Ran across an older study (The American Journal of Clinical Nutrition, Volume 83, Issue 5, 1 May 2006, Pages 1055–1061. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Carol S Johnston Sherrie L Tjonn Pamela D Swan Andrea White Heather Hutchins Barry Sears) which indicates that LDL is directly tied to BHB levels:

LDL cholesterol was directly correlated with blood β-hydroxybutyrate (r = 0.297, P = 0.025)

The study was only six weeks so it was too short a term to provide much of value in the critique of ketogenic low-carbohydrate diets. The main criticism was that people had a lack of energy on low carb during what we now know is the adaptation phase.

More details:

Compared with baseline, the 6-wk LDL concentrations increased in 5 KLC dieters (0.08, 0.13, 0.41, 0.44, and 0.52 mmol/L, respectively) and decreased in the remaining 4 KLC dieters (0.57 ± 0.18 mmol/L)

Another interesting point:

 Weight-adjusted REE increased in both diet groups over the 6-wk trial, but blood β-hydroxybutyrate concentrations were not correlated with REE (r = −0.014, P = 0.921), which indicates that the protein content of the diet, rather than the severity of the carbohydrate restriction, likely contributed to the elevations in REE.  These data support the contention that calorie-reduced diets high in protein facilitate weight loss, in part, by preserving the metabolic rate (7818).


Low-ish Carb Diet and Diabetes

A five week long study was conducted to determine the effect of a non-ketogenic but still low-ish carb diet on blood sugar numbers in diabetes (Diabetes 2004 Sep; 53(9): 2375-2382. Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Mary C. Gannon and Frank Q. Nuttall).

The study compared diets with two different macros. The carbohydrate:protein:fat ratio of the Low Carb diet was 55:15:30. The test diet ratio was 20:30:50. Again, note this was not ketogenic levels of carbohydrates. The diet was “weight-maintaining”.  Assuming this is a 2000 calories a day diet that would be 2000 * 0.2 = 400 calories or 100 grams of carbohydrates a day.

The subjects were tested and their Plasma and urinary β-hydroxybutyrate were similar on both diets indicating that the lower carb group was not in nutritional ketosis.

The results were favorable for the Low Carb group.

The percentage of glycohemoglobin (HbA1c) was 9.8 ± 0.5 on the control diet and 7.6 ± 0.3 on the Low Carb diet. It was still decreasing at the end of the Low Carb diet. Thus, the final calculated glycohemoglobin was estimated to be ∼6.3–5.4%.

The reason they estimated the final HbA1c numbers would be lower was that:

The mean 24-h integrated serum glucose at the end of the control and LoBAG diets was 198 and 126 mg/dl, respectively.

Carbohydrate Control is the Key to Blood Sugar Control

As the study noted:

Data obtained in our laboratory (1–3) as well as from others (reviewed in 4) indicate that glucose that is absorbed after the digestion of glucose-containing foods (carbohyrates) is largely responsible for the rise in the circulating glucose concentration after ingestion of mixed meals. Dietary proteins, fats, and absorbed fructose and galactose resulting from the digestion of sucrose and lactose, respectively, have little effect on blood glucose concentration.

The study did increase protein by 2x but a previous study had isolated the protein affects on HbA1c:

We previously reported that a diet in which the protein content was increased from 15 to 30% of total food energy, with a corresponding decrease in carbohydrate content, resulted in a moderate but highly statistically significant mean decrease in glycohemoglobin (8.1–7.3%) after 5 weeks on the diet. This was the consequence of smaller postmeal glucose increases. The fasting glucose concentration was unchanged (12).

Thus, the increase in Protein did help the HbA1C due to the decrease in carbohydrates that came along with that increase.

The conclusion was unavoidable given the data:

Thus, the dietary modification that we refer to as the LoBAG diet has the potential for normalizing or nearly normalizing the blood glucose in people with mild to moderately severe type 2 diabetes.

Not as well as the ketogenic diet, but pretty good nevertheless. I did low carb some time back and get my HbA1C to 6.4 (with other meds). But I like my 5.2 number better now.


Calories In Calories Out – Revisited Again

Here’s some thoughts I have on the Calories In/Calories Out (CICO) model.

The CICO perspective has value but I think where Fung’s contribution worked for me and others was the role of Insulin in weight gain and carbs being the driving force in Insulin Resistance. Combining Low Carb with Intermittent Fasting made for easy compliance. The reduction of Insulin levels over extended periods of time frees the body to release body fat. The release of body fat reduces the need for calories from the diet since part of the fuel that body needs comes from the body rather than meals.

