Even heavyweights fall short: Prof. Tim Noakes on insulin resistance and Dr Reaven

In Part 4 of Professor Tim Noakes’ series on insulin resistance, Noakes turns back to Dr Gerald Reaven’s academic career. Noakes states that Reaven made one crucial error: “He failed to follow up Kuo’s seminal observation that the majority of patients with atherosclerosis exhibit carbohydrate-sensitive hypertriglyceridemia (CSHT) (22), the key abnormality Reaven would later include as the foundational abnormality when he described his very own medical condition, Syndrome X.” Part 4 provides another in-depth look at LCHF and the way in which even those who contributed extensively to the discovery of insulin resistance syndrome fell short.


By Prof. Timothy Noakes


In a previous column (1), I showed that by 1994, Dr Gerald Reaven, an MD and professor of medicine at Stanford University, had with his team clearly already established that a high-carbohydrate diet produces hyperinsulinemia, hyperglycemia, and carbohydrate-sensitive hypertriglyceridemia (CSHT, 2–13). He had also demonstrated that these conditions were made worse by sugar consumption (11, 12), and the conditions improved with dietary carbohydrate restriction, even if the dietary carbohydrate content was not particularly low (17–40% of total calories) (2, 14, 15). This evidence led Reaven to question whether CSHT – and not cholesterol – might be the more important risk factor for arterial disease in persons with Type 2 diabetes mellitus (T2DM).

As I also detailed previously (1), Reaven had started to make a tentative detour away from downplaying the significance of cholesterol to heart disease risk because making such a claim was potentially career-ending. He also had been powerfully influenced by the studies of Margaret Albrink and her colleagues (16–19) and those of Peter Kuo (20–22), which showed that triglycerides, not cholesterol, are more likely to be elevated in persons with coronary heart disease. Albrink and Kuo tentatively proposed triglycerides, not cholesterol, could be the more likely drivers of arterial damage. In Albrink’s publications, Reaven would have read the following:

The present report suggests that an error in the metabolism of triglycerides is the lipid abnormality operative in coronary artery disease. (16, p. 7)

There can be little doubt from the present data that the serum triglyceride concentration is more closely associated with coronary heart disease than is the serum cholesterol concentration. (17, p. 17)

At all ages, however, the vast majority of patients exhibit an increase in serum triglyceride concentrations as the most characteristic abnormality. (17, p. 21)

The low-density lipoproteins, which have been implicated in coronary artery disease, may be classified into two chief types or combinations thereof. In one, cholesterol is the predominant lipid component; in the other, the very low-density category, triglycerides are the major constituent. The first type … is associated with an increased risk of coronary artery disease, it is found in only a small number of all patients with coronary artery disease, and rarely over age 50. The second type, characterised by increased triglyceride concentrations with either normal or elevated cholesterol … is the commonest lipid abnormality in coronary artery disease … . Post-absorptive concentrations of serum triglycerides and very low-density lipoproteins are raised by increasing dietary carbohydrate and reduced by caloric restriction and by substitution of fat for carbohydrate in the diet … . The evidence is discussed for an association between overnutrition, increased serum triglyceride concentrations, impaired carbohydrate tolerance, and coronary artery disease (19, p. 156, my emphasis).

From Kuo et al., he would have read the following:

Although the majority of patients with atherosclerosis in this series were referred to us … (for the investigation) of hypercholesterolemia, only 8.4% were found to have essential familial hypercholesterolemia. More than 90% were found to have carbohydrate-sensitive hyper(tri)glyceridemia with or without hypercholesterolemia. Thus, it is reasonable to assume that with proper dietary preparation and appropriate laboratory studies, a high incidence of carbohydrate-sensitive hyperglyceridemia could be demonstrated in persons with atherosclerosis. (22, p. 106)

This information convinced Reaven to study the factors driving liver triglyceride production. Insulin, he discovered, was the key factor (23, 24). Since blood insulin concentrations are, in turn, determined largely by the carbohydrate content of the diet, he should have theorised that dietary carbohydrates might be playing a crucial but unrecognised part in the development of coronary heart disease.

This logic would havre taken him to the edge of what could become one of the most important recent discoveries in modern medicine. Would he be the one to make that discovery?


While Reaven on the West Coast of the US was beginning to seriously question the role of cholesterol in heart disease and also the value of high-carbohydrate diets for the management of T2DM, on the East Coast, Robert Atkins’ work on obesity and T2DM was attracting the attention of Eric Westman, a physician at Duke University in Durham, North Carolina. Westman’s patients were informing their doctor that Dr Atkins’ advice to eat more fat if they wanted to lose weight seemed to be working. In his disbelief, Westman visited Atkins. As I detailed previously (25), one critical outcome of this meeting was the development of the definitive studies from the Virta Health company two decades later, which showed that more than 60% of patients can put their T2DM into remission if they follow a low-carbohydrate diet similar to the one Atkins had ‘discovered’ (26, 27).

