Pre-Insulin treatment of diabetes: the non-pharmaceutical approach

My first introduction to diabetes specialist Richard K. Bernstein was from a YouTube video in which he debates registered dietician Hope Warshaw.  Bernstein handily puts Ms. Warshaw in her place. It is no injustice to Warshaw to characterize her approach to diabetes treatment as a pharmaceutical approach: “The vast majority of people with diabetes need medication.” But Bernstein says, “Large doses of insulin don’t work in a predictable fashion.” Bernstein’s solution is to greatly limit the intake of carbohydrate and protein, and to permit the patient to eat fat to make up any calorie deficit. This is quite clearly because protein and carbohydrate require an insulin response. But as he explains in his book, Diabetes Solution, the absorption rate of doses of insulin above 7 cc is unpredictable, and therefore it is necessary to keep numbers low: small amounts predictable quantities of protein and carbohydrate accompanied by small doses of insulin will help type 1 diabetics (and type 2 diabetics needing insulin) to maintain glucose control. In this manner, a type 1 diabetic has the best ability to eliminate diabetic complications and to live out a full and healthy life. Thus, Bernstein recommends that both type 1 and type 2 diabetics eat no more than 30 gm of carbohydrate, and also only enough protein in the diet to provide satiation.

Thus, Bernstein’s approach puts nutrition on equal footing with pharma–indeed, a higher footing in the case of type 2 diabetics and “prediabetics”  who can often control their diabetes through diet alone.

Now Bernstein’s approach is fully integrative of the old and the new.  It is entirely reductionist to believe as Warshaw that a pharmaceutical approach will make it possible for diabetics to eat what she calls healthy carbohydrates, e.g., fruit and whole grains.  While diabetics may “deserve” to be able to eat such things, before insulin, treatments of diabetes recognized the toxic nature of carbohydrate and protein in the diet, and therefore, placed very strict limits on the quantity of each.

In the pre-insulin study, The Starvation Treatment of Diabetes (1915), Massachusett’s General Hospital physicians, Hill and Eckman, explain their treatment of both adult (type 2) and juvenile (type 1) diabetes. The therapy consisted of starving diabetic patients on a strict diet of coffee and whiskey until they  stopped peeing sugar. At that point, they would gradually introduce extremely limited carbohydrate and protein into the diet of their patients until once again they urinated glucose, at which point they would once again cut back protein and carbohydrate from their diet to the point that sugar no longer appeared in the urine tests. The bulk of the calories which the patients would need for their daily energy requirements would come from fat. The whiskey therapy is a curiosity, but we can now scientifically verify its usefulness: the liver busily converts the alcohol to usable form, thus reducing concomitantly the liver’s production of glucose from protein (gluconeogenisis). Now, when the patients left the hospital, their dietary profile might look something like:  “Carbohydrate, 20 grams. Protein, 40 grams. Fat, 200 grams.”  This equals 80 calories from carbohydrate, 160 calories from protein, and 1800 calories from fat for a total, 2040 calories: certainly enough to live on. These numbers are similar to those in Bernstein’s Diabetes Solution.  Only today, we can also add drug therapy to greater enhance glucose control.

In 1922, 14-year old Leonard Thompson, was the first patient to receive insulin to treat his diabetes. This was an unquestionable breakthrough in diabetes treatment, and insulin treatment is undoubtedly, along with antibiotics for the treatment of infectious diseases, what has greatly established the reputation of the medical profession today. Child patients, who would otherwise die within a brief time, could now live into adulthood, and even carry out a normal life, almost. A devastating consequence of this breakthrough is the vast ignorance of the dieticians regarding the toxic effect of carbohydrate in the diet of diabetics.  As Warshaw suggests, just take insulin, and you can eat the food you deserve.  This approach has led diabetics to suffer decades of diabetic complications and death, because of still uncontrolled blood sugars.  Bernstein, in his own testimony (in Diabetes Solution), said that he developed his method in order to eliminate the multitude of diabetic complications from which he suffered, and his method has been very successful.

How great has the supplanting of the dietary approach been?  In her Diabetic Cookery (1917), Dr. Ruth Oppenheimer lists baking ingredients that even the internet knows not from what they are made: Casoid flour and Aleuronat flour. She writes regarding the former:

Casoid takes the first rank as a flour for diabetics, and therefore a special chapter is devoted to its use in the preparation of Bread, Muffins, Desserts, etc. Casoid, to a great extent, has solved the problem which confronts the cook as to a substitute for wheat bread, and, as a diabetic naturally craves bread, the substitute must come as near to the real article as possible.

