21st August 2018
One of the most common diseases in the world is type II diabetes, and it seems to be increasing inexorably. I feel I should quickly mention that I have a problem with calling a high blood sugar measurement a ‘disease’ but that is an issue for another time. Anyway, because type II diabetes also greatly increases the risk of CVD (by around 300 – 500% depending on which study you read) then I could hardly continue ignoring it, in a blog primarily focussed on CVD.
At present, the increase in CVD risk in diabetes is not explained by the widely accepted risk factors.
‘Patients with diabetes have increased vascular vulnerability to atherogenic insults, leading to accelerated atherogenesis. Although atherogenesis is in part due to the increased prevalence of traditional cardiovascular risk factors, these factors cannot fully explain the propensity toward vascular complications in diabetic patients.’1
This, in some ways, is a rather bizarre concept. Type II diabetes is a traditional risk factor for CVD. So why do we need to explain why a risk factor cannot be explained by other risk factors? Which, if you try to chase down the logic, provides a perfect example of the incoherence around the thinking on CVD.
Anyway, what is really meant here is that, whilst other conventional risk factors, such as blood pressure, are raised in diabetes (although not necessarily) most other ‘traditional’ risk factors are unchanged. LDL is certainly not raised, although there is usually a high VLDL/triglyceride level and a low HDL level. However, in my opinion – and the opinion of many others – the high VLDL and low HDL is a result of insulin resistance in the liver. It is not a cause of, anything2.
So, what causes the greatly increased risk of CVD in type II diabetes? What is the mechanism, or process going on here? You may be thinking to yourself, a high blood sugar must be damaging. Now that may well be true (although it could well be that a high insulin level is damaging, because you rarely find one without the other). But if a high blood sugar is damaging, how does it do the damage?
At this point I shall introduce you to the glycocalyx – never mentioned before on this blog. Not, I hasten to add, because I had never heard of it, but because it added another complication to the discussion so far. A complication that I felt was not needed. Now it is. Because you cannot explain how diabetes increases CVD risk without looking at the glycocalyx.
If you have ever tried to pick up a fish, you will find that it slips through your fingers. This is due to the slippery slimy layer that lies on top of the scales. This is glycocalyx, or at least the fish version of glycocalyx. It allows fish to swim faster, because the glycocalyx is almost frictionless.
Inside your blood vessels, and lining endothelial cells, we humans have a slippery, slimy layer that, under a powerful microscope looks like a billion tiny hairs. This is our glycocalyx. A slippery forest. It does many, many, different things. Yes, I know, the human body is just mind-bogglingly complicated.
What are these ‘hairs’? They are usually referred to as proteoglycans. Basically, long strands of protein and sugars bound together. You can look them up on Google images, if you wish. Lots of pictures to see.
Perhaps the best paper to read in this area is, the following: ‘Loss of Endothelial Glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.’ 3
Main functions of the glycocalyx:
- Protects the underlying endothelium from damage
- Maintains the endothelial barrier function
- Acts as a mechanical sensor for stress/shear stress
- Mediates nitric oxide (NO) release
- Anticoagulant (stops blood clotting) – many anticoagulant factors live here, including NO
- Prevents adhesion of white blood cells and platelets.
It should come as no surprise, therefore, that if you damage the glycocalyx, a number of very bad things are going to happen. Damage to the underlying endothelium, adhesion of platelets, loss of anticoagulation, severe disruption to nitric oxide synthesis etc. etc. And a high blood sugar level does ALL of these things.4
So, there you go. Diabetes/raised blood glucose greatly increases the risk of CVD by causing damage to the glycocalyx/endothelium, and a parallel increase in the risk of blood clotting. Which, as you may have noticed, is exactly the mechanism of action that I have been outlining on this blog for the last three years. And if you think it cannot be that simple. Well, it is.
I’ve been taking a supplement called Arterosil for the past year that is supported by several clinical studies showing that it protects the Glycocalyx.
I’d love to get you your take on the science behind this product.
where do you get it? I have tried a couple of places online, and neither seems operational. Am interested in beginning it.
As someone who had a heart attack two and a half years ago at 48, with no “traditional” markers (diabetes, high LDL, etc.), it came down to the probability that my high lp(a) was a foundational problem (180 mg/dl, or 96th percentile). In my journey to understand what really caused this, I have been studying your blogs for some months, and agree that it is in totality a clotting issue. My clotting issue probably has to do with lp(a) mimicking plasminogen, and making my clots harder to diffuse, and the remnants larger – and thus the occlusion occurred faster. However, I find it ironic that we have hard evidence that not only supports the above post and the importance of the glycocalyx, but it has been known since the 60s and 70s. Lester Morrison began studies of chondroitin sulfate in the 1960s (along with several Japanese scientists), and attained some amazing results in secondary prevention, to several orders of magnitude beyond anything that statins or other drugs attain. He postulated, and understood that these substances healed arterial problems and along with heparin sulfate, were building blocks of the glycocalyx. His reductions in future heart attacks were beyond anything else at the time, and were based on a loading dose for many weeks of about 6000 mg daily of chondroitin, and then maintenance of about 1800 mg/day thereafter. I have been on this for two years, and all scans show no advancement of any occlusion or plaque burden. I take effient and baby aspirin daily to limit clotting, and have been in a clinical study for the first drug (from Ionis Pharmaceuticals, and Dr. Tsimikas) for a drug that limits production of lp(a) at the genetic level in the liver. Interestingly enough (ironic really), several large studies have shown that people with high lp(a) do not tend to become diabetic like the general population, but have a higher rate of “early” CAD events. As with many other solutions, this warrior passed into history, and the pharmaceutical companies have made sure up to this point that chondroitin has not gotten press enough to stay relevant. I believe that its repression of inflammatory substances like Nf-KB is also part of its effectiveness. I hope that some of the future studies show a return to this substance, and several recent trials in older patients who have taken this drug for joint pain along with glucosamine, have the exact same reduction in events shown by Morrison almost 50 years ago.
Thank you for that information. I must look more closely at chondroitin sulphate. It is clearly an important player in protecting the glycocalyx
Does chondroitin sulphate have adverse effects?
When I was taking statins, I suffered severe joint pains ( had no idea at that time about statin damage) I looked for anything to help, as I had to stop driving ), and took to glucosamine. I then read that it could contribute to glucose interference, so stopped. I now understand statins also interfere with glucose, Double whammy!
I take a General multivit now, and last night’s telly warns that they are of no value and can ,in fact, contribute to lung cancer etc increase. Well, I just don’ know what to think now. Last week we learned that High carbs kill, Low carbs kill…..for goodness sake….
@Jennifer: ” I take a General multivit now, and last night’s telly warns that they are of no value and can ,in fact, contribute to lung cancer etc increase. Well, I just don’ know what to think now. Last week we learned that High carbs kill, Low carbs kill…..for goodness sake….”
There is a study on multivitamins, by EPIC Heidelberg and it clearly demonstrates that multivitamins lower mortality. But it also noticed that people who started with multivitamins during the study had a higher mortality risk. The explanation: People who suddenly start with multivitamins often do that because they are already sick. And of course it’s logical that these people have a higher mortality risk than fully healthy people who start taking multivitamins. This is called the “sick user effect”. Most studies with multivitamins don’t take into account this effect and therefore wrongly come to the conclusion that multivitamins are detrimental to health.
But please don’t overdo it: Generally a multivitamin containing 100% of the Recommended Daily Allowance is a good idea – and depending on your diet, you even can take a little extra, like a little more vitamin c, vitamin d or magnesium if needed.
Research clearly demonstrates that if you overdo vitamins and minerals, you can really make yourself sick, e.g. raise your cancer risk.
Thanks Leon. I use just what you mention in your response, and think I am doing the correct thing.But doubts persist yet again! So a prof from Harvard is now saying coconut oil is a severe toxin…..oh, well, the half a dozen jars in my store cupboard must be viewed in a different light now….I THINK NOT.
All this ‘research’ is causing confusion and upset, and to quote the new phrase….falls into the category of fake news as far as I am concerned.
I am using the wonderful discussions on this blog to hone in on what I consider to be good advice. That is all I can do, as I have little access to University-based research papers….thank goodness, and so far, so good, as they say.
Jennifer: The Harvard professor apparently has no idea how widespread the use of coconut oil has been as a food, and for skin and hair care for millennia, particularly among Pacific islanders, with only healthful effects. She cannot see beyond the giant SATURATED FAT BAD sign hanging from her forehead.
The following link is from the patent on a product called arterisol, which is a formulation of rhamnan sulfate (very similar to heparin analogues and chondroitin sulfate as well), now being sold. It includes information about testing that EXACTLY follows the method of clotting causing heart attacks that you postulate, and shows how this product (in theory) eliminates the ability of those clots to form on endothelium in the first place, and restores both glycocalyx and NO production in the endothelium as well. It is very interesting, and I plan to do more research as it looks to do many of the things that chondroitin does, and other things possibly better. The rhamnan sulfate comes from a brown algae called monostroma nitidum, and while it supposedly stops the clots from forming, it does not compromise other aspects of normal coagulation like some of the synthetic drugs do.
I too had nasty problems with statins – as you imply, they can be really debilitating, and it is a scandal that they are still being used as widely as they are.
I think my advice would be to take plenty of exercise until you feel the statins are flushed from your system (it too me 9 months to be completely rid of the side effects), and then reassess your health – do you need to take anything? If your blood glucose is still high, you may be able to lower it by simply cutting out sweet things (particularly sweet drinks).
If you look it up, glucosamine doesn’t seem to affect blood sugar levels, and I do take it to protect my joints. In any case a typical 0.5 gram glucosamine tablet isn’t going to be very significant compared with normal sugar intake. It certainly seems to work, but I’d need to clone myself and feed glucosamine to just one of us to be sure.
I would certainly switch back to butter, and eat normal food, rather than ‘low fat’ products.
Above all, don’t let the doctor scare you back into taking statins.
Sounds like bone broth would also be of benefit as it contains chronditin. Another win for paleo/animal foods.
Well, the health benefits of bone broth is well recognized and it has been the staple “drink” for some years now in our LCHF regimen and now I see a good reason to continue. For convenience a slow cooker is required since the cooking needs at least a day, if not a couple, to get “ready”.
Goran you should look into “instant pots”. Basically a modern day electric pressure cooker. I make wonderful bone broth in mine in an hour!
Made me think of this:
“Current (baseline) glucosamine and chondroitin use were associated with a decreased risk of total mortality compared to never use. The adjusted HR associated with current use of glucosamine (with or without chondroitin) was 0.82 (95 % CI 0.75-0.90) and 0.86 (95 % CI 0.78-0.96) for chondroitin (included in two-thirds of glucosamine supplements). Current use of glucosamine was associated with a significant decreased risk of death from cancer (HR 0.87 95 % CI 0.76-0.98) and with a large risk reduction for death from respiratory diseases (HR 0.59 95 % CI 0.41-0.83). Use of glucosamine with or without chondroitin was associated with reduced total mortality and with reductions of several broad causes of death. Although bias cannot be ruled out, these results suggest that glucosamine may provide some mortality benefit.”
I’m not certain but I think I saw other studies showing that the effect is bigger in women than in men. Also note the interesting *higher* risk for death from colorectal cancer in current users but lower risk in former users.
I too think Lester Morrison is an ignored hero of medicine..I too take Chondroitin sulfate every day as suggested by Lester Morrison in the early 1970’s. I have had NO ill effects at all. Here is a link to Lester Morrison’s published research paper of 1973.
I had reductions in Lp(a) using oral Vit C supp’s. Apologies as I have mentioned this before and I know its a sample of 1 but there are papers showing the same results and furthermore my reading went back up when off it for 6 weeks. My readings went from 31 down to 18
Although during his interview (I’m not sure if there were more than one) on the Nourish Balance Thrive podcast Dr. Kendrick stated that Lp(a) levels are static (without intervention)–“…it seems to be that level is just set.You’ve either got a high level or not.”–I wonder if that level can’t be a function of (the tendency to) endothelial damage. There are so many feedback loops in the body, why not this one.
We know one of the functions of Lp(a) is repair of the endothelial lining. Why is it unthinkable that Lp(a) goes up if there is more damage? That would explain that it goes down with increased vitamin C levels: there’s less damage in progress, hence decreased need for Lp(a).
Maybe people could look into (if not done already) the relation between tendency of atherosclerosis and Lp(a) levels. And then not only look at the influence of Vit C variable, but also other lifestyle factors, like eating less carbohydrates to name one.
Bone broth (collagen-rich), sea foods (particularly sea weeds) and offal are high in glucosamine and chondroitin sulfate, plus other important minerals that can help reduce joint pain and promote overall health.
F*^king love it Malcolm – as always 🙂
Love your reply Ivor, Shaza
I wonder if limiting the amount of glucose we put in our mouths might have any effect on blood glucose levels?
Just an ignorant layman speculating.
Of course it does.
No carbohydrates –> no glucose, apart from the glucose generated from proteins (neoglucogenesis–if I spelled that right).
The very low carbohydrate high fat diet (ketogenic diet, or VLCHF) is known for even curing diabetes type 2 (not type 1). See some youtube presentations by Dr Eric Westman for instance, who does this all the time. ( http://www.youtube.com/watch?v=__4TCZzeNeU )
Consistently (!) lowering the sugar load (carbohydrates generally) to a negligible level (less than 20 gram = 80 kCal per day) switches your body from glucose to fat (transformed into ketone bodies–hence the name ‘ketogenic’) burning.
At the same time, in order to obtain this effect, protein intake should be limited to max 30% of energy intake, in order for neoglucogenesis not to produce too much glucose, which seems to ‘destroy’ (explanation of exact mechanism needed) ketone bodies and keeps your body in glucose burning mode.
Warning: side effects are better cognitive function and loss of hunger feeling. 🙂
This diet reduces the amount of intramyocellular fat (fat inside muscular cells) that seems to block the insulin receptors, thereby reducing the insulin resistance.
I don’t have T2D (nor T1D–and I hope T3D neither) but was attracted by the promise of better brains, lost 1 kg in 2 months (that’s 100 g per day) and felt better indeed.
For comparison: assuming a daily energy consumption of 1800 kCal, knowing that 1 g fat when burnt produces 9 kCal heat, without eating anything, a person (without metabolic syndrome) would lose 1800/9 = 200 gram per day more or less, so I assume I was on heavy caloric restriction or a higher energy expenditure than 2000 kCal/d, didn’t feel hungry or starving though.
With time this diet cures T2Diabetes and in T1D reduces insulin dependence and blood glucose swings and therefore reduces the risk of hypoglycemia.
So yes, reducing carbohydrates AND proteins reduces blood glucose, and with a low enough value your body goes into ketone burning mode, curing T2D.
Sorry if this response is too much, given that a simple ‘yes’ would have sufficed. 🙂
(Please correct any mishaps in this ‘exposé’. 🙂
Well, it doesn’t exactly cure T2D, it reverses it, but it will always be there waiting in the wings should one revert to the bad old days of high/very high carb intake. Regarding T1D see Richard Bernstein – his book and YouTube presentations are well worth a look – he keeps his lifelong severe diabetes under strict control with LCHF and keeps his insulin input to the barest minimum – a minute amount because that’s all he needs. Last time I looked he was hale and hearty well into his 80s. I do hope he’s still going. He is an inspiration and source of hope to all diabetics.
100 g per day would give you 6kg in 2 months…
“Well, it doesn’t exactly cure T2D, it reverses it, but it will always be there waiting in the wings should one revert to the bad old days of high/very high carb intake”
“It’s waiting in the wings” for EVERYONE. If you eat too much of the wrong kinds of foods (sugar, starchy carbs, refined food and drink, etc.), you, me, Dr. Kendrick, the Dalai Lama, et al, will all get T2 diabetes. Q.E.D.
So, yes, the right diet can CURE T2 diabetes, because it’s a DIETARY disease.
I think it is too simplistic to call type II diabetes a dietary disease. There are a number of other things than can ’cause’ type II diabetes. Cushing’s, acromegaly, long term use of steroids, severe mental illness and depression, Beradinelli Siep Lipodystrophy, increased production of insulin (see under PIMA Indians), PTSD, HPA-axis dysfunction, spinal cord injury… I could go on. There is no doubt that ‘excess’ carbohydrate intake is also a driver, but if most certainly is not the only one. I would not disagree in the slightest that, carbohydrate restriction is a simple and effective way of lowering the blood glucose level. Whether or not it cures the disease we call type II diabetes depends rather on your definition of the words ‘disease’ and ‘cure’. Neither of which, in my opinion, are particularly well defined.
I place type II diabetes in the same pot as ‘essential hypertension’ ‘cryptogenic stroke’ and ‘idiopathic pulmonary fibrosis.’
These can be translated as: High blood pressure of no known cause, stroke of no known cause and pulmonary fibrosis of no known cause. They sound like real diseases, but they are not. Type II diabetes is, in my opinion (very often), raised blood sugar level of no known cause. Just giving something a fancy name does not make it a disease.
To: Dr. Kendrick
“I think it is too simplistic to call type II diabetes a dietary disease. There are a number of other things than can ’cause’ type II diabetes.”
Putting anyone in those categories on a LCHF diet (along with some intermittent fasting) will, almost without fail, reverse their T2 diabetes. So it may just be correlations with other conditions.
“Type II diabetes is, in my opinion (very often), raised blood sugar level of no known cause.”
Raised blood sugar does not necessarily always translate to T2 diabetes, as Dr. Kraft explains in his book. It’s all about insulin resistance and hyperinsulinemia. That is, a lot of people with blood sugar levels in their 70s and 80s mg/dL have T2 diabetes. People focus too much on BS, IMO. Hyperinsulinemia is the culprit. And the only way to find out your insulin level is with a 2-hour glucose tolerance test AND an insulin assay.
“The very low carbohydrate high fat diet (ketogenic diet, or VLCHF) is known for even curing diabetes type 2”
Nonsense. No cure at all. People with beginning diabetes, those in the gray zone, can (sometimes) reverse the process by eating a healthier diet, losing weight and exercise. Those with full-blown diabetes aren’t cured by by (V)LCHF. Put them back on a normal diet, with just a moderate amount of carbs, and you’ll see they are not cured.
This “low carb cures diabetes” claim is ridiculous.
If you need a tooth filling you could stop eating and drinking and not need a dentist anymore. Would you say it cured your tooth decay? Of course not.
You cannot cure something that is not a disease. You may, however, control a sign/symptom – which is not a bad thing
“You cannot cure something that is not a disease. You may, however, control a sign/symptom – which is not a bad thing”
Word play, dr. Kendrick. The Shorter Oxford English Dictionary gives the following definition of disease:
A disorder of structure or function in an animal or plant of such a degree as to produce or threaten produce detectable illness or disorder.
And correction: controlling a sign/symptom *may* not be a bad thing. In allopathic medicine you can find all kind of examples of how controlling symptoms leads to other problems. I already mention the (too) tight glucose control in diabetes patients that turned out not to be a good thing. There are stronger examples: you know all about statins and “controlling” cholesterol and the consequences it can have.
Don’t think too lightly about faulty diets. I find it quite amusing: on the one hand you say you don’t think diets have a big influence on disease and on the other hand it seems you are quite impressed by the low/carb keto diet.
Don’t get me wrong, I am not saying such diets have no place in treating some conditions but let’s please first find out for who and for which conditions the low carb/keto diet could be useful.
If it has some usefulness in diabetes, fine, but let’s call it what it is, let’s not mislead people and tell them it cures them.
Also when one reads a bit superficially in the internet, one might get the impression that the keto diet is a panacea for all cancers. Unfortunately it is not and it might harm a majority of cancer patients more than do them any good.
I think it is extremely important to be very clear about this, otherwise you’ll get patients who know absolutely nothing about medicine yet make a decision to make use of unproven therapies (diets in this case) that may harm them – even if they are warned.
I have another issue with extreme diets like the low carb and keto diet: I am sure many people will only adhere it for a relatively short period. Many people simply won’t have enough will power to adhere to such a diet all their life. It might well be possible that after “leaving” such an extreme diet, they might adopt a diet that is even worse than they had before (finally “freedom” to eat everything….).
Not word play at all. The Oxford English Dictionary may define disease as it wishes. I cannot imagine whoever put in that entry has ever given the concept of ‘disease’ a great deal of thought.
To: Leon Roijen AND Dr. Kendrick:
“Nonsense. No cure at all. People with beginning diabetes, those in the gray zone, can (sometimes) reverse the process by eating a healthier diet, losing weight and exercise. Those with full-blown diabetes aren’t cured by by (V)LCHF. Put them back on a normal diet, with just a moderate amount of carbs, and you’ll see they are not cured.
This “low carb cures diabetes” claim is ridiculous.
If you need a tooth filling you could stop eating and drinking and not need a dentist anymore. Would you say it cured your tooth decay? Of course not.”
So all those people who are reversing their T2 diabetes on a LCHF diet (with intermittent fasting) are just mirages? They don’t really exist? Really, you sound like the Flat Earthers, who still can’t come to grips with the fact that the Earth is not flat. And yes, if they revert back to whatever diet gave them T2 diabetes in the first place, they will once again get diabetes (see tooth filling comment below). But so would anyone, even if they have never had T2 diabetes.
I call that a cure, but cure is just a word. I don’t think the vast majority of people on the planet will much care if they are “cured” of diabetes, or if they no longer have it, or if it’s been reversed, or whatever you want to call what happened. The fact remains that they will no longer have to take medications or injections and all of their numbers will fall into the normal range. This is happening right now in clinics all across the US and Canada. Denying it is like denying gravity.
As far as your tooth filling example goes, if afterwards you continue to eat food and drink that contain a lot of sugar (think fruit juice, soda pop, refined foods, donuts, cereals, pizza, etc.), and don’t brush and floss regularly, etc. (the diet that caused your tooth to need filling in the first place) you stand a good chance of developing more plaque and even gum disease, that will eventually require the need to have the tooth refilled or pulled out altogether. Also, if you avoid those kinds of food and drink, and brush and floss regularly, all your life, there is a very good chance that you will need very few, if any, teeth to ever be filled. So, yes, your example was a good one, just not in the way you thought it was.
@ Dr. Kendrick:
The Pima Indians eat mostly sugar, white flour, and other refined foods (supplied by the government, of course!). That’s essentially a recipe for T2 diabetes. Those other conditions you listed are mostly *associated* with T2 diabetes, because they can impact a person’s diet. Especially depression, PTSD, mental illness, etc., where a person really might not care what he or she eats, and almost always, if left on his or her own, will choose crap foods. But those conditions are not the proximate causes of their T2 diabetes, their DIET is. If they eat a LCHF diet, with intermittent fasting, they will not get T2 diabetes, and if they already have it, they can reverse it in the same way anyone else can. And that includes the Pima Indians. Why? Because T2 diabetes is a DIETARY disease.
I urge both of you to read Dr. Fung’s great book, where he explains it far better than I can on a blog.
I think low carb/keto and also intermittent or long term fasting does “cure” T2 diabetes or at least place it into remission. There is ample evidence of this. See, for instance, Dr. Jason Fung’s many patients and their stories.
See Virta Health and their amazing transformations based on a keto diet:
Real life success stories of keto from the 2 keto dudes:
Personally, I’ve been low carb/keto for almost 5 years now. I don’t find it difficult, except when I go to someone’s house where they host (and think everyone eats carbs and low fat or no or little meat) or when I’m on vacation (when it can be a challenge to find meat/veggies when everything is based on bread and fried foods) or at certain restaurants (eg, pizza place/Italian).
Keto also helps with T1 diabetes: https://www.amazon.com/Dr-Bernsteins-Diabetes-Solution-Achieving/dp/0316182699
And taking too much insulin if T1 means you can develop T2, while keto means you take less insulin, therefore have less chance of T2.
Now, does going from high carb, low fat to higher fat, lower carb help with heart disease? It’s hard to tell. In my personal case, I’m down over 50 pounds (say 25 kilos), have boundless energy, and have reversed all measures of diabetes. Does this help me live longer? I’d need two of me to determine that. Is low carb/keto a cure all or for everyone? I don’t think so. But if you have an issue with carbs — you are insulin resistant/are carb sensitive/have a metabolism screwed up due to years of carb overdose — I think low carb/keto can be quite helpful.
“Not word play at all. The Oxford English Dictionary may define disease as it wishes. I cannot imagine whoever put in that entry has ever given the concept of ‘disease’ a great deal of thought.”
Then what is your definition of disease? And would you call hypothyroidism a disease, or not?
I’m clearly not a native speaker of English, but maybe the word “condition” is better for “diseases” like diabetes and hypothyroidism?
I think you want to avoid that conditions are given a fancy name and that the search for a true cause will be neglected?
On the other hand, what is a true disease? Bacteria, viruses? There are bacteria and viruses that only make some people sick. Does that mean that we cannot call these bacteria or viruses a disease, although they make some people very sick?
I think the word itself is relatively meaningless – like many words one can interpret its meaning in different ways. Essential hypertension = disease? Raised blood sugar level = disease? In my mind, a disease is the underlying malfunction(s) that then leads to an array or signs/symptoms/pathology. So, TB could be considered a disease, or perhaps more accurately infection with the tuberculous bacillus.
People, including the WHO, now define obesity as a disease. What is the underlying malfunction here? Obesity is clearly a ‘result’ of other things. It may then go on to cause other problems, but that still not make it a ‘disease’. At least not in my world.
