PSMF March 2018

I’ve got to start this out saying that I was already at a pretty good weight. My body fat percentage puts me well into the healthy range.

A friend decided to do a Protein Sparing Modified Fast (PSMF) and I thought I’d do the PSMF along with her. I set my goal to 15% Body Fat. This is the second time I’ve done this diet. Like last time, this has been pretty easy.

I used my PSMF calculator to figure my macros at the start. My starting point was:

Current Weight: 178 lbs
Current Body Fat: 17.8%, 31.7 lbs
Your current body fat % is already lower than your ideal body fat %.
Ideal Body Fat: 20.9%
Lean Body Mass (LBM): 146.3 lbs
Basal Metabolic Rate (BMR): 1682 cal/day
Total Daily Energy Expenditure (TDEE): 2313 cal/day

My PSMF Calculator macros to reach my goal (maximum fat loss) were:

Goal Weight: 172 lbs
Lbs from Goal Weight: 5.9 lbs

Your total calories from food should be 1331 calories per day for maximum fat loss.
Protein: 117.1 g (468.2 cals), 35.2% of calories
Carbs: 20 g (80 cals), 6.0% of calories (from leafy green vegetables)
Fat: 86.9 g (783 cals), 58.8% of calories
Initial Maximum Fat Loss: 0.28 lbs per day
At this limit you will use 982 calories from your body fat per day.
Estimated time to reach goal: 21 days
If you consume 196 g (1765 calories) of fat you will remain at your current weight.

Dietary Compliance – Macros

I set the starting target macros in cronometer and have been tracking for the past three weeks. Here’s my actual numbers vs the goal numbers from the past week  of eating. Note my fat number went up since I recalculated every week:

I exceeded my Protein each and every day. I often ate less fat and I stayed below my carbs number.

Weight Loss Results

Over the past three weeks I’ve lost almost 9 lbs. That’s 3 lbs a week or about 1/2 lb a day. The PSMF calculator had me at .28 lbs of loss a day so I’m exceeding that number . The extra losses were probably due to additional losses from water (steeper slope in the first week) and the effects of exercise. I also had some extra weight I had put on from the end of the Carnivore experiment.

I deliberately ate a bottle of olives March 22 and a bottle of pickles March 23. There was a couple of pounds increase March 24. That gain was from the excess salt and water weight. It came off over the next couple of days.

Caloric Compliance?

How did I do for calories? Most days I did OK. This chart has four weeks so I removed the first week or so. I did good the first five days then ate way too much one day (almost 3000 calories). The extra calories didn’t hurt my losses. I increased my calories on some other days with not much effect.

Goal Weight

My goal weight was 172 lbs. I reached 168 lbs this morning. I will start to increase my calories over the next few days with the goal of reaching maintenance.

Maintenance Numbers

The PSMF calculator gives my maintenance numbers as:

Numbers at Your Goal Body Fat Percentage

Goal Weight: 172 lbs
Lbs from Goal Weight: 5.9 lbs
You will need to consume (TDEE): 2237 calories
Protein: 117 grams, 21% of calories (minimum)
Carbs: 20 grams, 4% of calories (maximum)
Fat: 188 grams, 75% of calories (maximum, less if you exceed protein)

Note maintenance has the same number of Protein and Carbs as the PSMF did. Maintenance allows for additional fat calories.  Other than that it’s just the same. Part of the beauty of PSMF is that it sets you up with good habits (low carbs from veggies, right amount of protein from good protein sources) and just limits your fat intake.


Pork Rinds – A Good Keto Choice?

Pork Rinds are the skin of a pig. They are either loved or hated by most people. They can have a strong flavor but their crunch can fit a need for crunchy food in people formerly addicted to foods like chips.

Are Pork Rinds a good choice for keto? Depends on your view of what matters. As far as the primary criteria they are low carbohydrate. One nutritional label says:

They are not bad for fat (5g). The even have a good protein value. But note the note next to the protein number “Not a significant source of protein”. That doesn’t mean what it might appear to mean. It doesn’t mean that they don’t contain much protein. It means that the protein they contain isn’t a particularly great source of protein. From (Wikipedia, Pork Rind: Nutritional Value):

However, pork rinds are considered an incomplete source of protein because they contain very low amounts of some essential amino acids, including methionine, tryptophan and histidine.

So, if you care about the quality of your protein, eat Pork Rinds with care.

