Diabetes is a Vascular Disease – More on Joseph R. Kraft, MD

To quote pathologist Dr. Joseph R. Kraft, MD, MS, FCAP, the father of the insulin assay:

Those with cardiovascular disease not identified with diabetes… are simply undiagnosed.

One of Dr. Kraft’s conclusions, based on his illustrious career, is simple and provides a profound and ultimate truth: diabetes is a vascular disease. His career spanned decades and included unparalleled research performing insulin assays in over 14,000 subjects, thousands of autopsies, and collaboration with others medical experts searching for the root causes of chronic diseases including vascular disease. He also wrote a book about his research titled Diabetes Epidemic & You.


With Dr. Joseph R. Kraft at the Trump Tower Chicago


I was lucky enough to meet and interview Dr. Kraft this summer in Chicago along with engineer Ivor Cummins and family physician Dr. Ted Naiman. Ivor discovered Kraft’s work through researchers Prof. Grant Schofield and Catherine Crofts, PhD who now have Kraft’s entire database for analysis. Ivor was insistent to interview the doctor who recently turned 95 years, and so we did.


The Three Amigos


I wanted to share my thoughts from the experience and focus a bit on the cardiovascular implications of Kraft’s work. But first let’s briefly look at his insulin assay.

Dr. Kraft’s test is similar to the oral glucose tolerance test (OGTT), but it runs longer and includes insulin measurements. He confirmed and standardized the measurements using 14,384 subjects of all ages (a rather huge sampling). He identified one distinct normal insulin pattern (I) called “euinsulinemia” and three abnormal patterns (II-III-IV) of hyperinsulinemia, also called diabetes “in-situ”. Pattern (V), consistent with type I diabetes and loss of beta cell function was also identified but is not discussed here. Diabetes in-situ identifies diabetes at its earliest stage, illustrating how hyperinsulinemia manifests itself before hyperglycemia. Insulin resistance, a more common term used today, can be used interchangeably as both describe a similar metabolic defect.


Courtesy Ivor Cummins BE(Chem) CEng MIEI 2015


Kraft discovered that 83% of the subjects (not intended to represent the general population by design) failed his test thus meeting criteria for hyperinsulinemia (diabetes “in-situ”) based on the insulin assay. Comparing Kraft’s findings to a recent NHANES study, the new prevalence estimates including pre-diabetes and diabetes in adults are 49-52%. These estimates, though they’re getting closer to what Kraft predicted, are still based on the industry standard methods (SMs) of blood sugar measurement and are likely missing many. Clearly Kraft, by way of the insulin assay, was way ahead of his time recognizing the enormity of the problem and how ineffective are the industry SMs. To summarize:

  • 83% of subjects failed the insulin assay. They had hyperinsulinemia (diabetes “in-situ”)
  • A recent NHANES study estimates that 49-52% of adults are pre-diabetic and diabetic based on industry SMs of blood sugar measurement
  • A disparity between Kraft’s insulin assay and NHANES findings demonstrates how industry SMs of blood sugar measurement are still missing many

Furthermore, Kraft demonstrated that industry SMs of blood sugar measurement including normal fasting plasma glucose (FPG<100 mg/dl) plus normal oral glucose tolerance test (NGT, 2hr<140 mg/dl) missed 75% (weighted average) of subjects labeling them as ‘normal’ when indeed they were not normal. Let me explain.

Kraft includes fasting plasma glucose (FPG) measurement and plasma glucose measurements at specific time intervals over five hours after a 100g oral glucose challenge is given to all subjects (75g challenge also works). The insulin assay adds insulin measurements at specific time intervals and is considered the gold standard test. Kraft then compares the glucose results to the insulin results.

Kraft shows that the majority of subjects who pass the gatekeeper FPG test get labeled as ‘normal’. They generally don’t advance to the OGTT (further reducing overall sensitivity to rule in diabetes from ~50% to ~25%), but in actuality 76% of them are not normal and are missed. For the few that might advance to the OGTT, most also pass this test and get labeled as ‘normal’ (normal glucose tolerance, NGT) but in actuality 78% of them are not normal and are missed. Subjects’ having both a ‘normal’ FPG and OGTT (NGT) yields better overall sensitivity to rule in diabetes, but still 75% (weighted average) of them are not normal and are missed.

See the problem? Many are missed because industry SMs falsely label subjects as ‘normal’ when indeed they are not (statistically speaking that’s called “false negatives” or “1-sensitivity”). The insulin assay in comparison is telling. The bottom line is that industry SMs of blood sugar measurement (still the same today) provide a false sense of security and that’s not ok! To summarize:

  • 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 stage

Getting back to our discussion about vascular disease (atherosclerosis), Kraft noted that those with vascular disease, all of them, had hyperinsulinemia, and Kraft concluded that any and all patients with vascular disease if tested properly would fail miserably. He also suspected that those testing normal via his test would likely be free of vascular disease.