A raised blood sugar is a result of other things. You cannot just claim it to be a disease because it is associated with, may cause, downstream problems. What you have to do is to try and work out what causes it. Some people have decreed that a high carb diet is THE single cause. I would strongly disagree. A high carb diet is neither necessary, nor sufficient, to cause a high blood sugar level. So, what is the ‘disease’ in a raised blood sugar level? Others have decreed, the underlying disease here is insulin resistance. That is merely circular logic.
There is a raised blood sugar level
There is a raised blood sugar level despite a normal, or high, insulin levels
Aha, there must be resistance to the effects of insulin
Aha, we shall call this insulin resistance
Hmmmm. It’s thinking, I suppose, but not as we know it Jim.
The problem here, with deciding that insulin resistance is the ‘disease’ is that you stop looking, or thinking, any further.
I started looking at Beradinelli Siep Lipodystrophy and I realised that the thinking on the condition that we call Type II diabetes is completely wrong.
“As far as your tooth filling example goes, if afterwards you continue to eat food and drink that contain a lot of sugar (think fruit juice, soda pop, refined foods, donuts, cereals, pizza, etc.), and don’t brush and floss regularly, etc. (the diet that caused your tooth to need filling in the first place) you stand a good chance of developing more plaque and even gum disease, that will eventually require the need to have the tooth refilled or pulled out altogether. Also, if you avoid those kinds of food and drink, and brush and floss regularly, all your life, there is a very good chance that you will need very few, if any, teeth to ever be filled. So, yes, your example was a good one, just not in the way you thought it was.”
You’re like a missionary….sigh 🙂
I have repeated it over and over but now I give up: Nobody (at least here, I guess) promotes high sugar diets for health but in your zealous enthusiasm for the low carb diet you cannot even notice this.
Certainly my example is a good one – there is no need to become extreme: Even if you have some sweets now and then, or a soda once in a while, that doesn’t mean you will have bad teeth. Moderation is enough. Same with carbohydrates and especially sugar: To prevent diabetes, moderating their intake will do the trick. There is no need to go low carb. And some people will get diabetes whatsoever as diabetes is not only caused by diet (as Dr. Kendrick already remarked). And there is no proof whatsoever that following a low carb diet will save these people from getting diabetes.
Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?
Each type of diet that results overweight—diabetic individuals to eat less food and taking in less energy will initially result in weight loss, which in itself will lead to favorable metabolic and functional changes.
The available scientific literature shows that controlled diet studies (several weeks to 2 years), a general public evidence based recommendation to support KLCHF and LCHF diets as a preventive measure to help reduce risks of type 2 diabetes, seems premature. The role of long-term elevated consumption of fat combined with low-carbohydrate consumption warrants further study before general recommendations can be made.
The ketogenic/LCHF diet reminds me of the no-fappers: They urge each other to abstain but you wonder how many really don’t enjoy themselves 🙂
To: Leon Roijen
“You’re like a missionary….sigh.”
Yes, I’m on a mission from God. 🙂
You seem to be on a mission from General Mills, Nestle, Coca-Cola, etc.
That is, to help people lose weight and avoid T2 diabetes. Even to reverse it. Because if we don’t find a way to do that, and soon, the entire healthcare system is going to come down on our heads. We just can’t afford our obesity and T2 diabetes epidemics. Not financially, and not the toll they take on humanity.
Avoiding sugar, starches, refined food and drink, can do that. It *is* doing that. but you refuse to see it. And unless you actually enjoy visiting the dentist (can we get a show of hands on that?), it can avoid most (actually, almost all of them) of the trips there, too. Those things cause tooth decay and gum disease, especially when people don’t brush and floss. That’s an indisputable fact. So if you care about avoiding expensive dental care, or losing your teeth altogether, by all means, eat and drink as much of those things as you want. Your dentist is counting on it, in fact. And as with all addictions, they start out with just a “moderate” amount of addictive substance (coke, heroin, alcohol, sugar, etc.) until control is lost and your body is found lying face down in a gutter somewhere.
“Moderation is enough. Same with carbohydrates and especially sugar”
You’re totally ignoring the part that HORMONES play in becoming addicted to sugar, starchy carbs, and refined food and drink. All the obese and diabetic people out there surely didn’t plan on becoming obese and diabetic, did they? People who consume too much of that “stuff” eventually lose control. Their hormones take over (insulin, leptin, ghrelin, etc.) and demand to be fed more of it (glucose). Which is why people who eat a lot of carbs have to eat 5, 6, 7, or more times a day, just to keep their energy up. That’s because they can’t access their fat stores (body fat), so all those excess carbs are stored as FAT, and it just keeps accumulating. Until their doctor tells them one day that they now have T2 diabetes and will have to be on drugs for the rest of their lives, because T2 diabetes is a “chronic and progressive” disease. Which, of course, is totally false.
“Each type of diet that results overweight—diabetic individuals to eat less food and taking in less energy will initially result in weight loss, which in itself will lead to favorable metabolic and functional changes.”
So you still believe it’s just a calorie problem, eh? Well, the old “move more, eat less” or “calories in vs calories out” paradigm is what got us into this mess in the first place. By seriously reducing the amount of food we eat, our metabolism essentially collapses. And that eventually leads to overeating and regaining all the weight that was lost, and then some. Because you’re still eating the wrong kinds of foods: sugar, starchy refined food and drink. It’s also why all the winners on the TV show “Biggest Loser” don’t have reunions. Because they’ve gained all that weight back, and then some. Because they’re still eating all that crap. And that also means that I was right about you being a Flat Earther. 🙂
“The ketogenic/LCHF diet reminds me of the no-fappers: They urge each other to abstain but you wonder how many really don’t enjoy themselves”
Yeah, because it’s so damn hard to eat fat, juicy ribeye steaks, smothered in garlic and butter, with sides of fresh green vegetables, and even some fresh fruit. Or huge slices of sockeye salmon, smothered in garlic or dill, with sides of fresh green vegetables, and even some fresh fruit, or a roasted chicken (with the skin on, of course) with sides of fresh green vegetables, and even some fresh fruit. Until you’re FULL. You know. REAL FOOD, not something concocted in some laboratory at General Mills. And washed down with a little Lagavulin, single-malt Scotch whisky, too.
Oh, the inhumanity!
Really, you need to read Fung’s book, and ASAP. You might not have much time left. 🙂
“Let food be thy medicine, and medicine be thy food.” Hippocrates
I appreciate Leon’s contributions. It is healthy for us all to be kept on our toes by people with different views.
To: Dr. Kendrick
“I appreciate Leon’s contributions. It is healthy for us all to be kept on our toes by people with different views.”
Absolutely, Doc! I appreciate them, too.
And also the opportunity to challenge them.
If excess calories are supposed to be stored as fat but aren’t being, then the disease is ‘failing to get fat fast enough’ for which I nominate the word ‘obesitardia’. ;o)
@ Dr Kendrick: Thank you very much for your clarification of how you see “disease”. Within a scientifical context (as opposed to a linguistic one), if we really want cures or prevention, your view is the only right one, of course. I can understand that Big Pharma prefers keeping “diseases” chronic instead of curing or preventing them but it eludes me why scientists in general so often fail to dig deeper for the root cause(s) of (complex) diseases. Maybe because they have become so much dependent on technology and think that as soon as they can measure something, that they have found the cause of the disease?
@Joe: “You’re totally ignoring the part that HORMONES play in becoming addicted to sugar, starchy carbs, and refined food and drink. All the obese and diabetic people out there surely didn’t plan on becoming obese and diabetic, did they?”
Oh please… this terrible victim mentality. “I can’t help it that I eat so much”, “it’s not my fault that I am as fat as a cow”…. our culture is drenched with this mentality and THAT, combined with a great lack of willpower, feminism and an economical structure that makes it necessary for women to work outside the home instead of serving good food to their husband and children is the big cause of the growing diabetes problem. (Excuse me, dr Kendrick, for not following your interpretation of “disease” here 🙂
“Because if we don’t find a way to do that, and soon, the entire healthcare system is going to come down on our heads. We just can’t afford our obesity and T2 diabetes epidemics. Not financially, and not the toll they take on humanity.”
Joe, I suppose you wish you had the power to prohibit selling everything with sugar and carbohydrates in it.
Like those dictators who are calling for smoking bans everywhere, even if they are not disturbed by smokers in the slightest way (and no, I have never been a smoker myself).
Your financial argument is childlike naive: Like smokers, diabetes patients generally die much earlier than people who don’t have diabetes, resulting in much less pension needing to be paid. Maybe a harsh fact yet true.
If low carb works for you, fine, but don’t proclaim it to be The Truth – it’s just another gospel. Four is more than enough.
As for you wanting to save humanity, I’d like to recall another subject I didn’t plan bringing up again:
“Both the meat-based average American diet and the lactoovovegetarian diet require significant quantities of nonrenewable fossil energy to produce. Thus, both food systems are not sustainable in the long term based on heavy fossil energy requirements. However, the meat-based diet requires more energy, land, and water resources than the lactoovovegetarian diet. In this limited sense, the lactoovovegetarian diet is more sustainable than the average American meat-based diet.”
You and your low carb high meat fellows will simply destroy humanity 🙂
It’s really good to have someone like Leon contributing. Gives me the chance to point out the alternative facts.
Since many overweight people do make significant efforts to avoid weight gain, and to lose weight. What do you think is their problem? It is probably not what I suspect you think.
As for meat consuming excessive amounts of fossil fuels, I suggest you read “Meat – a benign extravagance” by Simon Fairlie. If meat was fed on grass the fossil inputs would be very small.
On the subject of meat eating, Graham Harvey, in “Grass fed nation” is also very good and readable.
To: Leon Roijen:
“Oh please… this terrible victim mentality. “I can’t help it that I eat so much”, “it’s not my fault that I am as fat as a cow”…. our culture is drenched with this mentality and THAT, combined with a great lack of willpower, feminism and an economical structure that makes it necessary for women to work outside the home instead of serving good food to their husband and children is the big cause of the growing diabetes problem. (Excuse me, dr Kendrick, for not following your interpretation of ‘disease’ here”.
Way to turn a scientific/medical discussion into a political screed, Leon. I can see why you’d want to do that, because I don’t think you know much about science or medicine. I think you should do some research on the effects of certain hormones on insulin resistance, appetite, fat storage, and weight gain, and how certain food and drink affects those hormones, because until you do, you’re going to be wrong about anything you say here regarding diet and diabetes. Fortunately, Dr. Fung’s book will explain all that for you, and cites the science that support it.
It saddens me, however, that you would seemingly blame a person’s obesity and diabetes on a lack of will power, or the “economical structure.” Tsk tsk tsk.
“Joe, I suppose you wish you had the power to prohibit selling everything with sugar and carbohydrates in it.
Like those dictators who are calling for smoking bans everywhere, even if they are not disturbed by smokers in the slightest way (and no, I have never been a smoker myself).”
Actually, Leon, that’s the last thing I would do. I’m a libertarian by nature. What I would do, however, would be to stress even more EDUCATION about this subject, starting in medical school, that hopefully would eventually spread to the general population. It would highlight the *fact* that T2 diabetes is a dietary disease, and should be treated with diet, and not with drugs. And that it can be reversed. Doctors receive little to no education in medical school on nutrition or diet, and we’re currently paying the price for that.
Once people finally realized that smoking can cause lung cancer (among many other health problems), the number of smokers plummeted. Doctors help to spread that message, and they can help out with obesity and diabetes, too. But not until they realize they’ve been wrong all along. And that’s very hard for a doctor to admit, unfortunately.
“Your financial argument is childlike naive: Like smokers, diabetes patients generally die much earlier than people who don’t have diabetes, resulting in much less pension needing to be paid. Maybe a harsh fact yet true.”
I don’t think you’re thinking this through, Leon. The average life expectancy (according to this article: https://www.sepalika.com/type-2-diabetes/how-long-do-diabetics-live/) for a T2 diabetic in the UK, for example, is between 77 and 81 years (which won’t make much of a dent in pensions), with some even reaching the age of 85. (I have no idea how accurate that is.) And during that time (whatever it may be), they’re responsible for sucking up the largest share of healthcare costs before they die. If you’re going to look at this problem through a financial lens, make sure you do it with valid assumptions.
“If low carb works for you, fine, but don’t proclaim it to be The Truth – it’s just another gospel. Four is more than enough.”
Actually, it works for everyone who tries it. Even you, Leon. And it’s something that everyone can find out for themselves through a simple N=1 experiment. Again, it’s all about the effect that various foods we consume have on our hormones, e.g., insulin, leptin, ghrelin (aka “The Hunger Hormone”), etc.
It’s not just gospel, it’s SCIENCE. You believe in science, right?
BTW: You’re here on Dr. Kendrick’s blog, so I presume you’re at least interested in “The Truth” when it comes to the cause of heart disease, right?
“As for you wanting to save humanity, I’d like to recall another subject I didn’t plan bringing up again:”
That was basically a joke, Leon, because you accused me of being a missionary. And if anyone is going to be a missionary, being a missionary from God is far better than being a missionary from General Mills, Nestle, Coca-Cola, etc, IMO.
“Both the meat-based average American diet and the lactoovovegetarian diet require significant quantities of nonrenewable fossil energy to produce. Thus, both food systems are not sustainable in the long term based on heavy fossil energy requirements. However, the meat-based diet requires more energy, land, and water resources than the lactoovovegetarian diet. In this limited sense, the lactoovovegetarian diet is more sustainable than the average American meat-based diet.”
That’s mostly propaganda, not science, and is based on the myth that saturated fat is unhealthy (which it isn’t), and that it raises cholesterol levels (which it doesn’t), and that it causes heart disease (see: Dr. Kendrick), and the influence of BigFood, BigPharma, and BigGov. Not to mention “global warming.”
Also, grass-fed cows only require good grasses upon which to graze (which is what they were originally designed to eat), instead of being stuffed with corn, soy, etc., while they restore the soil to healthy levels of nutrients that have been stripped from the environment by factory farming, monoculture farming, etc. You might want to look up Allan Savory, who has similar thoughts. He also has a video on the concept.
“You and your low carb high meat fellows will simply destroy humanity”🙂
On roughly the same diet that our ancestors ate for hundreds of thousands of years?
Yeah, riiiight. Tsk tsk tsk.
“Way to turn a scientific/medical discussion into a political screed, Leon.”
I can’t help it that *you* can see diabetes only one-dimensionally. One of the other dimensions of diabetes is societal. You call it “political”, well, thats fine with me.
“I can see why you’d want to do that, because I don’t think you know much about science or medicine.”
That’s cheap. I think it was your ignorance Dr. Kendrick had to correct:
I think it is too simplistic to call type II diabetes a dietary disease. There are a number of other things than can ’cause’ type II diabetes. Cushing’s, acromegaly, long term use of steroids, severe mental illness and depression, Beradinelli Siep Lipodystrophy, increased production of insulin (see under PIMA Indians), PTSD, HPA-axis dysfunction, spinal cord injury… I could go on. There is no doubt that ‘excess’ carbohydrate intake is also a driver, but if most certainly is not the only one.
“I think you should do some research on the effects of certain hormones on insulin resistance, appetite, fat storage, and weight gain, and how certain food and drink affects those hormones”
I know about these things and damn, I suffer from isolated hypoglycemia and for months I haven’t been sleeping for more than 4 hours most nights, so I definitely know what these hormones can do. So I think I can honestly say I have some experience myself and that will power is part of the equation, too.
“It saddens me, however, that you would seemingly blame a person’s obesity and diabetes on a lack of will power, or the “economical structure.”
That’s fine with me, the truth needs to be told. As said, will power is part of the equation. There are a few people with obvious medical problems that makes them get obese more easily, but the overwhelming majority of people truly has a lack of will power when it comes to food or a “I don’t care” attitude, until it is too late.
As I said will power is one part of the equation. Hormones that make you want to eat more, advertisements or even simply a dispute with your partner are other (possible) parts of the equation.
The economical structure certainly isn’t helpful: When both partners come home from a long working day I don’t think it is that strange that they more often opt for easy food.
“It would highlight the *fact* that T2 diabetes is a dietary disease”
Read above. Dr Kendrick already corrected you on that.
“and should be treated with diet, and not with drugs. And that it can be reversed.”
Wait, not too quick: People who are about to get diabetes, can reverse it, sometimes, absolutely not always. Let’s be clear about that before you start saying diabetes is always a person’s own fault.
Paying attention to diet is always a good thing, and certainly with diabetes. But as I already demonstrated above, it is about weight loss, some calorie restriction, exercise and moderation of carbs, and cutting out most refined carbohydrates, especially sugar.
No need for an extreme diet like the low carb one.
And if people with diabetes really want to (and can!) adhere to such an extreme diet and it helps them with controlling glucose and other parameters (NOT curing diabetes), then I am absolutely fine with that. It’s not my business in the first place. But don’t try to pass it as a cure.
“I don’t think you’re thinking this through, Leon. The average life expectancy (according to this article: https://www.sepalika.com/type-2-diabetes/how-long-do-diabetics-live/) for a T2 diabetic in the UK, for example, is between 77 and 81 years (which won’t make much of a dent in pensions)”
That’s only best case scenario. If a diabetes patient will live till 77 while the average is 80, that is 3 years of pensions and other assistance less. Now I don’t know about the pensions in the UK, but nevertheless I think it represents a lot of money that is saved and theoretically could go to health care. I am not saying that is how we should deal with diabetes and diabetes patients, but I just want to make clear that the assertion that diabetes will break the health system is simply not true.
“It’s not just gospel, it’s SCIENCE. You believe in science, right?”
Got a credible meta-analysis (for example from Cochrane) that demonstrates beyond doubt that your low carb diet cures diabetes? I think not.
“That was basically a joke, Leon, because you accused me of being a missionary. And if anyone is going to be a missionary, being a missionary from God is far better than being a missionary from General Mills, Nestle, Coca-Cola, etc, IMO”
“Also, grass-fed cows”
Oh no, the grass fed cows again… I’m not going into that again – shouldn’t have started it again – my fault 🙂
“On roughly the same diet that our ancestors ate for hundreds of thousands of years?”
When “humanity” was not 7 or 8 billion people but 1 or less.
One cannot sustainably feed 7 or 8 billions of people with grass fed cows.
But please before you write a lot of paragraphs again – let’s agree to disagree, ok?
To: Leon Roijen
“I can’t help it that *you* can see diabetes only one-dimensionally. One of the other dimensions of diabetes is societal. You call it “political”, well, thats fine with me.”
I look at diabetes through a scientific lens. Period. And the science is pretty clear that hyperinsulinemia causes T2 diabetes. And hyperinsulinemia is caused by consuming excessive amounts of carbohydrates, especially sugar, starches, and refined food and drink. And consuming those kinds of foods dramatically affects insulin and other hormones, whereas protein and fat do not. And when your hormones are essentially always begging you to feed them more carbohydrates (glucose), it’s not a matter of willpower. It’s a matter of IGNORANCE. Ignorance about what those kinds of foods are doing to you, because the Standard American Diet, etc. recommend eating those foods and avoiding fat. Fat, which essentially has no effect on insulin levels, thus cannot cause hyperinsulinemia. Only carbohydrates can do that.
“That’s cheap. I think it was your ignorance Dr. Kendrick had to correct:”
I think you display your ignorance of science and medicine (especially as it pertains to diet, nutrition, and T2 diabetes) every time you make a comment here. And with all due respect to Dr. Kendrick, whom I admire greatly, he’s simply wrong about this subject, IMO, and I tried to explain why I think so. But you apparently missed that part, right? So I won’t do it again, but you can easily find my reply regarding his comments.
“I know about these things and damn, I suffer from isolated hypoglycemia and for months I haven’t been sleeping for more than 4 hours most nights, so I definitely know what these hormones can do. So I think I can honestly say I have some experience myself and that will power is part of the equation, too.”
Since I know virtually nothing about your medical history, I won’t even hazard a guess as to why you are experiencing episodes of hypoglycemia. Only your doctor can do that, and I urge you to find out why, especially if you don’t have diabetes.
“Hormones that make you want to eat more”
Yes, and they are stimulated to do that by what kinds of food you eat! If you eat a lot of carbs, you’re going to want to eat a lot more of them. If you eat a good amount of fat, however, you won’t. Because fat affects those same hormones much differently than carbohydrates. So, again, it has very little if anything to do with willpower. It has to do with IGNORANCE.
“The economical structure certainly isn’t helpful: When both partners come home from a long working day I don’t think it is that strange that they more often opt for easy food.”
But “easy food” doesn’t have to be sugar, starches, and refined food and drink. In fact, even if you don’t or can’t cook, even fast-food restaurants have LCHF versions.
“Read above. Dr Kendrick already corrected you on that.”
Again, Dr. Kendrick is entitled to his opinion, and someone I greatly admire, but I think he’s wrong on this one. And I explained why. If the good doctor would like to go into it further, I’m open to that. But here’s another question for you to ponder: If something like dementia, PTSD, etc. are proximate causes of T2 diabetes, why can a LCHF diet, along with intermittent fasting, reverse their diabetes (i.e., eliminate their need for medications, and return their numbers to the normal range)? The same applies to bariatric surgery, even if the patient is morbidly obese.
“Wait, not too quick: People who are about to get diabetes, can reverse it, sometimes, absolutely not always. Let’s be clear about that before you start saying diabetes is always a person’s own fault.”
People who have had T2 diabetes for 20-30 or more years, and are on every medication for diabetes there is, can have it reversed in a matter of months. It’s being done right now. And they can get off drugs, and have all labs in the normal range.
Bariatric surgery can do it, even for *morbidly* obese individuals. Which essentially proves that T2 diabetes isn’t a “chronic, progressive” disease that needs to be “treated” with drugs. And it proves that obesity isn’t the cause of T2 diabetes, either, because the person may still be morbidly obese only a few months after surgery, but no longer diabetic. And so can a LCHF diet with intermittent fasting, but not quite that fast, albeit without all the risks associated with surgery.
And it’s all included in Dr. Fung’s great book on T2 diabetes. And google is your friend.
“Paying attention to diet is always a good thing, and certainly with diabetes. But as I already demonstrated above, it is about weight loss, some calorie restriction, exercise and moderation of carbs, and cutting out most refined carbohydrates, especially sugar.
“No need for an extreme diet like the low carb one.”
But it isn’t about weight loss (as explained above, re: bariatric surgery). Nor is it about exercise. But it is about consuming excessive amounts of carbohydrates, especially sugar, starches, and refined food and drink. In fact, if people avoid those kinds of food and drink, they can sit in their BarcaLounger all day and still lose weight. No exercise is required. Just a LCHF diet and some intermittent fasting. Exercise is good for us, of course, but it’s not necessary for weight loss or for reversing T2 diabetes.
“And if people with diabetes really want to (and can!) adhere to such an extreme diet and it helps them with controlling glucose and other parameters (NOT curing diabetes), then I am absolutely fine with that. It’s not my business in the first place. But don’t try to pass it as a cure.”
There’s nothing “extreme” about it. It’s the way that human beings have always eaten, before the advent of agriculture, BigFood, BigPharma, and BigGov. And it’s the only way to prevent or reverse T2 diabetes. Because T2 diabetes is a dietary disease. And by changing their diet, they can get off of all drugs for diabetes, get their labs back in the normal range, and no longer be diagnosed as diabetic. That’s a cure in anyone’s book. You just don’t want to admit it.
“but I just want to make clear that the assertion that diabetes will break the health system is simply not true.”
Then check out the costs associated with T2 diabetes, heart attacks, kidney failures, blindness, liver damage, amputations, strokes, Alzheimer’s, etc. for yourself. And then project out a few years, because most of those conditions are increasing, and then try to figure out where the money is going to come from, when healthcare is already being rationed virtually everywhere.
“Got a credible meta-analysis (for example from Cochrane) that demonstrates beyond doubt that your low carb diet cures diabetes? I think not.”
I’ll tell you what, Leon, you can wait around for those “studies,” or you can do your own n=1 experiment and see for yourself; yes, whether you already have diabetes or pre-diabetes, and the effect it has on your BS and insulin resistance. And if you get off all your medications, and your numbers all check out in the normal range, and your doctor tells you that you no longer are diabetic, why would anyone want to wait for a Cochrane “study”?
“Oh no, the grass fed cows again… I’m not going into that again – shouldn’t have started it again – my fault”
Tsk tsk tsk.
When “humanity” was not 7 or 8 billion people but 1 or less.
One cannot sustainably feed 7 or 8 billions of people with grass fed cows.
Sure we can, but we really don’t have to. We have other kinds of animals to eat, too. Like goats, sheep, pigs, chickens, deer, fish, and on and on, plus lots of healthy green veggies, some fruits, seeds, nuts, etc. And we can even wash it all down with some single-malt Scotch, like Lagavulin. What’s not to like?
“I look at diabetes through a scientific lens. Period. And the science is pretty clear that hyperinsulinemia causes T2 diabetes.”
Sorry, you read too much pseudoscience and now think that you know it all while in reality still very little is known as to the causes of diabetes (type 2).
Obviously you don’t know the difference between associations, risk factors and causes.
Diabetes Australia states: “We do not know what causes type 2 diabetes.”
Dr. Kendrick does give some “causes”:
“There are a number of other things than can ’cause’ type II diabetes. Cushing’s, acromegaly, long term use of steroids, severe mental illness and depression, Beradinelli Siep Lipodystrophy, increased production of insulin (see under PIMA Indians), PTSD, HPA-axis dysfunction, spinal cord injury… I could go on.”
“And hyperinsulinemia is caused by consuming excessive amounts of carbohydrates, especially sugar, starches, and refined food and drink.”