Added 2018-10-06

This study shows how Protein quality matters for Lean Mass preservation (Oikawa SY, McGlory C, D’Souza LK, Morgan AK, Saddler NI, Baker SK, Parise G, Phillips SM. A randomized controlled trial of the impact of protein supplementation on leg lean mass and integrated muscle protein synthesis during inactivity and energy restriction in older persons. Am J Clin Nutr. 2018 Oct 4).

Protein supplementation did not confer a benefit in protecting LLM, but only supplemental WP augmented LLM and muscle protein synthesis during recovery from inactivity and a hypoenergetic state.

American Diabetics Association – Standards of Care (Nutrition)

The Standards of Medical Care for Diabetics contains the best practices at the time of publication based on the reading of the science. The following is from the (American Diabetes Association, Diabetes Care 2014 Jan; 37(Supplement 1): S14-S80. Standards of Medical Care in Diabetes—2014):

Carbohydrate Amount and Quality

  • Monitoring carbohydrate intake, whether by carbohydrate counting or experience-based estimation, remains a key strategy in achieving glycemic control. [1]

  • For good health, carbohydrate intake from vegetables, fruits, whole grains, legumes, and dairy products should be advised over intake from other carbohydrate sources, especially those that contain added fats, sugars, or sodium. [2]

  • Substituting low-glycemic load foods for higher-glycemic load foods may modestly improve glycemic control. [3]

  • People with diabetes should consume at least the amount of fiber and whole grains recommended for the general public. [4]

  • While substituting sucrose-containing foods for isocaloric amounts of other carbohydrates may have similar blood glucose effects, consumption should be minimized to avoid displacing nutrient-dense food choices. [5]

  • People with diabetes and those at risk for diabetes should limit or avoid intake of sugar-sweetened beverages (from any caloric sweetener including high-fructose corn syrup and sucrose) to reduce risk for weight gain and worsening of cardiometabolic risk profile. [6]

I added the numbers in square brackets above for commenting below:

  1. How many grams of carbs are you eating in a day? You need to track the grams of carbohydrate you are eating in a day. Tracking is not a pill and your doctor won’t do it for you. Unless you track you probably have no idea how many grams of carbohydrates you are eating in a day.
  2. Real sources of carbohydrates should be eaten rather than empty carbohydrate calories. An empty calorie is one that only provides calories with very little other nutritional value (vitamins, minerals, etc). Some of the listed items have more carbohydrates than others. Tracking will give an idea of how many grams each item has.
  3. Low Glycemic foods don’t increase your blood sugar as much as higher glycemic index foods. This guidance is helpful but most people don’t know what it means, including doctors.
  4. Eat fiber because it buffers the blood sugar rise you get from carbs in food. While I disagree with the need for whole grains they are certainly preferable to processed flour products.
  5. It’s obvious to most people that a cup of broccoli might have the same number of calories, or even grams of carbs, as a few jellybeans but the two are not of nearly the same value. This is not an IIFYM (If It Fits Your Macros) approach.
  6. Staying away from soda which has sugar avoids many problems. A single soda or two in a day can double your carbohydrates. Eat carbohydrates at a level which supports weight loss, not gain.

Note that there’s no upper or lower recommendations for carbohydrates here. A Very-Low Carbohydrate diet fits within these standards.

References Section

There are five studies of Low Carb diets which are listed in the references section of the standard. I think that a Standard of Care is pretty darned important. The standard of proof for studies used to make the Standard of Care should be high.

Let’s look closely at a couple of the studies for their weaknesses/strengths.

Larsen, et. al.

This may be the worst study I have ever seen referenced in anything important. The title of the study is misleading since the study did not even control for carbohydrates. This was not a metabolic ward study nor was compliance verified in any meaningful way. Dietary advice was given at the start and the results assessed 3, 6, and 12-months later. Further, there was no determination of what low-carb meant – although it appears to just mean not high-carb. In spite of that, the Conclusion stated:

These results suggest that there is no superior long-term metabolic benefit of a high-protein diet over a high-carbohydrate in the management of type 2 diabetes.

Nothing in the conclusions that support the title. In fact, someone who eats a “high-protein” diet may well be avoiding fat and eating low fat cuts of meat and eating high carbohydrate amounts. Looking closer at the actual data shows that at 12-months the High Protein group was eating 41.8% of calories from carbohydrates and 48.2% for the High Carbohydrate diet. That is hardly low carb levels.

Davis, et. al.

This was another poorly formulated study. In spite of that this study also found similar results between low-fat and low-carb diets. Once agaqin, dietary compliance was not done by putting people into a metabolic ward. Macros were checked by asking for the 24-hour food consumed – presumably from the day before.

