many people who provide further in sights – many eyes providing useful information.
Heart Disease root causes – good talk
David: Thank you! What an outstanding presentation.
Style and substance from Ivor Cummings is so good. Same fabulous easy on the ear as Dr Kendrick. Both could do stand up.
I too agree – outstanding presentation.
Thank you for putting me on this track 🙂
Everyone should watch Ivor Cummings lecture!
since we seem to be reading the same books, may I recommend this one:
The Modern Nutritional Diseases and How to Prevent Them (English Edition) Format Kindle
de Alice Ottoboni (Auteur), Fred Ottoboni (Auteur)?
It is very clear and well explained
Yes, everybody should. It’s extraordinarily good. He is a highly articulate communicator. Also watch his interview with Dr. Kraft. Pathologists can tell us a great deal about disease process.
In my mailbox today I just received the book “The Modern Nutritional Diseases” by your recommended authors Alice Ottoboni and Fred Ottoboni
The most recent Fat Emperor interview with Prof Tim Noakes is equally rivetting, not least on the causes of heart disease.
This is another interesting article:
Cholesterol, longevity, intelligence, and health.
Mike. Thank you so much for that link, what an interesting article and plainly put!
This is very off-topic, but so terrible I bring it to your attention. I first picked this up on Zoê Harcombe’s blog, posted by Barry:
When you read what the commissioner of the FDA was allegedly up to, and that Levaquin was responsible for 5000 deaths, perhaps, like me, you will conclude that the best medicine is no medicine!
mr Chris: I read that story, too, but was not shocked. The federal government is utterly and thoroughly corrupt. I agree that the best medicine is no medicine. I am successfully weaning from my only “medicine” thusly: three weeks at a half dose daily, followed by seven weeks of a half dose every other day (this represents how many pills I had left when I made my decision). I have finished the first two weeks of this regimen, and there will be no looking back. I simply no longer think my BP needs to be treated other than with lifestyle intervention.
My doctors have not been much help when I have had to taper off a drug that did not help or stopped working. I followed one tapering instruction from the doctor, and ended up with a severe reaction. Some others I was on a low dose of a drug, and the doctor said I could just stop cold turkey. I taped off any way, but hard to know exactly what was best and how. There are a lot of articles on ghost writing studies by drug or food companies. My doctor or any of us can be misinformed and not sure what to do. I would read the small print given with a drug. found out I was hit with a severe,rare side effect that was listed. Other side effects from drugs, were not on the sheets then, but are listed now. I am much more cautious and informed now that I have the internet, that I did not have then.
Cindy C: My doctor doesn’t yet know that I am tapering and will stop altogether. I will let her know in one month when I for my semi-annual visit. She’s really a good sport, and I’m sure will accept my decision once I explain it (I’ve been going there more than 25 years). I simply am as certain as it is possible to be that my BP is not such that it should receive pharmaceutical treatment. I have reached this conclusion from reading and understanding Dr. Kendrick, Dr. Graveline, Dr. Kauffman, and several others, but the decision is mine alone, not influenced by these fine folks, but by understanding the knowledge they have freely shared with the public. I was once on four drugs, and have long since dropped the others; this is the last one. This one can cause kidney damage, which is enough for me to swear it off. I enjoy excellent health and do not live in fear, so it was an easy decision to make. Food and exercise, gardening and cooking, reading and solving puzzles are my medicine.
I have not taken any drugs to lower my blood pressure for about 10 years now. With me, it was moderately high because of stress and chronic pain. When I got those more under control, no need for the drugs. My doctor is aware of the connection, so does not insist on drugs. More studies now show aggressive lowering of blood pressure and blood sugar in the elderly with drugs, some times using multiple drugs, can be harmful. Adult coloring books are now popular to reduce stress.
Cindy C: Yes, the stressors in my life are long gone. I feel wonderful, eat only high-quality food, exercise vigorously and stay active and mentally engaged, have no aches or pains, except minor ones, and sleep like a rock, so I don’t need drugs.
Which drugs are you trying to get off.
Lee I would like to get of BP meds. How do you taper off them without getting a reaction.