But you come with the silly, super simplistic assertion that carbohydrates are behind all this.
“And consuming those kinds of foods dramatically affects insulin and other hormones, whereas protein and fat do not.”
Nonsense. It’s all about obesity/adipose tissue:
“It appears that fat tissues evolved primarily as a safe harbor to store energy in times of plenty and to provide fuel when food sources become insufficient. However, in addition to serving as purely a storage depot, adipose tissue is now recognized as the body’s largest endocrine organ, controlling many aspects of systemic physiology by secreting hormones (adipokines), lipids, cytokines and other factors (Gesta et al., 2007; Nawrocki and Scherer, 2004; Spiegelman and Flier, 2001). Although many of the regulatory molecules are not yet identified, they control a wide variety of biological actions, including appetite, glucose homeostasis, insulin sensitivity, aging, fertility and fecundity, and body temperature.”
You Joe, you have no idea what you are talking about. You simply parrot the author of a (popular?) book. That’s all.
“Fat, which essentially has no effect on insulin levels, thus cannot cause hyperinsulinemia. Only carbohydrates can do that.”
Sorry to say but you talk nonsense, again, Joe.
As shown above, it’s about adipose tissue and not only carbohydrates but fat and proteins can equally contribute to this tissue.
“I think you display your ignorance of science and medicine (especially as it pertains to diet, nutrition, and T2 diabetes) every time you make a comment here.”
That remark would be funny if it weren’t you yourself making a fool of yourself here.
“And with all due respect to Dr. Kendrick, whom I admire greatly, he’s simply wrong about this subject”
And with “all due respect”, considering the great intellect and original thinking I have seen demonstrated by Dr Kendrick and the parotting of super simplistic ideas by you, it’s beyond doubt that the only one simply wrong here is you.
Please note that being wrong and arrogant is an ugly combination, Joe.
Leon, your points would be more persuasive if you left out the adjective and personal attacks. Those things make the case look as though the writer is insecure. Just saying.
I have been getting a little concerned about the increasing vehemence on both sides of this discussion. I hope we can proceed in a spirit of mutual regard.
Yes, Dr. K., Me too. It’s all very off-putting (and rather rude.) please play nicely, boys.
Lots of love from your mother(s)
Have you ever noticed how people who in the past posted sporadically suddenly burst into flame so to speak and post away rapidly, three or four times a day? What are they smoking?
Hello JanB. yes, the blog suffers such annoying episodes every few months…score pointing, and not helping with the discussion. I feel that there is the occasional troll out there infiltrating this great blog.
I am sorry that I responded, (unwittingly), and thus added fuel to the fire.
Hi Leon, re causes of diabetes
“There are a number of other things than can ’cause’ type II diabetes. Cushing’s, acromegaly, long term use of steroids, severe mental illness and depression, Beradinelli Siep Lipodystrophy, increased production of insulin (see under PIMA Indians), PTSD, HPA-axis dysfunction, spinal cord injury… I could go on.”
All these causes appear to have high glucose at the root. Result of a quick google.
Andy. High glucose is the measurement used to diagnose type II diabetes. Ergo, high glucose IS type II diabetes. That is not questionable. The question is, what is causing the glucose to be high. That, is not simple.
“I have been getting a little concerned about the increasing vehemence on both sides of this discussion. I hope we can proceed in a spirit of mutual regard.”
I’m afraid the mutual regard is gone when someone tells you “I don’t think you know much about science or medicine.” And even more or less repeats it in a next message.
I also don’t know where that insult comes from. Yes, I am not a medical doctor nor am I a trained scientist but I can keep up well with doctors and veterinarians in discussions and because of that I was asked if I work in healthcare myself several times already.
I proved one veterinarian to be wrong with his (faulty) diagnosis of Cushing diease (saving my dog from life-long treatment with rather harsh medication) and another dog that did have Cushing disease I -in collaboration with our veterinarian- treated with an alternative medication (not “alternative” as in “alternative medicine) usually not used in dogs, with very good results. Our veterinarian congratulated me.
By doing research with pubmed, I succeeded in solving several of my health problems. For example I discovered a small, seemingly unsignificant study that showed honey could control my eczema. I put it to the test and now I don’t need the cream that doctors prescribe (and can severely irritate the eyes) anymore.
I’m not one who likes to boast and I think it is shameful that I have to defend myself against such a claim as made by Joe.
I can accept the fact that I played my part in this heated dicussion and for that I offer my apologies.
To: Leon Roijen
“Sorry, you read too much pseudoscience and now think that you know it all while in reality still very little is known as to the causes of diabetes (type 2).
Obviously you don’t know the difference between associations, risk factors and causes.”
Diabetes Australia, American Diabetes Association, and Diabetes UK are all parts of the problem, not the solution. With a little help from their friends (BigFood, BigPharma, and BigGov) they are the reason we currently have obesity and T2 diabetes epidemics. Their livelihoods depend on perpetuating the myth that T2 diabetes is preventable and reversible, and that it’s a “chronic, progressive disease” that can only be treated with drug$.
Ignaz Semmelweis was a 19th century physician who NOTICED that if physicians delivering children would wash their hands with chorinated lime solution, deaths from “childbed fever” could be virtually eliminated. Other doctors ridiculed him and refused to wash their hands. Of course, that was long before Pasteur and Lister proved him correct. But only after thousands of babies (and who knows how many other lives?) could have been saved in the interim….
And you’re the person who doesn’t understand what associations, etc. are. It’s not me.
“Dr. Kendrick does give some ’causes'”:
No, *those* are associations. And without going into each of them, let’s talk about the Pima Indians. They are basically subsidized by the U.S. government (starting in the middle of the 19th century), and what they are fed is sugar, white flour, vegetable oils, and canned goods, among other crap. That’s essentially a recipe for T2 diabetes and obesity. And until they became wards of the U.S. government, T2 diabetes was essentially non-existent. Thus, feeding them a LCHF diet, with intermittent fasting can reverse/prevent their T2 diabetes, too. Because T2 diabetes is a dietary disease. Prior to their resettlement, they lived on wild fish, game meat, beans, corn and squash, and were thin and healthy. And they ate no sugar, and no refined goods. Thus, a return to their traditional diet can prevent or reverse their diabetes. Or essentially any LCHF diet, with intermittent fasting, will do the trick. This is a perfect example of epigenetics in action.
“Nonsense. It’s all about obesity/adipose tissue:”
But that’s not true. It’s what made them obese in the first place. Excessive consumption of carbohydrates, primarily sugar, starches, and refined food and drink. If the proximate cause of T2 diabetes was obesity, then why can bariatric surgery (some forms of this surgery are better than others) of even *morbidly* obese patients with T2 diabetes be reversed within 2-3 months after surgery, while they are *still* morbidly obese? This can also be done with a LCHF diet and intermittent fasting, but it takes longer.
Now try to explain how obesity could be the proximate cause of T2 diabetes, and without bringing up Dr. Kendrick’s name.
“You Joe, you have no idea what you are talking about. You simply parrot the author of a (popular?) book. That’s all.”
I’m not parroting anyone. I’m trying to explain that “seeing is believing.” If it works in Dr. Fung’s clinic, and Dr. Hallberg’s clinic, and in many other clinics across the US and Canada, it can work anywhere. On the other hand, I implore you to read Dr. Fung’s book, because it’s a crash course in how to prevent and/or reverse T2 diabetes, and explains why he’s able to do that, using SCIENCE. Doctors should have listened to Dr. Semmelweis, and they should also listen to Dr. Fung, et al.
“And with ‘all due respect’, considering the great intellect and original thinking I have seen demonstrated by Dr Kendrick and the parotting of super simplistic ideas by you, it’s beyond doubt that the only one simply wrong here is you.”
I loooove Dr. Kendrick. He’s definitely one of the good guys. But even good guys can be wrong. If he were right, it would be impossible to reverse T2 diabetes with a LCHF diet and intermittent fasting, in all those people, But it’s being done, right now, as we speak, in clinics across the U.S and Canada.
“Please note that being wrong and arrogant is an ugly combination, Joe.”
Oh, the irony contained therein…
Tsk tsk tsk.
Right, can we please play nice.
I would only say that there is no cause of type II diabetes, because it is NOT a disease. It is a blood sugar measurement. When the blood sugar reaches some arbitrarily defined level the ‘disease’ of type II diabetes is diagnosed. Many different things can raise your blood sugar level in the short term. Some can raise it in the longer term.
Many things can lower the blood glucose level e.g. insulin, or exercise, or metformin, or starvation. Have they cured an underlying disease. No, because the moment you remove them, the blood glucose will go back to exactly the same level as before. it is like claiming you can cure high blood pressure by prescribing a blood pressure lowering agent. ‘Look the blood pressure has gone down, you are cured.’ Until tomorrow, if you forget to take your tablet.
Clearly, if you do not eat any carbohydrates this will help to bring the blood sugar down, but have you cured anything by doing so? I have spoken to many people who can keep their blood sugar levels below the figure arbitrarily defined as ‘diabetes’ by eating a high fat low carb diet. If they eat carbohydrates again, their blood sugar goes back up to previous levels. Many of these people have been very thin.
We cannot agree on very much, if we cannot agree as to what type II diabetes is. I refuse to believe that a high blood sugar measurement is a disease. Although, clearly, I have written about it, as though it is. This is because the entire way of talking about and discussing this area is set in stone. I despair.
Dr K. your explanation seems perfect to me. I do not accept everything on this blog, but I think we are in the realm of ‘there are none so blind as those who refuse to see, and none so deaf as those who refuse to listen’. As with religion:- to those who believe, no explanation is necessary, and to those who do not believe, no explanation is possible.
That should not deter research into all forms of diabetes, but it would be nice to have an international consensus with terminology; then some of the antagonism might reduce.
To: Dr. Kendrick
“Ergo, high glucose IS type II diabetes.”
If that were true, Dr. Joseph Kraft must be wrong. Because he found T2 diabetes in people with entirely normal blood glucose levels. Why? Because of hyperinsulinemia. Which requires an oral glucose tolerance test and insulin assay to detect.
76% of subjects having a ‘normal’ FPG fail the insulin assay
78% of subjects having a ‘normal’ OGTT (NGT) fail the insulin assay
75% (weighted average) of subjects having both a ‘normal’ FPG and ‘normal’ OGTT (NGT) fail the insulin assay
FPG as a screening tool alone, is of little value
Those with a ‘normal’ FPG generally don’t advance to the OGTT, further reducing overall sensitivity to rule in diabetes from ~50% to ~25% using SMs
‘Normal’ FPG and OGTT provide a false sense of security (many false negatives)
Hyperinsulinemia occurs before hyperglycemia
The insulin assay is “gold” when it comes to detecting diabetes at its earliest
Diabetes in-situ identifies diabetes at its earliest stage, illustrating how hyperinsulinemia manifests itself *before* hyperglycemia.
Dr Joseph Kraft has simply decided to re-define type II diabetes as a raised insulin level. Fine, I have no problem with him attempting to do this. He may struggle to get the rest of the medical profession to agree with him. Especially as, at least in the UK, insulin is never/very rarely directly measured. Type II diabetes is a diagnose made purely on the HbA1c.
I am not sure I am keen on diagnosing 75% of the population as having type II diabetes, along with the 80% with hypertension, and the 75% with high blood sugar levels. We are all ill, and going to die.
I fully agree that hyperinsulinaemia occurs before hyperglyceamia. This, however, changes nothing in any causal model.
Dr. Kendrick this talk of insulin just reminded me why keeping a low level is beneficial: AUTOPHAGY, the path to cell rejuvenation via mTOR inhibition. Protein also involved in mTOR signalling. Low carb, moderate protein the way to go.
“The observation that mTOR inhibition extends lifespan and delays the onset of age-associated diseases in mammals has led many to speculate that mTOR inhibitors could be used to enhance longevity in humans.”
“It is now clear that the mTOR pathway plays a central role in sensing environmental conditions and regulating nearly all aspects of metabolism at both the cellular and organismal level.”
me: “Dr. Kendrick does give some ’causes’”:
you: “No, *those* are associations.”
There you go again, you accuse me of not knowing much about science and medicine, but you yourself simply have no idea what you are talking about.
Corticosteroids for example, one cause Dr Kendrick named, can **cause** diabetes, i.e. start the process of getting obese and diabetic.
” Steroids affect your metabolism and how your body deposits fat. This can increase your appetite, leading to weight gain, and in particular lead to extra deposits of fat in your abdomen”
The intake of excessive carbohydrates, but also fat and proteins can lead to extra deposits of fat.
I’ll stop the discussion here, it’s impossible if you cannot understand this, cannot differentiate between associations and causes and stubbornly keep to your carbohydrate story which clearly demonstrates tunnel vision.
To: Dr. Kendrick
“Clearly, if you do not eat any carbohydrates this will help to bring the blood sugar down, but have you cured anything by doing so?”
Well, you certainly don’t have to forgo all carbohydrates, but, yes, you have to essentially eliminate sugar, starches and refined/processed food and drink.
On the other hand, if by doing so, you get your blood sugar back in the normal range (and, ideally, pass an oral glucose test and insulin assay), no longer have to take any medications, that’s a cure in my book. Can you return to eating whatever you want? No. But neither can the rest of us.
“I refuse to believe that a high blood sugar measurement is a disease.”
Agreed. It’s a bit like fever, a consequence , a symptom if you want, something like that.
To: Leon Roijen
“Corticosteroids for example, one cause Dr Kendrick named, can **cause** diabetes, i.e. start the process of getting obese and diabetic.”
No, it’s a contributing factor. The success of bariatric surgery has already proven that obesity does not cause T2 diabetes, otherwise even morbidly obese people would not have their T2 diabetes reversed on 2-3 months, while *still* morbidly obese.
Empty out those cells already laden with sugar (perhaps from their own diets)and the T2 diabetes will reverse. And the best way to do that is with a LCHF diet and intermittent fasting.
“The intake of excessive carbohydrates, but also fat and proteins can lead to extra deposits of fat.”
Fat does not affect insulin levels. Protein can affect insulin levels, but only moderately, and only when it’s not being used by the body to build muscles, etc. because then the excess is stored as fat. Excess carbohydrates burned are always stored as fat. So the best way to minimize their effects on INSULIN (the hormone that ultimately determines how fat we get), is to eat a lot of fat, a moderate amount of protein, and minimize the level of carbohydrates, especially sugar, starches, and refined/processed food and drink. Please note, there are no essential carbohydrates, unlike fat and protein.
“I’ll stop the discussion here”
That’s your best comment yet.
“Excess carbohydrates burned are always stored as fat”??
Excess CALORIES that ARE NOT USED are stored as fat. Whether those calories come from carbs, fats or proteins, if they are in excess, they will be stored as adipose tissue.
Sasha, I don’t think that is entirely true. Eating excess calories from fat, esp saturated fat does not seem to cause weight gain, whereas excess calories from carbs do. We must all be eating an excess of calories, otherwise the converse would be true, and a deficiency of calories would mean we get thinner. So there must be a process that allows for disposing of the excess calories.
I’m inclined to agree with you. I eat mountains of cheese, lots of butter, cream, eggs, fatty meat, fatty fish but very little carb and I never gain weight. I’m very slender, which is a polite way of saying ‘thin.’
Diet again – sorry folks.
I am not sure what this proves. I know an Italian guy who eats pasta 3-4 times per week and he often eats it with bread! If I ate like that, I would have a big belly. He is thin as a rail. The same goes for his wife who skips the bread with pasta but otherwise eats as much pasta as him.
That’s probably because it’s much harder to consume extra calories when the bulk of them comes from fat. You end up consuming less calories overall. If you can eat carbs and proteins, especially if you allow yourself sweets and processed carbs (breads, pasta, etc), calories add up pretty quickly, even if a gram of fat packs nearly twice the amount energy per gram versus carbs and proteins.
In 2010 Chris Voigt, director of Washington State Potato Commission decided to go on 21 day potato only diet to protest the decision by the US government to remove potatoes from the list of vegetables it will pay for in its food assistance program. Here’s a quote from the book The Hungry Brain: “Voigt contended, correctly, that potatoes are actually quite nutritious – in fact, one of the few foods that provide a broad enough complement of nutrients to sustain a human in good health for months at a time. He documented his journey on a web site titled 20 Potatoes a Day, which refers to the number of potatoes he would have to eat to maintain his weight… Despite Voigt’s goal not to lose weight, the pounds melted off. He lost 21 pounds over 60 days, much of it from his waistline. According to physical examinations before and after, his blood glucose, blood pressure, and cholesterol levels improved considerably”.
And here’s another quote from the same book:
“In popular media, there’s a perennial debate over whether sugar or fat is responsible for the obesity epidemic. This has led some people to view obesity research as a team sport rather than a scientific discipline. Allow me to end the debate by stating what most researchers find quite obvious: It’s both.”
Which once again makes this question interesting: How is it that many Italians eat pasta daily or almost daily while maintaining some very impressive health metrics?
Sasha, the answer could be in the type of oil consumed on a regular basis. Pasta with soybean oil or other PUFA’s might pack on weight faster than pasta with olive oil. Please check this out and report back.
Andy: how does that make sense? Let’s say I am eating pasta and not moving much for a net caloric surplus. As long as I use PUFAs my body follows the laws of physics. But once I bring in the magic of olive oil, those laws no longer apply?
Because this idea about PUFAs sounds like another post hoc explanation. Many on this blog stick to the hypothesis that wheat or carbs are universally bad and when met with black swans to this theory (Kitavans and starchy tubers, Italians and pasta, Okinawans and sweet potatoes, and many other societies) all sorts of post hoc explanations come out: olive oil, sunshine, Bon dances… Sounds an awful lot like cholesterol theory and its defenders, just another side of the coin.
And, btw, you never answered my other question to you. You said that the mystery of disappearing calories has been solved in high fat vs regular diet and weight gain. Can you give a plausible physiological mechanism to how this happens?
dietary composition/gut bacteria/mTOR/mitochondria – determines where calories from a meal end up
gut bacteria and weight gain
Olive Oil-derived Oleocanthal as Potent Inhibitor of Mammalian Target of Rapamycin: Biological Evaluation and Molecular Modeling Studies
Mitochondria Can Either Spur or Stop Obesity
Click to access Thomas2.pdf
mTOR Complex1–S6K1 signaling: at the crossroads of obesity, diabetes and cancer
I’ll chip in here. I’ve been a PT and interested in nutrition for years I also understand the science. But in reality from experience excess calories of any macronutrient equals weight gain and conversely decrease of any calories leads to weight loss. No matter what the science has uncovered in support or against, visually and practically altering energy expenditure has always resulted in weight loss or weight gain.
I agree. Any other result would violate the first law of thermodynamics which I don’t think can be done.
The first law of thermodynamics refers to a closed system which the human body isn’t. You need to look instead to the 2nd law which takes into account heat loss and entropy (ie energy used up in producing energy). Carbs, proteins and fats use up different amounts of energy to produce useable energy.
Thank you for that correction, I will look it up.
Sasha: Richard David Feinman explains this (thermodynamics) well in “The World Turned Upside Down.”
Thanks, Gary. I will read it
Mystery of disappearing calories solved. Gut bacteria have to eat too. Keep i mind what their requirements are when deciding what to eat. Their health affects our health.
Can you please walk me through the physiology on this? Let’s say I am eating carbs and you don’t or you eat very little of them. Different kinds of bacteria proliferate in our guts, mine more carb dependent than yours. Both of us consume more calories than we spend yet, if I understood you correctly, I am gaining weight while you don’t.
Can you explain the physiology? How is it that my extra calories turn into adipose tissue while your extra calories don’t?
Start by googling “gut bacteria and weight gain”.
One result was :
Gut bacteria also affect other things besides weight, an interesting and important topic.
Andy, I agree that gut bacteria affects our weight and other things but that doesn’t explain the mechanism of what you said.
My carb dependent bacteria metabolize carbs into sugar and, because I consume more calories than I spend, the body turns excess into adipose tissue. I gain weight.
You have different gut biome because you consume little or no carbs and your energy source is primarily fat and protein. But you also consume more calories than you spend.
What happens to the fats and proteins your gut biome metabolizes and where do excess calories go?
In other words, how is it that you can consume more energy than you spend without your body turning it into adipose tissue? What is the mechanism here?
The mechanism for whether you store excess calories as fat is the action of the hormone insulin. Raised insulin levels tells the body to store fat. You can also only burn fat if insulin levels are low as the body will burn sugar first. If you have a predominantly fat and protein diet (although protein also raises insulin levels to a certain extent) then the body does not get the signal to store fat. If you have eaten excess calories, they will not be stored but will instead be used up by your body speeding up its metabolism, increasing your heat expended, doing extra repair jobs etc or it will be broken down and urinated and breathed out.
I’d recommend reading Dr Zoe Harcombe’s book The Obesity Crisis or Gary Taubes, The Diet Delusion if you want a more in depth explanation than I can give.
Sharon and Andy: thanks. The information you give conflicts with what I read earlier in “The Hungry Brain” but I will read it and see what it says.
Sasha, other possibilities for mysterious calorie loss: poo, pee and parasites
The Characterization of Feces and Urine: A Review of the Literature to Inform Advanced Treatment Technology
Andy, are you saying that LCHF diet leads to more fecal and urinary output than in diet containing grains? Or that those contain more protein, fats, etc? Because the paper you linked says that people in low income countries have larger bowel movements than people in high income countries. It also says that undigested fiber and polysaccharides increase fecal output and those are high in cereals and starches respectively. And I doubt any of the low income countries followed LCHF.
And what about parasites? How is that different in LCHF vs non-LCHF?
“Experts Temper Their Enthusiasm
Two experts were invited to review the paper and came up with similar feedback about the value of the postprandial assay. While the concept is sound, the practicality of employing this level of testing makes widespread use unlikely. As well, there is a need to be clear about what action to take in patients when insulin is found to be high.
“The reasoning behind the researchers’ argument, ”has been understood for decades,” said Elena Christofides, MD, FACE, chief operating officer of Endocrinology Associates in Columbus, Ohio, told EndocrineWeb. However, she indicated that “while someone with elevated insulin levels may be metabolically unhealthy, we can’t say why. While insulin levels typically correlate with levels of metabolic ”unfitness,” the patient may or may not be prediabetic, but there’s no way to be certain.”
So measuring insulin in people who don’t have elevated glucose is pretty useless with regard to diabetes.
To: Dr. Kendrick
“I think I need to to a blog on this – which shall be highly controversial.”
Yes! But please finish the blogging about the causes of heart disease first. It’s been a long journey already, and I’m running out of supplies. 🙂
“On the other hand, if by doing so, you get your blood sugar back in the normal range (and, ideally, pass an oral glucose test and insulin assay), no longer have to take any medications, that’s a cure in my book.”
Uhm right: HIV patients who are treated can have an undetectable virus load. Are they cured? No, when they stop their medication they will develop full blown Aids.
Same with diabetes patients: stop the treatment (medication, diet) and the glucose goes up again.
Only charlatans call this a “cure”.
Your chap “Jason Fung” calls it “reversal” and I guess why: especially in the US he probably would face legal problems calling something a cure that isn’t.
In one of his video’s ( https://www.dietdoctor.com/how-to-reverse-diabetes-type-2-video-course ) he says that we are told that complications like blindness, nerve damage, amputations, heart attacks, stroke, kidney damage, dialysis are inevitable.
Doctors tell patients to loss weight, follow a diet, take medication and monitor their diabetes and health in general. This cannot wholly prevent complications, but it certainly lowers the risk.
Nobody says all diabetes patients go blind or get amputations. It’s really RIDICULOUS. But it is obvious why Fung is so dramatic: he charges 429 USD a year for membership at his website…
Makes him very believable….not.
To: Leon Roijen
“Same with diabetes patients: stop the treatment (medication, diet) and the glucose goes up again.”
That’s untrue. Because if they eat a LCHF diet with some intermittent fasting, their BS will drop dramatically. Why? Because T2 diabetes is a DIETARY disease. And by changing the diet, you eliminate the disease. You no longer require medications to deal with your high BS, because there is no longer a high BS to deal with.
“Only charlatans call this a ‘cure’.
Your chap “Jason Fung” calls it ‘reversal’ and I guess why: especially in the US he probably would face legal problems calling something a cure that isn’t.”
1. relieve (a person or animal) of the symptoms of a disease or condition.
He uses both terms interchangeably. Why? Because they’re interchangeable.
But feel free to sue him. Tsk tsk tsk.
“In one of his video’s ( https://www.dietdoctor.com/how-to-reverse-diabetes-type-2-video-course ) he says that we are told that complications like blindness, nerve damage, amputations, heart attacks, stroke, kidney damage, dialysis are inevitable.
No, it’s entirely truthful. Why? Because those are the traditional complications of T2 diabetes. And by insisting it’s a “chronic, progressive” disease, all of those complications, plus a few more, should be expected, depending on how long you’ve been diabetic. He’s not suggesting that everyone will experience all of those complications. But that they are all possible in a “chronic, progressive” disease. Which no one disputes.
And I hope people will actually watch that video and decide for themselves.
What’s ridiculous is why anyone would ever want to board that particular train when another train, one that essentially promises a total reversal/cure, is reading for boarding, too.
To: Leon Roijen
“But it is obvious why Fung is so dramatic: he charges 429 USD a year for membership at his website…”
No he doesn’t. It costs $9 a month. And it has a free 30-day trial period, and you can cancel at any time.
And you get a lot of hand-holding for that amount. Some people need it, some people don’t.
“Makes him very believable….not.”
Tsk tsk tsk.