Here’s the protocol. The flaws should be obvious:

  • Participants signed up for the study.
  • Participants were given nutritional advice as part of a study.
  • Participants were interviewed at 6 and 12 months.
  • Participants knew their appointment is coming up the next day to check on how they did with the diet.
  • The researchers then asked Participants what they ate the day before.

Do you think that they followed the advice they were given a year earlier? Probably to the best of what they remember from the year before. And maybe they ate “better” that last day.

The real test is in the actual data. The Low Carb group said that they ate 1642 calories a day and the Low Fat group said that they ate 1810 calories a day (10% less calories is glossed over). The Low carb group ate 33.4% of their calories from fat (do you see a theme here?) and the Low Fat group said that they ate 50% of their calories from fat. Again, not really a test of a low carbohydrate diet. In spite of that, the “Low Carb” diet was no worse.

Guldbrand, et. al.

The macro levels used for this study were much closer to actual Low Carb levels (20% of calories from carbohydrate). The conclusions stated:

Weight changes did not differ between the diet groups, while insulin doses were reduced significantly more with the LCD at 6 months, when compliance was good. Thus, aiming for 20% of energy intake from carbohydrates is safe with respect to cardiovascular risk compared with the traditional LFD and this approach could constitute a treatment alternative.

This study was done in Sweden and may have been a part of the change to the Swedish dietary guidelines towards Low Carb.



High or Low Carb Diets for Diabetics?

Here’s a valuable older study (JAMA. 1994. Effects of Varying Carbohydrate Content of Diet in Patients With Non—Insulin-Dependent Diabetes Mellitus. Abhimanyu Garg, MBBS, MD; John P. Bantle, MD; Robert R. Henry, MD; et al Ann M. Coulston, RD; Kay A. Griver, RD; Susan K. Raatz, MS, RD; Linda Brinkley, RD; Y-D. Ida Chen, PhD; Scott M. Grundy, MD, PhD; Beverley A. Huet, MS; Gerald M. Reaven, MD) which looked at carbohydrates vs Metabolic Syndrome markers. From the study:

Objective.  —To study effects of variation in carbohydrate content of diet on glycemia and plasma lipoproteins in patients with non—insulin-dependent diabetes mellitus (NIDDM).

Design.  —A four-center randomized crossover trial.

Setting.  —Outpatient and inpatient evaluation in metabolic units.

Patients.  —Forty-two NIDDM patients receiving glipizide therapy.

Interventions.  —A high-carbohydrate diet containing 55% of the total energy as carbohydrates and 30% as fats was compared with a high—monounsaturated-fat diet containing 40% carbohydrates and 45% fats. The amounts of saturated fats, polyunsaturated fats, cholesterol, sucrose, and protein were similar. The study diets, prepared in metabolic kitchens, were provided as the sole nutrients to subjects for 6 weeks each. To assess longer-term effects, a subgroup of 21 patients continued the diet they received second for an additional 8 weeks.

Main Outcome Measures.  —Fasting plasma glucose, insulin, lipoproteins, and glycosylated hemoglobin concentrations. Twenty-four-hour profiles of glucose, insulin, and triglyceride levels.

Results.  —The site of study as well as the diet order did not affect the results. Compared with the high—monounsaturated-fat diet, the high-carbohydrate diet increased fasting plasma triglyceride levels and very low-density lipoprotein cholesterol levels by 24% (P<.0001) and 23% (P=.0001), respectively, and increased daylong plasma triglyceride, glucose, and insulin values by 10% (P=.03), 12% (P<.0001), and 9% (P=.02), respectively. Plasma total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels remained unchanged. The effects of both diets on plasma glucose, insulin, and triglyceride levels persisted for 14 weeks.

Conclusions.  —In NIDDM patients, high-carbohydrate diets compared with high—monounsaturated-fat diets caused persistent deterioration of glycemic control and accentuation of hyperinsulinemia, as well as increased plasma triglyceride and very-low-density lipoprotein cholesterol levels, which may not be desirable.(JAMA. 1994;271:1421-1428)

This diet wasn’t particularly low carb since the difference between the high-carb (55% of calories from carbs) and so-called low-carb (40% of calories from carbs) wasn’t all that much (15% differences). But the results were impressive nevertheless. And it was important since the high-carb diet is close to the Standard American Dietary recommendations.