So it would take 20 years for the efficacy of Atkins’ low-carbohydrate, high-fat diet to finally be proven beyond doubt, finally laying to rest the allegations that the diet is ineffective and dangerous (28).

But what was Reaven up to during that time? And how did his work aid or delay the discovery of the truth about the Atkins diet?

Already by then, Reaven was highly regarded by the elites in his profession; something Atkins never achieved in his lifetime. A full professor of medicine at Stanford University, Reaven’s very special status was confirmed in 1988, when he was invited to deliver the most prestigious lecture in medical endocrinology: the Banting Lecture (29), named after Frederick Banting, the Nobel laureate and co-discoverer of insulin.

Were this a two-horse race to the truth, clearly already in the 1990s, Reaven appeared to have established an unassailable lead over Atkins. But would Atkins’ greater practical experience with obesity and T2DM allow him to discover a truth hidden from his more highly regarded peer?


To study the evolution of Reaven’s thoughts on diet during this period, we can review the two editorials he wrote in 1980 (30) and 1988 (31) alongside the relevant contents of his popular book published in 2001 (32).

The first important point about the 1980 editorial was its title. The title was not ‘How Low the Carbohydrate?’ Instead it was ‘How High the Carbohydrate?’ In other words, despite the extensive evidence he had already collected showing the detrimental effects of carbohydrate ingestion, especially in those with insulin resistance or T2DM, he was not yet willing to abandon the still popular idea that carbohydrates are an essential component of a healthy diet. I will argue that his bias (and the blindness that it induced) was not driven by any special belief in the divine health benefits of carbohydrates. Rather, it was simply an inherited bias that led him to believe carbohydrates are less toxic than the real dietary devil, saturated fat.

The 1980 article begins with a restatement of the conventional wisdom that “the incidence of atherosclerosis is increased in proportion to fat consumption” (30, p. 409). As a consequence, he noted, most individuals including diabetics with Type 1 or Type 2 diabetes, are advised to eat a diet that contains “50–60% carbohydrate” (33).

However, while there was “no evidence that restriction of dietary fat will impede the development of atherosclerosis in patients with diabetes” (p. 409, my emphasis), he was very uncomfortable with the suggestion that the higher the dietary carbohydrate intake, the better off the patient would be. He was uncertain this belief could be supported by the published evidence.

He began his argument by addressing studies showing that an increased dietary carbohydrate intake can (modestly) increase “insulin sensitivity” in both normal persons and those with T2DM. He argued that most of this (modest) improvement occurs when the percentage of carbohydrate intake increases from about 10 to 40%. However, when carbohydrate intake is increased from 40 to 85%, there was little further change in insulin sensitivity.

But then he made the obvious point: “However, the crucial question is not whether high carbohydrate diets improve insulin sensitivity, but whether high carbohydrate diets will lead to lower glucose concentrations in patients with diabetes” (p. 410). To answer this question, he referred first to the studies of Harold Himsworth (34) and Himsworth and RB Kerr (35).

Those studies found the response to a glucose tolerance test differed between diabetic patients who were either insulin sensitive or insulin insensitive. Thus, Himsworth wrote:

When more carbohydrate is given to a healthy subject, the body responds by rendering itself more sensitive to insulin. Now it has been shown in the previous section that when more carbohydrate is given to an insulin-sensitive diabetic, the insulin requirement does not increase and glycosuria does not appear. I have shown elsewhere that this apparent increase in efficiency of the injected insulin can satisfactorily be explained on the basis that these patients react to the increased amount of dietary carbohydrate by becoming more sensitive to the injected insulin. But in the case of the insulin-insensitive diabetic increased intake of carbohydrate results in glycosuria and consequent increased insulin requirement. Thus these patients are abnormal in being unable to react to increase in dietary carbohydrate by increase in their sensitivity to insulin. It appears, therefore, justifiable to regard the insulin-insensitive type of diabetes as being due to a lack of that same unknown factor which in the normal subject produces sensitivity to insulin. (34, p. 1597)

In his final paper a decade later, Himsworth cited JP Peters, who had written: “No condition approaching the gravity of the disorders of metabolism encountered in severe spontaneous human diabetes (i.e. T2DM) has been produced in man by destruction or removal of the pancreas (i.e. T2DM)” (37, p. 468). Peters’ point was that the insulin insensitivity of the tissues in T2DM produces a more complex disease than occurs as the result of a pure insulin deficiency in untreated T1DM. Thus, he concluded, “It thus appears that we should accustom ourselves to the idea that a primary deficiency of insulin is only one, and then not the commonest, cause of the diabetic syndrome.” (p. 472).

In the 1980 paper, Reaven cited two of his own studies, completed in 1974 (3) and in 1976 (4). He also cited a third study by Himsworth, which measured the same variables in those with diagnosed hypertriglyceridemia when they ate a high-carbohydrate diet (36).

