Mice on an Ad Lib Keto Diet

Here is a nice paper from 2009 on mice fed an ad libitum ketogenic diet (Kennedy AR, Pissios P, Otu H, Roberson R, Xue B, Asakura K, Furukawa N, Marino FE, Liu FF, Kahn BB, Libermann TA, Maratos-Flier E. A high-fat, ketogenic diet induces a unique metabolic state in mice. Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1724-39. Epub 2007 Feb 13).

The study looked at:

C57BL/6 mice animals were fed one of four diets:

1) KD;

2) a commonly used obesogenic high-fat, high-sucrose diet (HF);

3) 66% caloric restriction (CR); and

4) control chow (C).

Calories were the same but weight was lower on the ketogenic diet.

Mice on KD ate the same calories as mice on C and HF, but weight dropped and stabilized at 85% initial weight, similar to CR.

In fact, they moved mice from the High Fat High Carb diet to the Ketogenic diet and had the following:

Animals made obese on HF and transitioned to KD lost all excess body weight, improved glucose tolerance, and increased energy expenditure. 

Even more along my own area of interest:

KD fed mice had a unique metabolic and physiological profile, exhibiting increased energy expenditure and very low respiratory quotient

The macronutrient composition of the diets was interesting:


Note this was not a high protein KD. I.e., The dietary advantage wasn’t protein. The percentage of calories from protein was the lowest on the KD – by far. This is a much higher level of fat than most people will tolerate and the protein level is pretty low.

Most telling was the body composition changes (Table 5).


The Chow fed mice were a bit over 10% heavier but at a lower % of Body Fat (13.5%) vs the Ketogenic fed mice. This can be attributed to the much lower protein consumption of the KD.

A contrasting study (Protein Leverage Hypothesis Counterpoint) showed an inflection point around 70% for fat where additional fat did not result in additional weight. In my opinion (study needed) – substituting protein for some of the fat should not be an issue.

The study concluded:

the effects that diet composition can have on metabolism and found that diets high in fat and low in carbohydrate do in fact lead to weight loss by increasing energy expenditure. 

Remarkably, animals eating ketogenic diet lost a small amount of weight and achieved the same weight and body composition as animals that were calorie restricted to 66% of usual daily intake.

In a related paper (Bielohuby M1, Menhofer D, Kirchner H, Stoehr BJ, Müller TD, Stock P, Hempel M, Stemmer K, Pfluger PT, Kienzle E, Christ B, Tschöp MH, Bidlingmaier M. Induction of ketosis in rats fed low-carbohydrate, high-fat diets depends on the relative abundance of dietary fat and protein. Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E65-76) noted the same issue with KD :

One problem with ketogenic LC-HF diets is that it is difficult to attribute observed effects (e.g., loss of body weight) to either the presence of ketone bodies or to the normally very low protein content of these diets.

The ideal ketogenic diet for research purposes would be a LC-HF diet that is ketogenic but ensures the sufficient supply of protein at the same time. However, until now, it is not clear whether the absence of dietary carbohydrates per se or the absence of carbohydrates in combination with a specific abundance of the two other macronutrients, fat and protein, is required to induce ketosis.

Fat Stores Where/How?

Peter at the Hyperlipid BLOG has an interesting analysis of an interesting paper on fat storage in mice (On phosphorylating AKT within visceral fat). The study he looks at is (Narita T, Kobayashi M, Itakura K, Itagawa R, Kabaya R, Sudo Y, Okita N, Higami Y. Differential response to caloric restriction of retroperitoneal, epididymal, and subcutaneous adipose tissue depots in rats.  Exp Gerontol. 2018 Apr;104:127-137). The study looked at ad lib feeding of mice and the storage of fat in three White Adipose Tissues (WAT) depots in rats: retroperitoneal (rWAT), epididymal (eWAT) and subcutaneous (sWAT).