An earlier study had similar results (N Engl J Med 1988; 319:829-834. Comparison of a High-Carbohydrate Diet with a High-Monounsaturated-Fat Diet in Patients with Non-Insulin-Dependent Diabetes Mellitus. Abhimanyu Garg, M.B., B.S., M.D., Andrea Bonanome, M.D., Scott M. Grundy, M.D., Ph.D., Zu-Jun Zhang, M.D., and Roger H. Unger, M.D.). The results were:

As compared with the high-carbohydrate diet, the highmonounsaturated-fat diet resulted in lower mean plasma glucose levels and reduced insulin requirements, lower levels of plasma triglycerides and very-low-density lipoprotein cholesterol (lower by 25 and 35 percent, respectively; P<0.01), and higher levels of high-density lipoprotein (HDL) cholesterol (higher by 13 percent; P<0.005). Levels of total cholesterol and low-density lipoprotein (LDL) cholesterol did not differ significantly in patients on the two diets.

These preliminary results suggest that partial replacement of complex carbohydrates with monounsaturated fatty acids in the diets of patients with NIDDM does not increase the level of LDL cholesterol and may improve glycemic control and the levels of plasma triglycerides and HDL cholesterol.

Again, neither of these diets reached ketogenic levels. They did achived significant improvements in glycemic control but not enough to reverse diabetes.


Get Fat Eating Fat?

Digging deeper into the Carb-Insulin-Hormonal-Obesity Theory. This site  (INSULIN…AN UNDESERVED BAD REPUTATION) criticizes the theory:

MYTH:  Carbohydrate Drives Insulin, Which Drives Fat Storage

FACT:  Your Body Can Synthesize and Store Fat Even When Insulin Is Low

One of the biggest misconceptions regarding insulin is that it’s needed for fat storage.  It isn’t.  Your body has ways to store and retain fat even when insulin is low.  For example, there is an enzyme in your fat cells called hormone-sensitive lipase (HSL).  HSL helps break down fat.  Insulin suppresses the activity of HSL, and thus suppresses the breakdown of fat.  This has caused people to point fingers at carbohydrate for causing fat gain.

However, fat will also suppress HSL even when insulin levels are low.  This means you will be unable to lose fat even when carbohydrate intake is low, if you are overeating on calories.  If you ate no carbohydrate but 5,000 calories of fat, you would still be unable to lose fat even though insulin would not be elevated.  This would be because the high fat intake would suppress HSL.  This also means that, if you’re on a low carbohydrate diet, you still need to eat less calories than you expend to lose weight.

Ignoring the n=1 experiments where people have eaten 5,000 calories a day of fat and maintained or even lost weight is this a practical case? I think it’s probably the case that it is hard to lose weight when eating 5,000 calories of fat a day. After all, why would your body free it’s own fat while there’s plenty of dietary fat available.

But it still may be possible to lose weight on a 5,000 calories a day of fat diet. It depends upon the feeding schedule. If the food was spread all day and into the night without any time to draw from body fat it might be possible to not lose weight.

Here’s the study that was cited (Am J Physiol. 1999 Feb;276(2 Pt 1):E241-8.
Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism. Evans K, Clark ML, Frayn KN.).

We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001).

I’m not sure the following supports the claim (it may, I am just not sure):

There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids.

So the body fat, it seems released fatty acids in response to the meal.

There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.

Non-Alcoholic Fatty Liver Disease and Diabetes (NAFLD)

From this study (Nutrients. 2013 May; 5(5): 1544–1560. Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease. Melania Gaggini, Mariangela Morelli, Emma Buzzigoli, Ralph A. DeFronzo, Elisabetta Bugianesi, and Amalia Gastaldelli):

NAFLD is more prevalent among obese subjects and also in patients with type 2 diabetes independently of degree of obesity. The prevalence increases to 57% in obese subjects, 70% in diabetic subjects and 90% in morbidly obese people.

Even though this is very common it goes un-diagnosed in Diabetics. The reason is the patients:

have normal liver aminotransferases and clinicians do not suspect the potential presence of NAFLD

It turns out that:

…Insulin resistance is a characteristic feature of NAFLD

many studies have highlighted the association between NAFLD and several factors of metabolic syndrome, especially abdominal obesity, insulin resistance, increased serum triglycerides and small dense LDL and low HDL

It has been shown that up to 85% of subjects with NAFLD compared to 30% in controls are insulin resistant and have abnormal glucose metabolism, i.e., prediabetes or T2DM, of which they were unaware

NAFLD is associated with features of metabolic syndrome and is more prevalent among obese subjects and patients with type 2 diabetes independent of degree of obesity. The increased risk for cardio-metabolic diseases in NAFLD is caused by different factors among which hepatic overproduction of glucose, VLDL, inflammatory factors, C-reactive protein (CRP), and coagulation factors and by the presence of insulin resistance. Large trials that investigate the incidence of CVD and related mortality in subjects with NAFLD are needed to confirm this observation.