The first study evaluated the effect a dietary change from a standard diet to a diet somewhat higher in carbohydrate would have on glucose control and blood lipid concentrations in healthy persons. The standard diet was comprised of a carbohydrate-fat-protein ratio of 43: 42:15%, and the higher-carbohydrate diet had a ratio of 55: 30: 15%. The study found the dietary change caused a “relatively modest” increase in blood glucose concentrations but approximately a 40% increase in the plasma insulin response to the noon-time meal. Reaven and his co-author, JM Olesky, concluded, “Since ingestion of a low-fat-high-carbohydrate diet led to increases in glucose and insulin levels, the advisability of recommending such diets as general prophylaxis against the development of atherosclerotic heart disease must be reconsidered.” (3, p. 151).

In the second study, a similar dietary change produced a 41% increase in fasting blood triglyceride concentrations in 26 of 27 subjects without any change in blood cholesterol concentrations (Figure 1). Postprandial triglyceride, glucose and insulin levels were also higher on the low-fat (higher-carbohydrate) diet. Again, Reaven and his co-authors concluded:

Since hypertriglyceridemia is a significant risk factor for the development of coronary heart disease, and since our data indicate that the moderate increase in dietary carbohydrate associated with a low fat diet will elevate plasma triglyceride levels, we believe that more caution is necessary before recommending the wide-spread use of low fat diets for heart disease prevention. (4, p. 729)

insulin resistance

Figure 1, top panel: The change from a diet containing a carbohydrate-fat-protein ratio of 40:45:15 to one with somewhat more carbohydrate (55:30:15) caused a 41% increase in fasting blood triglyceride concentrations (left) without any change in blood cholesterol concentrations (right). Bottom panel: Following a meal at noon, post-prandial blood glucose (left) and insulin (right) concentrations were significantly increased when subjects ate the higher-carbohydrate diet. Reproduced from reference 4.

The third study (36) found that an increase in dietary carbohydrate intake from 45 to 85% of total calories increased the fasting blood glucose concentration and the 24-hour urinary glucose excretion of persons with T2DM.

All these studies supported a uniform interpretation; specifically, that increased carbohydrate intake is detrimental to glucose control in persons with T2DM. Worse, by raising blood triglyceride concentrations, a high-carbohydrate diet will increase risk for future cardiovascular disease in persons with T2DM.

Reaven then reviewed a series of papers that argued the opposite: that higher-carbohydrate diets improve glucose control in persons with either T2DM or T1DM.

Of these papers, the most historically influential is that by RW Simpson, Jim Mann and colleagues from Oxford University (39). Dr Mann, who taught me at the University of Cape Town Medical School, became an ardent advocate of the value of dietary carbohydrates for all (40) and high-carbohydrate, high-fibre diets, particularly for the management of both obesity and T2DM. Mann eventually became the senior author of a large meta-analysis published in 2019, apparently showing the great value of a daily dietary fibre intake of >30 grams (41). (In fact, that study found that 100 people would have to eat 30 grams of dietary fibre/day for life for one person to benefit.)

In short, Mann has spent his life as a carbohydrate-loving sugar denialist, advocating the theory that a lack of dietary fibre (not an excess of carbohydrate or sugar) causes both T2DM and coronary heart disease. This is known as the Burkitt/Trowell hypothesis (42). The hypothesis remains unproven to this day. Some argue the hypothesis was popularised, perhaps at the behest of the sugar industry in the 1960s, to divert attention from a competing theory gaining popularity at that time: the theory that sugar (not dietary fat or a lack of dietary fiber) is the dietary factor causing an increase in many chronic diseases, including obesity, T2DM, and cardiovascular disease, among others (43, 44).

In the Simpson/Mann study, patients with T2DM increased their daily carbohydrate intake from 34 to 61% of their calories for six weeks. The only positive measurable outcome was a reduction in HbA1c from 9.5% to 8.3%, indicating a modest effect of the higher-carbohydrate diet (see Figure 2 below). However, patients were still extremely poorly controlled, even though they were using powerful anti-diabetic medications (sulfonylureas). (Recall that the gold standard for a T2DM dietary intervention is an HbA1c of <6.5%, with a reduction in medication use, as achieved in the modern Virta Health studies (26, 27).)

In another study (45), any supposed benefits of the high-carbohydrate diet were lost, and HDL-cholesterol levels were significantly lower on the high-carbohydrate diet. But this would not deflect Mann from his lifelong carbophilia (40). Himsworth’s message (34–37) that patients can be divided into those who are either insulin-sensitive or insulin-insensitive is not something Mann has ever been able to incorporate into his personal belief systems. According to Mann’s worldview, carbohydrates are uniquely healthy for all humans.

From these studies, Reaven concluded a high-carbohydrate diet may not worsen glucose control in T2DM patients who are using medications. But he was not particularly confident that a high-carbohydrate diet would produce any long-term beneficial effects on glucose control or future health.

What he could not know at that time was that the levels of blood glucose control that Simpson and Mann considered acceptable in 1979 were merely the best that could be achieved with the medications then available for treating T2DM patients who were advised to eat high-carbohydrate diets. He did not then know that a diet very low in carbohydrate might lead to the reversal of T2DM in some (26, 27).