A lot of “high” BP appears to be related to insulin resistance. Stopping eating fructose (i.e., fruit) helps, as does (for me anyway) intermittent fasting (IF). These both help reduce fatty liver and fatty pancreas, and cause BP to go down. I’ve reduced my systolic BP by 10-15 mm Hg using mainly IF (on top of low carb, high fat). I have the confounder of losing about 30 pounds too, though. Also, I lost another about 20 pounds using low carb prior to trying IF, but that didn’t have the same effect as what was caused by IF. (Again: there’s a confounder of losing a total of about 50 pounds between LC and LC+IF, though.)
And salt intake is basically meaningless, and lowering salt too much is likely worse than “high” BP.
BobM: I fully agree, and this is largely what I have done. For me IF means simply fasting each day for 15-16 hours. Having adapted to a high-fat diet, I never get hungry to the point where I can’t delay eating for the 1-2 hours it takes to prepare the meal, or before about 10:00 a.m. (I arise at 5 a.m.). I gave up sugar and industrial food years ago, but what really had a big impact was giving up grains. What small amount of belly fat I had melted away, and I discovered I have abs. I’ve stabilized at 63-64 kg (175 cm) over about a two year period. I have exceptional health, so I’m not going to bother checking my BP, except at the sawbones. We do too damn much measuring and testing!
How many hits can statins take. From American Heart Ass. – patients treated with statins, but have repeatedly failed to reduce cardiovascular events. http://atvb.ahajournals.org/content/36/5/777.abstract
The abstract states: “However, therapeutic interventions such as niacin, cholesteryl ester transfer protein inhibitors increase HDL cholesterol in patients treated with statins, but have repeatedly failed to reduce cardiovascular events.” Does anyone know if lowering lp(a) with niacin has an effect on cvd and/or total mortality?
Niacin is controversial, something about liver toxicity I think, so I said to myself why take it. By the way I take many supplements but not niacin and have lowered my triglycerides to 1.2 from a border line high level before taking suppls.
Hi, which supps do you take. Any for high blood pressure
I just watched fat emperor’s interview with Dr. Kraft. What great information! Does anyone know of a reputable lab in Philadelphia, USA to get Insulin Assay test?
Has anyone noticed that they are going to spend £1million on a new study to decide if statins cause muscle pain.
“The new trial will involve 200 patients who have stopped or want to stop using statins due to muscle pain or fatigue.
It will investigate whether muscle issues are more common in those using the statins than those taking a dummy drug. ”
I know of one person who will not be volunteering to try that out!
If we believe in the scientific idea of cause and effect and accept the overwhelmingly convincing facts telling us that indigenous people tuned to their natural foods for many thousands of years didn’t carry ANY of our modern diseases – basically not a single case has been reported except among those people that had acquired the agriculture – there must be a “common” underlying cause behind all these diseases and related to our “western style of life” well documented by e.g. Weston Price 80 years ago.
The common cause is, within 10 – 20 years, manifested in our diseases like CVD, cancer, diabetes, arthritis, depression and many others. The main driver seems to be the carbs, notably plain sugar, but especially the cereals, and recently (last 100 years) enhanced by the vegetable oils with the PUFA omega 6. My guess is that our physiology is responding homeostatically through inflammation to alleviate the foreign stress imposed.
So – you don’t solve the problem by fighting the inflammation in the long run. It is like fighting the fire brigade instead of fighting the present rampant corporeal pyromania.
Well said, Goran. You think like a scientist. Too many scientists don’t it seems.
This dogma is not about to lie down and die – letter in The Times this morning!
“Sir, Dr Andrew Bamji’s unfortunate and misleading comments on statins (letter, May 14) cannot remain unchallenged. There is a very large body of evidence from well-conducted clinical trials that show that statins reduce the incidence of cardiovascular events and mortality in those at increased risk. Their risk reduction is clearly related to the observed reductions in blood cholesterol. How that risk is assessed is a different question.
Stains, used correctly, remain one of the true advances in modern medicine.
Professor Robert Elkeles”
“a very large body of evidence from well-conducted clinical trials that show that statins reduce the incidence of cardiovascular events and mortality in those at increased risk.”