But if you need more than a little hand-holding, you can retain Dr. Fung (and other doctors on his staff) to consult with your own doctor:
And if you live in the following cities, you can visit a doctor who already subscribes to Dr. Fung’s approach:
But it’s interesting to note that you apparently expect Dr. Fung to do all this work for free. Do you know any other doctors who work for free?
I didn’t think so.
To: Leon Roijen
“However, she indicated that “while someone with elevated insulin levels may be metabolically unhealthy, we can’t say why. While insulin levels typically correlate with levels of metabolic ‘unfitness,’ the patient may or may not be prediabetic, but there’s no way to be certain.”
Of course she can say why. All she has to do is look at the patient’s DIET.
And there IS a way to tell if a person has high insulin levels, and that’s with a OGTT and an insulin assay. Which she essentially admits. But it’s supposedly “not practical.”
Tsk tsk tsk.
@Sasha: You’re right, it actually was 6 kg. Sorry for the typo.
And ignoring ‘mainstream’ dietary advice reduces your Stress… which keeps blood glucose from climbing…
@Andy, @Dr Kendrick
“Andy. High glucose is the measurement used to diagnose type II diabetes. Ergo, high glucose IS type II diabetes. That is not questionable. The question is, what is causing the glucose to be high. That, is not simple.”
I cited this before:
““It appears that fat tissues evolved primarily as a safe harbor to store energy in times of plenty and to provide fuel when food sources become insufficient. However, in addition to serving as purely a storage depot, adipose tissue is now recognized as the body’s largest endocrine organ, controlling many aspects of systemic physiology by secreting hormones (adipokines), lipids, cytokines and other factors (Gesta et al., 2007; Nawrocki and Scherer, 2004; Spiegelman and Flier, 2001). Although many of the regulatory molecules are not yet identified, they control a wide variety of biological actions, including appetite, glucose homeostasis, insulin sensitivity, aging, fertility and fecundity, and body temperature.”
Now look at the “causes” you cited:
” Cushing’s, acromegaly, long term use of steroids, severe mental illness and depression, Beradinelli Siep Lipodystrophy, increased production of insulin (see under PIMA Indians), PTSD, HPA-axis dysfunction, spinal cord injury”
What seems to be the common factor? Obesity, or at least a high(er) chance of getting obese.
Consequently the adipose tissue, as “the body’s largest endocrine organ”, gets dysregulated.
For the moment, I believe that’s the best explanation available.
Of course it cannot be the only one as there are also thin people with diabetes (type 2).
No. A chronically raised blood sugar level is due to an inability to store energy. Beradinelli Siep Lipodystrophy (BSL), for example, is a condition whereby the person has no adipose tissue. These people cannot become obese, it is impossible, as they have no fat cells. Yet they all – every single one – have sky high blood sugar levels. Why? Because their liver is full of glycogen, their muscles are full of glycogen, the liver has to turn any ingested carbohydrates into fat – but cannot – because the liver is now full of fat. They have nowhere to store excess energy, anywhere. So, it ends up in their bloodstream as sky-high VLDL/triglycerides, sky high blood glucose and suchlike – including sky-high insulin. Those with BSL are the model for ‘type II diabetes’. They are people who rapidly reach a point where they cannot store excess energy. Others, with better developed adipose tissue take a lot longer to get there, but they do – in the end.
I think I need to to a blog on this – which shall be highly controversial.
“No. A chronically raised blood sugar level is due to an inability to store energy. ”
You’re saying people with a chronically raised blood sugar level don’t gain weight anymore unless by excessive fluids accumulation?
To: Dr. Kendrick
“Dr Joseph Kraft has simply decided to re-define type II diabetes as a raised insulin level. Fine, I have no problem with him attempting to do this. He may struggle to get the rest of the medical profession to agree with him. Especially as, at least in the UK, insulin is never/very rarely directly measured. Type II diabetes is a diagnose made purely on the HbA1c.”
Yes, it’s a struggle, as this very thread demonstrates. But changing medical paradigms always do, as you’re finding out for yourself when it comes to heart disease, cholesterol, etc.
“I am not sure I am keen on diagnosing 75% of the population as having type II diabetes, along with the 80% with hypertension, and the 75% with high blood sugar levels. We are all ill, and going to die.”
Well, then a lot of people are going to die before their times, if we ignore the fact that T2 diabetes starts a lot earlier (including the damage it causes our arteries) than usually thought. And it should have some application in your search for the cause of heart disease.
“I fully agree that hyperinsulinaemia occurs before hyperglyceamia. This, however, changes nothing in any causal model.”
Well, I think you’re wrong. And a lot of doctors would agree. Fortunately, a lot of that hyperinsulinemia would never occur in the first place, or would stop occurring, by recommending a LCHF diet and intermittent fasting to more people (like *before* they become obese and diabetic), instead of virtual prescriptions for T2 diabetes, in the form of the Standard American Diet, Food Pyramid, etc.
It goes on………
you are right, it is very complicated.
Interesting that you bring up the question about glycocalyx. I came across the importance of this layer by a Swedish professor, Karl Arfors, who told me about his research on this subject many years ago when he developed special microscopic techniques necessary for the proper study. According to him it was a very tricky task to get “successful” and producing nice pictures as the one shown here.
He has produced a lot of papers together with his students on this subject.
As he claims as essential about his own research: ”A critical advance in understanding inflammation was data showing that leukocytes must adhere to microvascular endothelial cells to cause tissue damage in response to inflammatory stimuli.”
Anyway, he tured into a front figure for LCHF and his speciality is now to advocate the importance of NO through beet juice which he claims has a very strong rejuvenating effect on arteries.
Hello, may I ask, is beet juice beetroot juice and if so isn’t beetroot high on the glycemic index making it a food to use with caution for diabetics who use diet rather than drugs to control their diabetes?
Beets are naturally rich in nitrates which the body changes to nitric oxide. Nitric oxide improves blood flow and blood pressure, thus likely countering the negative effects of beet’‘s sugar content.
Yes, it is beetroot juice but as far as I understand and doing a net search health claims are abundant. It though seems like all (?) red berries, like lingonberries here in Sweden, carries the same (?) health benefits. Perhaps it is all about NO?
But you are right. Beetroot juice is a sweet drink to my taste and a limited amount is recommended.I take myself a small glass occasionally.
As mentioned in a comment on ‘book chapter’ 52 ( https://drmalcolmkendrick.org/2018/08/16/what-causes-heart-disease-part-52/#comment-101669 ) citrulline 750 mg/day would help also.
Georgina Wrelton: “Beet” and “beetroot” are two names for exactly the same thing. I take mine fermented (about 1/2 cup in the morning). I may be wrong, but as I understand fermentation, the process converts some of the sugars to lactic acid. I’m convinced that the benefits of the nitrates outweigh the concerns about the small amount of sugars.
Beet juice contains a lot of nitrate, the substance that could help lowering your blood pressure. Drinking it everyday in quantities high enough to lower your blood pressure, will lead to a higher than recommended daily intake of nitrate. Of course it’s everybody’s own decision. I wouldn’t do it.
Carrots are high in sugar, but people have cured their cancers by drinking high volumes of carrot juice because carrots have superb antifungal properties.
Also, fermentation is powered by sugar, therefore kvass has a much lower sugar content than beets or beet juice.
This well known connection between diabetes and CVD also reminds me of Dr. Kraft who clinically measured blood glucose and serum insulin simultaneously on 16 000 patients and he claimed that a CVD patient who was not considered diabetic was just un-diagnosed.
Here is an great interview with D®. Kraft by Ivor Cummins
My surprising takeaway from this interview with this awesome man (that bright at 95) is that ‘high cholesterol’ is a proxy for hyperinsulinemia.
It is more nuanced than just “high cholesterol is a proxy for hyperinsulinemia.” I would say that dyslipidemia (ie, high Trigs and low HDL) can be used as a proxy for hyperinsulinemia. High cholesterol is pretty much useless for anything without any sort of context.
Oh yes, Harry. I was diagnosed with type 2 and advised to consume 55% carbs ( no advice as to what constituted ‘healthy’ carbs, or ‘unhealthy carbs’.) I was then found to have high cholesterol readings and put on statins…and the upward spiral of poor health began in earnest. Up went the Hba1c, and more hypoglycaemic meds….and up went. the total cholesterol….no breakdown done to illustrate fractions. I kept saying to the Practice Nurse ( little chance of getting through the gate to a Dr), that I was chasing the diabetes with ever raising meds, and failing to control the cholesterol with ever raising meds. The way I got out of the dreadful situation was by changing my diet, much to the delight of the endocrinologist, and ultimately removing all meds. I said I was reverting to what I learned in the 1960s when approaching adulthood, and ultimately dismissing the fads of the NHS, and Big Pharma. So despite some bloggers here, whose thoughts I consider closely, to me diet is at the root of the modern day unhealthy conditions raging through our wonderful globe.
His book suggests that a person can be fully diabetic (with all its attendant complications) with blood sugars in the 70-80 mg/dL range! There’s an awful lot of people out there who have no idea that they have T2 diabetes.
Yes, this is actually what Dr. Kraft claims – fasting glucose tells very little or nothing about your diabetes status.
BTW He also claims that medicine doesn’t actually know “what” the diabetes disease “is”. This is in my eyes weird with 500 millions of diabetics world wide.
It is because the have the causal model all twisted the wrong way round, and will never, ever, change their minds.
“It is because the have the causal model all twisted the wrong way round, and will never, ever, change their minds.”
I’m seeing changes: 5 types of diabetes: https://www.livescience.com/61917-diabetes-five-types.html
Of course it’s still completely unsignificant, but maybe a little new start.
The “metabolic syndrome” is an amusing concept, too 🙂
Correct. And I love this description:- ‘ Cause of Death for 95% of diabetics is heart/circulation problems, for the rest, it’s a falling grand piano.’
Do you have any idea if “isolated” hypoglycemia can cause damage to the glycocalyx, too?
The glycocalyx stuff is fascinating, but article you reference is about microvascular complications in Type I diabetes. Macrocascular disease such as atherosclerosis doesn’t appear to be impacted by glycemic control.
Not sure on this one, it is undoubtedly complicated. My own view on this – not really ever stated up to now – is that it is not actually/necessarily the blood glucose that is the factor that damages the glycocalyx. In type II diabetes, many other things are perturbed – clotting factors, FFAs, glucagon, insulin and suchlike. I think the focus on blood sugar, alone, is not necessarily helpful. Thank you for your comment, which does open up other lines of thinking on the exact factor, or factors, that may be damaging to the glycocalyx.
I would hope I do not give the impression that I have all the answers, because I most certainly do not.
If glucose is a primary factor in damage, would that not explain why only arteries are affected? Because glucose levels in venous blood must be lower after the cells have consumed a chunk of it for energy.
“is that it is not actually/necessarily the blood glucose that is the factor that damages the glycocalyx”
This is actually the main point of Dr. Kraft (and Ivor Cummins) in the linked interview above – worth the time looking and listening in my eyes. Believing what they claim, it seems to be all (?) about hyperinsulinemia or insulin resistance though in an obscure pathological rationality.
The focus on blood sugar (BS) has evidently wrecked sound thinking about diabetes though my wife and myself are happy noting our BS to be “under control”. Her severe diabetes, ten years ago, seems to have been basically reversed today. Her night vision is restored and her neuropathy is evidently history today with both her eye-diagnosis. Her eye bottoms looks today perfect on the photographs we have taken.
“I would hope I do not give the impression that I have all the answers, because I most certainly do not.”
Something for which I immensely respect you.
I’ve seen research, including I think a paper from the ADA, which relates HbA1c with microvascular complications, and postprandial glucose spikes with macrovascular damage.
Here’s the problem – HbA1c is dependent on the lifespan of blood cells which may vary for numerous reasons. Worse than that, they are initially glycated reversibly, so A1c fails to register brief glucose spikes. Other tissues are not that lucky and are immediately damaged irreversibly. Not sure if that includes the glycocalyx but I suspect so (how did you get that photograph of my lawn???)
Then insulin itself may damage the endothelium among other things. High insulin from chronic insulin resistance may exist for years before the pancreas starts to lose beta cells (Kraft) and by the time diabetes is actually diagnosed around half the beta cells have gone. There were enough to generate several times as much insulin as normally required and even when half of them are lost there is still the capability to generate hyperinsulinemia, just not so extreme.
Type 1 diabetes is a catastrophic loss of beta cells by autoimmune attack. Type 1s used not to have insulin resistance unless they took steroids or other drugs. Now “double diabetes” has become common, probably resulting from the current philosophy of eating a “normal diet” and jacking up the insulin to cope with all the carbs, and more and more Type 1s are being prescribed not only metformin but other “Type 2” drugs.
Then there are MODY and other such genetic types of diabetes, such as I suspect I have, which mainly affect insulin response. I probably never had a proper Phase 1 insulin response but still have a fairly decent Phase 2 level, as long as I low carb to keep the IR down. A recent find was a gene/deletion affecting GLP-1, the relay that switches Phase 1 insulin on and off. Lots of other factors also affect incretins.
“Classic” Type 2 used to be largely a disease of ageing aided by high levels of IR over prolonged periods almost literally “wearing out” the pancreas. Now like so many diseases since low fat diets were invented it has become common and widespread. It is still blamed on being fat, which is blamed on eating fat, which is the justification for high carb diets. Yet 20% of Type 2s are not overweight and 80% of obese people are not diabetic. Count Pareto may have had something to say about that.
Up and coming is the belief that diabetes is caused by meat, or eggs, which a moment’s thought will show is a nonsensical notion, as Peter Cleave said it is ridiculous to blame ancient foods for a modern disease.
Here’s a fascinating talk by Michael Eades who has distilled down a lot of Peter (Hyperlipid)’s highly technical posts about mitochondria and protons
now this is something which HAS changed greatly in the last half century.and may explain why the level of carbs eaten in our past and by some other societies was not toxic then and is now.
If mitochondria are damaged this affects pretty much all tissues.
Thanks, Chris. I agree. The notion that correction of hyperglycemia by medications, particularly insulin and the secretagogues, lowers CV mortality risk, is wrong based on science and clinical experience. No interventional prospective trial of blood glucose lowering has shown this. Focusing on treatment of hyperglycemia, rather than the underlying insulin resistance, is at the heart of what’s wrong with current treatment models. Treatment goals should be reversal of diabetes via low carb diet, and normalization of insulin levels. Tragically, we rarely even measure insulin levels.
Yes I suspect the meds may decrease damage from hyperglycemia while increasing damage from hyperinsulinemia. Really you don’t want hyperanything in the blood.
Interesting! Thank you. Is the endothelial glycocalyx something that can repair itself if a type II diabetic switches to a diet that keeps blood sugar in a normal range?
Do I remember correctly that statins can increase your blood sugar?
Dearieme: Yes, they increase diabetes risk.
Methinks you do.
Quote from atorvastatin package information leaflet ” other possible side effects with Atorcastatin Common: may affect up to 1 in 10 people
increases in blood sugar levels………
Possible side effects reported with some statins (medicines of the same type):
Diabetes. This is more llikely if you have hjigh levels of sugars and fafts in your blood, are ovewrweight and have high blood pressure. Your doctor will monitor you while you are taking this medicine”
(once a year here!!)
Yes Dear, they do. But we don’t speak of it in ‘Polite Society’
In what sense does the glycocalyx “sense”?
Mechanical? Usually one thinks of innervation as the mediator for sensing.
What is the result of stress sensing?
I imagine, though I do not know, that they have a biomechanical sensory function. I would imagine if it is wobbling about a lot, this sends a chemical message to the endothelial cell.
If that biomechanical sensing results in a chemical message to enlist inflammatory cytokines, might the damage to the endothelial cells be due to the action of those (overenthusiastic) cytokines?
The Endothelial Glycocalyx: A Mechano-Sensor and -Transducer
“The apical surface of endothelial cells (ECs) is decorated with various membrane-bound macromolecules that constitute the glycocalyx (GCX). As the most apical structure on the EC, the GCX senses the force (shear stress) of flowing blood and transmits the force through the cytoskeleton to sites where transduction of force to biochemical response (mechanotransduction) may occur. In this presentation, we review the structure of the GCX and experiments that demonstrate its role in mechanotransduction and vascular remodeling. Experiments with enzymes that degrade specific glycosaminoglycan components showed that the GCX mediates the shear-induced production of nitric oxide, a central process in cardiovascular control, whereas the same enzyme treatments do not affect shear-induced production of prostacyclin, another hallmark of EC mechanotransduction. These experiments reinforce the concept of distributed sites of mechanotransduction in EC. The characteristic remodeling of the EC cytoskeleton and intercellular junctions in response to shear stress are dependent on the GCX as well, and we present the experiments and theories that support the role of the GCX in these processes. The GCX is a fascinating structure whose role in EC function is only beginning to be appreciated.”
‘Apical’ definition: in cell biology the surface of a plasma membrane that faces inward to the lumen
Cells are necessarily somewhat rounded in shape, so on a micro scale the arterial wall would resemble a cobblestone surface. Presumably the gel part of the glycocalyx fills in the joints and makes the knobbly surface hydraulically smooth. The hairy part would retain the gel against the rush of blood, and transmit shear stress to the endothelial cell.
As blood flows faster the shear stress increases, and nitric oxide is released. NO is a vasodilator. It tells the blood vessel muscles to relax so the blood vessels widen, reducing the flow speed of the blood and hence the shear stress. So NO is a control mechanism and not a ‘cry for help’ as I had elsewhere surmised.
Very interesting – thank you
I’ll be sharing with my appraiser next month.
Sent from my iPhone
Could anyone provide an answer to a question that has been puzzling me for a while please?
The damage to the glycocalyx and subsequently to the underlying endothelial layer is caused (amongst other things) by hyperglycaemia (prolonged raised levels of blood glucose), the LCHF dietary approach removes the source of hyperglycaemia by restricting the carbohydrate burden on the body, removing the roller coaster rise and fall of glucose as it peaks and falls in response to the subsequent insulin surges. The tracking of one’s dietary intake of carbohydrate, protein and fat is a simple matter of weighing and recording whatever goes into your mouth, allowing a reasonably accurate estimation of the proportion of kilocalories provided by C:P:F.
How then to account for a glass or two of wine or beer ? The majority of the energy content is provided by ethanol (alcohol) which is dealt with directly by the liver – does this arrival of ethanol in the bloodstream trigger an insulin response equivalent to having ingested a similar amount of carbohydrate? If so, would that mean that heavy drinkers / alcoholics also suffer increased rates of CVD ?
Thanks in advance for any clarification provided.
This is a very good point you are making in my eyes.
There is another great lecture by a reward winning professor, Roger Unger – BTW about the same advanced age as Dr. Kraft. It doesn’t hurt to view this lecture a couple of time since it is a “block buster” in explaining blood sugar regulating mechanisms. Again it is all about insulin and not least glucagon.
Three words: Oh.My.God… This is one of those talks that give me goose bumps.
Yes, it kind of trips everything upside down in your mind. A feeling that I love, but a lot of people hate.
What I have understood so far is that ethanol is ‘neutral’ to the ketogenic diet, i.e. doesn’t raise blood glucose levels. However, it provides an energy equivalent of 7 kCal/g ethanol, to this amount has to be taken into account if caloric restriction is one of the targets.
I think (someone please correct me if I’m wrong) that if the fats (and proteins) that you eat have a higher caloric value than the daily expenditure, increased weight still occurs.
I think that the ketogenic diet works so well for weight loss because
a. the hunger feeling (there is none) doesn’t fight against your caloric restriction,
b. the low insulin levels don’t make you store fat instead of burning it up (which was part of the metabolic syndrome: feeling tired because the insulin tells your body to store fat and to stay inactive).
Harry, when you stop secreting insulin, you don’t just stop storing fat, but your body is allowed access to your stored energy — body fat.
It seems such a pity that people who want to lose weight are never told that insulin has to be ‘turned off’ before stored fat can be used.
@Stephen T: Yes, that thought was included in my mentioning the metabolic syndrome (“…and to stay inactive”–which is short for not being allowed to burn your fat).
To: Martin Thompson
“The tracking of one’s dietary intake of carbohydrate, protein and fat is a simple matter of weighing”
It’s not really necessary to do that. Just avoid starchy carbs, sugar, and refined foods. It’snot really a calorie-in, calorie-out situation. Eat until your full. Mostly protein and fat.
“How then to account for a glass or two of wine or beer ?”
Actually, you pretty much have to say goodbye to beer and wine. Fortunately, you can have some whisky, vodka, tequilla, etc. 🙂
Aren’t vodka, tequila,etc metabolized into sugar in the body? Also, if you consume more calories than you spend (even if through protein and fat), what happens to excess calories?
Excess calories will be stored as fat
That’s what I thought too. I was asking because of “Just avoid starchy carbs, sugar, and refined foods. It’snot really a calorie-in, calorie-out situation. Eat until your full. Mostly protein and fat.”
In some ways it is a “calorie in, calorie out situation”.
I’ve been low carb for several years now. I’m usually in ketosis, and find that a glass of red wine, and once in while several (lol) doesn’t kick me out of ketosis. Your mileage may differ.
“I was asking because of “Just avoid starchy carbs, sugar, and refined foods. It’snot really a calorie-in, calorie-out situation. Eat until your full. Mostly protein and fat.”
It’s a well known fact that fats and proteins keep you full longer and therefore high carb diets with little fat are not a good idea because you’ll be more hungry more often, and though carbs contain less calories per gram (4) compared to fats (9), you probably will consume more calories with a high carb diet.
For proteins the story probably is a bit mixed: some proteins are able to provoke a rather big inuslinemic response.
With all that said, it’s a myth to believe that a fat laden diet can make you loss weight.
As we say in Dutch: “every pound goes through the mouth”.
I’ve been a PT for years and reducing intake and increasing output always leads to weight loss. This is always the case with thyroid issues, sleep issues, hormones it’s simply more difficult. When we talk about weight loss in the gym I work at we mean fat loss and this means resistance training and increased protein of course. Rightly so processed foods should be minimised and avoided if realistic to ones lifestyle and carbohydrates mainly from vegetables and whole grains also based around activity levels. Together with loads of other strategies, it eventually becomes a lifestyle. The most successful results I’ve seen are through tracking. People learn so much about food through a few months of tracking and then never need to use it again. I see tracking as a learning tool and it works for the most.
Leon, in Afrikaans there’s a saying, “Wat nie doodmaak nie maak vet.” (What doesn’t kill you makes you fat.)
“Leon, in Afrikaans there’s a saying, “Wat nie doodmaak nie maak vet.” (What doesn’t kill you makes you fat.)”
Hello Afrikaans cousin 😉 Nice saying – I love Afrikaans (‘n baie snaakse taal 🙂
This depends on how sensitive to carbohydrates you are.
Officially, I am on the borderline of pre-diabetes/Type II diabetes. I’m pretty sure I have actually been diabetic for several years, but the fact I already ate hardly any sugar on my previous diet disguised this fact. Wholemeal bread (47.1 % C H O) savoury sandwiches were probably the main source of the carbohydrates which may have caused my problems.
To keep my blood sugars fluctuating in the near-normal range, I have to weigh all non-animal food and some dairy products to the gram. I test before and once, at varying intervals, after meals as absorption times change a lot. I am keeping to 50 – 70 grams of carbohydrate a day, with the odd small lapse. I don’t believe I can be cured and expect to be on this sort of diet for the rest of my life.
I have been on a low carbohydrate, high fat diet for 21 months and have lost around 3 stone in weight. The best thing about this diet is the lack of the hunger pangs which in the past have prevented me complying with any diet for more than about six months. Then I would regain the weight with interest.
I like to drink dry white wine, 0.6% C H O, 80 ml with 170 ml sparkling mineral water as a spritzer in hot weather, and red wine, (0.3% C H O) with some meals. Some beers are around 3.0%
C H O so a 200 ml glass is allowed sometimes. It would help, if by law the % carbohydrate content had to be on the label like the alcohol one. Remember, treats are essential when keeping to any diet, even a strawberry and smoked salmon one.
The main problem is getting sufficient fat intake so as not to feel hungry. Supermarkets now trim the fat off meat and getting hold of beef dripping or lard is practically impossible. I fry most of my meat in olive oil or butter and eat a plenty of Jersey double cream and assorted cheeses.
It is important to remember that anything vegetable always contains carbohydrates, even lettuce, and it all adds up. Joe’s method underestimates the amount of carbohydrate I eat by about 50%. I know, because I used to use it until I stopped losing weight and my Hba1c went back up. I love fresh fruit but have to restrict it to two small portions a day as it contains a lot of sugar. And onions, a mainstay of savoury dishes are 10.1% C H O and are surprisingly heavy.
My GP’s original advice was to lose weight. He left it to me how I did it and has been supportive.
My blood pressure is now the lowest it has been for over 20 years and I may be able to reduce my BP medication soon.
Tracking one’s carbohydrate intake is not that simple, even with a computer spreadsheet formula to do the calculations. It is easy to make errors and any dish with multiple ingredients is much more of an approximation as they rarely mix uniformly. Sharing such dishes with my husband also increases the inaccuracies.
I reckon we two people spend about £20 a week more on this diet. My husband does not weigh his food and takes more carbohydrates than me, but eats much the same otherwise. We can still afford it but I realise many people, especially other pensioners and those with young families, cannot.
This is probably the core problem. Healthy food, especially meat, fish and dairy, is expensive and food loaded with carbohydrates is much less so. It might become necessary to heavily subsidise healthy food to make it cheaper than unhealthy food to improve the overall health of the population. Might this be a effective use of part of the NHS budget?
martin T: Binge drinking raises diabetes risk, raises cvd risk:
Thanks for this Leon, interesting stuff.
fascinating, thank you.
