Obesity and Diabetes

There’s a common definition of the word “obese”. We think of people who are really fat as being obese. I was one of them. 

What is Obesity?

Obesity has a technical definition which is somewhat arbitrary. It is a function of weight and height and is known as BMI (Body Mass Index). The US government definition is (NCHS Data Brief ■ No. 288 ■ October 2017):

Obesity: BMI was calculated as weight in kilograms divided by height in meters squared, rounded to one decimal place.

Obesity in adults was defined as a BMI of greater than or equal to 30.

BMI Weaknesses as a Metric

BMI (and obesity) does not take into account body composition such as body fat or lean body mass.  Two people can have the same BMI and be technically obese and one be solid muscle with little body fat and the other have significantly more body fat.

However, for the “average” person BMI is a decent measurement of fatness.

Obesity and Health

Generally, obesity and health are inversely related but there are people who are obese (by BMI) but are healthy. There are also people who are not obese but have poor health. This observation has led to the concept of personal fat threshold (PFT). This is described in (Taylor R, Holman RR.  Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond). 2015 Apr;128(7):405-10) (PDF).

Personal Fat Threshold (PFT)

The Personal Fat Threshold concept is that there’s a level of fatness which the individual can tolerate before their health is impacted. This concept is tempting but has some problems.

PFT is not all that useful in the a-priori sense. There is no objective test to see if someone is at or near their PFT. Obesity isn’t useful as a metric. Neither is body fat level.

The only use of PFT is to support the medical advice to patients of weight loss as a tool for management of Type 2 diabetes. The PFT concept doesn’t actually contribute much since it has been believed (before the PFT concept was developed) that weight loss of about 15% resolves diabetes (Reversing Diabetes with Weight Loss: Stronger Evidence, Bigger Payoff).

Until there’s an a-priori means of measuring PFT the approach seems to be not all that useful. No medical doctor can tell you that you are 10 lbs away from your PFT. The point is completely hidden until it manifests. All it says that is if you are not technically considered to be obese and you are diabetic it is because you have gone over your personal fat threshold. 

PFT – My Own Experience

There are three lines of reasoning from my own experience that call into question the PFT theory.

One was from my own experience with Insulin as a Type 2 Diabetic. I put on 40 lbs in a short time when I was put on Insulin. Conversely, when I got off Insulin my weight dropped quickly. Teenage females who are Type 1 diabetics and want to lose weight are well aware of this relationship. Weight increases followed Insulin increases (Skovsø S, Damgaard J, Fels JJ, Olsen GS, Wolf XA, Rolin B, Holst JJ. Effects of insulin therapy on weight gain and fat distribution in the HF/HS-STZ rat model of type 2 diabetes. Int J Obes (Lond). 2015 Oct;39(10):1531-8). not Insulin followed weight. Eventually, stasis is reached in weight and Insulin amount – at least in the short term.

Increasing dietary carbohydrates requires pumping more Insulin. When you stop eating dietary carbohydrates you don’t have to inject extra insulin for the meal. 

The second reason was the increase in Insulin that is required over time to maintain blood sugar levels. I started at about 40g of Insulin and had good blood sugar controls. By four later my weight was stable but the amount of Insulin to keep blood sugar stable kept increasing to about 120 units. More particularly, the amount of insulin to cover carbohydrate loads increased. In my own case 1 unit of Insulin could cover 15 grams of carbs when I started Insulin and by four years later 1 unit wasn’t enough to cover 8 grams. All of this was at a stable weight (after the initial gain) and the same level of carbohydrates.

A third reason is my own weight history. I was at 285 lbs and non-diabetic for years. Then I mysteriously lost 50 lbs down to 235 lbs over the course of about six months. This is a common occurrence with Type 2 diabetics (Unexplained Weight Loss and Diabetes). After six months of this unexplained weight loss, I was then diagnosed with diabetes.

Perhaps this is the body pushing back from the PFT but it does call the concept into question – or at least indicate the real issue is much more complicated. After being put on Metformin my weight stabilized at around 10 lbs higher (although Metformin is said to lower weight). As my diabetes got worse my doctor tried different medications some of which added weight and some (like Byetta) caused small weight loss. Finally, the addition of Insulin added 40 lbs to my weight.

I did low carb while on Insulin but it only took my HbA1C down to 6.4. It wasn’t until I did low carb plus Intermittent Fasting that I was able to get off Insulin and my weight fell very quickly. My last HbA1C was 5.2 which is a normal non-diabetic number.

Carbohydrate Insulin Relationship

At the very least, if the PFT concept is salvageable, it needs to be modified for increasing Insulin Resistance levels. If the best treatment for diabetes is weight loss the best way for Type 2 Diabetics to lose weight is to reduce insulin levels. The best way to reduce insulin levels is to the insulin load of the diet. For a Type 2 Diabetic who is on Insulin this results in a loss of a lot of weight in a very short period of time.