The diet Simpson and Mann studied was essentially vegetarian and high in fibre, with 42% of daily calories coming from wholemeal bread. Reaven’s bemused comment on this dietary choice was the following: “Although I can’t comment upon the practicality of this as a long-term diet in Oxford, I can raise the possibility that long-term compliance with this diet would be difficult to achieve in Palo Alto” (30, p. 411).

Indeed, Reaven’s group had already shown that increasing the dietary fibre content of a high-carbohydrate diet from 11 to 27 grams per 1,000 kcal did not influence any measure of glucose control, or blood cholesterol or triglyceride measures in persons with T2DM (46). And the second study from Mann’s group had essentially confirmed this (45), although the authors did their best to avoid this conclusion.

For the sake of completeness, it is important to include a brief comparison with another study of the vegetarian diet in T2DM and to compare these results with those of the truly low-carbohydrate (ketogenic) diet advocated by the Virta Health company (Figure 2).

Figure 2 compares changes in blood HbA1c concentrations in three studies: Simpson and Mann’s vegetarian diet (39); Neal Barnard et al.’s vegan diet (47); William Yancy et al.’s original low-carbohydrate ketogenic dietary intervention (48); and the low-carbohydrate ketogenic diet of the Virta Health company (26, 27).

insulin resistance

Figure 2: Glycated haemoglobin (HbA1c) concentrations in persons with T2DM following either a high carbohydrate vegetarian diet (39), a vegan diet (47), or a low-carbohydrate ketogenic diet (26, 27, 48) for periods of either six, 16, 56, 74, or 112 weeks. Only the low-carbohydrate diet reduced blood HbA1c values into the non-diabetic range (<6.5%). Redrawn from the original publications.

It is clear that of the three options, only the low-carbohydrate ketogenic diet is effective in producing a reversal or remission of T2DM. High-fibre vegetarian or vegan diets remain of unproven long-term value in the management of T2DM. In fact, on the basis of the evidence presented in these studies, they are essentially ineffective.

In concluding his review, Reaven asked a highly relevant question: “If diabetic control does not seem to change substantially in many patients on high carbohydrate diets, is there any reason to avoid the high carbohydrate approach as a method to decrease dietary fat in all patients with diabetes?” (p. 411). He then listed his three concerns.

First, he was concerned that many would interpret a high-carbohydrate diet as one allowing an increased intake of simple sugars.

Second, he was concerned about the effects of high-carbohydrate diets in diabetic patients who are either untreated or poorly controlled. Again, he was not to know (although he might have surmised) that the driver of such bad control is the high-carbohydrate intake itself. Yet, his point was correct.

His third concern was the problem of carbohydrate-sensitive hypertriglyceridemia (CSHT).

He referred to Albrink’s statement that hypertriglyceridemia is “the hyperlipidemia par excellence of the diabetic” (49) and continued:

On the other hand, one could argue that hypertriglyceridemia is not a primary risk factor for the development of coronary disease (50), so why worry. I would submit that this position may be too cavalier. In light of the increased incidence of both hypertriglyceridaemia and coronary artery disease in diabetics (17, 51-56), and the evidence from prospective studies that hypertriglyceridaemia may well be a risk factor (57-62), I would argue that considerable caution should be exercised before embracing a therapeutic programme that could accentuate this metabolic problem. (p. 412, my emphasis)

His solution was to call for more research before high-carbohydrate diets would be routinely prescribed for persons with diabetes. Since the evidence was not available, he wrote, “I don’t see how it is possible in its absence to advocate the routine use of high carbohydrate diets in all diabetics.” (p. 412)

Instead, he suggested patients should consume diets containing 15–20% protein, with the remainder (80–85%) divided equally (40–45%) between carbohydrate and fat. The carbohydrate, he advised, should be low in sugars, and the fat should be low in cholesterol and saturated fat.

In summary, he argued, “The kind and amount of carbohydrate and fat in the diabetic diet must be based upon sound experimental data. It is obvious that I have considerable doubts that this criterion has been met in the case of the use of high carbohydrate diets in the treatment of diabetes.” (p. 412)

Reaven’s advice had a long-lasting effect on dietary guidelines for persons with T2DM. Over the years, a low-carbohydrate diet has been defined as one containing 40% carbohydrate or less. Yet, the reality is that in the 1950s and ‘60s, the standard American diet contained 40% carbohydrate (63). As a result, a diet containing 40% carbohydrate could not have been labelled “low carbohydrate,” since it was the standard US diet right up to the 1970s.

Nowhere in this editorial does Reaven explain why he considered a 40%-carbohydrate diet a “low-” rather than “normal-carbohydrate” diet. His failure to study truly low-carbohydrate diets containing less than 40% carbohydrate had profound consequences for the health of the world.

For whatever reason, this blindness prevented him from asking a critical question: If increasing the carb content above 40% is shown to be detrimental for the reasons he described, what would happen if the dietary carbohydrate content was lowered to below 40%?

By failing to ask that question, he delayed the adoption of truly low-carbohydrate diets (<10%) for the treatment of T2DM by another 40 years. This failure also diminished his otherwise monumental contributions to medical science.