Another great thought provoking article. Little hairs on endothelial wall. That was new. Certainly explains a lot. Amazing bodies we do have. You’ve stated before that the endothelial wall is in constant repair. Does this ring true in this area also?
Thank you for yet another lucid explanation, Dr K. It seems to follow that those who advocate low sugar/low carbs have the rights of it, even if it’s the insulin excess resulting from too much intake of foods that cause rises in blood sugar that damages the glycocalyx and endothelium?
Can I ask what the process is? How does raised blood sugar levels damage the glycocalyx?
My understanding is that raised blood sugar interferes with the bonds in the proteoglycans. I may not be right on this
Really interesting…thank you. My husband has type 2 diabetes so I am particularly interested.
Excellent! So what part does Insulin play in glycocalyx destruction, if any?
I don’t know, for sure. I do know that high levels of insulin are not good, but I have not yet seen a mechanism of action for glycocalys destruction. Maybe I have not looked hard enough
And yet still…insulin levels are not measured routinely by NHS.
Ok I did read something on Insulin and Glycocalyx after I heard you on Nourish Balance thrive podcast, I will try to find it again and post, but Insulin is destructive to glycocalyx from memory.
A friend asked his (cynical and sarcastic) doctor why insulin was never measured
“We’d find so many diabetics it would bankrupt the NHS”
Thank you. Another little bit of the human body I’d never heard of. I’m sure there are many more. I remember asking my GP about chondroitin years ago when it was all the rage for osteoarthritis. From memory his reply was that it was just another protein and was metabolised as such, therefore had no more effect on arthritis than any other protein. Hadn’t found your excellent blog at that time.
Malcolm thank you again ! It is so good to read lucid, science in language we can all understand. Wonderful !
And of course you do not know everything..But you lead and encourage thinking, questioning, discussion among us here.. That too is rare and wonderful.
So, all those years when the allopathetic medical establishment was demonizing fat, and the food industry was busy producing low-fat “food” (made palatable by replacing the removed fat with sugars) really boosted the pharma industry — more type II diabetics, more prescriptions sold. And the push to get everyone on statins continues the trend. Sweet deal if you invested in pharma stock.
Invest in Big Pharma. Use the profits to buy grass fed meat and vegetables. Oh and cheese.
Brilliant. Thank you.
Is there any chance that Linus Pauling’s talking about lysil groups ‘sticking out of the damaged (scurvic) endothelium’, catching on to Lp(a), leading to plaque, is somehow related to this glycocalyx explanation?
Yes, I think it probably does
Then was he maybe also right about taking L-lysine (together with) vitamin C in order to ‘occupy’ those lysil groups, thereby preventing the Lp(a) from ‘sticking’ to them?
I have to say I tried it for a few months: 10 g vit C + 3-5 g L-lysine per day, and my shortness in breath totally went away when doing some incidental heavy exercise (climbing up a steep hill).
It was amazing, but also a sample size of merely 1.
(Only after that I learned that in man vit C gets, partly, recovered through the blood making, such high doses unnecessary. And what is the disadvantage of lowering Lp(a)?)
That ws most interesting. I have 2 questions, does the hyperglaecia episode in T2 also apply to T1?and re statins, do they have any affect on the hairs? I only ask as when I was on statins my hair, which was longish, became incredible dry and started breaking off, so much so I had to have it cut much shorter. This had not happened to me before so I blamed the statins assuming they somehow removed oil/fat from my hair. My Gp did bloods and it was not low thyroid.
Deborah, my hair became very thinned on statins, particularly at the temples. In passing, I asked a doctor about this and he told me, no, statins don’t do that. HOWEVER, when I eventually ceased taking the rotten things within two weeks new hairs were sprouting at my temples. A while later it was a total transformation. Hurrah!
This also clearly explains why bald men have greater incidence of heart attacks 🙂
That’s encouraging, thank you. However I think I didn’t make my question clear, I wondered whether statins,( if they could affect hair quality/quantity on the head) could also affect the glycocalyx hairs?
Once again a big thank you Dr Kendrick, and to all the invaluable informative comments another big thank you!
In today’s Times newspaper is an obituary of Professor Gerald Russell, a renown psychiatrist and leading authority on eating disorders. A fitting observation in the article was:
“He was notably open-minded as a scientist, changing his opinion when the facts changed: he had been convinced that anorexia was a condition of the hypothalamus, an area of the brain, but when presented with evidence that the hormonal changes followed the starvation, he happily discarded the hypothesis.”
What a shame that this is not the approach shown by the majority of scientists and medical ‘professionals’ today.
Many thanks for all your digging – keeps the hunt for answers alive.
I wonder if glycation is causing the Glycocalyx breakdown: Free glucose readily reacts with proteins present in the blood (the mechanism behind HbA1c as long term blood sugar biomarker) If the Glycocalyx hairs are a) made of suitable protein and b) sufficiently small in diameter to form an active glycation site then maybe this could be a reason for the observed damage. Perhaps glycation end products can be seen locally?
I am curious to know the scale on the picture of glycocalyx (another thing I didn’t know existed). There is what looks like a scale in the bottom right, but no numbers or units are visible.
Does this stuff coat plaque as well as healthy endothelium?
It sticks out of endothelial cells. You can see a single endothelial cell under the glycocalyx in the picture
Does the glucocalyx line all vessels including veins?
Including the lymph system?
Thanks Malcolm – I had totally the wrong scale in mind as I looked at that picture, because the base looked somewhat concave, I thought that was the curvature of the blood vessel wall!
Malcolm, is pre-diabetes, with only moderately increased blood glucose and elevated insulin levels, also correlated with increased CVD?
Money quote from David Ludwig
“Prediabetes isn’t really pre-anything”
It might be pre-tasting-sugar-in-urine I suppose. Is that what happens when kidneys dump sugar at 7mmol/ml?
Fascinating piece of the puzzle. This makes me ponder the idea that the glycocalyx is one of the important keys to understanding what causes CVD. If its main role is protecting the endothelium, and endothelial damage the key driver of atherosclerosis, leading to unstable plaques which can cause MI, it seems logical that damage to the glycocalyx is the beginning of the process.
That is what I believe to be the case.
I see a rising hypothesis that sleep problems contribute to CVD. Do you have any idea of the mechanism behind it, based on your explanation of CVD?
This primarily becomes a raised stress hormone issue, with additional hypoxia
Also because of the effects on leptin, ghrelin, and probably a bunch of other hormones. Dr Rhonda Patrick on FoundMyFitness had an interesting interview with a neuroscientist who studies sleep. He talks about them in the interview.
There’s also a book “Lights Out” which makes some wild claims on what the advent of electricity did to us as a species. That and moving away from agrarian/ hunter gatherer lifestyles. Dr Patrick’s interview touches on that too.
An excellent twist to the long running discussion.
I had no idea of the presence of the glycocalyx. This subject is finally starting to make sense. The comparison to the slimy feel of fish is apt. In fact, there have been trials with military submarines to carry a polymer/water mix to be emitted forward, surrounding the hull, to provide a speed burst, made possible by reducing the frictional drag. The solution affects the turbulent boundary layer, just as it does on a fish.
Aside from the molecular interactions made possible by the glycocalyx, one of the prime purposes must be to reduce viscous shear stresses at the surface of the endothelial cells by changing the kinematic properties of the boundary layer. If the glycocalyx system is damaged you get a more direct exposure of the endothelial cells to a pressure pulsed flow, which is probably turbulent and cyclical, depending on the artery cross section and resulting flow rate. Note that cyclic stresses have fatigue limits in terms of cycles, and this is a common engineering design consideration. That bridge that fell down in Italy probably exceeded its limits. This explains why you do not get diseased arteries in the rest of the body. Even if the glycocalyx is damaged in the rest of the body the consequences are less severe. Note that the cyclic fatigue limits in the rest of the body are infinite, but not in the main arteries; the stresses are too high, especially if the glycocalyx is degraded.
Thanks for your input.
DR K, I heard you mention glycocalyx in a recent podcast and wrote it down and researched it! I wracked my brain trying remember which podcast! Then I remembered: http://www.nourishbalancethrive.com/podcasts/nourish-balance-thrive/why-cholesterol-levels-have-no-effect-cardiovascul/ You snuck it in but I caught it! I was amazed when I researched it! Here is time stamp for anyone interested, it was a wonderful talk [00:10:20] Endothelium, glycocalyx.
SW: Thanks for the link! Great fun to read this morning. Lots of gems, such as the fact that EPC’s can become monocytes which can become macrophages, which I remember from an earlier post, but had forgotten. Handy little devils to have coursing through our veins. And it reminds me of a question I thought of as I was nearing slumber last night: Do EPC’s exist in the circulation with the glycocalyx already formed, or does that come after they are emplaced as endothelium? I suspect after, but then I wonder, how would we know? Another gem: “I have yet to meet a doctor who knows the difference between relative risk and absolute risk.” A bit unsettling, that. And finally the best explanation for why peer review should be abolished: peer review. . .”is the greatest system for maintaining the status quo.”
Not understanding the difference between relative risk and absolute risk drives me mad. I had a conversation with a friend GP recently regarding vaccinating boys against the HPV virus to prevent oral cancers. She was pushing for us all to vaccinate our boys as oral cancer has increased by over 30% since the early 1990s. I pointed out that this was a relative figure and that in absolute terms taking into account population growth over that time period it had actually only increased from 0.016% to 0.018%. Of the 0.018% of the population contracting oral cancers each year, a third were female and 75% were over 65 years old. The small number that was left also didn’t strip out those caused by smoking etc. The likelihood therefore of my son contracting oral cancer at any point over the next 50 or so years tends towards zero and I have no intention of putting foreign substances in a pubescent body that is changing rapidly on a daily basis. The response was “yes but it’s gone up by over 30%. That’s a big number”…
Sharon, My grandaughter was assaulted with the HPV vaccine because her mother is paranoid about cancer, and has the view that it’s best to do everything you can to prevent it. Arrrrgggghhhhh! How do you get absolute risk into peoples heads? My grandaughter was screaming that she didn’t want the jab, but still she got it. I gave her mother a lecture on amorphus aluminium hydroxyphosphate sulphate, of course she had never heard of it, so she gave “permission” for the assualt without having been informed, or having done any research.
Despite the pulsatile nature of flow in arteries, laminar blood flow is silent. Thus, no sound is normally heard via a stethoscope placed over arteries. Constriction of the vessel, or obstruction of the vessel lumen, disrupts laminar flow and leads to turbulent blood flow… Turbulent blood flow is noisy and can be heard by using a stethoscope placed over the artery at or distal to the point of constriction or obstruction. Laminar and turbulent flow provide the physical basis for the auscultation method of blood pressure measurement using a pressure cuff placed over the upper arm (to cause vessel constriction) and a stethoscope placed over the brachial artery (to listen for the noise of turbulent flow when the vessel is constricted). The sounds heard by this method are referred to as the Korotkoff’s sounds. — http://www.physiologyweb.com/figures/physiology_illustration_Gxr9bSdjRij69DSavoTbjWtiQ44Pw3aM_laminar_versus_turbulent_flow_in_blood_vessels.html
I note mention was made of the glycocalyx by Anthony Sanderson back in Parts 36 and 38 in September 2017, here is what Anthony wrote:
“On the issue of pressure/turbulence/bio-mechanical stresses being involved in the location of arterial plaques . . .
Recently I read a paper “Hypothesis: arterial glycocalyx dysfunction is the first step in the atherothrombotic process” https://www.ncbi.nlm.nih.gov/pubmed/18319293 FREE
Some of its points:
“Blood flow in arteries is associated with a shear stress at the glycocalyx, which signals the underlying endothelial cells to release nitric oxide (NO), an anti-atherogenic factor.”
“Sites of low shear stress in the arterial tree are more susceptible to atheroma due to lack of NO generation through this mechanism, whereas exercise, by increasing blood flow and shear stress, is protective.”
Counter intuitively the sites of least surface shear stress are the bifurcations in arteries where there is turbulence. (I would also guess that the inside curve, rather than the outer part, of an arterial loop would have lower shear shear stress and guess plaques should form there.????)
They seem to be saying that protienaceous hairs extend from inside the cytoplasm of the endothelial cells into the protective glycocalyx, and it is these that stimulate the production of protective NO, relaxing the smooth muscles – but mainly where the shear stress is high – where the NO need is highest??
I ponder on . . . why are veins, one assumes with super low shear stress . . . are not jammed with plaques? Perhaps they do not have the same demand on them as arteries, so are less needy of NO?”
“Good points about the roles of l-arginine and l-citrulline in the NO pathway . . . but it is worth bearing in mind that the impulse for the epithelial cells to producer NO is the shear force of the blood on the proteinaceous hairs that connect to the epithelial cells’ cytoplasm and extend through the glycoprotein matrix of the glycocalyx.
It is the forces on the glycocalyx and its hairs that are transmitted to the epithelial cells that stimulate the NO production. So, compromising the glycocalyx is all that is required to prejudice the power of the epithelium to producing protective NO.
“High Glucose Attenuates Shear-Induced Changes in Endothelial Hydraulic Conductivity by Degrading the Glycocalyx” 2013
It does seem odd that something that on the face of it might seem very destructive, like high sheer forces, in fact, is just the thing that stimulates the protective NO.”
I know. I love it. Counter-intuitive thinking. By far the vest sort of thinking that there is.
So, based on that way of thinking, it would seem that repairing the glycocalyx/endothelium with chondroitin, vitamin C, lysine, heparin sulfate, or whatever would be one step, then ramping up NO production with l-citrulline, etc., would be a very solid plan to move forward with secondary prevention, because the natural shear stresses already have the body primed to do just that. Very interesting, and so far out in left field the established medical community cannot grasp it. I asked a dr. about transcytosis not being able to be done on LDL because of the blood brain barrier issue, and he just looked at me like I had a third eye.
Yes, my thinking has moved a little away from the mainstream.
Martin: Thank you very much for reminding us of this! I remember reading it at the time, and tucking it into the “value of vigorous exercise” box in the ever-weaking-with-age memory bank.
Its interesting to speculate how the endothelium might heal itself. Presumably the new cell binds to its neighbours, then grows the hairs seen in the illustration, then exudes the glycocalyx gel. All done while the blood is rushing past. A tricky repair job.
NO appears to be a “cry for help” by the endothelium. But an intact endothelium needs no help. So I would assume that if an endothelial cell goes missing, its neighbours emit NO to summon endothelial progenitor cells to repair the gap.
If this is true then a high NO count could be considered a sign of a failing endothelium. But on the other hand it could be a sign of a vigorous endothelium replacement policy, resulting in a generally younger, more sturdy endothelium.
Pathological shedding of the glycocalyx occurs in response to mechanical cellular stress, endotoxins, inflammatory mediators, atrial natriuretic peptide, ischaemia-reperfusion injury, free oxygen radicals and hyperglycaemia.
Atrial natriuretic peptide (ANP) or Atrial natriuretic factor (ANF) is a peptide hormone which reduces an expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized, and secreted by cardiac muscle cells in the walls of the atria in the heart.
I was introduced to the dramatic effects of atrial natriuretic peptide about eight years ago. It wasn’t fluid volume that triggered it, though. It was distressingly symptomatic paroxysmal atrial fibrillation. As explained to me by my electrophysiologist, it’s the system’s attempt to correct what it sees as extreme high blood pressure as the atria are fibrillating and the ventricles are attempting to keep some kind of pace. The result is pee urgency every twenty minutes or so over a few hours. At a liter per pee, that’s pretty dramatic. It leaves one pretty “washed out” with extreme low blood pressure after the 2 to 3 hour paroxysm. It’s a natural diuretic. (BTW, most ANP is produced by the left atrial appendage.)
This article makes me think that, at least in part, those episodes contributed to the over 1,500 CAC score I got years after ablations stopped the AF paroxysms. All that ANP must have played havoc with my slimy glycocalyx.
Entresto is a comparatively new drug that’s given for congestive heart failure, It containing sacubitril and valsartan.
Sacubitril inhibits the degradation of the enzyme neprilysin whose duty it is to break down atrial and brain natriuritic peptides.
So, ANP and BNP continue their work!
Makes me wonder if this “wonder” drug is causing harm to CHF patient by effectively stripping their glycocalyx.
But, perhaps it’s no worry, what with all the valsartan recalls.
JD—What an intense experience that must have been—2 to 3 hours—more than just exhausting—thanks for the insight—
Does this paper go on to say what we can do to keep
our glycocalyx healthy or to rejuvenate it if damaged?
I am certain it is always trying to rejuvenate. As with everything else damage > repair – you have a problem. Repair > damage, you are OK
William—no it doesn’t—it is focused on perioperative fluid maintenance—-I try to focus on inflammatory mediators and hyperglycemia—–control carbs—–take various anti-oxidants.
I love that algorithm: Damage > repair – you have a problem. Repair > damage, you are OK.
It really seems to be the simple answer to the question, What causes heart disease?
It also may explain why age is a factor in CVD. As repair mechanisms succumb to senescense, damage exceeds repair, and down we go.
It is not what you know, that you don’t know, but what you don’t know you don’t know!
Slippy hairs wow! I love your blog, I have learnt so much this last 5 years 🙂 Thank you
Do Diabetics II need more insulin?
Not if high glucose is accompanied with high insulin ie insulin resistance caused by glycated insulin receptors. Glycated forever.
Rapid Non-Enzymatic Glycation of the Insulin Receptor under Hyperglycemic Conditions Inhibits Insulin Binding In Vitro: Implications for Insulin Resistance
“The IR rapidly glycates under hyperglycemic conditions resulting in significantly decreased INS binding under in vitro conditions. If this effect also occurs in vivo, the clinical implications of rapid glycation under hyperglycemic conditions may be to cause interference with binding of INS, IGF, and related hormones to their receptors that would last for the lifetime of the ligands and their receptors. Direct measurement of IR, IGFR, and glucagon receptor-glycation might provide more accurate and sensitive means for evaluating the effects of hyperglycemic episodes in diabetes than does hemoglobin A1C.”
These studies indicate that glucose adversely affects the glycocalyx by causing it to shed hyaluronan:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023224/ in the kidneys
http://diabetes.diabetesjournals.org/content/55/2/480 in human trials
https://pdfs.semanticscholar.org/a70e/681012531b1e3e2ce4fb206f366164aa8524.pdf in hamsters
It also seems from those studies that externally administered hyaluronan will only be replenished to the glycocalyx if chondroitin is injected with the hyaluronan.
The hyaluronan shedding reduces the thickness of the glycocalyx. Presumably this means that the hairs are flattened – administration of hyaluronan/chondriotin restores the glycocalyx quicker than I would imagine it could regrow. So how would this allow the endothelium to be damaged? I looked up the velocity of blood, and was startled to see that in arteries it’s up to half a metre per second. If the endothelial layer is to be damaged mechanically by the components of the blood eroding it, you’d expect to see plaque build up (the repair mechanism) more at bends in the arteries – which is exactly what happens.
What else indicates blood glucose as a culprit? From The Great Cholesterol Con MK says that stress is a major factor for CVD. Stress is also a factor in high blood sugar. And that the only three factors known to reduce the incidence of CVD are exercise, green vegetables 😒 and alcohol 😋. All three of which are known to be able to reduce blood sugars (alcohol for up to twelve hours after ingestion, through its action in the liver).
Do you have links to (preferably meta-)studies that support green veggies and alcohol against CVD. Much as I’d like to believe in these two, I thought there was no conclusive evidence for either.
Eggs ‘n beer:
The first study is an epidemiological (epi) study, therefore it’s worthless.
The second study is a meta-analysis of epi studies, therefore it’s worthless.
The third study is a meta-analysis of epi studies, therefore it’s worthless.
Epi proves correlation, not causation (that is, unless you hit the Bradford-Hill criteria, and these studies are nowhere near that level).
By contrast, here’s an RCT. In the Women’s Health Initiative Dietary Intervention Trial, they took 49,000 women and put them into two groups. The control group ate whatever. The group under test ate less red meat (by 20%, a statistically significant amount), more fruits and vegetables, less saturated and total fat, and fewer calories. Yet, at the end of 8 years and 400+ million US dollars, there was no statistically significant differences between the two groups. And this includes cancer, which the study was specifically designed to test. (This is one of the ONLY two RCTs I know of that tested reduction in red meat and cancer, both of which indicated red meat did not cause cancer.) (And it includes heart disease.)
If vegetables are so good for you, they’re remarkably bad in RCTs of proving it.
By the way, although a lot of people put trust in meta-analyses, this trust is misplaced. All they do is combine epi studies. Garbage in still equals garbage out. Furthermore, one can simply decide what they want the result to be, add and remove studies until they get that result, and then make the starting criteria such that only those studies that they put in to meet their goals are included.
BobM: All good points. I think that Dr. Kendrick is correct that diet matters little in health. By “diet” I mean macronutrient ratios. The evidence is in the wide variety of foods healthy populations consume, as noted by Dr. Weston A. Price and others. What does matter, in my opinion, is the quality of the foods, their nutrient content and cofactors they contain which aid in the bioavailability and function of those nutrients. A donut may have the same carbohydrate and fat composition as a purple Okinawan sweet potato swimming in butter (which we had last night), but the physiological effects of the two have to be quite different. I haven’t the science to prove it, but the Okinawans seem to live a long time, the donut eaters not so much.
BobM: Today’s Lancet has an article concerning alcohol and disease burden worldwide. They call alcohol the seventh leading cause of death and disability, or something of that sort, and recommend zero consumption. I say the hell with them, and will continue to enjoy my glass of wine, one is enough, in the evening.
Well; I seem to be on the right track – just now sipping on a glass of wine after a wild caught salmon/broccoli dinner with friends when I also had the opportunity to demonstrate my razor sharp scythe in the garden.
Sorry for unrelated post:
The force of indoctrination is strong with this one…
Eric: The drivel will never cease.
If only it were merely drivel. Such PR is designed and effective in sowing confusion and division in the ‘enemy’ that threatens Notional Security, and is crafted to deliver its payload as a headline with an opening paragraph of association with expertise, followed by ‘small print’ that effectively operates defence against litigation. But the post truth world is both a lack of substance in those asserting their ‘consensus’ narrative AND a lack of ability to recognize and remain free of deceits – much of which is targeted directly to your fears or fear-driven wishes.
However I hold that just as the body is a complex alignment to a unified purpose (your life experience), so also with living ‘systems’ of communication. That is to say that balance is a dynamic alignment within wholeness – and imbalance a symptom of exclusion, rejection and conflict.
The latter is the nature of our current thinking and behaviour and so we generate more imbalance or dis-ease by attempting to ‘control’ conflict as if this can enforce ‘balanced order’ in selected areas of a ‘dalek’s eye view’ of life as mechanism. This ‘wrong turning’ serves learning what doesn’t work and cannot work, so as to release it for what does. But only to those who accept and align in such purpose. A false guide is highly effective as a means to delay or avoid the feared true.
To lean away from toxicity and persistent stress/strain while leaning into the life giving or indeed the joyful, is to take from one and give to the other. There are many vectors or ’causes’ by which diseases and other negative experience can manifest in our lives. Not all will be found in the body – just as not all remissions or release of disease can be ‘explained’.
A pencil’s function is not to be a perfect point – so much as to serve creative and meaningful expression. How much of our ‘health concern’ is doublespeak for sickness worship? Or in old speak how much of our ministrations are magical attempt to appease or mitigate gods of terror?
If life was meant to be manually managed we would communicate virtually instantaneously in every facet of our whole being (as of course living biology does). But not as linear verbal mental concepts. My sense is the the journey (of self-doubt) opened by asking ‘what am I?’ will in one way or another bring us each and together back to our beginning – perhaps to know it for the first time as our conscious appreciation.
The ‘answer’ to conflict is ‘stop doing it’ but no one can change what they are not the owner of.
While the demand is to ‘see causes’ ONLY outside ourselves we want the conflict out there as the displacement from trouble at home. The intensity of our denied conflict – and the burden of it makes not dying of CVD somewhat miraculous. Keeping a block against what cannot be tolerated is part of the ‘survival’ of a surface sense of control. This can be seen inter personally and interpersonally – as in the use of social engineering (PR) to defend the ‘narrative identity’ from exposure as the construct of (fig-leaf) thinking that it is.
Whether she is right or not, I resonate with Seneff’s view that the body operates meaningfully with regard to maintaining core functions. Her perspective is free of the narrative projection of evil intent or inadequate and faulty nature onto the body or its parts, but not from the recognition of consequences arising from our thought, behaviour and experience.
It is certainly very dangerous drivel. For example, school children in California are (grudgingly) allowed only a tiny bit of fat in their milk. It is so dreadful that most of it goes into the dumpster.
There is a need to skillfully avoid crap. One would not step on it in he street. Why dirty the & brain & mind with crap ?
… But it will, eventually; One Funeral at a Time
I have been with you since #1… not always understanding but loving the information. This #53 has been one of the best…Thanks! You picture of the glycocalyx looks sort of like an arm with hair. With our more hairy ancestors body hair did provide a protective layer, can’t say as much for today. Maybe our skin adapted over the years as it shed hair .
With age and with “some” extended experience of our official health care system I have turned into a profound sceptic against Big Pharma simple pharmacological solutions and turned more and more open to holistic attitudes as in “natural herbal medicine” based on extended “popular” experience over millennia.
