Competition for Calories

Here is a very new paper which has an interesting way of looking at nutrient partitioning (Archer Edward, Pavela Gregory, McDonald Samantha, Lavie Carl J., Hill James O. Cell-Specific “Competition for Calories” Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals. Frontiers in Physiology, v9:2018, 1053):

…we posit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity and metabolic diseases is engendered by apparent deficits (i.e., false signals) driven by the asymmetric inter-cellular competition for calories and concomitant differential partitioning of nutrient-energy to storage. These frameworks, in concert with our previous theoretic work, the Maternal Resources Hypothesis, provide a parsimonious and rigorous explanation for the rapid rise in the global prevalence of increased body and fat mass, and associated metabolic dysfunctions in humans

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).

The Right Goal

Weight loss alone should never be your goal. Fat loss should be your goal. This can be demonstrated from the numbers. If you have 25% body fat then the weight you want to lose should come out of that 25% of body fat and not from the 75% of lean body mass. If you lose weight and most of the weight comes from your lean body mass you have not done yourself any favors.

Maximum Fat Loss

The fastest way to lose fat is to greatly reduce your carbohydrates and fat intake. Protein should never be reduced. For most people protein should be increased.

Macros for Fat Loss

There is a pretty simple set of macros for maximum body fat loss.

  • Protein at 1 gram per lb of goal weight. 
  • Carbs at less than 30 grams net. 
  • Fat at less than half the grams of protein. 

Macros Calculator

I made a calculator for maximum fat loss. The calculator estimates your current body fat and asks you to say what percentage body fat you want to reach.

Protein

The recommended daily protein minimums are pretty low. I suggest much more. If you have normal kidney function that is no problem.

You need enough protein in your diet to replace the protein your body will eat up during the diet. You also need some for gluconeogenesis. Since you will be eating at a caloric deficit any extra protein won’t be a problem – it won’t turn into chocolate cake.

Protein has essential nutrients. Eating 3 grams of Leucine (found in about 30g of protein) is a good goal to hit with every protein meal. That’s around 5 ozs of skinless chicken breast.

Carbs

Eat the carbs as green leafy veggies. Broccoli is a great choice for micronutrients. You don’t like the taste? Get over it. It’s good for you. And you will eventually grow to like the taste.

Fat

If you want to lose fat faster, eat less fat. If you are losing too quickly, eat more fat. The fat you eat doesn’t come off your body. The fat you don’t eat in your diet comes off your body. Any fat you eat is stored on your body very efficiently. Fat has few essential nutrients.

Even a low fat diet is still relatively high fat. The fat is just coming off your body. You can’t stay on a low fat diet forever. You have to increase your fat over time as you reach your goals.

It’s a good idea to take a couple of fish oil capsules every day to get more of the good fats.

Studies on this Diet

This is also known as a variant on the Protein Sparing Modified Fast. It is well studied and effective. The PSMF is often done at very low (20g) of fat.

Ketogenic Infants

From (Settergren G, Lindblad BS, Persson B. Cerebral blood flow and exchange of oxygen, glucose, ketone bodies, lactate, pyruvate and amino acids in infants. Acta Paediatr Scand. 1976 May;65(3):343-53):

Mean values from 12 infants (age 11 days-12 months) were: CBF 69 ml/100 g0min-1; cerebral uptake (in mumoles/100 g-min-1): oxygen 104, glucose 27, acetoacetate 0.9, D-beta-hydroxybutyrate 2.3; cerebral release: lactate 2.4 and pyruvate 0.8. Significant uptake of amino acids was found only for histidine 0.95 and arginine 0.7. Significant correlations between arterial concentration and cerebral exchange were found for: ornithine, arginine, phenylalanine, aspartic acid, serine, glutamine and acetoacetate. CBF and substrate exchange were unrelated to age within the group.

Infants had higher mean CBF and greater uptake of ketone bodies than has been reported in adults.