In 1988, the New England Journal of Medicine published a 28-day metabolic ward study comparing the effects of a high-carbohydrate (60%), low-fat (25%) diet and a high-fat (50%), low-carbohydrate (35%) diet on blood glucose control and cholesterol and triglyceride concentrations in 10 persons with T2DM treated with insulin (64). The study’s publication occasioned an invite to Reaven to publish an editorial (31) in the same journal.

The main finding of that study was that the low-carbohydrate diet was associated with reduced insulin requirements; lower mean plasma glucose, triglyceride, and VLDL-cholesterol concentrations; and higher HDL-cholesterol concentrations without any difference in either total or LDL-cholesterol concentrations. The authors concluded that the partial replacement of complex carbohydrates with monounsaturated fatty acids in the diets of persons with T2DM might improve glycemic control and blood lipid levels without increasing blood cholesterol concentrations.

Of course, the study that was really required was one in which there was complete replacement of all dietary carbohydrate with fat. But this was still one step too far. The closest these authors came was a “lowish” (40%) carbohydrate, “highish” (45%) fat diet compared to one in which carbohydrate content was 55% and fat 30% (14).

In his 1988 editorial, Reaven repeated many of the points raised in the previous editorial. He began by stating that an increased blood cholesterol concentration “does not appear to be characteristic of persons with T2DM (65, 66) and it has been difficult to define any relationship in such patients between an increase in plasma concentrations of LDL cholesterol and coronary artery disease” (31, p. 863).

He continued with his well-established argument that lowering blood triglyceride concentrations and raising blood HDL-cholesterol concentrations while improving blood glucose control would seem to be important goals in the management of T2DM. But his point was that this would not be achieved with a low-fat, high-carbohydrate diet since his studies (8, 9, 12) and others (64) showed high-carbohydrate diets produce exactly the opposite result: They worsen glucose control while increasing blood triglyceride and lowering HDL-cholesterol concentrations. Thus, he wrote, “It seems appropriate to question the routine use of such a diet in these patients on both theoretical and practical grounds.” (p. 863) 

Once more, he concluded that high-carbohydrate, low-fat diets continue to be prescribed to persons with T2DM because clinicians fail to question whether elevated blood triglyceride concentrations signify increased risk of coronary heart disease.

In contrast, his position was that without definitive evidence that raised blood triglyceride concentrations are not harmful, “physicians should be aware of the potential untoward effects of a low-fat, high-carbohydrate diet in patients with T2DM and realise that there are alternative methods of lowering the intake of saturated fat.” (p. 864). He continued, “If patients are advised to follow a low-fat, high-carbohydrate diet, they must be monitored to see whether this diet leads to metabolic changes that could increase or decrease the risk of coronary artery disease.” (p. 864)

In summary, by 1988, Reaven was certain a diet that impaired blood glucose control and raised blood triglyceride concentrations while lowering HDL-cholesterol concentrations was far from ideal for patients with either insulin resistance or T2DM. The clear evidence then was that diets containing more than 35% carbohydrate produced these undesirable effects. But no one had yet considered it important to study the effects of diets with much lower carbohydrate contents of the kind promoted by Blake Donaldson, Alfred Pennington, John Yudkin, and Atkins (25).

Reaven’s plea that physicians who prescribed high-carbohydrate, low-fat diets to patients with T2DM should monitor their patients for “untoward effects” was ignored then, as remains the case today.

Instead, the American Diabetes Association (ADA) continued to prescribe high-carbohydrate diets with the focus on controlling blood cholesterol concentrations while ignoring blood triglyceride concentrations because they were still considered essentially irrelevant (67).

Thus, the ADA’s 1970 guidelines for diabetics stated, “There no longer appears to be any need to restrict disproportionately the intake of carbohydrate … Diabetic patients appear to respond to reduction of saturated fat with a lowering of circulating cholesterol, as do non-diabetic persons.” (67, p. 394)

The 1976 guidelines emphasize “low cholesterol and high polyunsaturated fat choices” (p. 396), while the 1979 guidelines state, “The percentage of carbohydrate in the diet should be 50–60%” (p. 397). The most recent guidelines continue along the same lines. Yet, even in 2019, as SJ Hallberg et al. note, the “ADA guidelines recommended eating patterns fall short of rigorous standards of scientific review according to state-of-the-art systematic review and guideline creation practices.” (68, p. 1769)

So, at the time, Reaven was clearly fighting against a medical mainstream that chose to ignore – and continues to ignore – the long-term health consequences of carbohydrate-sensitive hypertriglyceridemia.


When he published his popular book over a decade later in 2001 (32), Reaven still considered it necessary to stress that “coronary heart disease risk factors in normotensive, non-diabetic individuals include more than a high LDL cholesterol concentration. (p. 50) 

“It became apparent,” he explained, “that you could have a heart attack even if your LDL cholesterol was within the normal range.” (p. 50) He then continued: “We’ve long been puzzled by the fact that many heart attack victims do not have elevated LDL cholesterol concentrations, even though it is a major risk factor.” (The meaning here is not quite clear. Either cholesterol is a risk factor present in all patients or it is not. It seems to me you cannot have it both ways.)