The recommendation that losing 15% of body weight does not seem plausible to a diabetic like myself. I’ve lost more than 15% from my peak weight and not been able to control my diabetes. I lost weight with Low Carb by itself but not enough to get off Insulin. At it was more than 15% of weight loss.  If I was told that losing 15% of my body weight would control my diabetes I would have told my doctor that I tried it and it didn’t work.

I lost much less than 15% of my weight in the beginning of Low Carb plus Intermittent Fasting and was able to get off Insulin completely. It was getting off Insulin which allowed me to lose weight. And it was reducing my body’s Insulin needs by the Low Carb diet and Intermittent Fasting which worked for me.

See (Obesity and Insulin Resistance).

Low Carb Hypothesis

Low Carb diets often result in greater weight loss than low fat diets – this BLOG has linked to many of these studies.

One explanation hypothesized for the greater weight loss on Low Carb diets is the Low Carb diet is said to have an inherent metabolic advantage. This metabolic advantage should manifest itself in a greater resting energy expenditure. The paper looked at two possible mechanisms – triglyceride cycling and glyceroneogenesis.

The critics of the Low Carb diet say that the advantage is that the comparisons aren’t done by holding protein constant. Overfeeding protein is not the same as overfeeding carbs or fat since protein stimulates 24 hour energy expenditure and fat doesn’t (Overfeeding Protein – Carnivore Diet).

Look to the Science

A short term (6 weeks) small (4 subjects) study was done on obese women to compare the Low Carb and Low Fat diets which held energy (total calories) and protein constant ( Segal-Isaacson CJ, Johnson S, Tomuta V, Cowell B, Stein DT. A randomized trial comparing low-fat and low-carbohydrate diets matched for energy and protein. Obes Res. 2004 Nov;12 Suppl 2:130S-40S). The study concluded that there is no significant differences when controlling for protein.

Our results showed no significant weight loss, lipid, serum insulin, or glucose differences between the two diets. 

The study was a decently formulated study but there were weaknesses:

  • Small study – only 4 subjects
  • No control group
  • Older obese females only
  • Very short duration (6 weeks)
  • Low fat didn’t get super-low (20% of calories from fat)
  • The Low Carb diet results in more weight loss but the study was too small to have statistical power

The good parts of the study were:

  • Controlled feeding
  • Matched total calories and protein – varying carbs and protein
  • Decent protein level (30% of calories)
  • Low carb was 5% of calories – good level
  • Randomized control trial
  • Cross-over design so the subjects ate both foods in random order
  • Starches and fruit were the carbohydrate choices (not jelly beans)
  • Deficit was relatively small (200 calories below REE which is a fairly large amount below TDEE depending on activity level)

At the end of the study they gave the participants the choice to continue on for a year. They were given the choice of the two diets and three of the four participants chose the Low Carb diet. However, the Low Carb participants raised their carbohydrate amount from 5% to 23% over the rest of the study so their weight loss partially reversed. There were several distinct advantages for the Low Carb diet.

Lipids were dramatically reduced on both diets, with a trend for greater triglyceride reduction on the VLC diet. Glucose levels were also reduced on both diets, with a trend for insulin reduction on the VLC diet

This fits my own experiences with protein and Low Carb. I’ve seen people stall for a long time and then break the stall by increasing their protein (and dropping their fat). My conclusion is that the ketogenic diet advantage does come from the higher protein intake of the diet. The diet often causes people to increase their consumption of meat which a high quality food.

Just Eat More Protein?

Protein alone doesn’t produce the same advantage that protein and Low Carb have together. This is shown in studies which substitute carbohydrates for protein (Blatt AD, Roe LS, Rolls BJ. Increasing the protein content of meals and its effect on daily energy intake. Journal of the American Dietetic Association. 2011;111(2):290-294).

This study showed that varying the protein content of several entrées consumed ad libitum did not differentially influence energy intake or affect ratings of satiety over a day. When the appearance, taste, fat content, and energy density were controlled, simply adding meat to lunch and dinner entrées to increase the protein content within commonly consumed amounts was not an effective strategy to reduce daily energy intake.

Sigma Nutrition Radio

Here’s a good program on this subject (SNR #64: Are Low-Carb Diets More Effective For Fat Loss?). tl/dl – Low Carb probably has better adherence than Low Fat diets.

Calories-In and Calories-Out

Does Calories-In and Calories-Out work on Keto? In the last 162 days I have averaged 2391 calories a day. My weight is the same at the end of these 162 days. My total energy expenditure (TDEE) is calculated at 2232 calories a day. This is only 159 calories a day from my TDEE or 7% off the calculated amount and that’s less than half the assumed measurement error in the food (typically assumed to be 15%).