Fat Jimmy

Jimmy Moore is a prominent advocate of the Low Carb/High Fat diet and lifestyle. Jimmy Moore is presented as proof that the Calories-In/Calories-Out model is correct and that obesity is not hormonal. Jimmy’s hormones are said to be entirely in order, but Jimmy is still fat.


I am not publishing this to shame or ridicule Jimmy but to look at reasons that Jimmy might still be obese as well as offer some possibilities for helping Jimmy with his obesity.

Jimmy’s Weight Loss History

Jimmy is no stranger to weight loss nor self discipline. Jimmy has written that he previously lost 170 lbs in nine months using the Low Fat diet (SATURDAY, DECEMBER 24, 2005. Low-Fat: Been There, Done That, Made Me Fat. Jimmy Moore.). Jimmy says his starting weight (before the Low Fat Diet) was 410 lbs. Jimmy stated that he regained the weight and got “above 400 pounds towards the end of 2003”.

Jimmy goes on to state that found Low Carbs and he lost 100 lbs in his first 100 days on Atkins and that he went on to lose a total of 180 lbs in that year (by the end of 2004). So that would put Jimmy at about 240 around Jan 2005.

Jimmy’s own biography on his website has many photos which show Jimmy at many different weights (Meet Jimmy) and here (Before & After) with the most recent being 2012 (chest up).

Jimmy’s Current Weight/Health

I do not know Jimmy’s current weight. What seems clear is that Jimmy has lost a lot of weight and kept much of it off. But I will concede that I have seen recent pictures of Jimmy and he is still fat.

Jimmy has tried various hacks such as Extended Fasting (Link) to lose weight and they don’t seem to be all that effective.

Most importantly, Jimmy’s claim is that he is now healthy (off medications, etc). Jimmy has posted blood sugar numbers as screenshots so I believe he is healthy (as far as diabetes and blood sugars).

Jimmy did post one weight loss chart on his page (ending ca May 2013) which correspond to a food elimination diet to see why he was still fat.

Jimmy’s Hormonal Profile

The claim is Jimmy has low resting Insulin rates. (Updated Jimmy has since confessed that his fasting Insulin is more like 14 – about 19:40 into the program). Assuming Jimmy adheres to the Low Carbohydrate diet he probably does. The counter-claim is that since Jimmy is fat it is proof that the Carb-Insulin-Obesity hypothesis is false. The problem is that it oversimplifies hormones and reduces them to a single hormone.

I’ve never seen a copy of Jimmy’s hormone test results, but the fact that Jimmy is overweight implies that he has excess female hormones (they come along with obesity) and a lack of sufficient male hormones (they come along with leanness). Jimmy’s insulin levels may be OK, but Jimmy probably has messed up sex hormones (part of the hormonal profile).

Helping Jimmy

imbalances in the hormone Insulin aren’t the only cause of obesity. There are a lot of food/hunger related hormones. Jimmy has done a number of shows focused on Leptin (example: Dr Rosedale who views Leptin disorders as the cause of diabetes not Insulin).  Jimmy’s answer to obesity could still be found in a hormonal disorder.

The hormonal-obesity theory rather than the insulin-obesity theory may provide some insights to what could help Jimmy. From (Obesity and hormones):

Hormones are chemical messengers that regulate processes in our body. They are one factor in causing obesity. The hormones leptin and insulin, sex hormones and growth hormone influence our appetite, metabolism (the rate at which our body burns kilojoules for energy), and body fat distribution. People who are obese have levels of these hormones that encourage abnormal metabolism and the accumulation of body fat.

A system of glands, known as the endocrine system, secretes hormones into our bloodstream. The endocrine system works with the nervous system and the immune system to help our body cope with different events and stresses. Excesses or deficits of hormones can lead to obesity and, on the other hand, obesity can lead to changes in hormones.

I’d like to see Jimmy look harder into other hormonal possibilities being the root cause of his continued obesity. If Jimmy has exhausted the hormonal tests, that would be worth knowing.

Fat to Satiety

Jimmy eats “Fat to satiety” (Link) but what exactly does that mean to Jimmy. Leptin is a hormone that controls hunger. As an example there’s something called Leptin receptor deficiency which causes obesity. Maybe Jimmy satiety mechanism is broken?

Jimmy Doesn’t Count Calories

To make the claim that Jimmy disproves the hormonal-insulin-obesity model it is necessary to know just how many calories a day Jimmy consumes. After all, since Jimmy is still fat he must be overeating calories, right? But Jimmy doesn’t count calories. Nor does Jimmy publish food diaries so it’s speculative to guess how many calories a day Jimmy eats.