So, with the newsletter from Dr. Mercola this morning the herb yarrow appears and it is very related to this blog post about bleeding and healing of injured tissues. I didn’t know about this effect of yarrow although I occasionally take a twig from my garden where it grows abundantly and to add it to my herbal tea. It is though claimed that heat destroys the “beneficial” effect of the herb.
Goran, yarrow is great to staunch bleeding. If I have deep cut (the type that just won’t stop bleeding) I chew a few bits of yarrow into a poultice and apply to the cut. The bleeding stops in no time.
Interesting. The name Achillea reminds us of the Greek guy with the heel who, according to lore, used it to staunch his bleeding.
Known as Schafgarbe in German, it has been used in herbal teas (for cough and congestion) and digestive liqors for a long time.
Its family, asteraceae, sports a few other traditional herbs.
Anaesth Intensive Care 2017 | 45:3Endothelial glycocalyx: basic science and clinical implicationsN. L. Pillinger*, P. C. A. Kam
Very interesting from surgical point of view and stresses importance of protecting glycocalyx, which insulin has a role in if I skim this correctly… Enjoy the read!
That’s a very good article. I saw it after my earlier post on blood sugars. It mentions bs also affecting the heparan sulphate levels, how much hep sul is in the glycocalyx (50% to 90%) and how strong the hep sul -ve charge is. If hyperglycaemia sheds the glycocalyx of substantial elements of -ve charge (hep sul and hyaluronan) then that further weakens its protection against -vely charged elements in the blood such as platelets. i.e. a negatively charged glycocalyx repels a negatively charged platelet just as two magnets will repel each other’s identical poles.
They also postulate maintaining normoglycaemia for maintaining the integrity of the glycocalyx.
Not sure of insulin’s rôle in doing that. If there is more glucose in the blood than the body needs, more insulin won’t help as I don’t think that the cells won’t take up more glucose than they need.
Insulin says NO to cardiovascular disease
Qiujun Yu Feng Gao Xin L. Ma
Cardiovascular Research, Volume 89, Issue 3, 15 February 2011, Pages 516–524, https://doi.org/10.1093/cvr/cvq349
Published: 04 November 2010 Article history
It is well recognized that insulin resistance found in patients with type 2 diabetes and obesity is a major risk factor for cardiovascular disease. Since its discovery in the 1920s, insulin has been used as an essential therapeutic agent in diabetes for blood glucose management. Recent studies demonstrate that insulin signalling is essential for normal cardiovascular function, and lack of it (i.e. insulin resistance) will result in cardiovascular dysfunction and disease. Moreover, insulin is the key component of glucose–insulin–potassium cocktail and exerts significant cardiovascular protective effect via a phosphatidylinositol 3′-kinase–protein kinase B–endothelial nitric oxide synthase (PI3K-Akt-eNOS)-dependent signalling mechanism in addition to its metabolic modulation, which renders it a potent organ protector in multiple clinical applications. This review focuses on insulin-initiated PI3K-Akt-eNOS survival signalling, with nitric oxide as an ‘end effector’ delivering cardioprotection in health and disease (especially in ischaemic heart disease), and highlights the impairment of this survival signalling as a key link between insulin resistance and cardiovascular disease.”
SW, interesting article about role of insulin and NO. If insulin receptors are damaged via glycation then insulin will not be able to signal cell to produce NO and also initiate GLUT4 transport to cell surface. This is insulin resistance in action, high insulin and high glucose.
AGE’s also gum up the process:
Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression
This is from the book “The 10,000 Year Explosion: How Civilization Accelerated Human Evolution”:
“In 1980, Italian researchers found that a man from Limone sul Garda (a small lakeside village in northern Italy) had very low levels of HDL (“ good” cholesterol) and high levels of triglycerides, yet showed no sign of heart disease. Both of his parents had lived to advanced ages. Their curiosity whetted, the researchers performed blood tests on all 1,000 inhabitants of Limone and found a total of 43 people with this same unusual blood-lipid profile. The local church had birth records going back centuries, and the researchers were able to determine that all those individuals could trace their ancestry back to the same couple (Giovanni Pomaroli and Rosa Giovaneli), who had married in 1780. This genealogical pattern suggested that these villagers shared a mutation, which turned out to be a change in the protein called ApoA-I (Apolipoprotein A-I), a major component of high-density lipoprotein (HDL)… ApoA-IM is much more effective at scouring out arteries than the standard version of the protein is, and carriers have substantial protection against atherosclerosis. They have a much-reduced risk of heart attacks and strokes, and they often reached an advanced age. Not only that, these effects of the ApoA-IM mutation have been duplicated in mice, and it protects them against artery plaque as well. Preliminary tests show that intravenously administered synthetic ApoA-IM actually shrinks preexisting artery plaque in humans: Nothing else we know of does that.”
I wonder if anyone else has heard of this research.
I wrote about it in the Great Cholesterol Con. It is utter twaddle.
By twaddle do you mean the idea that IV administered synthetic ApoA-IM reduces plaque? Or that carriers of that mutation have reduced risk of CVD despite low HDL and high trigs? Or both?
Follow the story further along. In the end, it did nothing to plaque. The findings of the first study were contradicted, and this product has hit the buffers.
Thank you. I will have to reread the book…
Thank you Malcolm, I must read your book again. All this information can be, er………, overwhelming.
Thank you Sasha, that’s fascinating.
Did you read this study out of China this week. Glycated lipoproteins rather than LDL correlate with CAD. Rather showed LDL was more likely protective against CAD.
J Clin Lab Anal. 2018 Aug 12:e22650. doi: 10.1002/jcla.22650. [Epub ahead of print]
Study on the levels of glycosylated lipoprotein in patients with coronary artery atherosclerosis.
Luo W1, He Y1, Ding F1, Nie X1, Li XL1, Song HL1, Li GX1.
I did, thanks. So much stuff comes out every day, that it can become overwhelming
Too true. How do you cope? It’s a fair task just keeping up (ok, I don’t really keep up, just skim to pick out some bits) with this blog, let alone reading all the linked pages.
Looks lige high blood glucose does a lot of bad things: glycates LDL, insulin receptors, insulin beta cells, and increases ROS and endothelial cell apoptosis.
In conclusion, this study has provided the first definitive evidence and measurement of glycated insulin in the plasma of patients with type 2 diabetes. Using the eugly- cemic clamp technique, a pure and chemically character- ized glycated insulin has been shown to exhibit an 70% decrease in glucose-lowering action in normal humans compared with physiological concentrations of native insulin. These observations support a role of glycated insulin in glucose toxicity and impairment of insulin action in type 2 diabetes (4,5).
Type 1 diabetes has raised blood glucose and absent insulin other than injected treatments. They have a horrific increase in systemic arterial sclerosis.
The glycosylated lipoproteins may be an indicator of high blood glucose in general, just like HgbA1C, or glycated haemoglobin, is a marker of chronic high blood glucose levels.
Gary, just read the whole article out of Chengdu. Very interesting, as one who lives in HK half of each year, I am so wary of Chinese data. But I hope it is not fudged. If not, it is excellent. Wiley is ok… thanks so much for posting
The HbA1c test may not be all it seems?
Point of clarification: My understanding is the glycocalyx is not the hairs in the illustration, it is the thin, gel-like layer lining the inside of the blood vessel into which the hairs protrude.
Glyco- is sugar-related, a calyx is a cup-shaped object. I don’t see how a film of gel gets a name like that.
Martin Back: In botany, the calyx is the protective cover over the petals of the flower, although some entirely lack it.
Yes, but it’s called a calyx because it’s cup-shaped, not because it’s a protective layer.
Martin Back: Thanks. Yet the question remains, why glycocalyx? In my dictionary definition 2 says, “in anatomy, a membraneous sac, enclosing each papilla of the kidney, opening at its apex into the pelvis of the kidney.” I had no idea the kidney has a pelvis. Looking again at the picture above, the glycocalyx appears more than anything like a six-month growth of beard, and nothing at all like a cup.
I think at the micro-level they look more like ferns, than cups. I think the word just means glucose/glycogen + protein. Not sure about the actual derivation
In summary, it can be said that in relation to the vascular damaging effect of air pollution, particulate matter plays a prominent role,” commented Professor Thomas Münzel. “We are especially worried about ultrafine dust. These particles have the size of a virus. When ultrafine matter is inhaled, it immediately enters the bloodstream through the lungs, is taken up by the vessels, and causes local inflammation. Ultimately, this causes more atherosclerosis (vascular calcification) and thus leads to more cardiovascular diseases such as myocardial infarction, acute myocardial infarction, heart failure, and cardiac arrhythmias. Of particular interest is the fact that with regard to the much-discussed diesel exhaust emissions, particulate matter and not nitrogen dioxide (NO2), both of which are produced by burning diesel fuel, have a negative effect on vascular function,” Münzel continued.
‘Good’ Cholesterol (HDLs) Found to be Bad in New Study
HDL (High-Density Lipoprotein) Metrics and Atherosclerotic Risk in Women
Do Menopause Characteristics Matter? MESA
Samar R. El Khoudary , Indre Ceponiene , Saad Samargandy , James H. Stein , Dong Li , Matthew C. Tattersall and Matthew J. Budoff
Originally published July 19th 2018 American Heart Association journal:-Arteriosclerosis, Thrombosis, and Vascular Biology. 2018;38:2236-2244
OT: This Russian troll thing is getting ridiculous. Next think Dr. Kendrick will be outed as a Russian troll.
Russian trolls ‘spreading discord’ over vaccine safety online — https://www.theguardian.com/society/2018/aug/23/russian-trolls-spread-vaccine-misinformation-on-twitter
Martin, I note in your link the mention of the current/coming measels outbreak in Europe being blamed on lack of uptake of vaccination. As I undestand diseases, they occur in cycles, just as the population of every organism occurs in cycles. It is good to blame errant members of the population for not taking up vaccines as a cause for the outbreak as it gives TPTB someone to blame, despite the fact that cycles have always happened, and will continue to happen, IMO vaccines do nothing for disease progress in general, they just make short term adjustments, which nature then stabilises and goes on relentlessly to impose the normal cycles. People make the assumption that disease = bad. Stephanie Seneff has shown that is not the only view.
Do we know how many of those who were infected with measles were fully vaccinated?
A wild gues here, but I think the authorities do not publish those figures as they see them as irrelevant. After all, it will be those that did not get vaccinated that caused the vaccinated (protected?) ones to catch measles. They know where the blame lies.
If we look at figures (Suzanne Humphries) for pertussis in the US, 86% of those who caught the disease were vaccinated.
How ever did we survive before vaccines (who mentioned the smallpox fraud?)
The West constructed the internet without any regard to security, and what security there now is, has been bolted on later, and clearly doesn’t work that well.
Presumably Russia has hackers of various sorts, just as we do, but whereas we call our own hackers criminals (or sometimes praise them), we call Russian hackers agents of their state and use them to keep East-West relations bad (arms sales are important, you know). The truth is that the internet is a brilliant tool for leaking secrets, and far too much of modern life is based on trying to conceal dissent instead of engaging in open debate – think MMR, Cholesterol, Statins, LFHC vs HFLC, ‘climate change’…….
As Malcolm just said, “Do we know how many of those who were infected with measles were fully vaccinated?”. Presumably we don’t, and we won’t be told because that information might complicate the message Big Pharma wants to put out!
David Bailey: That’s right, they won’t tell us, but it is likely many were, since even the high priests of vaccine policy acknowledge that vaccine-induced immunity to measles wanes after as few as five years, whereas natural immunity is considered to last the lifetime (as well as reduce the risk of CVD and stroke). The majority of those in the minor 2015 California outbreak (which led to the loss of informed consent here) whose vaccination status was known were vaccinated. The measles-vaccine era has changed the demographics of measles, from the roughly 6-15 age group, where it is relatively benign, to infants and adults, where it carries greater danger. Virtually the entire cohort of women of child-bearing age today have been vaccinated, have never had measles, and thus lack the immune factors to pass on to their infants in nursing, which once offered them protection. Another case, like statins, where Medicine has gone off the rails. The most dangerous produced in this era, in my opinion, is the HPV with its large load of neurotoxic aluminum salts (used as adjuvant). A marvel of technology, but dangerous if administered to people. Thanks to the Nordic Cochrane group for reminding us of this, and astonishing that BMJ published their paper!
Then there is personal proximity & population densities. EU compared with US, Australia / NZ. Plus confounding environmental factors such as climate during school year, air pollution ( diesel in EU) glyphosphate use affecting the gut microbiome etc – and flouridation for good measure !
This vaccine issue makes me confused.
My basic understanding of immunology is there but there is so much contrary information around which also makes sense in my eyes, the adjuvants e.g. but also that vaccines appears “untimely” in relation to epidemics.
Is this something on par with the statin “issue”?
Big big money?
Goran, how could you suggest Big Pharma is only interested in Big Money? 🙀
Goran: Yes, big money. Forbes magazine published an article a few years ago which described vaccines as pharma’s growth leader, since most natural biological agents have already been discovered. With mandates, FDA, CDC, WHO, and the EU on board they have minimal advertising and marketing costs, and a vast number of patients to deliver them to.
I don’t know about vaccines, but I support Comrade Kendrickoff in his efforts to overturn the diet-heart conspiracy and thwart the Western imperialist statin-mongering monopolists. ;o)
Thank you for the reminder of Stephanie Seneff a brilliant researcher and “sceptic” and an old time sharp mind favorite of mine. She brings a lot of food for your thoughts about toxic agents and especially the glyphosate. Sulphur and magnesium seem to be the key element.
Here is a great interview with her.
And this very early morning I was “hit” by another newsletter from Dr. Mercola who announced a new film about the effects of the glyphosate to produce birth defects on children i Argentina – GMO-monocrop country. You easily understand why a scientist as Stephanie Seneff, with other notable researchers receive the “quack” stamp by Big Pharma and not least Big Agro.
Monsanto just got hit with $200 million plus judgement against them in a lawsuit by a school groundskeeper who developed Non-Hodgkins because of Roundup. They are appealing, of course, but it may possibly open a floodgate. There’s now something like 8000 lawsuits against that company.
“As I undestand diseases, they occur in cycles, just as the population of every organism occurs in cycles. It is good to blame errant members of the population for not taking up vaccines as a cause for the outbreak as it gives TPTB someone to blame, despite the fact that cycles have always happened, and will continue to happen, IMO vaccines do nothing for disease progress in general, they just make short term adjustments, which nature then stabilises and goes on relentlessly to impose the normal cycles. People make the assumption that disease = bad. Stephanie Seneff has shown that is not the only view.”
That’s full ignorance or craziness.
Thank god I live in a time in which the polio virus is virtually eradicated.
But of course you with your vitamin C gurus believe vitamin C can cure this and almost any disease….sigh.
Leon, Where do you get the idea polio is virtually eradicated? Go to India, 60,000 plus cases a year. Not the old natural virus, but the nice new vaccine generated one. They told Bill Gates to sling his hook when he tried to get his product in, they have enough problems. And before the vaccine, Klenner was curing polio in the 1940s with, er……., IV sodium ascorbate.
Leon Roijen: You speak of ignorance. What is your knowledge of the history of infectious diseases and vaccination? I can give you an extensive reading list, but I suggest you begin as I did, with “Dissolving Illusions,” by Suzanne Humphries, M.D., and Roman Bystrianyk. One snippet: (source: Journal of the American Medical Association, vol 172, February 20, 1960, pp. 807-812) In the 1958 Michigan polio epidemic, virological and serological studies of 869 fecal specimens. . .”yielded no virus in 401 cases, poliovirus in 292, ECHO virus in 100, Cocksakie virus in 73, and unidentified virus in 3 cases.” “In a large number of paralytic as well as nonparalytic patients poliovirus was not the cause. Frequency studies showed that there were no obvious clinical differences among infections with Cocksackie, ECHO, and poliomyelitis viruses.” Also see http://www.cdc.gov/vaccines/vpd-vac/polio/in-short-both.htm. It is nearly impossible to learn anything of value in science in the popular press. One must dig deep, and remain always skeptical.
The story about polio, the vaccine and cases of paralysis in India is a bit different:
“The weak form of the polio virus is used to activate an immune response in the body, which then protects the child when challenged by WPV. But when a child is immunised with OPV, the weakened vaccine-virus replicates in the intestine. During this time, the vaccine-virus is also excreted. In areas of inadequate sanitation, this excreted vaccine-virus can quickly spread in the community and infect children with low immunity. This excreted vaccine undergoes genetic changes as it circulates in the community and causes VDPV.”
“To be clear, the problem is not with the vaccine itself, but low vaccination coverage. That VDPV is circulating in the community that is under-immunised marks the failure of the Central government — which even in best case scenarios has achieved only 70 per cent immunisation coverage, leaving a massive cohort susceptible to poliovirus, vaccine derived or otherwise.”
There you have it: inadequate sanitation and insufficient vaccination coverage.
Your Klenner was a quack:
“After Annie Klenner became Fred’s full-time nurse, the couple managed their clinic with no other help. They developed a strong personal bond with many of their patients. “When you were around them, you became very, very secure about whatever illness you had,” remarked a patient and family friend. “You also became dependent on them. It became almost like a love affair.” Dr. Klenner brought his religious fervor into his medical practice. Quoting bible passages to his patients, he prayed for them and promised to keep doing so. He handed them prayer cards that offered protection from evil. He even sprinkled some with what he called holy water from a Catholic shrine in France. “He got all the chronics,” noted Phil Link, an admiring Reidsville pharmacist. “He got all the ones the others had given up on.””
Feeling secure whatever the ilness is, becoming dependent, holy water, prayer cards that protect against evil….damn, if that is not the prototype of a guru/sect leader !
Also this is typical for quacks:
“He recommended that patients be given “large doses of vitamin C in all pathological conditions while the physician ponders the diagnosis”
“Dr. Klenner diagnosed more and more cases of multiple sclerosis. Other medical doctors—as well as the National Multiple Sclerosis Society—rejected his nutritional therapy. Some doctors criticized Klenner for over-diagnosing multiple sclerosis, claiming he cured non-existent diseases with his vitamins.”
It seems you believe everything “alternative” they feed you.
Critical thinking is a very good thing as shows Dr. Kendrick, but please don’t get carried away by utter nonsense.
I think you will tire of this blog soon, having to put up with posts from so many people who have got it wrong will prove too stressful for you. Best wishes for an eventual recovery.
“I think you will tire of this blog soon, having to put up with posts from so many people who have got it wrong will prove too stressful for you. Best wishes for an eventual recovery.”
It’s certainly not you and the like that keeps me here.
I’m here to read the excellent and highly intelligent exposés by Dr. Kendrick and contributions from a few other highly intelligent posters.
I cannot reason with people who believe in charlatans who sprinkle holy water and hand out prayer cards.
Both my sons were immunised against measles in infancy, just measles, MMR had not then been introduced. My eldest then caught the disease aged five. He was quite ill for two days and had a terrible rash. He was fully recovered days before he was allowed back into school. His younger brother aged four was unaffected.
I caught measles aged thirteen in the 1960 s before measles jabs were introduced. I was in bed for three weeks and off school for a term. I was semi-conscious for several days and got very dehydrated. My mother called the doctor initially, but once she knew it was measles she did not think it necessary to call him again when I got worse. I have little memory of this time. When I came to my senses I realised I had lost my hearing. It came back slowly but it was never as good as before. Since then, I could not follow group conversations in noisy settings like the classroom or the pub, only one to one exchanges. Also I was much slower mentally which affected my school work, especially in maths, where I had been at the top of my grammar school year. Hard work made up much of the deficit, but it was always there. Also all my hair fell out, which was mortifying for a teenage girl.
People have forgotten how serious these childhood diseases can be. In the 1950 s almost everyone wanted their children immunised to protect them. Two of my school friends had been affected by polio, one’s hands and feet stopped growing aged eight, and one had a severely wasted leg, though she still played a mean game of hockey. My husband had a cousin who died from polio aged 5. A few months after the epidemic which affected my school friends the whole school was immunised against polio as part of a national scheme.
Years ago I nursed an old lady in intensive care who died of tetanus, which she caught after she was pricked in the leg by a rose thorn while gardening. She had never had a tetanus jab.
Parents are not in the position to weigh the benefits of immunisation against the risks. Doctors should be equipped with up to date national figures of the number of children immunised, the number of children who suffered serious reactions to the injections, the number who caught the disease, whether of not they were vaccinated and the number who suffered serious effects of the disease. With this information, the parents can make a more informed judgement for the benefit of their children or take the doctor’s advice if they prefer.
It is my understanding that MMR vaccine can cause ‘shedding’, and this can cause an outbreak of measles. If the vaccine is effective, why are unvaccinated people blamed for outbreaks among the vaccinated? Also, the measles virus has mutated since the vaccines were introduced. To me, the most interesting point I have read is that a natural case of measles apparently gives us some quite specific immunities against other viruses during our lifetime, a protection not given by vaccines.
Back when I was young, mothers used to hold “measles parties” to ensure that children caught the measles, mumps and chickenpox as soon as possible.
In my case this wasn’t necessary, just going to school did the trick. I soon caught mumps, then chickenpox back to back before I came out of “quarantine”. then measles soon after I returned to school.
Sometimes I wonder if it was this viral load that affected my long term health. Measles can actually be quite dangerous and a number of Type 1 diabetics appear to have developed the disease soon after measles (and in some cases flu) both of which have also been associated with other autoimmune diseases.
In retrospect most of my symptoms from then until thirteen years ago have been symptoms of diabetes and conditions that are “common in diabetics”. Genealogical research shows a significant number of diabetics and also early deaths from CVD, mostly in males along one specific line of my family BUT NOT EVERYONE which makes me ponder what factor makes some people succumb/express the gene(s).
Measles especially seems to have become more virulent when it occurs despite vaccination. I’m definitely not “anti-vax” but can’t help wondering if it couldn’t be done better.
Further ramblings: streptococcus seems to have become a much milder infection while staph has escalated to MRSA. What other factors are affecting our immune system and can they also affect the virulence of viruses in the same way antibiotic resistance has affected many bacteria?
In the USA all College students are *Fully* vaccinated as a condition of admission, – apart from the dwindling few who carry a legal exemption.
However, these would be the lucky ones if exposed as they’d then gain a home-grown Lifetime Immunity. The vaccinated will require top-up$, which Big Pharma is happy to provide !
Best not go to college. If everyone took that position, the evil ones would have to back down.
Any thoughts on how stents might interact with glycocalyx?
Not very well, I would imagine. Stands are a pretty brute force solution, although in an acute situation they can be life saving. How re-endothelialisation can occur, of what happens to the natural anti-coagulation system of the glycocalyx has not been studied – as far as I know.
Having been fitted with a single 3mm x 27mm stent into an artery on the right side of my heart in 2015, I hope (and pray) that the endothelium has grown through the mesh and re-established full coverage with its corresponding glycocalyx.
Otherwise, all the good advice on this blog and positive changes on my part will have been for nought 😟
Martin, I would imagine that the test of success of your positive changes revolves not so much around what has changed at the site of your stent but in the health of your vasculature in general. I made changes to my lifestyle since having five stents fitted nine years ago but have seen further decline in my vascular wellbeing, though not recently.
This is the first that I’ve seen of the glycocalyx so offers new hope of recovery. Just need to work out how without resorting to drugs or supplements over the long term, as I believe my CVD, or should it be hypoglycocalyxaemia, to be a lifestyle disease
Thanks for your response Dave – sorry to hear you had 5 stents fitted. You mention that your vascular condition deteriorated in the years following the surgery: may I ask how you know this ? Have you had angiograms to detect the deterioration?
More intriguing – you mention that your vascular condition hasn’t deteriorated further recently – to what do you attribute this success?
Very best wishes
Martin, I’ve had no additional tests. My vasculature decline is evident in some finger extremities being numb and blue or white and being susceptible to chilblains. And not everything works. I think it has stabilised as the chilblains are less frequent than they were and the numbing/discoloration hasn’t progressed.
I attribute the stabilisation to a whole food diet with lots of meat, seafood, vegetables and cheese, and regular, moderate exercise – walking around 5km per day. I steer away from sugar and wheat, eat nose to tail. I maintain a healthy gut, which I believe is very important for Vit K2 synthesis
With regard to this topic, I wonder what it is that I’m doing that might be damaging the glycocalyx. The two possibilities that come to mind are excessive protein (something in the order of 100g/day) and excessive alcohol (>=250ml wine/day). Think I’ll try reducing both
Hi Dr Kendrick. Great work. It’s always bugged me why I had my CAD only in my RCA which occluded in 2015 too when I was 42 and got 2 stents. 3 year anniversary on 9/11. I suppose what seems to be the case is that once damage occurs it generally continues in that area?. I work in stressful environment have always been incredibly active, heavy binge drank, all of which are stressors. Always been well apart from in mid twenties I had a bit of hepatitis A,. then shortly afterwards I started getting chillBlaine and occasional rashes
I now wonder whether this was the start of the damage.?
frustratingly though I was considered an outlyer by my cardiologist and was told remodeling and cholesterol were what we would tackle. So I went dr esselstyn vegan (not so strict now) and was given ramipril. Came off the ramipril as I just felt fatigued even in lowest dose bp around 90-100/60-70, For me now it’s finding out enough to protect my son and keep myself healthy for the family.
Keep up the great work and thanks to all the posters too as it’s all brilliant info
Wow! Are there any similarities between the glycocalyx lining the endothelium and intestinal cilia?