As a result, Reaven also had some strong words about the dietary advice that was being offered to those with the condition he discovered, Syndrome X (also now known as Reaven’s syndrome) (69). Thus, he presented the following points:

  1. “But looking at the world through cholesterol-colored glasses can prevent you from seeing other potential dangers to heart health, such as risk factors associated with Syndrome X. You can have a healthy LDL cholesterol and still be hit with a heart attack induced by the syndrome.” (p. 65)
  2. “This means that, for tens of millions of people, cholesterol is not the underlying problem leading to heart disease. And that’s why, if you have Syndrome X, simply lowering your total cholesterol or LDL ‘bad’ cholesterol is not enough to shield you from a heart attack.” (p. 17, my emphasis)
  3. “Even stranger, to most people, is the idea that one way to guard against Syndrome X is to ignore the ‘best’ medical advice, to shun the low-fat, high-carbohydrate diet everyone ‘knows’ is good for the heart. If you have Syndrome X – and 60–75 million Americans do – that ‘good’ diet can be deadly. If you have the syndrome, carefully dieting to lower your total cholesterol or LDL cholesterol won’t solve the problem. In fact, conscientiously doing so may make a heart attack even more likely.” (p. 17–18)
  4. “[T]he Syndrome X culprit isn’t red meat or butter, it’s carbohydrates.” (p. 18)
  5. “Insulin resistance is at the heart of Syndrome X. That’s why simply lowering total cholesterol or LDL ‘bad cholesterol’ won’t solve the problem. And that’s why the low-fat high-carbohydrate diet so highly recommended by most physicians and health organisations is so dangerous for those with this disorder. Remember, carbohydrates become glucose, and glucose must be herded into certain cells. That result requires insulin. More carbohydrate equals more glucose equals more insulin. That’s the formula for disaster for those with this ‘unknown’ syndrome.” (p. 19–20, my emphasis)
  6. “The more carbohydrate an insulin-resistant person eats, the more insulin the pancreas must secrete to prevent the blood glucose from climbing too high. The higher the blood insulin levels, the greater the production of VLDL (triglyceride), and the more the (blood) triglyceride will rise.” (p. 49)
  7. “In other words, the more insulin resistant one was, the greater the negative impact of a high-carbohydrate diet.” (p. 50)
  8. “Elevated total cholesterol, which many people are concerned about, doesn’t even appear on the Syndrome X risk factor list.” (p. 65)

Given Reaven’s understanding that “the more carbohydrate the insulin-resistant person eats,” the worse would be his or her features of Syndrome X, it seems obvious that he would have to conclude that the best treatment for this condition would be a diet restricted to as little carbohydrate as possible. In other words, the Stefansson-Donaldson-Pennington-Atkins diet Atkins was then promoting in New York. A no- or very low-carbohydrate diet would produce the lowest blood insulin concentrations. Therefore, according to Reaven’s logic, such a diet would be the most effective. But Reaven would never risk venturing down that path.

Although he personally believed Syndrome X, caused by eating too much carbohydrate in those with insulin resistance, is the commonest trigger of coronary heart disease, he could never completely divorce himself from the other, more popular explanation: the conventional Ancel Keys lipid hypothesis that eating “artery-clogging saturated fat loaded with cholesterol” causes coronary heart disease.

His fear became that a diet very low in carbohydrate would be too high in fat, including saturated fat, and would elevate artery-clogging blood cholesterol concentrations (which he had repeatedly said are not the cause of arterial disease in those with Syndrome X). This was simply too great a personal or professional risk for him to consider, so he chose to sit squarely on the dietary fence, a ‘revolutionary’ unprepared to go for broke. Thus, he dismissed Atkins’ low-carbohydrate diet as harmful:

The Atkins diet … is based on the idea that carbohydrates are bad but everything else is terrific. Bring on the steak, eggs, cheese and butter, says Dr Atkins. Hold the bread or anything else with carbohydrate. With only 40% of its calories from carbohydrate and protein combined, the Dr Atkins Diet can actually be an effective treatment for Syndrome X. After all, 60 percent of its calories comes from fat, which does not stimulate insulin secretion. If the 60 percent fat calories were low in saturated fat, and if the diet were nutritionally balanced, it would work well for Syndrome Xers. No such luck. The Atkins Diet sample menus and recipes contain roughly 25 percent artery-clogging saturated fat and are loaded with cholesterol. (p. 76, my emphasis)

The result was that Reaven ended up providing dietary advice that was less than ideal for the optimum management of Syndrome X and IR. His “low-carbohydrate” diet provided 45% of energy from carbohydrate, 40% from fat, and 15% from protein. The consequence was that his work fell short of a Nobel Prize-winning finding: that a properly structured LCHF diet can – simply, effectively, and cheaply – prevent and reverse all the medical conditions caused by IR (26, 27). Instead, the fat content of his Syndrome X diet was far too low and its carbohydrate content far too high to effectively treat those with insulin resistance.

