Low Carb Against the World

Pete Ahrens was objecting already in 1957: "When unproved hypotheses are enthusiastically proclaimed as facts, it is timely to reflect on the possibility that other explanations can be given for the phenomena observed."

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Ahren's own research had opened up another line of inquiry, suggesting that the carbohydrates found in cereals, grains, flour, and sugar might be contributing directly to if not actually causing obesity and disease. And he correctly predicted that a fat-reduced diet would only increase our consumption of these foods. 

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The highly controlled liquid-formula feeding experiments that he conducted from 1951 to 1964 consistently revealed that these trigylcerides shot up w henever carbohydrates replaced fat in the diet. A majority of patients showed the clouding because of a "normal chemical process which occurs in all people on high carbohydrate diets," Ahrens wrote.

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“But let’s talk about Pete Ahrens,” he volunteered. “Pete Ahrens! He was always a big roadblock on everything! I used to have vigorous discussions with Pete.”

Mockingly, Stamler proceeded to channel Ahrens: “No, We’re researching this, give us another five years. We have to do balanced studies. We have to figure it out. We don’t know.”

“He always opposed any statement. I would say, ‘Pete, what you’re saying is that the present American diet is the best diet you can conceive of for the health of the American people.’ ‘No! No!’ ‘But Pete, please, the logic!’ Anyway, he’s dead and gone now.”

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Listening to Stamler talk, I could almost picture his spear. “And Yudkin!” Stamler nearly bellowed to me, referring to the British doctor who promoted the rival sugar hypothesis. “I was part of shooting him down!” And of Michael Oliver, a prominent British cardiologist and critic of the diet-heart hypothesis, Stamler repeatedly said that he was a “scoundrel.”

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Nina Teicholz - The Big Fat Surprise - Page 59, Page 60

In 1958 William Daughaday commented on behalf of the American Dietetic Association that ‘uncertainty exists in the minds of many physicians today concerning the therapeutic role of diet in diabetes’. He could find only three arguments to support its role: first, that it is a valuable educational procedure leading to optimal nutrition; second, that it can avoid the need for insulin; and third, that properly spaced food intake can reduce the risk of hypoglycaemia. Glucose control and prevention of vascular disease are notably absent from this list of benefits. He proposed that carbohydrate should provide no more than 40% of total calories, avoided discussion of free diet, and dismissed the high carbohydrate regimen with the comment that carbohydrate restriction is an essential feature of the diabetic diet [28].

https://link.springer.com/article/10.1007/s00125-008-1203-9

Before the discovery of insulin, the primary controversy in diabetes was what kind of reductive diet to use—rice diet, rancid fat diet, vegetables “cooked three times in their own water,” and so forth. All were restrictive and essentially treated diabetes by starvation. For type 2 diabetes, they probably worked out, in that they no doubt led to weight loss. (Perhaps we should try some of these again.)

With the advent of insulin, the problem of diabetes was thought to be solved, and indeed, those with type 1 diabetes did just fine, for a while. It didn’t take long, however, for those now living longer to begin to develop vascular and neurological complications. And thus began a new round of controversy.

This controversy, which began in the 1930s, raged on for the next 60 years and was often very heated. The issue, simply put, was whether the vascular and neurological problems associated with diabetes were a genetic concomitant of the disease (and thus inevitable and unalterable) or instead were associated with the metabolic abnormalities of diabetes, such as high blood glucose levels (and thus preventable). Which side one took on this issue had great ramifications regarding the method of diabetes management one’s practice adopted.

A classic debate on this topic took place in New York in the 1940s between Dr. Elliott Joslin and Dr. Edward Tolstoi. The debate, which was recorded and is available at the New York Hospital, Cornell University School of Medicine, was reenacted a few years ago.

In the late 1930s, Dr. Robert L. Jackson, then a pediatrician at the University of Iowa School of Medicine, joined the debate. Dr. Jackson, supported by his wife, who was a nutritionist, questioned why the diets of children with diabetes were restricted in carbohydrate and calorie content. He observed that, with such restriction, children were not growing well. The diet of restricted calorie and carbohydrate contained a high fat content so that smaller or fewer doses of insulin would be required. (Only regular insulin was available then.)

Dr. Jackson began to experiment with a regular meal plan (he did not care for the word “diet”) and four injections/day of regular insulin and found that his method could control blood glucose levels in children while still allowing them to grow. He had the foresight to also document the effects of his method on the health of organs usually damaged by diabetes (eye and kidney). And, in the 1950s, he published landmark research1,2 documenting the prevention of retinopathy in children with well-controlled diabetes. Unfortunately, Dr. Jackson’s data were not well received. This was in part because there was not a good method of measuring glucose control at the time, but primarily because both patients and doctors recognized how hard it was to achieve glucose control.