I’d challenge the advocates of Calories-In/Calories-Out to publish Jimmy’s food logs. Otherwise, they are begging the question they are attempting to prove (question-begging fallacy). It could very well be possible that Jimmy eats relatively low calories but is still obese due to a metabolic disorder (other than insulin related).

Missing Protein

An important part of Jimmy’s Low Carb lifestyle is relatively low protein. So the problem may be that Jimmy just doesn’t get enough protein. Again, without a food log it’s impossible to know what Jimmy is eating.

Low Carb/Low Fat (Protein Sparing Modified Fast)

Jimmy has written that it is bad to do both low carb and low fat at the same time. This diet is the Protein Sparing Modified Fast. It’s pretty clear that Jimmy has not tried both at the same time. Added to Jimmy’s self-imposed limit on protein consumption it’s pretty likely that Jimmy has not ever tried this hack.

Jimmy didn’t like Low Fat diet because he was always hungry on the diet. What Jimmy is missing is that the hunger was due to his continued consumption of carbohydrates. If a person is doing low carb then low fat is also possible without feeling hungry.

Jimmy could try one of his famous n=1 experiments and do PSMF for a few weeks. I believe Jimmy would adapt and do pretty well on the diet.

(2018-05-04 Jimmy did PSMF – here’s my view of what he did).


(2018-06-05 CarbSanity – Jimmy Moore — Big Fat Liar — Steps in it AGAIN! It Was NOT a Joke, He Is!)

What you eat matters for your Calories-Out

Somebody asked the question of whether or not the composition of a diet matters for Calories-Out. After all, if a calorie is a calorie it shouldn’t matter if that calorie is sugar or steak.

Turns out there was a well designed study to figure out whether different diets had different effects on Energy Expenditure. Here’s the study (JAMA, June 27, 2012—Vol 307, No. 24 2627. Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance . Cara B. Ebbeling, PhD, Janis F. Swain, MS, RD, Henry A. Feldman, PhD, William W. Wong, PhD, David L. Hachey, PhD, Erica Garcia-Lago, BA, David S. Ludwig, MD, PhD).

Compared with the pre–weight-loss baseline, the decrease in REE (Resting Energy Expenditure) was greatest with the low-fat diet (mean [95% CI], –205 [–265 to –144] kcal/d), intermediate with the low–glycemic index diet (–166 [–227 to –106] kcal/d), and least with the very low-carbohydrate diet (−138 [–198 to –77] kcal/d; overall P=.03; P for trend by glycemic load=.009). The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86] kcal/d, respectively; overall P=.003; P for trend by glycemic load.001).

In layman’s terms that means that your metabolism gets hurt the least with a low carbohydrate diet. Basically, the low carb diet didn’t drop the body’s energy expenditure much at all. That’s good news if you want to preserve your metabolism. Also, from the comments section of the study:

The results of our study challenge the notion that a calorie is a calorie from a metabolic perspective. During isocaloric feeding following weight loss, REE was 67 kcal/d higher with the very low carbohydrate diet compared with the low-fat diet. TEE differed by approximately 300 kcal/d between these 2 diets, an effect corresponding with the amount of energy typically expended in 1 hour of moderate-intensity physical activity.

300 calories a day is 31 lbs a year difference in weight maintenance. That’s very significant.

A study looked at the Resting Energy Expenditure to determine the effect on weight gain (N Engl J Med 1988; 318:467-472. Reduced Rate of Energy Expenditure as a Risk Factor for Body-Weight Gain. Eric Ravussin, Ph.D., Stephen Lillioja, M.B., Ch.B., William C. Knowler, M.D., DR.P.H., Laurent Christin, M.D., Daniel Freymond, M.D., William G.H. Abbott, M.B., Ch.B., Vicky Boyce, R.D., Barbara V. Howard, Ph.D., and Clifton Bogardus, M.D.). From the study:

The estimated risk of gaining more than 7.5 kg in body weight was increased fourfold in persons with a low adjusted 24-hour energy expenditure (200 kcal per day below predicted values) as compared with persons with a high 24-hour energy expenditure (200 kcal per day above predicted values; P<0.01). In another 126 subjects, the adjusted metabolic rate at rest at the initial visit was also found to predict the gain in body weight over a four-year follow-up period.


Calorie-In/Calories-Out Math Matters

Let’s do the math of Calorie-In/Calories-Out (CICO).

