Objections to the Keto Diet – Part 14- No Long Term Benefits to Weight Loss

This last objection by a dietitian (Dietitians Weigh in on the Low Carb/Ketogenic Diet) actually has some merit but it’s not really all that important since it emphasizes weight loss and not glycemic control.

…though ketogenic diets [sic: short term] were found to produce the greatest weight loss compared to other diets, in the long term there was no difference

This is not really an objection to the ketogenic diet. If it’s more effective short term and no less effective long term then what’s the problem? Most people would love to have a short term loss particularly if it didn’t cause a long term problem.

The issue is compliance and the ketogenic diet is easier to stick with long term since it is more satisfying.

 

Objections to the Keto Diet – Part 12 – Consistent Carbohydrate Diet is Better

This response by one of the dietitians (Dietitians Weigh in on the Low Carb/Ketogenic Diet) is something I’ve not heard of before (at least by this name). The suggestion is that this alternate diet is better for diabetics. Here’s the comment:

I would consider suggesting the Consistent Carbohydrate Diet.

Here’s the Consistent Carbohydrate Diet (Int J Pediatr Endocrinol. 2009; 2009: 469623. The Origin of the Constant Carbohydrate Diet. Charles Herbert Read, Jr.). I believe this is what the dietitian I visited in the 1990’s was teaching (or something similar). This diet was developed in 1951.

The developer of the diet had “children with insulin-dependent diabetes” as patients and their mothers had trouble figuring out the standard ADA diet for diabetics. It was just too complicated back in 1951.  From the history above:

This prestigious ADA exchange diet was taught in virtually all the diabetic centers in Canada and the United States. Its concept was that any food which contains an equivalent amount (within 3 grams) of carbohydrate, fat, and protein could be substituted for a similar food if they were in the same food group. The groups were Milk, Meat (sometimes divided into high- or low-fat subgroups), Vegetables, Breads, and Fats. For example, if an eight-ounce glass of skim milk was substituted for an eight-ounce glass of whole milk containing 10 grams of fat, where would one find the 2 fat exchanges that were needed.

The implication was that the insulin need was related to the total calories ingested.

The last line is a solid objection. No need to inject for fat.

It made little sense to me that while insulin is necessary to produce fat, it has a negligible role in its catabolism. So why to pay attention to fat in so far as the insulin requirement is concerned?

The author also observed that people tend to eat a consistent amount of protein so that could be held constant day to day. Remember that Type 1 diabetics typically injected for half the grams of protein (as compared to carbohydrates).

This was an astute observation in that in the end it meant that people who inject insulin only need to track carbohydrates. They will be giving variable amounts of Insulin based on carbs and a constant amount (basal amount) based on the protein levels. So this insight was to keep carbs constant day to day.

I concluded that because insulin is required for the metabolism of the dietary carbohydrate, an appropriate diet for diabetes is one in which the carbohydrate content of each of the meals, although different in amounts at breakfast, lunch, and dinner, would be the same from day to day. Variations in the protein and fat content are ignored.

The method in a nutshell is:

Only the carbohydrate is counted, so any food may be included in the diet by referencing a Carbohydrate Guide and staying within 3 grams of the decided amount of carbohydrates at each eating time. This is the Constant Carbohydrate diet.

This all led to increased compliance in Type 1 diabetics.

After she had used this diet for several months, Adams [] noted that although at first the mothers were confused by this seemingly drastic change, they and the patients easily and even happily adapted to this new way of thinking and doing, especially those of different ethnic origins. Her reaction was typical of the responses of each dietitian who subsequently began using the diet.

From that I would conclude that there’s nothing inherently contradictory between a Low Carb diet and a Constant Carbohydrate diet. The Low Carb diet is just less than 20 or 30 grams of carbs a day.

The insights of the author are probably part of my own thought process. Controlling carbs is good. Keeping carbs at low levels is good. Most problems come from large amounts of carbs.

 

Objections to the Keto Diet – Part 10 – Carbs are not nutrients

This objection from a dietitian (Dietitians Weigh in on the Low Carb/Ketogenic Diet) is funny since it’s true on one sense but not what the dietitian intends:

Ketogenic diet emphasizes on one macronutrient (Fat) while ignoring the importance of others (carb, protein and natural sources of vitamin & minerals). Thus, leading towards nutritional deficiencies if followed long term.