In later years, endocrinologist Gerald M. Reaven, MD gained some traction along the same path. Famous for his Sir Frederick Banting lecture in 1988 and discovery of the first method to quantitatively measure insulin mediated glucose uptake (called the insulin suppression test), he coined the term Syndrome X, which today is more commonly known as Metabolic Syndrome. Like Kraft, Reaven also quantified hyperinsulinemia and insulin resistance and further demonstrated its’ central role in the development of Type II diabetes and cardiovascular disease. Surprisingly, Kraft and Reaven never collaborated.

What troubles myself and other colleagues who address proper nutrition, is that despite this well established relationship between hyperinsulinemia and vascular disease, most doctors still view diabetes as just a loosely associated risk factor. Most healthcare professionals fail to recognize how insulin and other hormones, via various metabolic pathways, play pivotal roles that lay at the root cause of many chronic diseases including vascular disease. Ignore these pathways and watch those blood vessels go up in flames! So then why are so many doctors disconnected?

Sadly, traditional cardiovascular risk assessment tools lead us astray, steering us away from the root cause of atherosclerosis, namely inflammation. These tools including the 2004 NCEP ATP III guidelines and the 2013 CV risk calculator provide doctors with “muddy” and statistically noisy predictors based on rather loosely associated Framingham risk. The focus of the guidelines has a central theme: to simply lower serum cholesterol concentration (more specifically serum lipoproteins including total cholesterol and LDL-C) via a low saturated fat diet and or medication. Although diabetes gets a mention, it’s clearly underemphasized. It’s all about lowering cholesterol, and nothing more.

Without a well identified mechanism, cholesterol remains an elusive associated risk and yet orthodoxy says that too much is bad and requires remedy. Hyperinsulinemia, insulin resistance and the metabolic syndrome, on the other hand, provide irrefutable mechanisms that describe vascular disease (atherosclerosis) as an inflammatory process. These mechanisms include adiposity, inflammatory cytokines, free fatty acids, and oxidative stress that inflame the blood vessel wall, the cholesterol and the lipoprotein lying within the plaque itself. Addressing the quality of cholesterol rather than the quantity is key based on these mechanisms.

inflamation and adiposity

Hyperinsulinemia, Inflamation & Adiposity


Many large epidemiological studies challenge the approach to lowing cholesterol. The Get with the Guidelines study in 1998 showed that 75% (the majority) of patients hospitalized with acute coronary syndrome (ACS) had actually met cholesterol lowering targets at time of admission. Why then were they having heart attacks? A large recent review titled Towards a Paradigm Shift in Cholesterol Treatment demonstrated that people with higher cholesterol live longer. These observations suggest that current guidelines addressing cholesterol concentration are indeed problematic.

Framingham might predict a two to three times increased risk in some, but looking at diabetes as an independent risk factor paints a different picture. A recent study presented at the European Society of Cardiology noted that younger diabetic women are six times more likely to have a heart attack. Combining this with Kraft’s findings, that many with diabetes are being missed, it’s clear that we’re not properly addressing cardiovascular risk as well. If you truly want to properly address CV risk, forget the Framingham tools and focus on the root cause, hyperinsulinemia. It’s a sure bet.

Some have asked why Kraft’s work has gone largely unrecognized and the sad truth is that “Big Pharma” never found a way to cash in (GLP1 analog class of drugs changes that picture today). Reaven also didn’t draw much attention from “Big Pharma” as he identified diet and carbohydrate restriction as the primary intervention. Kraft admits that he mostly avoided the dietary debate but he did tell us in Chicago that reducing carbohydrates in the diet certainly was important and that there was never any basis to recommend reducing saturated fat in the diet. It’s clear, however, based on insulin metabolism, that a low-carb high-fat (moderate protein) diet should be the default for those pre-diabetic or diabetic.


Dr. Gerber and “Cameron” are drawn to the little girl in the white dress – Ferris Bueller’s Day Off – Sunday Afternoon on the Island of La Grande Jatte by Georges Seurat 1884 – The Art Institute of Chicago


Pragmatically, the 5hr insulin assay is tedious to perform in the clinical setting. What’s important is for doctors to recognize the importance of properly addressing insulin metabolism, cardiovascular disease, and proper diet while deemphasizing traditional Framingham risk assessment. Dr. Ted, myself and other like-minded physicians don’t do 5hr insulin assays but we do proactively address hyperinsulinemia and insulin resistance early, which is what’s important. Better standardized testing can help to recognize hyperinsulinemia including, HbA1c, fasting insulin (<5 uIU/ml normal), c-peptide, screening 2hr OGTT including a 1hr glucose measurement (<155 mg/dl normal), 2hr insulin (<30 uIU/ml normal), lipid ratios and lipid particle size.