I see Fung’s advice as focused on his patient population which as a kidney doctors is many older diabetic patients. He found that his patients were compliant with Intermittent Fasting and Low Carbohydrate diets. Probably much more so than the standard population because they were seeing a kidney doctor to begin with. Faced with the possibility of failing kidneys or eating OMAD/Low Carb the alternative seems pretty bad.

Also, there are differences in body composition between various diets. Some are more effective than others at shifting the lean mass/fat mass proportions. http://www.ergo-log.com/paleo-diet-makes-fat-cells-lazy.html

I think they do matter but not so much at the start of the diet. Eventually we have to pay attention to them when we stall with lazy keto. But I got from 285 to around 220 with being completely lazy keto. Never would have reached goal weight, though.

Put another way when we have 100 lbs of body fat that’s 3100 calories a day of fat we can easily pull from our fat stores. Easy to do a caloric “deficit” since we have plenty of surplus to draw from in our bodies.

I’ve been looking into the three compartment theory of diabetes and it seems to have legs to me. First our body’s fat cells fill up. Then our liver fills up with fat. Last our pancreas gets choked with fat which keeps us from making enough Insulin. When that happens our fat backs up into our blood in the form of very high triglycerides. When I was Dx with T2D my triglycerides were over 5000. In fact, they couldn’t get an assay on the number since it was too high. Putting someone on Insulin gets them over that by allowing the fat cells to get even fatter. I gained 50 lbs when the doctor put me on Insulin and my diet was not any different.

This has application in this situation since the fat cells stay locked closed due to high Insulin. There are studies which show CICO doesn’t exactly apply in these cases. Diabetics take more Insulin and eat less calories but still gain weight. There’s a strong relationship with Insulin and body fat.

Intermittent fasting and Low Carb break that relationship by lowering basal Insulin levels and allow the liver to begin dumping the fat. That only takes about a week. The pancreas gets less fatty within 2 weeks and the body’s fat cells drop thereafter.

To me the key is the role of Insulin and that’s Fung’s “contribution”. He’s not a researcher but applied what he learned in the clinical setting.

Bottom line is that if someone is Type 2 Diabetic they can get off meds very quickly by following Fung’s approach of Intermittent Fasting and Low Carb. They can learn to count calories/macros later on when they stall if they want to get lower in weight (and some of them may not care about their weight, they just want to be no longer diabetic).

The reason I think CICO matters later on is that our hormones, particularly Insulin, get in order and then the standard model applies.

There are studies which also show CICO is not matched by the data. For example: https://academic.oup.com/jcem/article/88/4/1617/2845298

The mechanism of the enhanced weight loss in the very low carbohydrate diet group relative to the low fat diet group is not clear. Based on dietary records, the reduction in daily caloric intake was similar in the two groups. For the greater weight loss in the very low carbohydrate group to be strictly a result of decreased caloric consumption, they would have had to consume approximately 300 fewer calories/d over the first 3 months relative to the low fat diet group.

I think Protein is the power multiplier between Low Carb and SAD. In part it has something to do with the Thermic Effect of Food with Protein using about 25% of the calories to process and fat and carbs being much less. So Calories in and Calories out need to take into account the source of the calories.

I’m eating about 2800 calories a day now on Carnivore diet with around 280g of Protein a day. Far in excess of my “Needs”. Some of that we just eliminate as Urea – again outside of the CICO model.

Or maybe the CICO model is just really, really complicated compared to what we see on the standard calculators?

My guess is that the standard calculations for BMR and TDEE are inherently based on the SAD macro ratios. They don’t correct for overconsumption of protein nor do they correct for underconsumption of carbohydrates. They don’t take into account hormonal factors either nor medications such as Insulin.

They are good first order approximations. Eat and track macros and by extension calories. Watch the scale. If you are gaining you need to cut back. If you are maintaining then things are set pretty close. If you want to lose you need to cut.

In my case my methodology is:
Less than 20 g of carbs
At least 1 gram of protein per lb of Lean Body Mass
Enough fat to fill the gap between the first 2 and what I want to lose.

Here’s the calculator I wrote to calculate macros.


Carbs After Workouts?

If you are exercising to improve your insulin sensitivity, then Carbs after workouts are bad. Here’s the science (Nutrients. 2018 Jan 25;10(2). pii: E123. PostExercise CarbohydrateEnergy Replacement Attenuates Insulin Sensitivity and Glucose Tolerance the Following Morning in Healthy Adults. Taylor HL, Wu CL, Chen YC, Wang PG, Gonzalez JT, Betts JA.)

In this study they put participants on a 90-minute treadmill at 70% of their VO2max. At the end they gave the participants either a placebo (no carbs) or maltodextrose that matched the caloric expenditure. Researchers then measured the glucose and insulin responses with an Oral Glucose Tolerance Test (OGTT) the following day and found that the participants who had the carbohydrates had reduced Insulin Sensitivity and increased blood glucose levels.