I’ve already tackled the protein question earlier in this series (Objections to the Keto Diet – Part 7 – Keto is Low Protein).

No one has ever demonstrated that a lack of carbohydrates leads to nutritional deficiencies in the long term. I did look at the long term studies which show no such deficiencies (Objections to the Keto Diet – Part 4 – Long Term Consequences Are Unknown).

But this charge is more serious. It’s not that the consequences are unknown but they that keto will lead to deficiencies. I’ve not seen any studies showing that and I suspect that there is no basis for this charge other than bald faced assertion.

Produce the evidence or retract the charge. Show me what I am missing in my typical keto micronutrients. I publish them here – my last seven days averages. Show me yours, Dietitian. I bet I do better on keto than you do on your diet.

I do put salt in my coffee and don’t log it so my sodium is fine (just in case they care).

Want to see my other macros? OK. Here’s my last 7 day’s averages. What’s missing, dietitians? 30g net of veggies. 222g of fat. 161g of protein. They will probably tell me I am eating too much protein.

Objections to the Keto Diet – Part 9 – Low Blood Sugar

This objection from one Dietitian (Dietitians Weigh in on the Low Carb/Ketogenic Diet) is particularly ironic:

there is the possibility of low blood sugar, or hypoglycemia, from restricting carbs too much

There are people who afraid of low blood sugar but diabetics aren’t at risk for this. However, a diabetic who is on medication will require adjustment in their medications to lower them as their blood sugar goes down on the keto diet. But remember the definition of diabetes is high blood sugars…

Incredible the scare tactics being used here.

Don’t do keto because your high blood sugar won’t be high anymore.

Don’t these dietitians consider the alternatives? In spite of being on 100 units of Insulin and even being relatively lower carb (under 200 grams of carbs a day) I had horrible control of my blood sugar with numbers ranging all over the place.

With low carb/keto my blood sugar is very steady and constant. Plus being keto fuel fired my blood sugar can get even lower and it isn’t a problem. Remember these curves?

Blood sugar drops and stabilizes in the case of starvation. Eating low carb doesn’t drop blood sugar farther than starvation would.

I would suggest that dietitians develop some sense of compassion and put themselves into the shoes of diabetics who don’t have good control of their blood sugar and help them adjust meds over the week or so of induction.

 

Objections to the Keto Diet – Part 5 – A “Slew of Risks”

This objection from a dietitian (Dietitians Weigh in on the Low Carb/Ketogenic Diet) actually has some truth in it but in the most serious charge is way off base. Here’s the objection as it was written:

…comes with some a slew of risks. These risks can start with symptoms such as headaches, fatigue, fogginess and if left untreated, possible coma and death. There biggest risk is diabetic ketoacidosis which is the result of too many ketones in the blood, a lack of insulin and blood glucose spiking too high. Left untreated, diabetic ketoacidosis can be potentially fatal.

Keto Flu Symptoms

It is true that the diet has various symptoms during the withdrawal from carbs. The symptoms of keto flu are “headaches, fatigue, fogginess” and they can last a couple of days to as much as a week. And they cause many people to tap out. That’s why it is important to help people understand and treat these symptoms.

These symptoms are similar to the withdrawals from any addictive substance. Sugar is no different. That could cause some who is going through them to ask the question why when they stop eating carbs that they go through the symptoms of heroin withdrawal (albeit in a smaller way)?

If carbs are so good then why am I going through these sorts of symptoms? The first reason comes from the switching of fuel sources from glucose (which drops quickly) to ketones which take a few days to kick in.

This can be seen in studies of starvation. The curve on the left is the blood glucose which falls in the first few days and then levels out. The fact is well all feel worse as our blood sugars drop. That is a normal condition. I felt best when my blood sugar was around 300 (normal is around 85) and unless you are testing your blood sugar you don’t know that you are still just fine.

Around day 2, the ketone bodies start to kick. They are your new fuel and it will take a few days for them to reach sufficient levels to meet your needs.

The reason people feel bad when going into keto is that their body was normally accustomed to being fueled by glycogen and that fuel source is limited.