Addressing cardiovascular risk begins with properly addressing hyperinsulinemia and insulin resistance and we have to thank Dr. Kraft for his work in this arena. The treatment is primarily nutritional, using low carb diets. Focusing on Framingham risk and cholesterol alone is a distraction and more doctors need to understand why.


A Stoic, Puritan Lookin’ Fat Emperor! – American Gothic by Grant Wood 1930 – The Art Institute of Chicago


Big thanks to Ivor our problem solving engineer who extracted Kraft’s numbers on all 14,384 subjects. He then created a huge spreadsheet breaking down the data by age and result allowing for proper analysis. And all that just for giggles!

Catherine Crofts, PhD:

  • David Mitchell

    You mention A1c test, a frustrating subject for a few. I’m LCHF for 2 years with TG/HDL going to 66/72 from 220/52, small LDL-p @ 217 with LDL-p slightly >1500 and LDL-C 140-170, bmi to 21 from 27, Naiman’s Homo-IR = 0.55 – all good except no change A1c 5.8-5.9 for last 5 yrs unchanged. From 1st glucometer 3/17 and many readings for various meals and fpg/bedtime, my estimate under most conservative assumptions for normal meals/ cheat meals / extended return to 95-100 up to 3 hrs PP when pasta is average fpg is no more 102 – not the 130-133 via formula from A1c results. My conclusion I am rare individual with very long extended life RBC. Should I be worried even though clearly I am IS (ogtt 75g insulin was 2.5, 24, 14, 23, 10 at 30 minute increments (post only 3 days carb upload after 1.5 yrs LCHF. Symptomatic I am healthy in all ways doing 30 mile day hikes AT, 100 mile backpack/day hike combo in Glacier NP and climbing Mt Whitney. I’ve never been on any meds other than 15 years of 10mg lipitor wasted before abandoning statins forever 2012. At M 67 I am EBT Agatston score or volume of about 165 9/16 with family history of CHD (father) and diabetes T2 (mother no insulin). Have you seen any patients with good everywhere except A1c? It appears to me there is nothing I can do to improve my A1c.

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  • Louise Corrans

    What a great read, and may I ask this: if insulin is pattern 2 or 3, would the patients blood sugar readings be normal but an HbA1c be elevated? I ask because my husband had a very high HbA1c reading (19%) but his fasting blood glucose was not that high, however his fasting insulin was a little higher than normal.

    • @louisecorrans:disqus I have never seen an A1c that high and confirms that his blood sugars would be sky high during a glucose challenge. He is probably a pattern 2 or 3 as only pattern 4 has a high fasting insulin.

      Across all Kraft abnormal patterns you can have totally normal sugars and A1c. The Kraft test would only confirm what you already know, that your husband is diabetic. The Kraft test wouldn’t add much information nor change the management. Does your husband have a weight issue? Kraft pattern 5 is one other possibility when someone isin’t producing insulin, called insulinopenic.

      Time to focus on reducing the foods that drive insulin, cut the carbs, processed foods and eat more natural fats.

      • Louise Corrans

        Thank you SO much for that reply. I appreciate you taking the time out to do so. We are, in fact eating LCHF now (we call it Banting in South Africa) following the book by Prof Tim Noakes, and then we will retest. I have also just never heard of such a high HbA1c. Thanks for the post and the info. And I was thrilled to see the picture of your heart after 15 years eating LCHF. Just thrilled. It proves what many ask about.

  • For those of you who wish to do the Kraft 5 hour insulin assay yourself: http://meridianvalleylab.com/Kraft-Prediabetes-Profile

  • Axel F Sigurdsson has a great post: Less Heart Disease Despite More Diabetes; The Role of Diet: http://www.docsopinion.com/2015/09/13/less-heart-disease-despite-more-diabetes-the-role-of-diet

  • Tim Heineman

    Your post says, “More on Joseph R. Kraft, MD” in the title but I searched your website for “Joseph R. Kraft, MD” and drew a blank. I enjoyed the post very much and would like more!

  • You’ve established that Insulin Resistance (IR) is bad. I completely agree. As I mentioned on Facebook, insufficient activity increases IR by down-regulating Glu-T proteins. It also raises Triglycerides & lowers HDL-c by down-regulating Lipoprotein Lipase. See http://blogs.plos.org/obesitypanacea/files/2010/12/Published-Paper.pdf

    LCHF diets ameliorate Insulin Resistance, but they don’t up-regulate Glu-T proteins or Lipoprotein Lipase. Is it therefore advisable to get patients with IR etc to modify their diets (to switch from mostly over-processed foods to mostly animal & vegetable produce) and increase their activity, to get the best results?