Suppose you gain 6 lbs over a year. Suppose that weight gain is spread over the year evenly. That’s 1/2 lb or 1750 excess calories a month. 1750 calories over 30 days is a miniscule 58 calories a day. If you’ve ever measured/tracked your caloric intake you know how hard it is to even accurately measure that small an amount of calories. Control of your diet

This also makes the point of how finely balanced the body is to maintaining weight. To be more accurate, the body maintains certain aspects of the body very tightly. As one person put it:

Without advanced technology, not even the most expert nutritionist could accurately assess an individual’s energy balance to within 350 calories a day by assessment of diet and physical activity level. A daily overestimate 1/10th that magnitude would cause obesity in a decade.

For that matter, if conscious control of calorie balance were so critical to weight control, how did humans ever manage to prevent extreme fluctuations in body weight before the very notion of the calorie was embraced a century ago? (Link).

For instance, gaining/losing bone mass happens at a very slow rate. Bone mass peaks around ages 25–30 years and declines gradually thereafter in both men and women (Oxford, Toxicological Sciences, Volume 55, Issue 1, 1 May 2000, Pages 171–188. Modeling Normal Aging Bone Loss, with Consideration of Bone Loss in Osteoporosis. Ellen J. O’Flaherty). While there are differences among the rates of loss of mass from different bones, which vary from 2 to 13%/decade (summarized in Mazess, 1982), the rate of loss of cortical bone mass in both women and men is generally reported to be 3–5%/decade. The more variable rate of loss of trabecular bone mass is commonly reported to be 6–10%/decade with some reports as high as 13%/decade and no clear-cut difference between men and women (Mazess, 1982).

Water weights shift dramatically over the course of even a single day. Muscle mass is also lost with age but can, like bone mass, be increased with resistance training.

What really matters is changes in fat mass.


How to Lose (or not Lose) Weight

There’s some controversy about the so-called Hormonal-Obesity model. I’d like to dig into some of the details here and this may get technical so bear with me if you want to get to the heart of the differences.

For the Hormonal-Obesity side let’s look at Jason Fung’s IDM site (12-Part Hormonal Obesity series). Some of the points from Fung’s position are:

  1. Exercise doesn’t result in weight loss (Exercise-Part 1).
  2. Caloric restriction doesn’t result in weight loss (Calories-Part 1).
  3. If certain foods (what to eat) or dietary habits (when to eat) affect metabolic rate, then a calorie is not simply a calorie (Calories-Part 2).
  4. The body tries to maintain a set-point and involuntarily raises Calories-Out to match Calories-In (Calories-Part 3).
  5. Fat stores are regulated by hormones (Calories-Part 4).
  6. Total Energy Expenditure drops when Calories-In are decreased (Calories-Part 5).
  7. Control of Calories-In, ie, portion control, is doomed (Calories-Part 6).
  8. The body will reduce expenditures even after the weight loss is done in order to regain the lost weight (Calories-Part 7).
  9. Weight loss stimulates hormones which cause the weight to be regained (Calories-Part 8).
  10. Viscous cycles of dieting and re-eating are the result (Calories-Part 8b).
  11. Low Fat-Low Calories have been shown in studies to not result in long term weight loss (Calories-Part 9).
  12. Overfeeding (eating more calories) results in increases in Total Energy Expenditure (Calories-Part 10).
  13. Dietary composition (macro ratios) determines weight loss/gain (Calories-Part 11).
  14. Historically, excessive carb consumption (starches and refined carbs) were recognized as the cause of body fat until fat became the villain in the 1950’s. (Hormonal Obesity-Part 1).
  15. Dietary goals were set by the US Government in 1977 which led food producers to change their products to be higher in carbohydrates and lower in fat and the result was people got fatter (Hormonal Obesity-Part 2).
  16. Obesity was hypothesized to be a hormonal dysregulation of fat mass.  That is, there is a hormonal signal from the body that controls fat mass.  For example, thyroid stimulating hormone (TSH) controls the thyroid.  Growth hormone (GH) controls growth of cells.  Sex hormones (testosterone and estrogen) control sexual maturation.  These are called endocrine glands and the substances that control them are hormones.  This is the hormonal Obesity Theory (HOT). (Hormonal Obesity-Part 3).
  17. Insulin causes Weight gain not Calories-In/Calories-Out (Part 4).
  18. We get fat because our insulin levels are too high. If we increase insulin, we gain weight.  If we decrease insulin, we lose weight (Hormonal Obesity-Part 5).

Throughout each of these pages, Dr Fung presented quite a few lines of evidence for each of his point. Many of them are formal studies and others are anecdotal but each has persuasive value. It is worth reading each article to see the lines of evidence that he uses for each point.