Electrolytes

Along with the drop in glycogen comes a very large drop in water weight. For every gram of glycogen your body stores 3-4 grams of water.  Along with this water loss comes a loss of electrolytes.

For me cramps in my legs (calves in particular) as I was falling asleep. This was my signal that I needed to have more magnesium, potassium and sodium.

This is very easy to treat. For most people just eating a small amount of salt will bring immediate relief. For others more electrolyte supplementation may be required. See this for more information (Electrolytes, Water Retention, Low Carb Diets).

Diabetic Ketoacidosis

This is a rare condition which is not a by-product of the ketogenic diet. Quite the contrary since it is a risk of untreated diabetes. And yes, it is often fatal. I have a personal friend who died from this. It is typically found in someone who is an undiagnosed diabetic.

It is accompanied by very high blood sugars. Remember what happens when you start a ketogenic diet (see above)? Your blood sugar drops. That is why diabetic ketoacidosis is describing a completely different condition. In the untreated diabetic both ketones and high blood sugar are present. In the ketogenic diet ketone levels don’t reach these deadly levels so both conditions for DKA are not present.

The diabetic who doesn’t do a ketogenic diet has a much higher chance of dying from DKA than a diabetic on the ketogenic diet. Again, just comparing the risks shows the dietitian’s claim is false.

 

Statins – Is the Cure Worse Than the Disease?

I was given statins years ago. I haven’t dug back to see when I got my first prescription for statins but I think it was before I first got diagnosed with diabetes.

My doctor prescribed statins for me according to the Standard of Care at the time (American Diabetes Association Indications for Statins in Diabetes: Is there evidence? Roy Eldor, MD and Itamar Raz, MD. Diabetes Care 2009 Nov; 32(suppl 2): S384-S391.).

…It appears that based on current available data, all individuals with diabetes should be treated with a statin unless they apply to very specific exclusion criteria. These criteria include a patient with type 2 diabetes under the age of 32 years (or 38 years in women), short duration of disease (<10 years), and no apparent CVD risk factors (including a baseline LDL >100 mg%). In individuals with type 1 diabetes, the age should be even lower, i.e., <30 years of age. To not be prescribed a statin, a patient will have to have all these exclusion criteria present…

Oops…

Turns out that the statins might have been bad for me after all (J Pharmacol Pharmacother. 2014 Jul-Sep; 5(3): 181–185. Statin induced diabetes and its clinical implications. Umme Aiman, Ahmad Najmi, and Rahat Ali Khan).

From the study:

Statins are one of the most commonly used drugs in the world based on their potential to prevent adverse cardiovascular events. These cholesterol-lowering drugs received a US Food and Drug Administration warning, in February 2012, regarding increased risk of incident diabetes and impaired glycemic control in patients who already have diabetes.

Here’s the FDA statement (FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs). Here’s the wording from the FDA statement:

Increases in glycosylated hemoglobin (HbA1c) and fasting plasma glucose

FDA’s review of the results from the Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) reported a 27% increase in investigator-reported diabetes mellitus in rosuvastatin-treated patients compared to placebo-treated patients. High-dose atorvastatin had also been associated with worsening glycemic control in the Pravastatin or Atorvastatin Evaluation and Infection Therapy – Thrombolysis In Myocardial Infarction 22 (PROVE-IT TIMI 22) substudy.18

FDA also reviewed the published medical literature.19-26 A meta-analysis by Sattar et al.,19 which included 13 statin trials with 91,140 participants, reported that statin therapy was associated with a 9% increased risk for incident diabetes (odds ratio [OR] 1.09; 95% confidence interval [CI] 1.02-1.17), with little heterogeneity (I2=11%) between trials. A meta-analysis by Rajpathak et al.,20 which included 6 statin trials with 57,593 participants, also reported a small increase in diabetes risk (relative risk [RR] 1.13; 95% CI 1.03-1.23), with no evidence of heterogeneity across trials. A recent study by Culver et al.,26 using data from the Women’s Health Initiative, reported that statin use conveys an increased risk of new-onset diabetes in postmenopausal women, and noted that the effect appears to be a medication class effect, unrelated to potency or to individual statin.