    RE Cholesterol: LDL-c is involved in atherosclerosis. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/

    • Hi @nigelkinbrum:disqus. Certainly cholesterol plays a role, but proper diet and lifestyle come 1st. We mostly agree about what makes up a proper diet. My point is that the cholesterol guidelines steer doctors away from addressing proper nutrition. Cutting carbs (sugar and processed especially) will most likely reduce your CV risk better than taking a statin.

      • What do you do with clients who are resistant to changes in diet and/or activity?

        • Modern medicine has me well trained and I still prescribe medications (including statins) when lifestyle fails.

          • Good. Too many MDs use medication as a first resort for treating T2DM, rather than a last resort if lifestyle modification efforts fail.

          • spfldo .

            Stains have dangerous side effects and although they may, in fact do, lower cholesterol, there is little to no evidence in support of the claim that statins decrease Cardiovascular events. LDL-C may show up at the scene of the crime but that’s like saying the ambulance that shows up at the traffic accident had something to do with the accident. Carbohydrate or the insulin response to a sugar load lowers HDL and reduces particle size, a very LC HF diet doubles my HDL and reduces the VLDL. Diet, that is, a low fat diet, can only influence TC by about 10% overall but most of the reduction comes at the expense of HDL. Statin drugs reduce my TC but I’ve suffered every side effect on the bottle, from temporal global amnesia, peripheral neuropathy to severe fatigue, muscle cramps and more. Since any proven benefits for statin use are quite slim, it would be stupid as hell to take them.

          • See http://1.usa.gov/1YNGhEI

            LDL-C is involved in atherogenesis, but not in the way it’s usually portrayed, and there are other factors involved. This means that it’s possible to have atherogenicity with a low serum LDL-C level.

            There is evidence that lowering LDL-C reduces the RR for CHD, but as you correctly point out, interfering with the non-sterol synthesis pathway by inhibiting the conversion of HMG coenzyme A into mevalonate with statins has unintended side-effects, including the reduced synthesis of coenzyme Q10 & dolichol.

            PCSK9‬ inhibitors look more promising, though they cost a fortune at the moment.

            Lowering LDL-C by diet & lifestyle modification is best, but some people are so brainwashed by the food product industry to over-consume over-refined food products, that they have difficulty making diet & lifestyle modification.

          • spfldo .

            Diet and lifestyle modification is indeed the best way to address CVD. Medicines have very very marginal benefits with very real, dangerous and COMMON side effects. You can only affect TC marginally (in either direction) through diet, generally about 10%. If you eat a LCHF diet which I’d recommend, TC will generally rise. The good thing with LCHF is, HDL, “the good cholesterol” also rises (mine doubled) and particle size will move into the “healthy” pattern A. If you eat a LFHC diet, TC generally declines but HDL drops and particle size will move toward the “unhealthy” pattern B. So, diet is key but diet doesn’t affect TC, generally no more than 10% one way or the other – there must be something else in the diet that affects CVD outcomes. Sugar is the most important factor as Dr. Linus Pauling theorized and Dr. Joseph Kraft maintains. Other critical factors in the diet are Omega 3 to 6 ratios, grain oils, transfats and processed foods void of nutrients. Some of us suffer from genetics which predispose us to CVD from eating the SAD diet e.g., LDL receptor and methylation problems resulting in high TC, homocysteine and low nitric oxide production. It is noteworthy that Myocardial Infarction was essentially nonexistent until about 1915 and even into the 1930s it was rare. Genetics haven’t changed in that timespan, so why were my ancestors who likely possessed the same Familial Hypercholesterolemia that I have, not suffer heart attacks? The SAD and SUGAR. HIGH TC is relatively innocuous without other antagonists at play. Some people, particularly medical doctors, are brainwashed or bought by pharmacological companies, The American Heart Association, The American Medical Association and others. Cholesterol is not a problem except a very limited number of people, even in my case (TC 400). Mark my words, statins are bad, won’t help and PCSK9 inhibitors will be worse. https://www.youtube.com/watch?v=UCk_vTkS6bU

          • ” If you eat a LFHC diet, TC generally declines but HDL drops and particle size will move toward the “unhealthy” pattern B.”
            That’s not correct. Studies by Dreon & Krauss had 50% of the carbs as sugars, and the other 50% (complex carbs) may have comprised a high proportion of rapidly-hydrolysed starches such as maltodextrin & amylopectin. As this is completely different from what people on whole, minimally-refined HCLF diets eat, the results are invalid.