Peter’s interest is in fat storage based on insulin levels. The study compared ad libitum to calorie restricted eating in the mice. Peter concentrated on the ad libitum eating of the mice (not being all that interested in calorie restricted diets). Peter points out that it takes insulin to store fat in subcutaneous tissues but very little insulin to store fat in visceral fat. The study put it this way:

In all WAT depots, CR markedly upregulated the expression of proteins involved in FA biosynthesis in fed rats. In visceral WAT (rWAT and eWAT), hormone-sensitive lipase (lipolytic form) phosphorylation was increased by CR under fed conditions, and decreased by CR under fasted conditions. Conversely, in sWAT, hormone-sensitive lipase phosphorylation was increased by CR under fasted conditions. CR enhanced the effect of feeding on AKT activity in sWAT (indicative of a positive effect on insulin sensitivity) but not in rWAT or eWAT. These data suggest that CR improves lipid metabolism in an insulin signaling-dependent manner in sWAT only.

As Peter puts it:

This looks very much like one of the intrinsic differences between subcutaneous adipocytes and visceral adipocytes is that visceral adipocytes maintain insulin signalling at much lower levels of plasma insulin than do subcutaneous adipocytes. You have to store calories which arrive without insulin somewhere. Looks like this is the place!

I’m still of the opinion that visceral fat is what matters the most in reversal of Type 2 Diabetes. The Low Carb diet gets insulin levels low which reduces fat in general. See this article (A Grand Unified Theory of Polyunsaturated Fatty Acid Misbehaviour in Inflammatory Disease).

This article is actionable as well (Fatty liver and its treatment).

Another Way to Reverse Diabetes

Here’s another way to reverse Type 2 Diabetes (E. L. Lim, K. G. Hollingsworth, B. S. Aribisala, M. J. Chen, J. C. Mathers, R. Taylor. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia, October 2011, Volume 54, Issue 10, pp 2506–2514). Here were the subjects:

Eleven people with type 2 diabetes (49.5 ± 2.5 years, BMI 33.6 ± 1.2 kg/m2, nine male and two female) were studied before and after 1, 4 and 8 weeks of a 2.5 MJ (600 kcal)/day diet.

Here are the results:

After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003).

Insulin suppression of hepatic glucose output improved from 43 ± 4% to 74 ± 5% (p = 0.003 vs baseline; controls 68 ± 5%).

Hepatic triacylglycerol content fell from 12.8 ± 2.4% in the diabetic group to 2.9 ± 0.2% by week 8 (p = 0.003).

The first-phase insulin response increased during the study period (0.19 ± 0.02 to 0.46 ± 0.07 nmol min−1 m−2p < 0.001) and approached control values (0.62 ± 0.15 nmol min−1 m−2p = 0.42).

Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2).

Pancreatic triacylglycerol decreased from 8.0 ± 1.6% to 6.2 ± 1.1% (p = 0.03).

Other interesting factoids from the study. In Type 2 diabetics:

Beta cell function declines linearly with time, and after 10 years more than 50% of individuals require insulin therapy.

Here’s the data from the study.

VariableControlsBaselineWeek 1Week 4Week 8
Weight (kg)101.5 ± 3.4103.7 ± 4.599.7 ± 4.5*94.1 ± 4.3 *88.4 ± 4.3*†
BMI (kg/m2)33.4 ± 0.933.6 ± 1.232.3 ± 1.2*30.5 ± 1.2*28.7 ± 1.3*†
Fat mass (kg)36.2 ± 2.739.0 ± 3.536.6 ± 3.6 *31.7 ± 3.7 *26.3 ± 4.0*
ffm (kg)64.7 ± 3.864.7 ± 3.063.2 ± 3.162.4 ± 3.0 *62.1 ± 3.0*
Waist circumference (cm)105.0 ± 1.5107.4 ± 2.2104.4 ± 2.2*99.7 ± 2.4 *94.2 ± 2.5*†
Hip circumference (cm)109.8 ± 2.4109.5 ± 2.9108.3 ± 2.7*105.0 ± 2.6*99.5 ± 2.6*†
WHR0.96 ± 0.020.98 ± 0.020.97 ± 0.020.95 ± 0.010.95 ± 0.01

It is remarkable that the people lost mostly fat. The Fat Free Mass loss was only 2.6kg (about 6 lbs). The fat loss was 10 kg (about 22 lbs). That’s a pretty decent drop.

Low Carb?