Based on clinical trial meta-analyses and epidemiological data from the published literature, information concerning an effect of statins on incident diabetes and increases in HbA1c and/or fasting plasma glucose was added to statin labels.

The Original Logic

The original justification to reduce dietary cholesterol was based on:

  1. Cholesterol is found in the arteries of people who die of heart disease.
  2. Reducing dietary cholesterol should lead to less cholesterol in the arteries.
  3. Therefore, everyone should eat low cholesterol foods.

There was never any evidence that eating foods like eggs (high in cholesterol) were causing heart disease. It was all based on the above chain of logic.

A Solution In Search of a Problem

Because dietary changes don’t make drug companies any cash, eventually the pharmacological industry came out with cholesterol lowering drugs, IE, statins. The logic was similar and based on the previous premises:

  1. Cholesterol is found in the arteries of people who die of heart disease.
  2. Reducing lipid (blood) cholesterol should lead to less cholesterol in the arteries.
  3. Statins have been shown to lower cholesterol.
  4. Therefore, people with high cholesterol should take statins which reduce cholesterol in the blood.

Again, there was never any evidence that lowering cholesterol in the blood would actually lead to a reduction in heart disease. Nor was there evidence that the lowering effect of the statins would lead to a reduction in heart disease. Plenty of studies showed no delivered benefit but that didn’t get in the way of the industry. This led to the practice of prescribing statins to anyone with “high” cholesterol. And the standard of high kept getting reduced.

In Come Diabetics

The move to prescribe statins for nearly every diabetic was something like this:

  1. Cholesterol is found in the arteries of people who die of heart disease.
  2. Diabetics often have higher cholesterol than non-diabetics.
  3. Stains reduce cholesterol.
  4. Anything we can do to reduce heart disease in diabetics should be done.
  5. All diabetics should take statins.

Same broken chain of logic. 

Now we learn that the same meds we were given to help us supposedly reduce our cholesterol (and heart disease by inference) may have contributed significantly to both giving us diabetes and making our diabetes worse.

 

Can Beta Cells be Healed?

This article lists studies showing that beta cells can be healed (Diabetes Self-Management. Can Beta Cells Be Healed? Published April 10, 2013 by David Spero, BSN, RN).

One interesting study gave Insulin to newly diagnosed Diabetics (Diabetes Care 2004 Nov; 27(11): 2597-2602. Induction of Long-term Glycemic Control in Newly Diagnosed Type 2 Diabetic Patients Is Associated With Improvement of β-Cell Function. Yanbing Li, MD, Wen Xu, MD, Zhihong Liao, MD, PHD, Bin Yao, MD, Xiahua Chen, MD, Zhimin Huang, MD, Guoliang Hu, MD and JianPing Weng, MD, PHD) and concluded that:

Short-term intensive insulin therapy can induce long-term glycemic control in newly diagnosed type 2 diabetic patients with severe hyperglycemia. The improvement of β-cell function, especially the restoration of first-phase insulin secretion, could be responsible for the remission.

So it may be that providing a “shock” of Insulin to newly diagnosed diabetics may give the pancreas enough of a break to let the pancreas recover.

 

Two Different Things That are the Same

There are two different things which are basically the same – at least for best course of treatment.

  1. Type 1 Diabetics Who Become Insulin Resistant
  2. Type 2 Diabetics Who Use Insulin

The Type 1 Diabetic is unable to produce Insulin in their pancreas. Some Type 1 Diabetics become Insulin Resistant (like a Type 2 Diabetic).

The Type 2 Diabetic was once able to produce more than enough Insulin but their body has become resistant to the action of Insulin and they have to give insulin externally. A Type 2 Diabetic who has high enough levels of blood sugar for a long enough time will suffer pancreatic beta cell burnout.

In the end, both have the same problem.  At this point they end up injecting more and more Insulin and get worse control over their blood sugars.

There is only one solution!

The solution is to reduce dietary carbohydrates to the maximum level possible. Less than 20 grams of carbohydrates a day as the goal.

 

DIRECT Trial in UK Shows Diabetes Reversal

From (Newcastle diet achieves type 2 diabetes remission after one year of DiRECT trial):

The Diabetes Remission Clinical Trial (DiRECT) study, co-led by researchers at the University of Newcastle and the University of Glasgow, followed around 300 patients from 49 primary care services in Scotland and Tyneside who have had diabetes for six years.