            See http://wholehealthsource.blogspot.co.uk/2008/08/cardiovascular-risk-factors-on-kitava_14.html
            “There is a theory of the relationship between blood lipids and CVD that can explain these data. Perhaps blood lipids, rather than causing CVD, simply reflect diet composition and other lifestyle factors. Both on Kitava and in the West, low HDL and elevated triglycerides imply a high carbohydrate intake. Low-carbohydrate diets consistently raise HDL and lower triglycerides. On Kitava, carbohydrate comes mostly from root crops. In the West, it comes mostly from processed grains (typically wheat) and sugar. So the blood lipid pattern that associates best with CVD and the metabolic syndrome in the West is simply a marker of industrial food intake.”

          • spfldo .

            Good luck with your fruits, grains and tubers. Unless you are one of the 25% in Dr. Kraft’s graph with good insulin response to a sugar load, you are going to have cardiovascular and diabetes problems. Dr. Barry Groves maintains, we are carnivores and I believe he’s right. The human digestive tract is similar to dogs. No, I’m not incorrect about Cholesterol response to sugars and carbs, I have like twenty two years of blood tests to prove it. Although, I’m n=1, crowd sourcing or the wisdom of the crowds back it up. You’d be wise to listen to the crowds. Again, statins don’t do crap for CVD. https://www.youtube.com/watch?v=qn5zdWucv6I http://www.spacedoc.com/articles/cholesterol-not-factor-heart-disease http://www.spacedoc.com/articles/why-the-cholesterol-causes-coronary-heart-disease-dogma-has-persisted

          • Luck has got nothing to do with it! I fixed my IR in 2008. See http://bit.ly/1OvsEPk You may be able to fix yours. If so, you’ll be more metabolically-flexible.

            Humans are not carnivores. The late Dr Barry Groves got that completely wrong. We are omnivores, like Chimpanzees.

            I don’t listen to crowds. I listen to evidence.

            “No, I’m not incorrect about Cholesterol response to sugars and carbs”
            It’s not you that’s wrong. It’s the bogus studies with fudged methodologies that are wrong.
            If you fix your IR and eat a diet based on whole, minimally-refined animal & vegetable produce, you’ll be healthy.

            “I have like twenty two years of blood tests to prove it.”
            What blood tests? Serum NEFA’s? Postprandial TG’s?

          • Pattern B particles are only unhealthy if LDL-P is high. If LDL-P is low, there’s no increase in CHD risk.

            As I previously mentioned, the Dreon & Krauss studies fudged the methodology to make carbs look bad. There’s bias in some LCHF research, just as there is in some HCLF research.

    • You like numbers Nigel – here’s some ‘associative’ fun ! http://www.thefatemperor.com/blog/2015/9/22/kraft-konfirmed-the-bizarre-result-of-the

  • Great article Jeff – here’s the excel file I put together to make sure I was happy with the numbers before interviewing him 🙂 https://www.dropbox.com/s/mrw01q59imri38g/1%20KRAFTY%20KRAFT.xlsx?dl=0

  • Yep. I’ve been saying this for years. Great article, Jeff.

    • Thanks Adam. I thought to add you to the docs I mentioned above who address hyerinsulinemia early on, but I decided to keep it short. Had you on my mind however!

  • Nagar J

    Kraft’s theory that diabetes is the real cause of CVD is fascinating. But haven’t rates of CVD dropped dramatically just as rates of diabetes have exploded? Wasn’t CVD at its peak long before the diabetes epidemic really took off? How can the theory that diabetes —> CVD be squared with the epidemiology?

    • But, they haven’t tracked diabetes properly, that’s the point. Also, People with CVD live longer and die from other reasons (thus death attributable to CVD has been falling, thanks to modern medicine). CVD still remains the leading cause of death. http://www.heart.org/idc/groups/ahamah-public/@wcm/@sop/@smd/documents/downloadable/ucm_470704.pdf

      • Nagar J

        “But, they haven’t tracked diabetes properly, that’s the point.”

        Even so, isn’t it pretty clear that hyperinsulinemia, as described by Kraft, has massively increased in industrial societies since the 50’s and 60’s? We know that diabetes as conventionally defined has skyrocketed, as has “prediabetes,” so Kraft’s diabetes-in-situ almost certainly has, too, I’d think.

        “Also, People with CVD live longer and die from other reasons (thus death attributable to CVD has been falling, thanks to modern medicine).”

        I believe that CVD *incidence* has declined over the decades, not just CVD *mortality*. Some of that incidence decline is no doubt thanks to less smoking, and maybe (maybe) preventive medicine, but I don’t think that explains all of it.

        In any case, if hyperinsulinemia really primarily drives CVD I’d have expected an explosion of CVD during the runaway diabetes epidemic, which hasn’t happened. I’m not saying that disproves Kraft’s theory. It certainly doesn’t, due to all the possible confounders such as smoking rates. But it raises a good question I think.