How long it will take for this myth to die. Michel de Lorgeril had an interesting article in the Journal of Controversies in Biomedical Research last year debunking the “well-conducted clinical trials” claim.
I picture the statin proponents all standing around with their fingers in their ears, singing, “La-la-la-la-la-la-la, I can’t hear you. La-la-la-la.”
I hope you all get a chance to read the latest post by Dr. Feinman (Prof. of Biochemistry at SUNY USA). One of the best posts I have seen, right up there with all of those which employ science to support their statements, something so lacking in so much of what we are offered as “proof”. Here is the link.
And if you are up to the science, check the post by Peter Dobromylskij called “uncoupling and weight loss” at this link – http://high-fat-nutrition.blogspot.ca/. You will have to scroll down to find the right post. After reading Dr. Feinman’s post, what Peter wrote was much more understandable to me.
Thermodynamic happens to be one of my favourite subjects and to me the very idea that “a calorie is a calorie”, i.e. overeating being the cause for our weight gain over the years, is just an incredible ignorant stupidity that is proposed by our nutritional establishment. The stupidity, and the ignorance of basic thermodynamics, is the supposition that we are considered as being “closed systems” and calories in an calories out are unrelated variables. These guys wouldn’t even pass the simplest exam i physics.
General weight gain is about one kg per year rendering 20 + kilos when we have turned 60 and we are starting the weight gain when we are around 30. With this “closed system” view and the overeating hypothesis we are thus gaining about 3 grams per day and evidently “overeating’ those 3 grams. Thus, for whatever reason (bad self control?), we are evidently eating about a fraction of a percent to much food each day. “I don’t want to get fat!” “Well why don’t you just push away one gram from every plate you have in front of you? Then you would have a body at 60 as you had at twenty!” How much “brain” does it really take to understand that this, as THE explanation for people getting fat, is utter nonsense. No one can control his food intake with such precision.
I am eating “like a horse”, though not oats but LCHF, and dropped 20 kg in two years without effort or counting a single calorie and have never been hungry. My wife lost 12 but we were only interested in our health issues. While restoring our health the weight drop was then purely a bonus.
Thank you for an interesting link.
Though I must say that we are now entering into very deep waters and may easily be carried away by details.
By coincidence I just happen to be halfway through my current reading of “THE CELL” (Alberts) which happens to be chapter 14 “Energy Conversion: Mitochondria and Chloroplasts” and I am both intrigued and amazed by the scientific rigour here in the detailed depicting of the thermodynamic chain of events involved. Completely to my taste! This actually connects very well with what I now read in your link about the nutritional preference for saturated fats on this level of the mammalian metabolism.
Though, a necessary humbleness in front of the evolutionary complexities now hits me like a hammer and I realise that this also happened at the most basic level of biochemical understanding.
What about the complexity at higher levels, e.g. the cell level or at the interaction between different cells? Not to mention within higher order organisms.
What if I see a delicious cake and want it?
Then we are perhaps back at my favourite philosopher Schopenhauer with his “The World as Will and Representation” and the official nutritional nonsense.
Surely this is a joke:
Statins for unborn babies!
What has the world come to?
Saints preserve us!
Goran, I too love thermodynamics and have often used the “closed” system argument in previous discussions on CICO. What I found interesting and did not understand in the science of uncoupling was that these chemical processes essentially mediate the conversion of input energy to output energy. What this made me see is that the body controls how much food product is actually converted to output energy. This now explains why you can eat “like a horse” and not gain any weight. I have the same experience. Clearly this is not the only mechanism for weight gain, and the types of input calories matter. During the reading of the Ottoboni’s book I also realized that the pathway where fats are converted to ketones, excess ketones will be wasted if unused for energy. This in another mediating process in homeostasis. So, yes, there are a lot of other processes involved. Still learning a bunch.
” What this made me see is that the body controls how much food product is actually converted to output energy. ”
This statement needs some refinement. The body is not in control, rather its microbiome is.