Oppenheimer also employed ground almond, which is the most common substitution for wheat in today’s Wheat Belly cookbooks, and she claims that Casoid flour is better. So why would Casoid and Aleuronat flour have disappeared from our usage and knowledge? My guess is that apparently no one still saw the need for the best substitutions for wheat flour, because diabetics could, as of 1922, eat standard bread and shoot themselves with insulin. They weren’t going to die right away. But eventually, with such an approach, their unregulated blood sugar levels would cause them to die either of a diabetic coma from fatally low blood sugar or too high regular blood sugar which leads to such complications as retinopathy, kidney disease, peripheral neuropathy, cancer, heart disease and Alzheimer’s disease, to name a few. Clearly, an integrative approach, which implements the strict dietary approach of the pre-insulin treatment and judicious usage of insulin and other drug therapies, is superior. Hats off to Dr. Bernstein!

Which one of these two guys should take statins? Or, Is high LDL really a danger for those on a low-carb high-fat diet?

When I realized that I had multiple symptoms of diabetes, I started to follow Richard K. Bernstein’s Diabetes Solution and have attempted to control my blood sugar through an ultra-low carbohydrate, high fat diet.  I eat two eggs scrambled in two tablespoons of saturated fat, steak or bacon and sausage for breakfast, Korean soup with meat, kim chee and eggs for lunch, an avocado mixed with other salad and meat for supper, often with another low-carb vegetable.  For snacks I’ll have sugar-free cheese cake or sugar-free crust-less pumpkin pie, topped with copious amounts of whip cream and a few berries (~tablespoon) or a few nuts, boiled eggs with mayonnaise and salt, pepperoni, or other sausage.  I avoid all sugars, all grains (including rice) and all vegetables high in carbs (no potatoes, carrots or legumes).  I suppose my total carb count is between 30 and 50 gm per day and I assume that I am in a consistent state of ketosis.

My low carb high fat diet has begun to heal me.  I experience much less peripheral neuropathy, my arthritis has largely disappeared, my diabetic dermopathy is gone, and I have lost a lot of weight.  Here are the before and after pictures.

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Before December 2012

slimmer me

Today, after ten months of high fat low carb diet

Yet my doctor wanted to put me on statins because my cholesterol is very high, in her view, and needs to be brought down because I am at 10% risk of having a heart attack in the next ten years.

So here are the before and after numbers of my blood test: first number is ten months ago (American conversion in parentheses), and the second number (after the slash) my most recent test (two weeks ago):

  1. Total Cholesterol: 6.3 (243) / 9.21 (356)
  2. HDL Cholesterol:  1.0 (39) / 1.3 (50)
  3. Triglycerides: 2.34 (207) / 1.37 (121)
  4. LDL (calculated): 4.24 (164) / 7.29 (282)
  5. HBA1C: 6% / 5.5%

Here are some other markers not on the blood tests:

  1. Weight in pounds: 260 / 210
  2. Waist measurement in inches:  44″ / 36.5″
  3. Average blood sugar during previous three months (calculated from hbA1C):  7.7  (136) / 6.6 (118)
  4. Snoring has lessened both in frequency and decibels.
  5. No significant loss of lean mass.
  6. Blood pressure is now in the optimal range instead of borderline hypertension (without drugs).

My diet is healing me without the help of drugs.  The only marker that has worsened, at least in the eyes of the medical community, is LDL. Yet now my physician wants to put me on statins.  However, I refuse to go on statins, especially now that I’ve done a bit of research.  As for the blood work, the triglycerides are down 40% and the HDL is up 30%.  My HBA1C has improved, but it is still too high in my opinion, and this is likely because my liver over produces glucose (gluconeogensis), especially in the morning (dawn phenomenon), and so my metabolic disorder continues despite my strict diet.  Yet my family doctor is ill-equipped to help me with this particular marker, a true sign of metabolic syndrome and diabetes, and is only concerned to lower my LDL.  Having done a week’s worth of reading, several important facts have become clear to me:

  1. Elevated LDL is a marker only–it is not a disease.
  2. High Cholesterol or high LDL have no correlation with artery disease.
  3. High Cholesterol or high LDL are not proven causes of artery disease.
  4. The link between metabolic syndrome/diabetes and heart disease is far clearer and more convincing than any alleged link between cholesterol and heart disease.
  5. No one can answer the question of whether a person that has adopted a low carbohydrate lifestyle but has high LDL is really at risk.  No such long term study has ever been done.
  6. A person with low triglycerides but high LDL is more likely to fall into the “Pattern A”  than the “Pattern B” cholesterol.  My alleged VLDL (very low density lipids) has dropped from 41.4 to 24.2, suggesting that I am shifting from Pattern B to Pattern A.