        • @nagar_j:disqus Yes, CVD incidence has shown a decline over the decades. Sorry, I was not quite locked in on your question. @ivorcummins:disqus has some insightful comments and I agree that there are many confounders looking back. Pre-diabetes, diabetes and CVD incidence don’t seem to quite track as you say but it is hard to say they don’t.

          I just have to think that the under-reporting of pre-diabetes and diabetes which we still see today was also the case historically and needs to be considered. Today I see cardiac patients who are overtly type 2 and they nor their previous docs knew it. It creeps me out every time! The epidemiologist would have reported them as non-diabetic.

        • spfldo .

          Be patient, it ( CVD incidence ) is coming. Three out of four diabetics will die of MI or stroke, modern medicine will keep them struggling along with massive intervention for years. Then you’ll see a spike.

    • spfldo .

      Hyperinsulinemia is the driver of cardiovascular disease but there are/were other factors at play. Cigarette smoking has been cut in half and could well account for the reduction you allude to. Damaged arteries from hyperinsulinemia already – add three packs a day…..that’s trouble. Trans Fat has been recognized and banned for the artery damaging toxin it is and people are healthier for it. Pepsi and Coke have had declining sales for years now, with people opting for their diet sodas instead. I wouldn’t claim diet soda is good for you but it’s probably better than the nine to 12 teaspoons of sugar in the typical can of soda and could possibly be responsible for healthier arteries. Sizable numbers of people have learned of the damaging properties of grains and high Omega 6 grain oils and have made changes, witness the uproar of the Atkins Diet, the South Beach Diet and the Mediterranean Diet. At the same time people have added the Omega 3 ESSENTIAL for LIFE fatty acids to their diets, which were previously difficult to get in the Standard American Diet. Calling 911 and getting to the hospital quicker, where you can receive life saving clot buster drugs etc. result in many CVD survivors who wouldn’t have survived in the sixties and seventies.

    • The dramatic increase in cardiovascular disease from the early to mid 20th century had it’s origins in the cigarette smoking explosion, along with huge increase in sugar consumption, with a likely contribution from the ramp in omega 6 vegetable oils and trans fats. Epidemiology is a notoriously confounded discipline (though I hesitate at even using the word, given the way it is generally conducted).
      Incident atherosclerosis declined from the 80’s to the late 90’s (primarily driven by smoking abatement), then the trend reversed as the carb storm began to gather pace. No-one will really be able to decode the full picture due to the hilarious level of confounding involved. There is another possible confounder via potential exacerbation by infectious agents and industrial pollution, although this has never been proven out.
      So let’s look at the person who maintains euinsulinemia (via low carb, no sugar etc.), doesn’t smoke cigarettes or consume industrially produced omega 6 oils and trans fats, and keeps their magnesium and vitamin D levels at healthy evolutionary levels. They need not stay awake at night worrying about their love organ. Of the latter factors, avoiding hyperinsulinemia is the central plank. The others are belt and braces.

      • spfldo .

        Dead on Ivor.

    • @iv@ivorcummins:disqus, @s@spfldo:disqus Great replies!

      • @ivorcummins:disqus, that paper you found is another gem. @nagar_j:disqus asked an interesting question and this will add another layer of discussion for that presentation I’m working on.

      • Nagar J

        Epidemiology is interesting, but you have to be cautious. Another well known epidemiological finding: the Japanese love to smoke but have low rates of CVD. There’s a lot we don’t know. Explaining plummeting CVD rates with smoking reduction (or anything else) is, to me, still fraught with uncertainties. Some people believe widely fluctuating CVD rates reflect a fundamentally infectious origin. No idea if they’re right, but numerous explanations seem possible at this point.

        • I agree about caution @nagar_j:disqus, but your the one that brought up the epidemiology argument in the 1st place. The mechanisms make for a more powerful argument and I’m going with those.

          • Nagar J

            Touché, Dr. Gerber.

            As I said, long term CVD trends certainly don’t invalidate the Kraft hypothesis. But when such a strong epidemiological trend goes directly against the trend predicted by a hypothesis it should give pause—even if *possible* explanations for the unexpected trend seem plausible.

            My guess is that the diabetes—>CVD theory has a lot of truth, just like the smoking—>CVD theory. But far from the whole truth, with fundamentally multi-causal, context-dependent l phenomena. Lots left to learn. In the meantime, I’m sticking with low carb! (And I’m not taking up smoking.)

          • spfldo .

            Dr. Linus Pauling mentioned in one of his books that although he couldn’t prove it, intellectually, he thought that the rapid increase in CVD in the 20th Century was due to increased sugar consumption. After suffering with and reading about CVD complications for years, I too had come to that conclusion i.e., CVD was really misdiagnosed diabetes. Ivor Cummins “proved it” to me with Dr. Kraft’s research. My arteries are getting better and they were about as bad as anyone alive.