Do microbiotas warm their hosts? (Rosenberg, 2016)
“All natural animals and plants are holobionts, consisting of a host and abundant and diverse microbiota. During the last 20 years, numerous studies have shown that microbiotas participate in the ability of their hosts to survive and reproduce in a particular environment in many ways, including contributing to their morphology, development, behavior, physiology, resistance to disease and to their evolution. Here we posit another possible contribution of microbiotas to their hosts, which has been underexplored – the generation of heat. We estimate that microbial metabolism in the human gut, for example, produces 61 kcal/h, which corresponds to approximately 70% of the total heat production of an average person at rest.”
Diana: Yes, the microbiome is in charge. Our human parts are merely its high-rise housing. So keep them well fed and happy by giving them plenty of soluble fiber from vegetables.
This was also linked to the one Diana posted. I have read parts of this. There has been concern because fat changes the composition of the microbes. However, breast milk has mixes of fat, protein, carbs, and even has fiber. Some fatty acids act against microbes, which can be good to fight infection, while other part of the milk encourage some.
Sorry, but I don’t buy it. There is no way that the microbiome is generating 70% of the body heat at rest. In any case, this is irrelevant to the uncoupling issue which is taking place in the mitochondria. I suspect that you can kill all of the microbiome in the body and your body temperature will not drop. We are missing something here or the study is “bollocks” as you brits say.
I think that if you kill all the microbiome in your body, your temperature will drop and very quickly. Largely because you will be dead.
Although there is still lots to learn’t the idea that gut microbiota could be a diagnostic marker of coronary artery disease is worth considering.
Characterization of gut microbiota profiles in coronary artery
disease patients using data mining analysis of terminal restriction fragment length polymorphism: gut microbiota could be a diagnostic marker of coronary artery disease
It’s interesting also to note giving humans sufficient vitamin D3 to raise 25(OH)D to the natural levels found in indigenous peoples living now as human DNA evolved, improves the diversity and range of gut flora, reducing pathogenic while increasing beneficial forms.
Effects of high doses of vitamin D3 on mucosa‑associated gut
microbiome vary between regions of the human gastrointestinal
Thanks Ted. I just started reading this.
“Sorry, but I don’t buy it. There is no way that the microbiome is generating 70% of the body heat at rest.”
Haha, John. I love your categical opinion. Reconsider, to put it mildly.
“Sorry, but I don’t buy it. There is no way that the microbiome is generating 70% of the body heat at rest.”
What makes you think so? I suggest you reconsider.
I believe a calorie is a calorie. Remember the “Twinkie Diet”? A professor of nutrition lost weight on a diet composed mostly of cookies, demonstrating that it doesn’t matter how you get your calories, it is the amount that matters. Not sure about his general health, though.
The same article also reports on another diet experiment: They gave participants “diets with just enough calories to maintain their current weight but that varied the ratios of fat, protein and carbohydrates. After 33 days, those assigned to a no-fat diet were still at their pre-study weight. So were those who got 70% of their calories from fat. Percentages of carbs and protein didn’t matter either.”
Personally, I have lost 15 kg on a LCHF diet without effort or counting calories. We seem to have a built-in mechanism for controlling our protein and fat intake, but not one for controlling our carb intake.
For instance, a typical lunch for me would be two one-egg omelettes with a slice of cheese, tomato, sauerkraut, sprouts, maybe some broccoli. 350-400 calories. I know I couldn’t eat another omelette. Yet as a treat the other day I scarfed a 200g packet of biscuits with 75g chocolate, over 1300 calories, and hardly felt I’d had a meal. Somehow, those carb calories don’t register on the meter.
I think that’s right. We probably did not evolve with a lot of carbs around to eat, so we can just keep on eating them.
Dear Dr Kendrick,
I read in ch 9 of “Modern Nutritional diseases by the Ottoboni’s that Omega 6 EFA’s have an inflammatory effect, which, by inference is bad. If inflammation is a sign of a healing process taking place, is this inflammatory effect, the result of Omega 6 EFA’s, largely of plant origin causing some bad effect to which the inflammation is the body’s answer?