This was neither a Low Carb nor Low Fat diet. It was a restricted calorie diet (600 calories a day). The macros were 46.4% carbohydrate, 32.5% protein and 20.1% fat; vitamins, minerals and trace elements; 2.1 MJ/day [510 kcal/day]; Optifast; Nestlé Nutrition, Croydon, UK. This was supplemented with three portions of non-starchy vegetables such that total energy intake was about 2.5 MJ (600 kcal)/day. 

It is remarkable how much fat was lost from the liver in just the first week.

Hepatic triacylglycerol content decreased by 30 ± 5% during week 1 of intervention (p < 0.001), becoming similar to control values (p = 0.75). It continued to decline throughout the intervention period to reach the normal range for non-obese individuals [20] (2.9 ± 0.2%; p = 0.003; Fig. 1), i.e. a total reduction of 70 ± 5%.

Most interestingly, the study after the study noted:

Following the intervention, participants gained 3.1±1.0 kg body weight over 12 weeks, but their HbA1c remained steady while the fat content of both pancreas and liver did not increase.

The conclusion matches my own hypothesis:

The data are consistent with the hypothesis that the abnormalities of insulin secretion and insulin resistance that underlie type 2 diabetes have a single, common aetiology, i.e. excess lipid accumulation in the liver and pancreas.

Giving Monkeys Diabetes

I listened to an interesting Break Nutrition podcast (Episode 13 – What happens to fructose-fed monkeys?) on a study of Rhesus Monkeys who were fed fructose meals (Bremer AA, Stanhope KL, Graham JL, Cummings BP, Wang W, Saville BR, Havel PJ. Fructose-fed rhesus monkeys: a nonhuman primate model of insulin resistance, metabolic syndrome, and type 2 diabetes. Clin Transl Sci. 2011 Aug;4(4):243-52). (Full PDF).

…a high-fructose diet in rhesus monkeys produces insulin resistance and many features of the metabolic syndrome, including central obesity, dyslipidemia, and infl ammation within a short period of time; moreover, a subset of monkeys developed type 2 diabetes

A Rhesus monkey used in the study is closer genetically to a human than the typical mouse study.

Numerous animal studies, mostly conducted in rodents, have shown that diets high in fructose produce metabolic perturbations associated with the metabolic syndrome and T2DM. 

However, important metabolic differences exist between rodents and primates, particularly with respect to lipoprotein metabolism,the major site of lipogenesis (liver vs. adipose), and the physiology of thermogenesis.

Therefore, the results of metabolic studies performed in primates are substantively more applicable to human physiology and medicine than those from rodent studies, underscoring the importance of developing standardized nonhuman primate models of insulin resistance for the study of metabolic syndrome and T2DM.

Kimber Stanhope was one of the authors of this study. See her other study on Fructose (Not All [Sugar] Is Bad).

The charts in the study are very interesting. Gabor discusses them on the podcast.

Am I Still a Diabetic?

That’s a challenging question since by most tests I am not a diabetic. I no longer take diabetic meds and have good control of my blood sugars. The Type 2 Diabetes ADA Diagnosis Criteria are any of the following:

  1. A hemoglobin A1c (HbA1c) level of 6.5% or higher; the test should be performed in a laboratory using a method that is certified by the National Glycohemoglobin Standardization Program (NGSP) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay, or
  2. A fasting plasma glucose (FPG) level of 126 mg/dL (7 mmol/L) or higher; fasting is defined as no caloric intake for at least 8 hours, or
  3. A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test (OGTT), or
  4. A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with classic symptoms of hyperglycemia (ie, polyuria, polydipsia, polyphagia, weight loss) or hyperglycemic crisis

I have changed the bullet-ted list to a numbered list for convenience. I am on no diabetes medications to mask the results here:

  1. My last HbA1C was 5.2 so I pass this test.
  2. My fasting plasma glucose is less than 100 typically so I pass this test.
  3. I have not had an OGTT (more on this to follow).
  4. I have none of the symptoms of hyperglycemia at all and I have had no blood sugar measurements of 200 or higher (or anywhere near that level) since I started Low Carb.