        • spfldo .

          Smoking, as unhealthy as it may be, is particularly dangerous to arteries already being damaged by insulin overload. I’d bet smokers who eat a LCHF diet have much less smoking related complications across the board. Just my opinion.

  • Kok-Hong Wong

    It is amazing how much effort is needed to prove a simple, seemingly obvious relationship…diabetes IS a vascular disesase. Now someone has to go on to prove that carb overload IS the cause of diabetes. 🙂 Cut the carbs. #lowcarbs #LCHF

    • Johan Wallström

      Good luck proving that, lol. Choose healthy non refined foods and there is nothing wrong with carbs, as shown in a massive amount of studies. On the contrary, whole foods will increase insulin sensitivity. No need to demonize good carbs

      • I gave up carbs but I still smoke… only ultra lights. When are they gonna stop demonizing good cigarettes? 🙂

        • Johan Wallström

          That is a nonsense analogy. Whole food plant sources of carbs are consistently showing up as a protective against disease. My insulin level is fine

          • Check your insulin level again in a few years. That’s how we track our patients.

          • From http://www.ncbi.nlm.nih.gov/pubmed/10535381 :-
            “…serum insulin decreased with age in Kitava…”
            Kitavans got >70% of their energy from whole food plant sources of carbs.

          • @nigelkinbrum:disqus, there’s no way I’m going to tell my diabetics that they can routinely consume safe carbs. If it works for you, great. I would like to see your postprandial sugars and insulin. As the retired and wise engineer you are, time and diet may have eaten away at your beta cell function like it does to most. 🙂

          • I only linked to the above study to counter claims that carbohydrate consumption causes IR.

            Someone with T2DM has a “broken” metabolism, so a Kitavan diet wouldn’t be appropriate for them.

            Instead of a LCHF diet for life to manage T2DM, have you tried Prof. Roy Taylor’s 8 week LCLF diet to reverse T2DM (i.e. “un-break” the metabolism)? The patient would then have more flexibility in terms of diet (but still have to minimise consumption of the over-processed stuff that broke their metabolism in the first place).

            As I’m not very active (an arthritic right hip & knee joint has reduced my mobility), I’m not burning much carbohydrate, so my diet is mostly non-starchy veggies & meat, with some fruit.

          • I like your diet.

          • At my last OGTT (in 2008), my fasting blood glucose was 5.0mmol/L (90mg/dL) and my blood glucose 2 hours after swallowing 75g of glucose was 3.7mmol/L (66.6mg/dL). My beta cells are fine & dandy, thank you very much.

            That’s after having had IR & compensatory hyperinsulinaemia for 52 years! (until 2007, when I reversed my IR for good).

          • Janknitz

            Kitavans are omnivores. Look closely at their diet. They eat fish, seafood, and pork. And plenty of saturated fat from coconut.

          • “And plenty of saturated fat from coconut.”
            Kitavans eat a low fat diet (~20%E from unrefined fats) plus unrefined carbohydrates, whereas Americans eat a medium fat diet (~35%E from a lot of refined fats) plus a sh*t-load of refined carbohydrates.
            From http://www.staffanlindeberg.com/TheKitavaStudy.html
            ” The intake of vitamins, minerals and soluble fibre was therefore very high, while the total fat consumption was low, about 20 E% [28], as was the intake of salt (40-50 mmol Na/10 MJ compared with 100-250 in Sweden). Due to the high level of coconut consumption, saturated fat made up an equally large portion of the overall caloric intake as is the case in Sweden. However, lauric acid was the dominant dietary saturated fatty acid as opposed to palmitic acid in Sweden.”

        • spfldo .

          That’s right, some have better IR than others, probably about one in four as Dr. Kraft’s research shows. The rest of us better pay attention.

    • Sorry, but please stop beating this dead horse.

      • Emaho

        And thank you doctor and your fellow low carb doctors for attempting to raise the horse from the dead!

        • Sorry if you don’t like my idiom. With due respect to the ethical issues, vegetarians can also do low carb. However, I’d like to stay on topic.

  • spfldo .

    I came to the conclusion that “heart disease” was a form of diabetes, but not understood as such about four years ago. In the last six months I was introduced to Ivor Cummins’ excellent blog, thefatemperor.com and Dr. Kraft’s work, which explains and puts everything into focus. I read Dr. Kraft’s book, and your article does a fine job of condensing it into a form which I’ll be able to share with family and friends who wouldn’t buy or take the time to read. I also notice, the paintings you and Ivor are posing against are 85 to 130 years old – and nary a fat person to be found. That jibes with information that I’ve seen, that the rise in myocardial infarctions started about 1915 and really started to gather steam in the 1930s. Thanks for the fine article.