Yet, he understood that even this diet was sufficiently radical to become extremely unpopular with the diet dictators:

But it’s a controversial approach, flying in the face of accepted wisdom offered by venerable health institutions such as the American Heart Association, the American Diabetes Association and the National Cholesterol Education programme. These and other groups insist that low-fat diets are best for everyone but they aren’t! 

Don’t let that shake your resolve. Most well-meaning physicians, dietitians and organisations are simply unaware of Syndrome X and its ramifications. Their dietary advice doesn’t take the syndrome into account. The advice to all Americans to replace fat with carbohydrate is fine for many of us, but if you have Syndrome X too much carbohydrate can lead to trouble. (p. 69–70)

I suspect Reaven knew what would happen if he came out in full support of a high-fat, low-carbohydrate diet for the treatment of Syndrome X. He knew Professor Yudkin was at that time the only other scientist brave enough to have challenged Keys and the diet-heart hypothesis. He also knew Yudkin’s now iconic book, Pure, White and Deadly (44), for the first time exposed the dangers of sugar while at the same time attacking Keys’ lipid hypothesis. In the book, he proposed sugar, not fat, caused arterial disease (70–73), and thus, Yudkin had fallen afoul of his profession … and the sugar industry.

Those controlling the British scientific community simply destroyed Yudkin’s academic career. As Ian Leslie has written:

The book did well, but Yudkin paid a high price for it. Prominent nutritionists combined with the food industry to destroy his reputation, and his career never recovered. … He found himself uninvited from international conferences on nutrition. Research journals refused his papers. He was talked about by fellow scientists as an eccentric, a lone obsessive. Eventually, he became a scare story… . “They took him down so severely – so severely – that nobody wanted to attempt it on their own” … . He died, in 1995, a disappointed, largely forgotten man. (74)

During his work at the Stanford Medical School, Reaven was in close daily contact with some of the most influential physicians and cardiologists in the US and perhaps the world. They would not have taken kindly to their colleague’s suggestion that, to prevent heart attacks, they should prescribe a high-fat, low-carbohydrate diet rather than the low-fat diet dictated, then as now, by the US Dietary Guidelines for Americans (USDGA), the American Heart Association (AHA), and the American Diabetes Association (ADA).

Reaven’s solution, it seems to me, was to come up with a convenient compromise, a dualistic explanation for the mechanisms causing heart disease, one that incorporated his belief in the key roles of insulin resistance and Syndrome X but that did not alienate his colleagues in the mainstream by completely excluding the traditional Keys diet-heart and lipid hypotheses.

So he argued cholesterol was only a risk factor for heart disease if one did not have Syndrome X. If one did not have Syndrome X, then one should eat the higher-carbohydrate, very low-fat diet promoted by the USDGA, the AHA, and the ADA. But in the presence of Syndrome X, triglycerides and not cholesterol became the key factor driving ill health, so one would need to ‘risk’ eating more fat and less carbohydrate.

And that is Reaven’s Syndrome X Diet™.

As he described: “Imagine a diet that’s thoroughly enjoyable and easy to follow, lowers both elevated insulin and high LDL cholesterol levels, and can be used for either weight loss or maintenance. There is such a diet: the Syndrome X Diet™.”

He continued:

The key to this diet is the ratio of protein, fat and carbohydrate (15:40:45) and the kind of fat that’s consumed (mostly unsaturated) … . The two-step rationale behind this clinically tested approach is amazingly simple. First, insulin levels do not increase when you eat fat. Whether saturated or unsaturated, fat has no effect on insulin levels. Eat more, eat less (fat), your insulin levels won’t budge. However, if you substitute fat for carbohydrate, your insulin levels will fall. This means that, to a certain degree, more fat is good for those with Syndrome X. But not any fat will do, and that brings us to the second point: unsaturated fats don’t raise LDL cholesterol levels. Substituting saturated fat for carbohydrate, bite for bite, will keep your insulin under control but will elevate your ‘bad’ LDL cholesterol. That’s dangerous, whether you have Syndrome X or not. And that’s why this diet carefully replaces carbohydrates with unsaturated fats. These ‘good’ fats keep insulin and LDL under control, which means that this approach guards against the ‘new’ kind of heart disease caused by Syndrome X as well as the ‘old’ kind associated with elevated LDL. You win both ways.

Most Americans are already eating something very close to the Syndrome X Diet’s proportion of protein, fat and carbohydrate. It’s simply a matter of adjusting the fat intake, plus replacing some carbohydrates and most of the saturated fat with ‘good’ fats. (p. 73–74)


Unfortunately, in coming up with the Syndrome X™ Diet, Reaven failed to exercise his scientific mind as shrewdly as he might have.

First, the Syndrome X™ Diet was not rigorously clinically tested by Reaven or anyone else. The sole relevant study conducted by Reaven’s group was performed in 1994 (15) and based on a similar study published two years earlier (14). Yet, both studies only compared a (relatively high-carbohydrate) Syndrome X™ Diet with even higher-carbohydrate diets more compatible with the USDGA, AHA, and ADA recommendations. And both studies evaluated the effects of the diet on just four of the nine risk factors of Syndrome X identified by Reaven.