Is my doctor not guilty of straining a gnat and swallowing a camel?  She had little concern about the true risk factors for heart disease (camel):  high HBA1C, low HDL, high triglycerides, and visceral obesity (fat around the waist); but she was ready to kill the gnat, high LDL.  While she had the results of my earlier test, she manifested not the slightest approval in my improved numbers and was anxious only about my higher LDL; and she was more worried about me than the physician who went through the numbers with me ten months earlier.  The medical profession seems to have disordered priorities.  This is clear from a look at heart risk calculator that she used. Risks factored into the equation are as follows:

  1. Age
  2. Male or female
  3. Low HDL-C
  4. Total Cholesterol
  5. Systolic blood pressure
  6. Diabetes
  7. Smoker

According to her risk assessment, I have a 18.4% chance of cardiovascular disease in the next ten years.  Using the same assessment criteria, my earlier self (see “before” picture)  had a 15.6% risk.  My loss of 50 lbs around my fat belly counts for nothing; my lower triglycerides and lower HBA1C (because I’m not “diabetic”) count for nothing.  Yet which guy in the above pictures do you think has the more likely chance of a heart attack?

Now I am mostly happy with the results of the latest tests and I am very happy with the improved state of my health.  Here are my three options going forward:

  1. Take statins to reduce my LDL.
  2. Reduce my consumption of saturated fat to reduce the LDL.  Why?  My current diet is healing me.
  3. Continue as before trying to fine tune my blood sugar issues and shoot for an HBA1C of 5.0%, Triglycerides of 100, and HDL of above 60.  Reject my doctor’s anxiety about LDL, her dietery advice and her recommendation of statins.

I found the blog of Dr. Rakesh Patel in Arizona who himself decided to low carb using the Carbnite Solution (CNS) and was feeling much better after four months, but his LDL-P had skyrocketed.  What to do?  He decided to actually test himself for artery disease, because he believed that metabolic syndrome, not high cholesterol, was its likely cause.  He therefore did not want to treat something that is not a disease.  He himself had a Carotid Intima Media Thickness (CIMT) scan before the low carb diet and then at the four month mark his improvement was remarkable.

I had my CIMT done in 2006 on the Standard American “heart healthy diet” eating low fat, higher carb. You know those espoused by the ADA and AHA. My lipids were “normal” at this time. My thickness was 0.6 mm (about the 50th percentile). I also had two small “road bumps “ (minimal plaques) at my left carotid bulb both measuring 1.2 mm. I was not happy. I also had similar findings on a study in 1/2010.

Flash-forward to June 2012, about 4 months into CNS, my CIMT showed a thickness of 0.445 mm (13th percentile) and I had the vascular age of a 16 year old! And oh by the way, the “road bumps” were gone. All the while carrying an LDL-P of over 2500 consistently for over a year. I have also had a CT Coronary Calcium score that was zero.

Some primitive people who eat a diet rich in saturated fats and low in carbs never experienced problems with heart disease (like the Masai).  Saturated fat, and the resulting high LDL that occurs in some people like myself and Dr. Patel, does not seem to cause heart disease.  A diet rich in carbohydrates marked by high triglycerides, low HDL and high HBA1C causes metabolic syndrome, obesity, inflammation and artery disease.  This is why diabetics have a much higher risk of death by heart attack.  My maternal grandmother was diabetic and died of a third heart attack.  Yet stubbornly, most doctors will not recommend high fat low carb diet because they’ve been taught to fear fat and cholesterol.

Now to answer the first question posed in the title:  Which one of these guys should take statins? The guy in the before picture or the guy ten months later?  In my opinion, neither.  The guy in the first picture was eating too many carbs and needed to stop it.  The guy in the second picture has rapidly improving health already.  Why would you want to possibly destroy that with a potentially harmful treatment of a non-disease?

Offline Resources consulted:

Anthony Colpo, The Great Cholesterol Con, 2012
Jeff S. Volek, Stephen D. Phinney, The Art and Science of Low Carbohydrate Living, 2011.
Gary Taubes, Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health, 2007, 2008.
Richard K. Bernstein, The Diabetes Solution, 2011.