Martin, these diets were either just calorie sufficient or calorie deficit. There is every reason to believe that such diets will allow you to maintain or lose weight. No one is saying that calories don’t matter, especially where one is in deficit. If you burn all the calories that you consume, you will not gain weight. The problem is that you don’t know how many calories you need to maintain weight, and neither do wild animals who just eat what then can get and obviously don’t consider such things as being overweight. Our bodies are designed to be in homeostasis and to make this work the nature of the nutrients matter. If you consume more calories of carbs than you can burn in a short time, the nature of the processes involving insulin and glucose will cause any “EXCESS” glucose to be stored as fat.(Glucose is being stored on a continuous basis while it is in the circulation). Furthermore, if you are insulin resistant, you will still have higher than baseline insulin present in the circulation after the glucose is all gone from the circulation, so your fat cells will be shut down and not available to provide nutrition in the form of fatty acids to feed your body. So you will feel hungry and probably eat more and the cycle repeats. This does not happen when you eat fat instead of carbs because a lot less insulin is produced. So if you are not insulin resistant and you are not eating in excess of your “immediate energy needs” (whatever that my mean), you will not store as much in the form of fat and therefore gain weight. You fat cells will be available to provide the nutrition your body requires because insulin is low. No magic there, but no insight on how to prevent the obesity epidemic either. Typical high carb calorie restricted diets fail in the long run because the patients can’t stand the continuous hunger, not because they don’t work. All nutrients are not the same when it comes to metabolism. High fat diets work because hunger is a non-issue.
Do people who are not insulin resistent benefit from LCHF?
Hi Dr Kendrick
Do you think some Auto Immune illnesses like Lupus could be caused by Gluten damaging the gut lining? Whether Celiac disease is diagnosed or not?
Surely these illness arise from inflammation?
I may have already sent this but connection to $ is atrocious On 7 May 2016 10:38 p.m., “Dr. Malcolm Kendrick” wrote:
> Dr. Malcolm Kendrick posted: “Heart disease and inflammation. A few people > have sent me links to a recent paper called ‘Inflammation and > Atherosclerosis.’ This was published in Circulation, and the authors were: > Peter Libby, MD; Paul M. Ridker, MD; Attilio Maseri, MD. Remember two ” >
Sorry for this off topic comment, but while searching past posts I came across some responses to one of my comments to which I did not reply, because Dr. K issued a new post and I thought the other thread was over. The comment which I made was that I did not believe was that 70% of our body heat was being generated by the microbiome. I stated that you probably could kill all of the microbiome and the body temperature would not be affected. Perhaps that was a bit extreme as a response as probably temperature would be affected either up or down, don’t know which. Shasa thought that it would go down fast as the body would be dead. Diana asked why I thought so. Well I don’t have a scientific answer, but I thought that a newly born baby doesn’t have an established microbiome, but develops it over the course of time. So if one destroyed one’s microbiome with say antibiotics, would that necessarily drop your body temperature to the point that other processes would not be able to compensate?
Anyway that was my thinking. Sorry that I did not respond earlier.
John U: Appreciate your input. Dr. Kendrick’s blog is a process of learning for all of us. If an infant is swaddled because it cannot generate sufficient body heat, what implications does this have in your thinking?
“Well I don’t have a scientific answer, but I thought that a newly born baby doesn’t have an established microbiome, but develops it over the course of time. ”
Sorry, John. Sasha is right and you are wrong. I don’t know what you mean by “established” – probably something along “adult-like”? but neither foetus nor a newborn baby is sterile. Even (heatlhy) placenta is full of microbes.
Babies in the Womb Aren’t So Sterile After All (2015)
Developmental aspects of maternal-fetal, and infant gut microbiota and implications for long-term health (Neu, 2015)
Hello Dr Kendrick.
I have just been listening to a radio interview you gave last year. In it, you mention aspirin and the cost/benefit of taking it to reduce your chances of heart disease when it might cause a bleed. Do we know the chances of a bleed on aspirin compared to on prescription anticoagulants? And, if the latter carry a higher chance of a bleed, is it considered an acceptable risk when the danger is CVD or DVT/embolism? Finally, in the case of DVT, is it as “simple” as “just” lowering your clotting factors?