The nine Syndrome X risk factors listed by Reaven (32, p. 22, 43–45) are:

  1. Impaired glucose tolerance
  2. High insulin levels (hyperinsulinemia)
  3. Elevated triglycerides (hypertriglyceridemia)
  4. Low HDL ‘good’ cholesterol
  5. Slow clearance of fat from the blood (exaggerated postprandial lipemia)
  6. Smaller, more dense LDL ‘bad’ cholesterol particles
  7. Increased propensity of the blood to form clots (hyperfibrinogenemia)
  8. Decreased ability to dissolve blood clots due to elevated blood plasminogen activator inhibitor-1 (PAI-1) levels (hyperPAI-1emia)
  9. Elevated blood pressure (hypertension)

Yet, Reaven failed to evaluate the effects of the Syndrome X™ Diet on all nine factors, at best covering just four of these risk factors – factors 1, 2, 3, and 4 – so he could never claim his diet had been exhaustively tested.

Next, he only ever tested diets with a small range of carbohydrate contents. Critically, he failed to test a truly low-carbohydrate diet of the kind developed by the Stefansson-Donaldson-Pennington-Atkins experience.

This is particularly surprising since he understood better than anyone the carbohydrate effect: “Remember, carbohydrates become glucose, and glucose must be herded into certain cells. That result requires insulin. More carbohydrate equals more glucose equals more insulin. That’s the formula for disaster for those with this ‘unknown’ syndrome.” (32, p. 19–20)

And: “The more carbohydrate an insulin-resistant person eats, the more insulin the pancreas must secrete to prevent the blood glucose from climbing too high. The higher the blood insulin levels, the greater the production of VLDL (triglyceride), and the more the (blood) triglyceride will rise.” (32, p. 49)

Given this understanding that he, better than anyone else in the world, truly grasped, Reaven was uniquely positioned to ask and study the critical question: But what if we lower insulin secretion to an absolute minimum by having those with Syndrome X eat a high-fat, extremely low-carbohydrate diet?

Additionally, although he followed the party line by writing about the dangers of “artery-clogging saturated fats”, his writings do not give the impression that as someone interested in hard scientific evidence, he truly believed it. Why else would he write that there is “no evidence that restriction of dietary fat will impede the development of atherosclerosis in patients with diabetes” (30, p. 409)? If he truly believed the party line – the lipid and diet-heart hypotheses – why did he ever feel it necessary to write this in a major editorial in 1980?

And finally, and most importantly, why did he not take more notice of what Kuo had shown in 1967; evidence that effectively destroys the diet-heart and lipid hypotheses:

[Of] the majority of patients with atherosclerosis in this series … more than 90% were found to have carbohydrate-sensitive hyper(tri)glyceridemia with or without hypercholesterolemia. Thus, it is reasonable to assume that with proper dietary preparation and appropriate laboratory studies, a high incidence of carbohydrate-sensitive hyperglyceridemia could be demonstrated in persons with atherosclerosis. (22, p. 92)

The point is that if 90% of patients with atherosclerosis have Syndrome X, then Reaven should have focused on a diet that would minimise insulin secretion, the hormone he believed is the key driver of his syndrome (29, 69, 75), not on worrying about the unproven effects of a higher-fat diet in those with mildly elevated blood cholesterol concentrations.


In his utterly brilliant academic career (homage to which I will pay at great length in future columns), Reaven made one crucial error. He failed to follow up Kuo’s seminal observation that the majority of patients with atherosclerosis exhibit carbohydrate-sensitive hypertriglyceridemia (CSHT) (22), the key abnormality Reaven would later include as the foundational abnormality when he described his very own medical condition, Syndrome X.

And he should have but unfortunately failed to discover that the proper treatment of Syndrome X is a very low-carbohydrate diet of the kind Stefansson, Donaldson, Pennington, and Atkins had developed on the East Coast of the US between 1920 and 1970.

So, instead of backing to the hilt his theory that insulin resistance acting through CSHT is the most prevalent cause of atherosclerosis, he prevaricated and acted as if it was a less common cause that elevated blood cholesterol concentrations because of a diet full of “artery-clogging fats”.

The result is he fell between two stools – the Syndrome X™ Diet he promoted was really no different from what would become the AHA diet – the diet that since its global adoption has caused the rates of obesity and T2DM (and ultimately the arterial disease caused by T2DM) to soar in the US and around the world. Instead of preventing arterial disease, the Syndrome X™ Diet has produced a massive increase in arterial disease.

In the next column, I discuss how one of the very first victims of this false approach to dietary intervention was US President Dwight D Eisenhower, who suffered a heart attack while in office in 1955. He was one of the very first subjects placed on Keys’ low-fat, ‘heart-healthy’ diet, the diet that was as experimental in 1955 as it still is today, 64 years later.


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