So, yes, I conclude that Calories-In and Calories-Out do fairly closely match. At least in my particular case and macros.

So Why Keto?

Where Keto comes in is that I have maintained a 120 lb loss for the past 5+ months without hunger. My hormones are in balance. My insulin level is kept low. I don’t have the blood sugar roller coaster ride.

Here’s a good podcast covering this subject (Sigma Nutrition Radio #85: What Drives Fat Gain? – Thoughts on CICO, Insulin & Obesity).

Blood Sugar Rises

It is common and well documented by Cahill in his landmark studies on starvation that at the start of carbohydrate restriction blood sugar often goes up in the first few days before it starts to drop.

I’ve seen this myself with long fasts (greater than 4 days). The first few days result in your body making a lot of glucose in spite of low carbs in your diet.

It takes several days for your ketone production to kick in. That’s why the body dumps glucose.

I’ve also noticed an association between weight loss and blood sugar. My blood sugar is often up on the day before I drop in weight. In reverse, my blood sugar is lower when my weight goes up.

Diabetes and Weight Loss

A typical explanation for those of us who reversed our diabetes is that we did so because we lost weight. That can be found in a quite a few places like this (Nicola D. Guess. Dietary Interventions for the Prevention of Type 2 Diabetes in High-Risk Groups: Current State of Evidence and Future Research Needs. Nutrients 2018, 10(9), 1245).

Weight loss appears to be the primary driver of type 2 diabetes risk reduction, with individual dietary components playing a minor role. 

I don’t buy it. I got off Insulin in two weeks. Can it be based on weight loss? I don’t believe so. The reason is that I was diabetic over a wide range of weights – from the 230’s into the 280’s. At the time I went on LCHF + IF I was at 285. I didn’t drop below 230 in two weeks. Here is my weight loss chart. 

Associations

I’ve been meaning to write on bad associations for a long time but there are so many other good articles on it that I’ve saved my fingers until now. I really enjoy a lot of Marty Kendall’s Nutrient Optimising (British spelling) material but I’m getting a bit annoyed at some of the association data that is being put forward. I guess I should be as annoyed at the ketogenic community associations as well. None of them meet the Bradford Hill criteria

So I am going to play the same game. My theory is that fresh broccoli causes obesity.  Check out the blue graph below.

Here’s the chart for obesity.

Here’s a chart for the total calories in the food supply.

So it looks to me like obesity is caused by too much broccoli.

And when the rooster crows the sun comes up.

And fallacies go on and on.

Blood Sugar Roller Coaster – Part 2

A good small study comparing the blood sugar and insulin responses to breakfasts with different fat/carb/protein values at the same number of calories (Paula C. Chandler-Laney, et.al. Return of hunger following a relatively high carbohydrate breakfast is associated with earlier recorded glucose peak and nadir. Appetite. Volume 80, 1 September 2014, Pages 236-241).

Turns out that a Low Carb High Fat breakfast results in a lower Area Under the Curve (AUC) for Insulin and higher blood sugar levels hours after breakfast. The lower AUC makes sense since there’s less glycemic load from lower carbohydrates. However, the glucose response may be counter-intuitive. It happens because the problem with higher glucose in meals is a larger drop in glucose after the meal digests. Eating lower carbs results in less of a drop in blood sugar. And it also results in less hunger.

The study protocol was:

Overweight but otherwise healthy adults (n = 64) were maintained on one of two eucaloric diets: high carbohydrate/low fat (HC/LF; 55:27:18% kcals from carbohydrate:fat:protein) versuslow carbohydrate/high fat (LC/HF; 43:39:18% kcals from carbohydrate:fat:protein). After 4 weeks of acclimation to the diets, participants underwent a meal test during which circulating glucose and insulin and self-reported hunger and fullness, were measured before and after consumption of breakfast from their assigned diets.

The results of the study were:

The LC/HF meal resulted in a later time at the highest and lowest recorded glucose, higher glucose concentrations at 3 and 4 hours post meal, and lower insulin incremental area under the curve.

Participants consuming the LC/HF meal reported lower appetite 3 and 4 hours following the meal, a response that was associated with the timing of the highest and lowest recorded glucose.

Credit to Ted Naimam for pointing out this study.

Ancel Keys – History Lesson.

From this site

The story of Ancel Keys is told in a way intended to correct the predominent keto narrative of Keyes as Anti-Christ (Denise Minger. THE TRUTH ABOUT ANCEL KEYS: WE’VE ALL GOT IT WRONG). Denise includes a table that looked at all cause mortality and not just the fat/cardio chart that Keyes is infamous for producing. Read Denise’s excellent BLOG post for the background of this table.