    • @spfldo:disqus Thanks for your comments. Mission accomplished. Sometimes the stats can be daunting and I’m always trying to make it easy for all to understand including other healthcare professionals. The tie to CV risk is indeed an awakening and hopefully more will discover the importance of hyperinsulinemia and early recognition.

    • Annlee

      I grew up in the 1950s – and recall a norm that looked like the pictures here — http://www.shorpy.com/ … we’ve come a long ways, and not all of it has been good.

  • Pingback: Diabetes is a Vascular Disease – More on Joseph R. Kraft, MD | Primal Docs()

  • Axel F Sigurdsson


    Thanks for a great article on a very important subject. Really enjoyed reading. It’s good to see Kraft’s theories resurfacing. Great photos as well 🙂

    I’ve found the TG/HDL cholesterol ratio to be a cheap and helpful tool to assess insulin resistance in the clinical settings. However, I assume there are a lot of false negatives there as well, but probably very few false positives, e.g. those with a high ratio are very likely to have insulin resistance. I also frequently use fasting blood glucose and HbA1C, but less frequently fasting insulin.

    Do you think that using fasting insulin would add much to the clinical picture when already using fasting glucose, HbA1c and TG/HDL cholesterol ratio?

    How about adiponectin? Its inverse correlation with insulin resistance is very strong and hypoadiponectinemia might even be one of the possible underlying causes of insulin resistance. Do you think adiponectin is something we should be measuring in clinical practice?

    • Hi @docsopinion and thanks for your comments. Your way ahead, already as one of the few docs already triangulating in on hyperinsulinemia. That’s half the battle!

      Cholesterol ratios seem to be the 1st indicator but no test is perfect and false negatives do creep in. Iv’e been doing fasting insulin for years and we do see some with normal fasting blood sugars and yet have fasting insulin >7 uIU/ml. Kraft showed that the fasting insulin by itself has to be fairly high to be telling. We actually had a patient today with a fasting insulin of 40!

      Leptin, adiponection, FFA all sounds like tests that could provide useful info but in the US cost and standardization need to be considered.

  • melancholyaeon

    I’m sympathetic to your argument, and even I have trouble rallying much interest in data that appears to be 30-40 years old now. How is this still relevant? Thanks.

    • erdoke

      Why do you think it might not be relevant? Exactly the same parameters are measured these days to determine who is diabetic and pre-diabetic. Based on Dr. Kraft’s findings a very significant portion if not the majority of people is still not diagnosed properly/timely.

      • Well said @erdoke:disqus

        • melancholyaeon

          Ty for your reply Dr. Gerber. I’m afraid however that instead of telling me why it’s still relevant you just simply assert that it is. 🙁 Which is not very convincing. I personally can’t think of any other biological science in which we just accept such ancient evidence without update or explanation. Best wishes.

          • Modern medicine is still catching up with Kraft’s “ancient evidence”. NHANES 2015, pre-diabetes and diabetes prevalence estimates 49-52%. Sorry…that’s old news and the study is a waste of money. That’s exactly what Kraft’s data predicts, but I guess that’s not “relevant”.

          • Nancy Jacobs

            Melancholyaeon, are you saying that since the data have been ignored for 30 or 40 years that we should continue to ignore them? And if we continue to ignore them they will not be true? I don’t understand your logic. But to set your mind at ease I will tell you that there is a researcher named Catherine Crofts who is working to test Dr. Kraft’s hypothesis. She will have brand new data!

          • Holly

            It’s not ancient science. Are you assuming that humans biological processes have undergone a significant metamorphism or genetic mutation that lab values that are younger than me are not relevant? So to restate your assertion, lab values that are younger than you are irrelevant and the fact that many of the people tested by Dr. Kraft are still alive, is also irrelevant as far as you are concerned.

    • spfldo .

      What data does rally interest with you, the latest and greatest in low fat vegetarian research? Maybe the sat fat cholesterol nonsense still propagated on the “current” research of Ancel Keyes? Much of the CURRENT research presented today is done by Big Pharma, Big Food, Big Agribusiness or government agencies which are controlled by them through the principle of regulatory capture. Since they employ some pretty smart chemists, they have a pretty good idea of how to set up the controls to get results they want. They used to do their “studies” and present the positives to the FDA and sh*t can the negatives, but after 60 or 80 thousand deaths from VIOXX, they aren’t allowed to “get away” with that anymore. Business, including big business has brought us a standard of living unparalleled in the history of the world, but when business allies itself and uses (buys) the power of government for favors and protections, the abuse, misinformation and propaganda begin. It’s quite ironic that the government stamp of approval by George McGovern and his Select Committee on Nutrition and Human Needs has killed more people with diabetes and heart disease than Stalin and Mao combined. I’d be highly skeptical of any current research. The wisdom of the crowds is where it’s at.