Putting Dr Fung’s Theory to the Test

Fung’s position is that efforts which lower fasting Insulin levels will inevitably result in weight loss, so his cure is two-fold. One part is a Low Carbohydrate, High Fat (LCHF) diet. The other aspect of the cure is restricted time eating, ie, Intermittent Fasting (IF).

Foods containing carbohydrates cause Insulin release so Fung limits them. Fat causes almost no Insulin to be produced by the body. Protein, while necessary, causes Insulin release so Fung limits protein to relatively low levels. This is all towards the goal of reducing Insulin release from the body to the least amount possible.

The only problem here is that reducing a diet to protein and fat almost always results in a caloric deficit. And when people up their caloric intake they often gain some weight even with Low Carb/High Fat diets (albeit not too much typically).

I know Fung’s approach matches my personal experience when I gained a lot of weight while I was on Insulin and lost an incredible amount of weight quickly as I got my Insulin levels down. I lost over 30 lbs in the first month of LCHF.

I did keep food logs in the beginning as well which show I was eating at a caloric deficit at the time and had plenty of body fat to offset the deficit from fat stores. I’ve also overfed many times and not had much weight gain.

The Diet that You Do is the One that Works

For me, compliance has been relatively easy with Low Carb/High Fat and Intermittent Fasting. I tend to slip into these eating patterns anyway.

The Other Side of the Issue

The other side of this issue contends that it’s not as much about hormones, rather it is all about calorie balance. In one sense, this can be seen as a cart/horse question. But which is the cart and which is the horse? Or is it a more tangled problem like a chicken/egg problem? Which came first?

Representative of the Other Side

For the other side, I picked Lyle McDonald because he has written on the subject in a thoughtful manner. From (Insulin Sensitivity and Fat Loss, September 5, 2008):

  1. Protein is a given with any diet (LM recommends 1-1.5 g per lb of Lean Body Mass for bodybuilders).
  2. Some people do well on LCHF and others do well on LFHC diets. There may be genetic differences between people which dictates which diet works better for which person.
  3. A link between diet effectiveness and both insulin sensitivity and insulin secretion after a meal has been proposed.
  4. Insulin is a storage hormone released in response to eating with carbohydrates having the largest impact on insulin secretion, protein having the second greatest and fat having little to no impact on insulin secretion.
  5. Insulin sensitivity refers to how well or poorly the body responds to the hormone insulin. Individuals who are insulin resistant tend to have higher baseline insulin levels because the body is releasing more in response to try and overcome the resistance.
  6. Some research suggests that a tendency to release too much insulin in response to feeding may predispose people towards weight/fat gain.
  7. High insulin secretion tends to make people eat more.
  8. Studies of diabetics find that decreasing insulin secretion with drugs tends to cause a spontaneously lower food intake.

All of those points are very helpful insights but honestly it is difficult to distinguish between Lyle’s position and Fung’s position from that article. Lyle’s position is that the right diet will result in calorie restriction and that caloric restriction will result in weight loss. Whether eating Low Carb lowers Insulin levels leads to weight loss (Fung) or eating Low Carb results in eating less resulting in weight loss (Lyle) is a difference that makes little difference in practice. And, it could be a combination of both.

From a later Lyle article (Insulin Resistance and Fat Loss, August 12, 2015):

  1. [The] analogy for how hormones work is the lock and key analogy…. insulin has an insulin receptor.  When insulin binds to that receptor, stuff happens …  And that insulin receptor is found all over the body, in the brain, in skeletal muscle, in the liver, and in fat cells.
  2. Think of insulin as a storage hormone.  Released in response to eating carbohydrate and protein (but not in response to fat, which can impact on insulin resistance in other ways) insulin puts the body in an energy storage mode.
  3. In skeletal muscle, insulin stimulates the storage and/or burning of carbohydrate for fuel.  In the liver, it shuts down glucose production.  In fat cells, it both stimulates the storage of calories and inhibits the release of fat (it inhibits lipolysis).
  4. When a fat cell becomes insulin resistant, that means that insulin not only doesn’t store calories but that insulin can’t inhibit fatty acid release as well.
  5. Chronic elevation of a hormone tends to cause receptor resistance itself.  So it becomes a bit of a vicious circle.

From (Endocr Pract. 2010 Jan-Feb;16(1). Identifying prediabetes using fasting insulin levels. Johnson JL, Duick DS, Chui MA, Aldasouqi SA.):

Further analysis using the area under the curve revealed that at a fasting insulin level > 9.0 microIU/mL, prediabetes would be correctly identified in 80% of affected patients.