Almost half of the participants managed to achieve and maintain diabetes remission at one year without medication using overall calorie restriction in place of standard guidelines.

After being on the 800-calorie diet plan and maintaining a healthy weight for a year, up to 46 per cent of participants managed to achieve diabetes remission, compared to only four per cent of participants in the control group.

Reduction of the body fat is a part of this solution.

In two previous pilot studies, the researchers showed that remission appeared to be related to a reduction in fat around the liver and pancreas which a low calorie diet helped to achieve.

Note that the DIRECT study was a Low Calorie study not a Low Carb approach.

Similar US Study

A US Study (Diabetes Care 2016 May; 39(5): 808-815. Very Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiological Changes in Responders and Nonresponders. Sarah Steven, Kieren G. Hollingsworth, Ahmad Al-Mrabeh, Leah Avery, Benjamin Aribisala, Muriel Caslake and Roy Taylor.)

A robust and sustainable weight loss program achieved continuing remission of diabetes for at least 6 months in the 40% who responded to a VLCD by achieving fasting plasma glucose of <7 mmol/L. T2DM is a potentially reversible condition.

The detailed results:

Weight fell (98.0 ± 2.6 to 83.8 ± 2.4 kg) and remained stable over 6 months (84.7 ± 2.5 kg). Twelve of 30 participants achieved fasting plasma glucose <7 mmol/L after return to isocaloric diet (responders), and 13 of 30 after 6 months.

Responders had a shorter duration of diabetes and a higher initial fasting plasma insulin level.

HbA1c fell from 7.1 ± 0.3 to 5.8 ± 0.2% (55 ± 4 to 40 ± 2 mmol/mol) in responders (P < 0.001) and from 8.4 ± 0.3 to 8.0 ± 0.5% (68 ± 3 to 64 ± 5 mmol/mol) in nonresponders, remaining constant at 6 months (5.9 ± 0.2 and 7.8 ± 0.3% [41 ± 2 and 62 ± 3 mmol/mol], respectively). The responders were characterized by return of first-phase insulin response.

It is worth examining the differences between the responders and non-responders in Table 1.

  1. Responders had diabetes for a shorter time than the non-responders.
  2. Responders had more pancreas function (ie, higher initial fasting plasma insulin level).

Why does the UK lead in a Low Carb approach?

The Low Carb Program in the UK is curing Diabetes. Even though the diet isn’t Very-Low-Carb, the reduction in carbohydrates is helping a great number of people (hundreds of thousands).

Diabetes.co.uk‘s low-carb program helps people start a liberal low-carb program (90-120 grams per day) during a structured 10-week education program.

This is not a government sponsored program, it is grass-roots (Thousands of diabetics adopt high-protein low-carb diet in backlash against official NHS eating plan).

 

Sulfonylureas and the Pancreas

Sulfonylureas are a class of diabetic medications which stimulate the production of Insulin. That seems like a good thing for a person with high blood sugar but we’ve shown that’s not the case. This is noted in studies (PLoS Med. 2008 Oct; 5(10): e215. Why Treatment Fails in Type 2 Diabetes. Anders Rosengren, Xingjun Jing, Lena Eliasson, and Erik Renström).

…Sulfonylureas, a group of insulin secretagogues, have long been cornerstones in the pharmacological treatment of type 2 diabetes. These compounds bypass the normal glucose-sensing mechanism in the pancreatic beta-cells and thereby initiate insulin secretion.

Sounds great, right? Not so much.

Unfortunately, this story does not end on a high note. Within a few years of starting treatment with sulfonylureas, the beta-cells show clear signs of fatigue leading to deteriorated blood glucose control. Eventually all patients need to take daily insulin injections to achieve acceptable control over blood glucose.

The study goes on to say:

 The possible clinical implications of this study are that failing insulin secretion in type 2 diabetes should not be treated with pharmacological compounds that stimulate insulin release in a tonic fashion. Instead, preference should be given to compounds with short half-life in the circulation and compounds that enhance normal pulsatile and phasic insulin secretion.