Oral Glucose Tolerance Test (OGTT)

I don’t know if I would pass an OGTT or not. I assume I would fail such at test in spite of losing 120 lbs, etc. The reason I assume I would fail is that I think part of being on a Low Carb ketogenic diet is that my body has developed peripheral insulin resistance.

Peripheral Insulin Resistance

PIR is a normal response to the ketogenic diet and happens as a response to lowered glucose availability. Here’s a mouse study which shows that Peripheral Insulin Resistance got worse under a ketogenic diet (Kinzig KP, Honors MA, Hargrave SL. Insulin sensitivity and glucose tolerance are altered by maintenance on a ketogenic diet. Endocrinology. 2010;151(7): 3105-14.). The study measured:

After 8 wk of consuming chow or KD, caloric intake after peripheral or central insulin and insulin and glucose levels after a glucose challenge were assessed. In a separate group of rats, glucose and insulin responses to either a low- or high-carbohydrate test meal were measured. Finally, rats maintained on KD were switched back to a chow diet, and insulin sensitivity and glucose tolerance were evaluated to determine whether the effects of KD were reversible.

That answers the test that I would want to do to determine if I would pass an OGTT. What happened to the mice?

Maintenance on KD resulted in decreased sensitivity to peripheral insulin and impaired glucose tolerance.

So after 8 weeks of not eating carbohydrates the mice had trouble eating carbohydrates. Not much of a surprise there. It would take a deeper dive to see how much worse their PIR and IGT became.

Furthermore, consumption of a high-carbohydrate meal in rats that habitually consumed KD induced significantly greater insulin and glucose levels for an extended period of time, as compared with chow-fed controls.

So the mice over-reacted to carbohydrate meals by producing more glucose and insulin.

Responsivity to central insulin was heightened in KD rats and associated with increased expression levels of insulin receptor mRNA.

Not sure how to understand that if the mice were more insulin resistant. But was this effect a permanent change or was it temporary and a side effect of the diet itself?

Finally, returning to a chow diet rapidly reversed the effects of KD on insulin sensitivity and glucose tolerance. These data suggest that maintenance on KD negatively affects glucose homeostasis, an effect that is rapidly reversed upon cessation of the diet.

Although 8 weeks isn’t that long to a human it’s a long time to a mouse. I don’t know the scaling factor but it’s reasonable to assume it is years rather than the two months of the study.

So, if someone is concerned about whether or not they would pass an OGTT it seems like they probably could stop the ketogenic diet for some time (weeks maybe?) and then take the test. Most of us who do LC / Keto won’t be trying it anytime soon.

The fact is your doctor is not going to order an OGTT for you if you don’t fail one or more of the other numbers. In fact, if you fail the fasting blood sugar test the doctor might order you an HbA1C test for confirmation. And then, depending on other factors, may just decide to keep an eye on it.

SlimFast Keto Products

Here are another set of products I am going to avoid.

SlimFast Keto Meal Bars

I imagine they could have done worse than they did. But it’s hardly very good.

I have no clue how the label says free from artificial sweeteners but the ingredients list includes Erythritol. I suppose technically it’s considered to be a sugar alcohol and not an artificial sweetener…

Stevia is another “natural” sweetener.

Cultured Dextrose? That’s sugar.

If Ted Naiman and the Protein Leverage Hypothesis is true, we are people in search of protein. Eating products low in protein just makes us eat more.
I get the convenience part, but what’s wrong with real food?

Glycogen Shifts

Working on a theory of glycogen and caloric surplus/matching/deficit. My theory is that glycogen stores are somewhat related to carbohydrate consumption (how full the tank gets) but also to caloric status. My theory is that eating at a surplus of calories even on low carb will fill the glycogen stores higher than the “normal” keto level.

This explains to me the wide fluctuations in weight that I and others see when we gain or lose 5-7 lbs in a few days. In fact, I think it’s pretty easy to gain in a day or two and might take some days to lose again what was gained in that day or two. The reason is that glycogen stores can get filled quickly but unless you are at a caloric deficit they won’t get drawn down.

Explains the “LBM gains” people have when they increase their caloric intake. Normal body water amount vary greatly along with the glycogen.

See (Keto Flush – How Body Water and Glycogen Affect Ketogenic Weight Loss).

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.


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.


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.


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.