Longer-acting insulins (protamine zinc insulin, globin, NPH, and the lente series) were becoming available in the ’40s and ’50s, and physicians trying to be nice to patients were prescribing one dose of insulin per day. Their reasoning was that if control didn’t make any difference anyway, why try to achieve it with numerous daily injections? This method of diabetes control was easier for patients and physicians alike, so it was easy to develop this mindset. Specialists were not needed, and anyone could do it, they said. Physicians with this mindset tended to demand strict scientific evidence that control mattered, while accepting data to the contrary without rigorous scientific scrutiny.

I entered the fray in 1964 when I began training with Dr. Jackson at the University of Missouri. It was about this time that an article was published on muscle biopsy specimens and measurement of basement membrane thickness (BMT) of capillaries.3 The article concluded that control of blood glucose made no difference because thickening had occurred even in those who had not yet developed full-blown diabetes. This solidified the position of the loose-control advocates and made the position of the tight-control advocates very difficult. Nonetheless, Dr. Jackson and I and others stuck to our guns and continued to advocate physiological control, but proof was clearly needed.

Thus began our involvement in Dr. Charles Kilo’s and Dr. J.R. Williamson’s research on BMT.4 We published an article showing conclusively that tight control would not only prevent BMT, but also reverse it when poor control was improved.5 We also published an article on prevention of retinopathy.6

Dr. Jackson retired in 1972, and his mantle fell to me as a spokesman for the physiological method of tight control. I participated in many debates throughout the country, often against multiple opponents, to advocate for better control. These debates certainly raised emotions, but, confident in our position, we persisted for the sake of the children.

The debate was finally put to rest by the Diabetes Control and Complications Trial (DCCT) results in 1993.7 But the underlying problem remained.

In 1996, I participated in a debate with one of the principle investigators of the DCCT, who conceded that I had been right that the course of vascular disease was related to the degree of control of the metabolic abnormalities but claimed that the degree of control necessary simply couldn’t be achieved. Tight control, he said, was too imposing on patients (more so than blindness or amputation?, I wondered), too labor intensive, and too costly.

There was also a respected fear of hypoglycemia, which was a concern, especially in children. However, we were finding that we had less difficulty with hypoglycemia when the methods we used brought about normal blood glucose levels more of the time.

Tools eventually became available to answer all of these arguments. Self-monitoring of blood glucose, hemoglobin A1c measurement, and insulin analogs have solved many problems. But still, in 2003, a decade after the DCCT, physiological control still is not universally accepted.

Today, the controversies are centered not so much on “why” as on “how.” Debates about how to get the most physiological management include:

• What kind of meal plan should we use—carbohydrate counting? Low-carbohydrate, high-protein diet? Calorie counting? Exchange lists?

• How should we monitor blood glucose levels—fasting and postprandial glucose measurements, or pre-meal and bedtime measurements?

• On what should we base our insulin adjustments—sliding scales, algorithms, or patterns?

Through the current debates, I remain an advocate of physiological diabetes management, as follows:

• A good, healthy, well-balanced meal plan

• Monitoring at fasting and 2 hours after meals

• Pattern control

• Either four doses per day of insulin using the bolus-basal concept, with lispro or aspart for bolus insulin and glargine for basal insulin, or bolus insulin injections with basal insulin administered with an insulin pump

I have been at this now for 40 years, and I will continue to insist that the closer to nature we can become in our management, i.e., the closer we can restore people with diabetes to physiological normalcy, the better off our patients will be.

We need to continue our research to find better ways to mimic nature and test all methodology, to look at the data critically, and to base management on scientific data outcomes. Why must we do this? Not simply to settle arguments and debates, but instead because the quality and length of the lives of our patients depend on it.

We must always look beyond the horizon to see how we can improve the quality of life for those we serve. If we always keep their welfare in mind, then there are no losers of debates, only winners—our patients.

Retinal studies were done in 181 postpubescent, insulin-dependent diabetic patients who developed diabetes before the age of 20. Retinal studies included serial direct ophthalmoscopic examinations, stereoscopic fundus photography and fluorescein angiography. At the time of retinal studies, muscle biopsies also were done to measure capillary basement membrane thickness (CBMT) as an index of early microvascular changes in skeletal muscles. Assessment of clinical metabolic control, interpretation of retinal findings, and CBMT were done independently. No retinopathy was detected in patients observed continuously and known to have been in higher degrees of metabolic control. Twenty-five patients in lower degrees of control for extended periods had retinopathy. CBMT was found to be labile and to progress or regress within a year depending on the degree of control. All patients in lower degrees of control with retinopathy had increased CBMT, but if they subsequently attained and maintained a high degree of control for a year, then CBMT diminished and there was no progression of retinopathy. Our study demonstrates that a high degree of metabolic control delays, and may prevent, microvascular changes, and confirms other studies indicating that most postpubescent, insulin-dependent diabetic patients will develop retinopathy within 15 years unless a relatively high degree of control is maintained.