A positive number is an association. The larger the number, the larger the association. Of course we know that association is not causation.  All cause mortality is associate the most strongly with carbohydrates (+0.396) and the least with calories from fat (-0.340).

This is also the subject of another paper (Pett, et.al. Ancel Keys and the Seven Countries Study: An Evidence-based Response to Revisionist Histories).

Here is another related BLOG post (From Ancel Keys and the diet-heart hypothesis to LCHF may not be a huge leap.).

Low Carb vs Reduced Calorie

An interesting study that took a look at an ad libitum Low Carb diet compared to a Low Calorie diet (Foster, Gary D. et.al. A Randomized Trial of a Low-Carbohydrate Diet for Obesity. New England Journal of Medicine, 2003, VI 348, pp 2082-2090). The groups were:

We conducted a one-year, multicenter, randomized, controlled trial to evaluate the effect of the low-carbohydrate, high-protein, high-fat Atkins diet on weight loss and risk factors for coronary heart disease in obese persons. The subjects were randomly assigned to follow either a low-carbohydrate, high-protein, high-fat Atkins diet or a high-carbohydrate, low-fat, energy-deficit conventional diet.

The Low Calorie group was pretty restrictive:

1200 to 1500 kcal per day for women and 1500 to 1800 kcal per day for men, with approximately 60 percent of calories from carbohydrate, 25 percent from fat, and 15 percent from protein

You’d think that with the Low Carb group able to eat what they want that the calorie restricted group would beat them hands down. The results were:

Subjects on the low-carbohydrate diet had lost more weight than subjects on the conventional diet at 3 months (mean [±SD], –6.8±5.0 vs. –2.7±3.7 percent of body weight; P=0.001) and 6 months (–7.0±6.5 vs. –3.2±5.6 percent of body weight, P=0.02), but the difference at 12 months was not significant (–4.4±6.7 vs. –2.5±6.3 percent of body weight, P=0.26). After three months, no significant differences were found between the groups in total or low-density lipoprotein cholesterol concentrations. The increase in high-density lipoprotein cholesterol concentrations and the decrease in triglyceride concentrations were greater among subjects on the low-carbohydrate diet than among those on the conventional diet throughout most of the study. Both diets significantly decreased diastolic blood pressure and the insulin response to an oral glucose load.

Satiety Index

There’s a study that was done of food satiety (Holt SH, Miller JC, Petocz P, Farmakalidis E. A satiety index of common foods. Eur J Clin Nutr. 1995 Sep;49(9):675-90) (PDF).

Isoenergetic 1000 kJ (240 kcal) servings of 38 foods separated into six food categories (fruits, bakery products, snack foods, carbohydrate-rich foods, protein-rich foods, breakfast cereals) were fed to groups of 11-13 subjects. Satiety ratings were obtained every 15 min over 120 min after which subjects were free to eat ad libitum from a standard range of foods and drinks.

A satiety index (SI) score was calculated by dividing the area under the satiety response curve (AUC) for the test food by the group mean satiety AUC for white bread and multiplying by 100.

Thus, white bread had an SI score of 100% and the SI scores of the other foods were expressed as a percentage of white bread.

The results were:

There were significant differences in satiety both within and between the six food categories. The highest SI score was produced by boiled potatoes (323 +/- 51%) which was seven-fold higher than the lowest SI score of the croissant (47 +/- 17%).

Most foods (76%) had an SI score greater than or equal to white bread.

The amount of energy eaten immediately after 120 min correlated negatively with the mean satiety AUC responses (r = -0.37, P < 0.05, n = 43) thereby supporting the subjective satiety ratings. SI scores correlated positively with the serving weight of the foods (r = 0.66, P < 0.001, n = 38) and negatively with palatability ratings (r = -0.64, P < 0.001, n = 38).

Protein, fibre, and water contents of the test foods correlated positively with SI scores (r = 0.37, P < 0.05, n = 38; r = 0.46, P < 0.01; and r = 0.64, P < 0.001; respectively) whereas fat content was negatively associated (r = -0.43, P < 0.01).

This goes a long way to explain the Kitavan diet which is largely sweet potatoes. Can you imagine eating sweet potatoes every day as a main staple? Even though they are high carbohydrates it would be tough to over eat them.

Added: Gary Taubes takes on the palatable foods cause obesity theory (CATCHING UP ON LOST TIME – THE ANCESTRAL HEALTH SYMPOSIUM, FOOD REWARD, PALATABILITY, INSULIN SIGNALING AND CARBOHYDRATES… PART II(E, AS IN “END” AND “ENOUGH ALREADY”). Gary has some good points about the usefulness of this idea.