In regards to ketogenic diets and cancer: there’s a recent podcast of Dr Rhonda Patrick on FoundMyFitness with Dr Longo. Dr Longo is the current director of the longevity institute at the University of Southern California and also director of the Oncology and Longevity Program at the Institute of Molecular Oncology Foundation in Milan, Italy. The podcast is called “Resetting Autoimmunity and Rejuvenating Systems with Prolonged Fasting and FMD”.
In the podcast he says that while some cancers love glucose others love ketone bodies…
Diabetes / met syn does more than just damage the glycocalyx and puts the endothelium at greater risk of injury.
There’s also this:
“Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures.”
Diabetes / met syn also retards the repair process. Double whammy.
Question for Dr K (because I haven’t been able to find an answer for this):
When an endothelial injury occurs, and the EPCs are migrating to the site, do they come with glycocalyx preformed, or does the glycocalyx develop after the EPCs have become new endothelium?
Basically, I wonder if there’s a period of time during the repair process where there is risk of further injury.
My theory – sugar and flexion. Sugar damages endothelial cells just google – sugar damages human endothelial cells. Caused by eating carbs. After eating a meal with carbs most of us are diabetic for a few hours. Watch a video of a beating heart. The veins feeding the heart bounce around very hard.
“After eating a meal with carbs most of us are diabetic for a few hours.”
The “new normal”… healthy people are sick… have yourself embalmed and mummified and thou will live forever. I enjoy my ice cream.
Can I put in a word for molasses sugar – the genuine unrefined cane sugar (e.g. Billington’s) which has a substantial quantity of molasses still in it? (It makes a mean chocolate cake with butter, eggs, ground almonds, cocoa/cocao powder and bicarb.)
Molasses contains antioxidants and
Niacin (vit B3)
+ sugar of course!
So it can’t be all bad – nice for treats.
TS – John Yudkin in his experiments found that when he fed his laboratory rats on ordinary sugar they didn’t thrive, yet they did and so did the babies when fed dark muscavado (molasses, as I understand it) sugar. As I remember, he was somewhat flummoxed by the finding. I always make my husband’s fruit cake with Dark Muscavado as I want him to thrive too.
Damn. Those little tick boxes are so small and close together. I meant to give your comment a thumbs up. 👍 Sorry.
I seem to remember you can undo the thumbs-down by pressing the thumbs up, or the thumbs down again or something. I don’t recall the details, but I was able to undo my mistake.
Thank you, AH. 👍👍👍 If only all mistakes were so easily remedied.
I suppose molasses sugar is the same stuff as jaggery, aka palm sugar, which resembles crystallized honey and has a strong molasses taste. I bought some to try and liked it so much I kept eating it straight from the container by the spoonful. I decided I’d better not get any more, otherwise my teeth and waistline would suffer.
I do take a teaspoon of blackstrap molasses most days. As someone said, molasses is healthy cane juice with all the nasty sugar taken out.
‘thumbs up / down’ – What Thumbs ??? Can’t see any on my page…
Randall, agree that a high post prandial glucose level mimics diabetes for a few hours. I used a glucose monitor and kept a food diary to avoid this problem. This is the only study that matters, the one that you do on yourself. Glucose is a modifiable risk factor.
This used not to be the case. Richard Bernstein used to test meter salesmen with their own glucometers and found their BG was usually around 5 +- 0.5. He guestimated 83 (US numbers) and was never far wrong.
10 – 15 years ago I knew many diabetics who had tested friends and family and found much the same.
Now CGMs are available people are finding more and more that their BG goes well out of range and even into diabetic numbers in nondiabetics. Michael Snyder had a recent study showing huge spikes after a “healthy breakfast” of cornflakes.
David Unwin tested himself and likewise found significant spikes, considering he was “not diabetic”. Giles Yeo did the same and concluded that since he was also “not diabetic” this meant that normal people like him also had glucose spikes. Er Giles, I have something to tell you . . .
The body normally maintains blood glucose very tightly and keeps around 5g glucose in the total blood volume at all times. This tight control is now being lost. I wonder why? Oh of course, it must be the meat.
When CGMs become more available, that’s when people will realize what’s happening to their bodies. I used a CGM to test what happens to my blood sugar while eating very high protein (150+ grams in a MEAL). (Short answer: nothing to me. However, Jimmy Moore got hypoglycemia from this.) But wearing that allowed me to see how high blood sugar goes for holiday eating. It goes unbelievably high. I also found some surprises. I was trying to be good and I had soup and fish from a Chinese restaurant for a “pre-holiday” meal with family. The soup caused my blood sugar to skyrocket. I was shocked. (It was likely corn starch, but I’m not sure.) By contrast, I ate one pound (1/2 kg) of ground beef and one can of anchovies, and my blood sugar did not move at all. When I say “at all”, I mean you could not determine when I ate. And that happened basically every time I ate all meat for a meal, unless the meat itself had carbs (shrimp, mussels).
“The body normally maintains blood glucose very tightly and keeps around 5g glucose in the total blood volume at all times. This tight control is now being lost. I wonder why?”
Yet another urban legend to promote the low carb – all nuts diet?
Luckily there is internet. Here, a study from 1976:
Blood glucose levels between 111-155 (6.2 – 8.6).
Yes agree CGMs could be a game changer as long as the results are interpreted correctly. I used a pseudo-CGM
and soon discovered that while my fasting BG was near normal and so was my 2 hour postprandial, my 1 hour postprandial approached or exceeded diabetic numbers while my 3 or 4 hour postprandials could be significantly BELOW normal, depending on the preceding spike.
Now my BG is almost a flat line. As a result of eating the exact opposite of what I was told, trigs dropped to 1/10 of what they were while HDL doubled and I have maintained this for over thirteen years now. LDL? Who cares . . . well actually trigs are mostly around 1/5 of what they were and trigs/HLD ratio is less than 1 (UK numbers) which suggests my IR has been defeated. I still don’t eat many carbs though, and hardly any in the morning. Why would I want to? Everything I eat has far more nutrition.
Yes I have been surprised on occasion, mostly when eating out. They stuff sugar and wheat into almost everything if you aren’t careful.
Thank you Leon for calling me, and my friends, and endocrinologist Dr Richard Bernstein, liars.Your agenda becomes clearer.
I don’t think you are as bright as you believe you are. Do you have any idea what else Mary Gannon and Frank Q Nuttall researched? Check out their LoBAG diet – low carb in all but name. They were originally funded by the ADA but when they kept coming up with the wrong results their funding went away and at one stage their papers were hidden in the ADA site. Well they were delinked but could still be found if you already had the URL.
This was also hidden in a similar way
“Perhaps the best paper to read in this area is, the following: ‘Loss of Endothelial Glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.”
I support the view that damage to the endothelium and glycocalyx is *the* cause of CVD, but I am not sure if that study is good evidence.
After all, it was carried out in healthy volunteers extremely raising glucose. Diabetes patients could have build up tolerance to the effects of glucose.
According to the American Heart Association (not my most favorite source):
Diabetes is treatable, but even when glucose levels are under control it greatly increases the risk of heart disease and stroke.
So obviously there is much more at play than just raised glucose.
“Now that may well be true (although it could well be that a high insulin level is damaging, because you rarely find one without the other).”
Hypoglycemia From a Cardiologist’s Perspective
(just a little citation from this Cardiologist’s Perspective)
“Hypoglycemia‐induced silent myocardial ischemia has also been suggested by multiple authors.20, 21 Desouza et al reported a statistically higher incidence of ECG and symptomatic ischemia during hypoglycemic episodes as compared with both hyperglycemia as well as normoglycemia in his study population.”
Hypoglycemia also raises the risk of cardiac arrhythmias: https://www.ncbi.nlm.nih.gov/pubmed/24757202
But as you said before, in diabetes a lot of things in the body can be off and it might be well impossible to disentagle all these variables.
And stress, of course, leads to a combination of temporarily higher blood glucose + extra mechanical stress with raised blood pressure.
And rapidly dropping blood glucose leads to a dump of counterregulatory hormones including but not limited to cortisol, epinephrine and norepinephrine, ie. stress hormones when glucagon is no longer up to the job of normalising it. Gloriously circular.
Apologies that this appears here – it is in relation to Dr K’s Q above:
‘Do we know how many of those who were infected with measles were fully vaccinated?’
I was flicking through Barry Groves’ book ‘Trick and Treat’* on the porcelain throne this morning and came across this on p118:
‘It’s the same story with vaccination …… Researches investigating a large outbreak of mumps in 2006, when 6,584 cases were reported among college students, discovered that almost every sufferer had been vaccinated against the disease – twice.’
* Trick and Treat (how ‘healthy eating’ is making us ill), Hammersmith Press, 2008 (reprinted 2014). For those that might never heard of the book (from the Trick and Treat title it would not be obvious what it is about). Part 1 of the book sets out the extent of corruption in the ‘health industry’ and Part 2 lists over 70 common, chronic, degenerative diseases providing evidence that those diseases owe their recent rise in numbers to the diet ‘we are told to eat’. A fantastic read packed with information (and it clear that Groves’ work has inspired other researchers and a number of other books that since have followed by others).
Clathrate: Indeed, the Jeryl Lyn strain of the mumps component of MMR (named for the daughter of Merck CEO Maurice Hilleman, from whence it came-he used a cheek swab from her to create the mumps component decades ago, and it is still in use) is at the center of a long winded qui tam lawsuit in New York federal court by the two scientists, formerly employed by Merck, who were tasked by Merck with fraudulently certifying its efficacy. It simply isn’t effective any more, like the acellular pertussis vaccine, the failure of which is responsible for recent whooping cough outbreaks.
Andy. I have always wondered why a high post prandial glucose level following consumption of carbs (and surely a perfectly normal state of affairs), has been decreed to be diabetic if not returned to a normal level within about 2 hours. Who declared that the 2 hour timing was appropriate? It is another one of those theories plucked out of the air, similar to ‘5 a day’, and as such, playing into the hands of Big Pharma by declaring the majority of us diabetic, ( and thus multiplying their profits considerably) Why not make it 1 hour, and increase the numbers needing medication? why not make it 3 hours….oh, goodness me NO….profits will plunge.
I do not claim that a raging high glucose level is good for anyone, but so long as it returns to an acceptable level before the next due meal containing carbs, then our bodies are coping. Or am I missing something here?
Hi Jennifer, from a consumer’s point of view; postprandial glucose spikes will cause endothelial damage even in non diabetics, the longer the spike the more damage. This is all one needs to know.
Thanks, Andy. Without sounding awkward, I actually agree with what you are saying, but my issue is that just because there is a glucose spike, ( which is perfectly normal), then it seems that we are immediately classed as ‘diabetic’ and given the first line of attack…medications. I think more needs to be done to educate the vulnerable public that by changing their diet, it will go a long way to improving their health. Big Pharma may well endorse that, but show me a medic nowadays who wouldn’t introduce Metformin asap. Even the endocrinologist who agreed with my decision to come off meds and change my diet, still wanted me to continue with the Metformin ( albeit asking me to reduce it from 2g per day, to 500mg…as he said, ‘to keep him happy’)..he just could not go that extra step to eliminate it altogether).
I really do feel that people are being labelled at the first hint of trouble, then medicalised before a more natural way is suggested to them.
Jennifer, postprandial glucose spikes should not be accepted as perfectly normal, they are damaging.
Well, if your blood sugars were high from one meal to the next, then when would they be normal?
Anna, if glucose levels are still high before the next carb meal is due I.e. normally 6/7 hours, then I would indeed say there is a problem with glucose metabolism, requiring investigation. But NHS decrees ‘diabetes’ ( type 2) within a 2 hour timescale , and looks no further. We know some folks never manage to wait 6/7 hours for their next appropriate meal, and munch on choccies, crisps, biscuits and sweets ( generally because their hunger pangs are never satisfied). I would say they are most certainly courting type 2, as the glucose level keeps bobbing along at an elevated level, and as such requires investigation, as to why the person is regularly eating carb related snacks.
But I would like an explanation as to what constitutes an accurate diabetes diagnosis if the glucose returns to an acceptable level, say after 3 hours. That is why I have long thought that testing insulin levels ought to be an imperative test before an individual is labelled type 2. This blog has discussed the Glucose Tollerance Test previously, but with little interest.
Am I being too pedantic?
Hmm, well you are suggesting 3 hours instead of 2. Most people don’t go 6 hours between meals. Maybe 5. At any rate, I suspect that routine fasting insulin levels is what should be tested at the doctor visits, not the glucose level, which is end stage.
You may be missing the insulin side of things!
CONCLUSION: Hyperlipidemia is not an important cause of coronary atherosclerosis. High glucose levels and glycosylated lipoprotein are of high importance in the development and progression of coronary atherosclerosis.
The raw, unsickly sugars, in order of molasses content, begin with molasses sugar with the highest, followed by dark muscavado. All others have a diminishing molasses content. If it is not a proper raw sugar (a clue is that the packet should have a country of origin, e.g. Mauritius, stated on it), it will be refined white sugar merely coated to look a bit healthy – and really no better than refined white sugar.
(Molasses sugar is also delicious with rhubarb!)
Hmm. I’ll look out for molasses sugar next time I shop. Must keep the old man in good health.
Daily Aspirin Fails as Primary Prevention in ARRIVE Trial https://www.medscape.com/viewarticle/901208
I have a little concern.
Almost all participants on this blog are sceptic towards Big Pharma/Big Agro today but does that turn us automatically into “low carbers”?
To be ‘low carb’ in today’s world, you need to eat less than 50% carbs. This is not low carb.
Zoe Harcombe commenting on Seidelmann SB, Claggett B, Cheng S, et al. Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis. The Lancet Public Health 2018:
‘We need to make a critical point up front: every headline using the words “low carb” was wrong. The first sentence of the paper was “Low carbohydrate diets…” This was also wrong. The full paper used the words “low carbohydrate” 40 times. That was also wrong – 40 times. Low carb diets have not been studied by this paper. Full stop. The average carbohydrate intake of the lowest fifth of people studied was 37%. That’s a high carb diet to anyone who eats a low carb diet. As we will see below, the researchers managed to find just 315 people out of over 15,000 who consumed less than 30% of their diet in the form of carbohydrate. The average carb intake of these 315 people was still over 26%. Not even these people were anywhere near low carb eating. Hence, if you do eat a low carbohydrate diet, don’t worry – this paper has nothing to do with you.’
Found here: http://www.zoeharcombe.com/2018/08/low-carb-diets-could-shorten-life-really/
Typical abuse of the “meaning” of a word by MSM and the medical community – by purpose?
To me, as a LCHF-adherent, low carb means to stay away from carbs as much as possible for health reasons and replace them with “healthy fat” from the animal kingdom and also to keep protein intake limited and aiming at 20 % protein and 80 % fat as a health aim.
To stay away from carbs in todays society is though, in my eyes, like going out in heavy rain and try to stay dry. I noticed this yesterday at a meeting with friends at a very nice local community handicraft market where almost everything offered seemed to be high, high carb “sweets”. My 82 years old diabetic friend who joined me and whom I “converted” ten years ago, is though tougher than me to keep “dry” what probably makes him stay alive – my guess. And he is rather ‘fit’ in my eyes as judged from his vigorous performance (compared to mine) on his bicycle
Am a doing my twelve mallards in the pond, i see through my bedroom window, a diservice (for my own pleasure) by feeding them with ‘unlimited’ amounts of oats? I now notice that they seem to be very addicted. Shouldn’t they prefer grass instead of the “sweet carbs” I offer. Don’t they have any “character”?
Perhaps they get sick on sweets as we do? Cows and perhaps even horses do if they get too much of the “sweet” stuff.
It strikes me that we all, including mallards, might have some sort of self perseverance (Is that why we are here on this blog?). After feasting on the oats in the early morning “my” mallards are now all swimming around and grazing whatever vegetables is growing at the bottom of the pond with there heads down in the water and their rear ends protruding above the surface.
Otherwise the rest on the shore, sleeping as it seems.They look a bit overweight (the feathers??) but they now easily take of on their wings. That is reassuring as the winter soon approaches and they should get south.
It is all very “amusing” and thought provoking at the same time!
Myself I am for sure also adding some green vegetables to my typical bacon and egg breakfasts.
“Eat your broccoli!”
Well, evidently the mallards can not refrain from the “carbs”.
They are on them again – vigorously !
They’ll probably get sick – diabetics?
Mallards need to build up fat for their long flight. Carbohydrate consumption is the best way of building up fat, which they will then lose on their travels.
Isn’t excess carbs the way to get pate de fois gras?
Hi Goran, cereals are “junk food” for waterfowl. They may not get CVD but likely a fatty liver and central obesity. Not good for flying south.
Well, the “heat” is certainly on attacking “low carb” from the medical establishment – “causing premature death”!
Here the Harvard attack is cut into pieces!
To my defense it is whole oat grains with hull and everything direct from a farmer friend of mine (not the breakfast cereal) I am now feeding them. This feat must though be more healthy for them.
The geese who deliver their fatty livers for the delicious French pate are actually force fed with grains – a disputed practice. But perhaps my mallards are as “stupid” as some people who don’t believe in the logic that it is the carbs and not the fat that adds to their undesired weight and can’t stay away from them. Mallard addiction?
As a general rule, wild birds cannot overeat.They are quite capable of eating a less than balanced diet if it is easily available, but the only bird species regularly known to overeat is the common wood pigeon, which is often seen to fill its crop so full that it becomes unable to fly until it has done some digesting. I suspect that vultures sometimes suffer from the same behaviour. If you were to take one of your wild mallard and prepare it for the table, you would be unlikely to find much fat on the carcase, unlike the domestic ducks reared for the table, and fed what is a less than optimum diet for a bird – high carb!
Thank you for this initiated comment about feeding habits of birds – reading your comment while I watch my 12 mallards being heavily on the oat grains again this very morning. It is enjoyable to watch them and especially when knowing I, as a low carber myself, am doing no harm to them.
And BTW, having my license for hunting and a few guns I am though not the least tempted to put one of the mallards on my plate even if they most probably would be delicious.
Small birds like Sedge Warblers can double their weight to fuel a Trans-Saharan migration (the exercise burns it all off again)
They do this by eating plum reed aphids which are basically little protein bags of plant sap – ie. high carb insects.
Other species may switch from insects to berries to gain weight in order to survive hard weather and fuel local movements
Conversely species like finches and buntings who are genetically adapted to eating seeds nevertheless usually feed their young on insects because they need the fat and protein to grow.
chris c, apparently domesticated birds can get diabetes on a high carb diet. They may need aerobic exercise to stay healthy. Consequence of deviating from a traditional diet. Applies to all animals including humans.
Remind ourselves of some comments made by Editors of (previously) prestigious Medical Journals… Two opinions in one link.
I have my own opinion as to which 50% that Damning the Dangerous Diet’ falls into.
Yes and livestock farmers have pointed out that while feeding grains fattens their animals, overfeeding grains, especially wheat, makes them ill. True for cows and chickens at least. And since high carb pet food, dogs and cats too.
“………… overfeeding grains, especially wheat, makes them ill.”
Apparently has little effect if you are Dutch. 🤭
I don’t know if it’s correct to compare livestock’s evolutionary history to that of humans. Livestock didn’t evolve to eat grains while wheat was one of the earliest grains to be domesticated by humans (9th century BCE or somewhere around there, I think). Plenty of time for humans to develop digestive enzymes to accommodate the new food, at least according to some evolutionary biologists. Not to mention that many hunter gatherers ate wild grains when they could get them.
Another indirect proof of this (at least to me) is that Italians have some pretty impressive longevity metrics despite eating large amounts of pasta.
Sasha, it could be the olive oil and sunshine not the pasta.
for grains lets be conservative, at 5000 BCE.
as for Italy, yes they eat a lot of pasta, and I have the impression that there are certainly well-rounded mama’s!
Chris and Andy:
I think there’s pretty solid evidence that wheat was one of the earliest plants domesticated, which would mean at least 10 thousand years ago.
So, are we saying that wheat isn’t good for you unless there’s also sunshine and olive oil?
And complex carbs aren’t good either unless you are on Okinawa?
Sasha, I am not saying that one should eat pasta outdoors in Italy. Not an expert on Italian eating habits. Sunshine is good, olive oil is good, wheat is bad.
I am definitely not a low carber even though I am sceptical about the claims of those two industries…
Neither am I. Had a plate full of spaghetti with vegetarian minced meat (Quorn) and Heinz Spaghetti sauce (some sugar in it) and a bit of delicious ice cream after it. I guess 22 grams of sugar and MUCH more carbs from the spaghetti. Can’t begin to imagine how boring low carb must be. And no diabetes (on the contrary, hypoglycemia) or overweight here. Life is good with carbs 🙂
Well, Leon, if your metabolism isn’t broken as mine is (I’m Mody3) then you can eat so much carb and not have a negative effect. So much carbohydrate as you have described would make me feel VERY ill indeed. I have adapted well to a low carb regime over the years – I was 15 when diagnosed- ‘mild diabetes’ then not MODY as MODY in its several forms hadn’t been discovered back in the 50s, well before the era of genetic testing – and I can tell you that a low carb lifestyle is far from boring. Life doesn’t crash if we can’t eat pasta. We are all different in body type and there is a lot of truth in the saying “one man’s meat is another man’s poison. Horses for courses.
By the way, should you be interested, there is an excellent website explaining MODY in its various forms – Phlaunt.com.
P.s. longing for the new Brussels sprout season. How weird is that?
For me a not low carb meal is what I just had: I mixed some good quality Russian sour cream with salt and adjika (that’s a mix of spices from Caucasian mountains – a region, incidentally, famous for long-lived people). I spread that mix on a whole chicken and baked it in the oven. I also cooked some millet, and on a side I had some tomatoes and onions which my friend grows.
I like pasta, unfortunately, it becomes harder to eat it, once you try it in Italy… But I wouldn’t have pasta with Heinz spaghetti sauce and fake meat, that’s a bad bad combination, IMO.
By the way, Leon, if you’re worried about meat eaters destroying humanity, think about the ecological footprint of the meal you just had as it compares to someone getting his foods (including meat) from as many sustainable sources as possible.
“Neither am I. Had a plate full of spaghetti with vegetarian minced meat (Quorn) and Heinz Spaghetti sauce (some sugar in it) and a bit of delicious ice cream after it. I guess 22 grams of sugar and MUCH more carbs from the spaghetti. Can’t begin to imagine how boring low carb must be. And no diabetes (on the contrary, hypoglycemia) or overweight here. Life is good with carbs 🙂”
You should try cheeses then. There are thousands of varieties, though I normally have only about 8 including Gouda. Very tasty, loads of saturated fat, plenty of minerals, and nutritious, or is that just another “urban legend” in your opinion? I also eat meat (low energy input) despite your incorrect assertion that it is necessarily high fossil fuel input. I eat vegetables, not much good unless they are organic, which are not too common. I eat loads of soft fruit with lashings of unpasteurised cream. I eat eggs, probably a couple of dozen a week, I eat 85% cocoa chocolate, and make my own of various flavours.
Yep, low carb certainly is boring, as everyone else who chooses low carb diets, who posts here will confirm.
I think not!
Our only hope is cheeses.
“Our only hope is cheeses.”
Shhhhh! The price will go up.
Yes, hopefully made from good milk and according to traditional methods))
Interesting article from down under on the positive effect of sun exposure on the gut microbiome in mice (increases the proportion of firmicutes, reduces the proportion of bacteriodes).
Good analysis of the latest Lancet rubbish on the risks of moderate drinking by David Spiegelhalter at WinstonCentre.
Goodness, you disappear for a few days and there are 253 comments on a new post. It so happens I am reading a very interesting book called Infectious Diabetes in which the author, Doug Kaufmann, who seems to be a nutritionist, lays out a very interesting, not to say compelling, case for fungal infections being at the root of many of our diseases and discomforts, including diabetes, and that of the three broad infective categories (viri, bacteria and fungi) we have almost ignored fungus even though fungus are everywhere and are opportunistic.
It makes sense of a lot of things.
‘ Former longtime (17y) Editor of JAMA and “ultimate insider” says “It’s Not the Fat that Makes us Unhealthy” Says he was involved in disseminating bad nutrition science but now realizes it was never true. ‘ OOPS
Former longtime (17y) Editor of JAMA and “ultimate insider” says “It’s Not the Fat that Makes us Unhealthy” Says he was involved in disseminating bad nutrition science but now realizes it was never true. THEN HE PRAISES DR KENDRICK AT THE END…
PS Dr K, you are referenced at the end of the video! I hope you can put it up, I can not figure out how https://www.medscape.com/viewarticle/900495?src=soc_tw_share
Fantastic find, well done.
Malcolm, he certainly lays it out for you, well done.
He is obviously a highly intelligent man 🙂
Hi SW, I saw the video as it was retweeted all over the weekend. We’ll worth spending 8 minutes to watch – it was under the headling ‘Former JAMA 17 year Editor* does a @ProfTimNoakes & then admits he was wrong. In a stunning reference he refers to Dr Malcolm Kendrick as hitting the nail on the head.’ (* Dr George Lundberg.)
In the recording, Dr GL mainly refers to Gary Taubes’ work (Good Calories, Bad Calories). His reference at the end to Dr K is specifically the blog entry of 3rd July 18:
Dr Lundberg will be following up with a Part 2.
Can whoever sees part 2 post it!
This is a great talk of a great man in my eyes!
Specifically he honors only two people for whom I have the greatest respect myself – Gary Taubes and Malcom Kendrick.
Gary Taube’s book “Good Calories & Bad Calories” is really a book to my taste (as a researcher in the natural sciences) and it was actually this book which “converted” me profoundly although I had already 1999 after my MI realized that it was my excessive sweet tooth that was partly to blame for my CVD and then by self perseverance I cut all sweets. Ten years later 2009 me and my wife (after reading the book) also cut all carbs and turned into strict LCHF with dramatic health benefits not least for my severely diabetic wife – her diabetics is now basically “reversed”.
Yes! A fine piece of work. Took me a while to find it, and Medscape is always hard to access because they never like the password I give, but find it I did, by typing drlundbergmedscape into DuckDuckGo. Up it popped. Looking forward to part two. What struck me was the statement he made about insulin, something to the effect that it is the regulator of fat storage and fat being metabolized for energy. Put that way, it is easy to remember.
Thanks, SW, for posting this.
I was curious about Dr. Lundberg’s background. A brief read suggests he is just the guy to “come out of the closet” and say what he thinks on the current state of dietary dogma. I’m sure there are others who share his views. Very nice he cites Taubes and Kendrick in his well-made presentation.
And he picked an excellent Kendrick post to cite (all Dr. Kendrick posts are excellent, but some are more excellent than others).
I am sure you all may have seen the news about Lorcaserin (spelling) the new appetite suppressant, another drug to be concerned about. A USA study assures us it will not contribute to heart disease. It does meddle with seratonin so that’s alright then! Will NICE embrace it, let’s hope not.
An interesting article from 2013 about the source of Endothelial Progenitor Cells (EPCs) and the fact that there are colonies of such cells in all three layers of the artery, these being clonogenic (able to produce clones of themselves) in order to proliferate to repair an area of damage. The authors Goligorsky and Salven explain that it isn’t so much the free circulating EPCs in the blood flow that initiate the repair, rather the EPCs already part of the intima that replicate to provide coverage of the site of damage.
Just as interestingly is the identification that EPCs in those with lupus erythematosus and in diabetic mice are rendered defective and “functionally incompetent”. This would suggest that the normal repair mechanism of the EPCs multiplying to cover the area of damage will be greatly reduced in these sufferers and reinforcing Dr K’s simplified explanation of “rate of damage > rate of repair = bad, and rate of repair > rate of damage = good”.
“Hyperglycemia has been reported to reduce survival and impair function of circulating EPCs”.
Hence I suppose why rates of CVD are so much higher in those with diabetes.
Click to access sct499.pdf
Martin, that’s a very interesting article I happened to bookmark the other day. It’s full of intriguing ideas, and I haven’t read and absorbed them all yet. For example, the authors cover the effect of aging on EPC’s, which certainly might help explain the connection between aging and CVD.
There’s also this:
“In aging animals, angiogenic competence is decreased. Mouse
aortic rings obtained from these animals show a 40% reduc-
tion in vascular sprouting induced by vascular endothelial
growth factor compared with young animals . A similar
defect occurs in prematurely senescent Klotho mice . Of
note, caloric restriction regimens rescue angiogenic compe-
tence of aortic rings obtained from 24-month-old rats by
I tend to read “caloric restriction” as “carbohydrate restriction”. To tie all this in with Dr. K’s current post, I’m coming to suspect the nexus between diet and CVD runs right through glucose tolerance.
I bet they will. As we know, you don’t need appetite suppressants, you need proper food.
Oh, geez. I think the whole high fat low carb diet makes a lot of sense and I’ve been a Weston Price type for years, but it seems that, other than the fact that all food is deadly and we ought to just stop eating, there are two very strong camps. One says that the blue zones are 95% plant based (I know that is off base) and that the way to cure cancer is to avoid all animal products, and the other is keto. What with the new understanding of cancer as a metabolic disease, keto ought to be in the lead, but so many people claim to have cured themselves eating raw fruits and vegetables. Well, the latter might be very cleansing for a time, and many fruits and vegetables have antifungal/anticancer properties. So today I heard on a podcast that eggs are horrible because cancer eats cholesterol. So I found this:
Not only is it true that never vaccinated moms don’t give protection in their breast milk, they also do not give it in utero to the fetus. This is the reason why young infants are getting it. It used to be that the immunity from the womb lasted around 6-8 months, so young babies were protected even if bottle fed.
Me, I have had 3 vaccines and recently was found to not have immunity. Isn’t that nice. Great to get measles when I’m old.
AnnaM: It is indeed a terrible tragedy. We know so little about the microbial world yet have the hubris to think, by altering one small aspect of it, there won’t be a multitude of downstream effects, or worse, ignoring them. Meanwhile, children all over the world are ill, not with short-lived infectious diseases, but with chronic conditions. The autism rate in the U.S. is now 1 in 36, this, for a condition which essentially did not exist prior to the 1930’s, when Hg was first widely used in lumber preservation, seed preservation, and vaccines. Autoimmune conditions are increasing at an alarming rate. A medical textbook, “Vaccines and Autoimmunity,” published in 2015, explains how this happens. In the case of autism, it is chronic microglial activation. The microglial cells in the brain, tasked in early neurodevelopment with pruning the excess synapses, never quit. The brain remains in a state of inflammation, its development hijacked. Now we have Forbes magazine blaming the knowledge many of have gained about the risks of vaccination on Russian trollbots! I’m not kidding. For the U.S. media, it is blame everything on the Russians. Getting desperate, they are.
AnnaM: “Me, I have had 3 vaccines and recently was found to not have immunity. Isn’t that nice. Great to get measles when I’m old.”
Did you actually get measles or were your antibodies for measles measured?
“Autoimmune conditions are increasing at an alarming rate. A medical textbook, “Vaccines and Autoimmunity,” published in 2015, explains how this happens. In the case of autism, it is chronic microglial activation. The microglial cells in the brain, tasked in early neurodevelopment with pruning the excess synapses”
Autoimmune conditions can be there for a lot of reasons/have many causes. It’s a bit simplistic to blame (just or mainly) vaccination.
And autism is a very complex condition with still unknown cause(s).
I’m certainly not saying vaccines are always harmless but it’s ridiculous all that is blamed on vaccines these days by uninformed people.
“……….I’m certainly not saying vaccines are always harmless but it’s ridiculous all that is blamed on vaccines these days by uninformed people.”
Not to mention by some very well informed people too, and denied by some people who happen to have financial interests.
Leon Roijen: I did not say that vaccines were the only cause of autoimmunity, nor the major cause, nor did I imply it. Read for yourself “Vaccines and Autoimmunity,” edited by Dr. Yehuda Shoenfeld of Tel Aviv University, the world’s leading expert on autoimmunity. What you will read is science. The cause of autism is known; it results from neuro-inflammation, from an immune-activation event at the wrong stage of development which may happen in utero or in early childhood, mainly before the age of three A great deal of research has been done, especially over the past 10-15 years. The media has fully suppressed public knowledge of this, but you can find it indexed on PubMed. Ginger Taylor has compiled a list of 151 scientific papers which show the connection between vaccines and autism. Once you’ve done diligent research we can have a discussion. In the meantime, CVD is my main interest here.
So, what can we learn from this:
New anaemia medications help in the recovery of MI in diabetics by boosting HIF (whatever that is!?).
It so happens I am reading a very interesting book called Infectious Diabetes in which the author, Doug Kaufmann, who seems to be a nutritionist, lays out a very interesting, not to say compelling, case for fungal infections being at the root of many of our diseases and discomforts, including diabetes, and that of the three broad infective categories (viri, bacteria and fungi) we have almost ignored fungus even though fungus are everywhere and are opportunistic.
It makes sense of a lot of things.
We soon get back to diet don’t we – but stress raises blood glucose levels no matter what we eat.
I’m not sure whom you are poking but I agree more and more – stress lowers the immune response, in part because of the increase in stress hormones which themselves lower immunity.
But if Doug Kaufmann is right that fungus is at the root of many of our problems including type 1 and 2 diabetes, then we look at food a bit differently, i.e., where does the fungal exposure come from? Of course, it is not only food.
And it is also interesting that many of the foods that are supposed to lead to heart disease due to sugar content are also vectors for fungus or their mycotoxins. That is, sugar, but also wheat and corn, peanuts, and sadly, probably alcohol.
I was not specifically getting at anyone – it’s natural that we should home in on food because it is a factor we can control. I mention food quite a bit myself anyway. But to get stressed about food is only going to complicate things considerably.
I have a huge respect for our microbes and yeasts and believe them to be capable of anything – especially after reading Giulia Enders’ “Gut”, written by such a young woman but informative (and amusing).
To quote her:
“Our gastrointestinal tract is home to more than a thousand different species of bacteria – plus minority populations of viruses and yeasts, as well as fungi and various other single-celled organisms….The vast majority of our immune system (about 80 per cent) is located in the gut.”
She also says,
“Blood group development is just one of the many immunological phenomena caused by bacteria. There are probably many more waiting to be discovered.”
“Taken together, our gut bacteria have 150 times more genes than a human being. ..The guts of obese people are often found to have more bacterial genes involved in breaking down carbohydrates. Older people have fewer bacterial genes for dealing with stress…. Every microbe contains many genes involved in breaking down carbohydrates or proteins, and in producing vitamins.”
“We humans are very proud of our particularly complex brains…The gut is the organ that is currently forcing researchers to rethink its role: in fact, scientists are cautiously beginning to question the view that the brain is the sole and absolute ruler of the body. The gut not only possesses an unimaginable number of nerves, but those nerves are also unimaginably different from those of the rest of the body…The gut’s network of nerves is called the ‘gut brain’ because it is just as large and chemically complex as the grey matter in our heads…We humans have known since time immemorial something that science is only now discovering: our gut feeling is responsible in no small measure for how we feel.”
They affect our metabolism, they affect our thyroids…. And when we’ve gone the way of the dinosaurs they will no doubt still be around.
Hats off to them!
And (back on specific topic) now it seems that there is an individually distinctive glycan coating each and every living cell, not only the glycocalyx of your endothelials . . . and directing its activity.
That includes the members of your gut community.
TS, I enjoyed “Gut” immensely, as well as the author’s earlier Science Slam presentation on youtube. Giulia Enders is so infectiously enthusiastic (no pun intended!) and funny. For me, Gut was the first of a trail of books and blogs that eventually led me to Dr Kendrick’s blog.
Just for a sad laugh—-headlines from Drudge
Deaths from drugs, alcohol, suicide now outpace diabetes…
Scientists discover genetic link between marijuana and SCHIZOPHRENIA…
1 in 7 adults on pot…
1 in 20 use e-cigs…
Half Americans can’t pay for basic needs?
Scientists discover mysterious new type of human brain cell…
Because of soil depletion, crops grown decades ago were much richer in vitamins and minerals than the varieties most of us get today https://www.scientificamerican.com/article/soil-depletion-and-nutrition-loss/
You are right!
There are though agricultural efforts to restore the soil the called Permaculture. Around the world there numerous activities in this way.
With likeminded friends I am in a week to visit such a successful farm in Sweden to see with our own eyes what they are up to. They claim success.
Richard Perkins, the enthusiast behind this farm, has written a very solid and interesting book about how they go ahead and a book which I am deeply in just now. They are just serious on this farm to say the least.
“Making Small Farms Work”
Ridage dalle Farm, yes thats it
You are right!
There are though agricultural efforts to restore the soil the called Permaculture. Around the world there numerous activities in this way.
With likeminded friends I am in a week to visit such a successful farm in Sweden to see with our own eyes what they are up to. They claim success.
Richard Perkins, the enthusiast behind this farm, has written a very solid and interesting book about how they go ahead and a book which I am deeply in just now. They are just serious on this farm to say the least.
“Making Small Farms Work”
Dr K, Blood clotting device being deveopled here in Aus , interesting http://www.abc.net.au/news/2018-08-29/blood-clot-detecting-device-could-cut-heart-attack-stroke-risk/10175390
“A new 3D-imaging diagnostic device could dramatically reduce the rate of heart attacks, strokes and other conditions by helping to identify people at risk of a blood clot, according to one of its developers.
Blood clots can cause any number of health issues, but the new bio-optic device being developed at the Australian National University could detect an imminent and dangerous clot before it happens.
Using a small sample of a patient’s blood, developers say the machine can map how platelets in the blood perform when damaged, creating a digital hologram of the microscopic reaction.
It does this by measuring the delay in the amount of time it takes for light to pass through the clot, also known as a thrombus….” Cool pictures too!
Thanks, will have a look. I love a cool electron microscope picture.
Have you picked up on this one https://www.telegraph.co.uk/news/2018/08/28/cheese-red-meat-back-menu-study-suggests-eating-twice-much-officials/
I found this very helpful in understanding the GCX: https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-016-0182-z
Various sorts of essential “sweet stuff” manage our bodies, directing proteins where to go, etc. There’s one sort all other mammals have and not us, so, when you eat red meat, you acquire this foreign glycan and it can do your heart harm.
So says this article:
“There have been many studies linking consumption of red meat with diseases like atherosclerosis and diabetes, but they have not been able to show why or how this occurs until recently.”
To avoid glycating my proteins I was about to go on an all meat diet. Now meat is bad again. There is something fishy going on.
It seems to be that there is an individually identifiable “glycocalyx” engineering the activity of every different sort of living cell.
Can’t ignore that any longer!
This is a new and ongoing field of research and, as with all such, “more research is needed before any recommendations can be made”. Standard maddening disclaimer.
Is it true about the malarial wipe-out?
Is the meat glycan take-over and its harmful inflammation true?
Is truth true?
re “glycocalyx’ on every cell: interesting topic
Time for another hypothesis. Diseases could be result of defective cell communication caused by glycated signal receptors. For example insulin resistance (diabetes) could be result of glycated insulin receptors. Composition of cell membranes and lipid rafts can be affected by diet and medications and not always in a beneficial manner. Accumulation of a “glycocalyx” on a cell could be a measure of an ageing cell.
I find it hard to blame red meat, which we ate for millennia, for diseases which only happened in the last century or so. Or am I just justifying the huge rump steak I just ate with an armful of runner beans?
(The steak could almost have walked here and the beans come from a friend in a nearby village. OK the oatcakes came from a factory but contain few ingredients, and the butter came from Somerset but could have come from Ireland or France, not a great carbon footprint there)
Rapid Non-Enzymatic Glycation of the Insulin
Receptor under Hyperglycemic Conditions Inhibits
Insulin Binding In Vitro: Implications for
Click to access ijms-18-02602.pdf
I suspect one of many pathways to insulin resistance, but something I did NOT know before is that insulin itself can be glycated
How do we know these diseases happened only in the last century or so? DM, for example, is described in the old Chinese medical texts. They called it “waisting and thirsting disease”.
Speaking from ignorance, having not read the article, my personal logic bump leads me to the conclusion that the only safe mammal to eat is humans. Other than that it is poultry all the way. Sorry, I have a funny tendency to take things to their logical conclusions – thgh I suspect that is better than so many of the experts who take things to illogical conclusions.
And those gut microbes may very well be the reason that I and others find it so difficult to give up foods like bread and sugar and other carbs. It seems quite plausible that they have ways to signal their hunger.
Yes, and stress affects our digestion and gut microbes. So many vicious circles.
Reason why wheat is added to foods and best to avoid consuming it.
“Wheat essentially acts like an opiate in the body, creating the desire to consume it again and again.”
“And those gut microbes may very well be the reason that I and others find it so difficult to give up foods like bread and sugar and other carbs. It seems quite plausible that they have ways to signal their hunger.”
To me it seems more plausible that the body needs them 🙂 Not the refined sugars but certainly the carbs.
And your body needs nicotine and alcohol as well –
but only those carbs and tobacco and booze have been ABUSED.
“…but only IF those…”
I have never gotten measles. I had a titer drawn for antibodies.
“I have never gotten measles. I had a titer drawn for antibodies.”
In that case you might not be at risk for measles at all.
I might be mistaken as I researched this subject more in dogs (as I have them and they need vaccinations), but I have two questions as to your titer results:
1) First of all, the reliability of the test. For dogs there is now such a test, too. But the test is not completely reliable. You might get false positives but also false negatives.
I wonder how sure the measles antibodies test is.
Doctors do a lot of tests and usually present the results as 100 % reliable (maybe even they themselves don’t give it much consideration that tests can be wrong), but a lot of medical tests have error margins, unfortunately.
2) Another thing, that is maybe even more important: The body, (at least in dogs that is the case, but also in humans, I guess), has memory cells. And even if the level of antibodies measurable in your blood isn’t high, these memory cells might be enough to fight off infection (simply put).
So, I guess you cannot say for sure you are unprotected.
Antibodies do not imply immunity, anymore than lack of antibodies mean lack of immunity.
According to Merriam-Webster, “to imply” means:
“to involve or indicate by inference, association, or necessary consequence rather than by direct statement”
As such, antibodies absolutely tell us something about immunity and immune status.
Are there exceptions? Yes, absolutely, like often in medicine.
It would make your arguments stronger if now and then you could show us some proof substantiating your claims instead of presenting us with a mere assertion.
I will no longer comment on your posts. As with posts from others commenting on your posts they are met with an unacceptable level of agression. It is possible to find support for any assertion, likewise it is possible to find conflicting views. There are references supporting statins on the internet. Why should any reference be believed?
“It is possible to find support for any assertion, likewise it is possible to find conflicting views. There are references supporting statins on the internet. Why should any reference be believed?”
By giving references, one can substantiate his claims and others can examine the references and then decide for themselves whether they think it’s good evidence or not. Dr. Kendrick (as a good scientist) does it all the time.
But you, you come up with long forgotten doctors who sprinkled holy water and gave out prayer cards and now you make a rather silly claim and call it “an unacceptable level of agression” when I ask you for references – that must be a joke.
I will not stop commenting on your posts when I think it’s necessary. “Alternative” thinking, questioning things is a VERY good thing, don’t get me wrong, but making all kind of unsound claims misleads people and could be dentrimental to their health.
You have commented strongly on this blog.
I, for one, am curious as to what you see as your personal qualifications to be the arbiter of what is necessary on this, Dr Malcolm’s blog.
Low-carb linked to dying young.” “Low-carb kills.” Dr. William Davis refutes that study. https://www.siliconinvestor.com/readmsg.aspx?msgid=31768640
Vascular disease is caused by endothelial dysfunction at the cellular level. Glucose at levels greater than the renal threshold ( 160 mg/dl) are toxic to the edothelium as well as other tissues notably the glomerulli in the kidney. The glycemic index of highly processed foods raises your glucose into the toxic level each time you eat that high glycemic food . Other toxic components such as pesticides, food additives also negatively affect the endothelium. Chronic high blood pressure damages the endothelium, Thus the livestyles of the “Western” cultures all affect the metabolism of the vascular lining. So ALL of the risk factors for vascular disease noted epidemiologically, relate to healthy (or not) membrane function of the endothelium.
I really love that Engineers involved in GCX research https://qmro.qmul.ac.uk/xmlui/bitstream/handle/123456789/24656/Lin_Miao%20PhD%20FInal%20061216.pdf?sequence=1
Interaction between the vascular endothelial glycocalyx and flow in vitroby Miao LinSupervisor: Professor Wen WangSubmitted for the Degree of Doctor of PhilosophySchoolof Engineering and Materials ScienceQueen Mary University of London2016
(Long read but worth it)
Dr K, when I donate blood a Red Cross here in Sydney, they do an on the spot CMV test in order to direct blood away from pediatric wards and heart transplant words. Fascinating that CMV causes Atherosclerosis to accelerate and babies to die. GCX of Blood Brain barrier must get destroyed via GCX as well as the virus perhaps degrading GCX in heart transplants, very interesting link I think https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801777/ animal model: https://www.ncbi.nlm.nih.gov/pubmed/28825336
FDA warns of flesh-eating genital infection linked to diabetes medication http://www.waow.com/story/38994444/fda-warns-of-flesh-eating-genital-infection-linked-to-diabetes-medication#
Glycocalyx not mentioned but explains effect of high glucose on endothelial cells.
Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
Great post. Very helpful!
I’ve read Zoe Harcombes book and understand what she is saying. But I see time and time again, overweight people who claim to be on a ketogenice diet. They may of course not be telling the truth but I honestly believe in reality excess calories from any macronutrient will be stored or cause the storage of another. It may feel like it’s harder to overeat on HFHP diet but people still do and they still put on weight. This is from observation and experience and I have also read the science to understand obesity but excess calories always lead to excess body weight.
“This is from observation and experience and I have also read the science to understand obesity but excess calories always lead to excess body weight.”
Refreshing to read someone (and a few others) with common sense on this blog.
Earlier I posted a link showing research that every diet with less caloric intake works and that a ketogenic diet is not different – inversely of course, every diet with too much calories will cause fat storage.
I think several years ago I saw a BBC documentary examining the claims of two persons: one claiming she could everything she wanted without getting obese, the other person claiming that every little bit of food made her obese.
They measured the caloric intake of these two persons very scientifically (not by diet records but using chemical tracers) and it turned out that both claims were simply not true:
The slim person really consumed much less calories than the obese person.
That would be interesting to see Leon. Science will be the nearest to fact that we will ever get and it’s correct to base good discussion with science on our sides. Nutrition research will always be far from reliable because the human body will respond differently, it could be badly recovered, high stressed, poor digestion, menopausal and so on. I have seen weight loss in all the types and more and with different nutrition strategies. All with one thing in common: A calorie deficit and when the body responded by slowing their output to accommodate the loss of fuel, they kept that body moving. It was hard and harder for some than others but all achieved weight loss.
But did they keep the weight loss off for any length of time? Have a look at the Minnesota Starvation experiment done during the 2nd world war (and by practically every yo-yo dieter since) to see why calorie restriction is not a good solution for long term weight stabilisation.
Exactly right Sharon, yo yo dieting is the issue. fat loss via calorie restriction with muscle retention is the key. Note fat loss (not weight loss) and keeping the metabolic engine of muscle as we age is the key to long term body composition and maintaining the best metabolic rate as we age. Of course it gets more challenging as we age as our bodies want to loose energy expensive tissue such as muscle and bone but we can keep them, just need to give them a reason to stay.
Leon and Sasha
Leon you answered Sasha’s question about disappearing calories, maybe they were not there in the first place. You have to look at the individual not an averaged group effect. We are all different with possibly different outcomes for the same input. There are too many variables.
Unfortunately I can’t find the original documentary anymore, but in this one they do the same experiment showing people who are obese often underreport what they eat:
Concerning the claims of those 2 people “one claiming she could everything she wanted without getting obese, the other person claiming that every little bit of food made her obese.” … “and it turned out that both claims were simply not true: The slim person really consumed much less calories than the obese person.”
Have you considered that these people might have been making true statements? If the slim person ate to her (presumably quite low) satiety level, then she actually was getting everything she wanted without getting obese. If the other person had a rather high satiety level, then their idea of a “little bit of food” would actually be little, compared to the amount they would be eating to arrive at their personal satiety level.
So was the real cause excess calories, or was it something else controlling satiety, like hormone balance?
Hormone imbalance certainly can lead an individual to overeating. They overeat calories and that leads to obesity. The pathogenesis of obesity in my eyes will never be explained but the result will be too many calories for that body and it’s activity levels. Of course it can work the other way. Less in, resistant train and keep moving as the body down regulates. It’ll just be harder with a hormonal imbalance.
Bill in Oz: Please don’t give up on this. It is an interesting issue. Macrophages seem to play multiple, and crucial, roles in physiology, and it seems the heart muscle contains lots of them. As I recall your original question was about the macrophages trapped in foam cells. This may be a dead end in the healing process, but since they are self, not other, perhaps they remain essentially inert in the plaque, and thus benign; nevertheless it is a topic worthy of discussion. I, too, am weary of the discussion of food issues. Other than quality, which matters a lot, dietary composition matters little in CVD, in my opinion. It is a matter of personal taste and availability.
Food choices affect glucose levels, too many carbs = high blood glucose= more AGE’s = atherosclerosis. This is in addition to the blood clot pathway to CVD. Have to check out formation of necrotic cores and relation to plaque stability.
“According to the results that most of the changes induced by AGEs are concentration dependent, our study emphasize the importance of good blood glucose control which can reduce AGEs levels both in blood serum and in arterial wall in prevention of diabetic atherosclerosis.”
The debate here seems to downplay the potential role of stress in causing higher blood pressure and higher blood sugar. Whether they are temporary or permanent, after a period of chronic stress, I do not know, but they seem to be a reality for some people. I also read somewhere of a group of medical students who became type 2 diabetic before their finals, due to exam stress. They were young, so I think it was reversible once the stress ended. Dr. Kendrick did discuss elsewhere the evidence that stress is linked to heart attacks and maybe to strokes.
I have discussed this, and will do again
Stress can do all sorts of bad things, including causing us to gobble sweets. I’m not for a minute minimizing the damage chronic stress can do, but what were those medical students eating to get through those finals?
Someone recently told me that her father, who served in Burma during WW2, had come home (after a decade away) with diabetes. His daughter understood this was common for returning WW2 soldiers.
Thanks for interesting article.
Malcolm, I listened to a number of podcasts Nourish balance thrive and Enduring health, you did with others. They are great. I started taking arginine 10 years ago for weight lifting and sports due to the Byrd study, I am 60 years old.
My cholesterol went up, not a problem. My problem on statins with spotty memory and severe muscle cramps. Thus, why I dumped atorvastatin in the rubbish.
My strength is coming back, memory is getting better. Thanks!
My only issue is my friends can’t understand the details when I send these podcasts. Can we do one where we dumb it down so the average Joe can get it. My daughter has a PhD in biology that helps me.
Also, her husband does podcasts. Maybe we can get you to produce your own for the average Joe podcasts.