The practical conclusion of this is that to maximize Insulin Sensitivity it is best to both eat low carb and take no carbs after exercise. Decreased Insulin Sensitivity is one of the markers that lead to Diabetes and increasing Insulin Sensitivity is an important part of reversing Diabetes.

This study is the first to show that feeding carbohydrate to replace that utilized during exercise can reduce insulin sensitivity and glucose tolerance the next morning in healthy adults, when compared to a preservation of the exercise-induced carbohydrate deficit. Furthermore, carbohydrate replacement suppresses subsequent postprandial fat utilization. The mechanism through which exercise improves insulin sensitivity and glucose control is therefore (at least partly) dependent on carbohydrate
availability, and so the day-to-day metabolic health benefits of exercise might be best attained by maintaining a carbohydrate deficit overnight.

For those people who are not particularly concerned about their risk of getting Diabetes it’s worth noting that if they refill their Glycogen stores quickly with carbohydrates they are not burning fat. If they let the Glycogen stores be low then their body will burn fat.

Want to burn fat? Work out and don’t eat carbohydrates after working out.


Blood Test Results

I got them back. 2015-09-04 was from before (while I was a diabetic). 2017-07-28 was my 1 year keto anniversary. The new test is about 18 months.

Test Range 2015
WBC 3.4-10.8 11.0 7.7 6.6
Lymphs (Abs) 0.7-3.1 3.8 3.1 2.5
Glucose, Serum 65-99 152 159 103
BUN/Creatinine 9-20 17 31 20
Protein, Tot, Ser 6.0-8.5 6.4 6.6 5.9
A/G Ratio 1.2-2.2 2 2.3 2.5
Total Cholesterol 100-199 159 Did not
Triglycerides 0-149 460 Did not
HDL Cholesterol >39 36 Did not
12.78 2.31
VLDL 5-40 Invalid Did not
LDL Cholesterol 0-99 Invalid Did not
HbA1c 4.8-5.6 7.5 5.8 5.2
Vitamin D 30-100 14.9 Did not
Did not
Testosterone 264-916 Did not
Did not

Interpreting the Results

Looking at the results – overall very good results. Most important of all my goal of hacking my Type 2 Diabetes has been accomplished. My HbA1C number is not even in pre-diabetic range. It is right in the middle of the healthy range.

The Triglyceride number is went from a very unhealthy 460 a couple of years ago to a healthy 118 now. And I was on statins for lipid issues back then. Much healthier now and I am on no statins.

My Testosterone number would be a good number for a young man. Libido from Keto – check…

To see an increase in LDL is not an unusual situation on keto.  The very important ratio is triglycerides to HDL. My ratio went from 12.7 to 2.3 which is a very dramatic drop in risk of heart disease. See (The American Journal of Cardiology Volume 94, Issue 2, 15 July 2004, Pages 219-222. Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Viktor Hanak MD, Julian Munoz MD MSPH, Joe Teague MD, Alfred Stanley Jr. MD. Vera Bittner MD MSPHc):

A triglyceride/HDL cholesterol ratio of 3.8 divided the distribution of LDL phenotypes with 79% (95% confidence interval [CI] 74 to 83) of phenotype B greater than and 81% (95% CI 77 to 85) of phenotype A less than the ratio of 3.8. The ratio was reliable for identifying LDL phenotype B in men and women.

Studies on the Ketogenic Diet and Blood Biomarkers

There’s a lot of studies which been done on the positive benefits of the Ketogenic Diet on Blood Markers.

Christmas Status Letter


Holidays provide time to reflect on the past year. It’s long overdue to circle back to the purpose of this BLOG. I started this journey of hacking my Type 2 Diabetes almost 18 months ago. In that time, I fixed my Diabetes and so much more.

No More Insulin or Medications

I am on ZERO medications. No diabetes medications. No hypertension medications. I still use a CPAP machine since I am afraid of quitting the machine.

Weight Loss

I have lost over 100 lbs. My starting weight was around 285 and it was 178 this morning. I’ve been in maintenance for a month now and my weight has stayed steady. I wish I had charted better in the beginning.

Added Exercise

After I lost most of my weight (around 80 lbs) I added exercise. I have been doing CrossFit for about four months now. I can lift weights that match the girl’s weights. I usually finish the Workout of the Day (WOD) last but I do finish – even the hard ones. I workout five days a week. The typical CrossFit workout is less than one hour. I take rest days Thursday and Sunday.

Blood Sugar Control

My blood sugar after working out last night was 65 (US units) which is really good. I most often see numbers in the mid 80s. My last HbA1C was taken this summer (before CrossFit) and it was 5.8 (which is at the bottom end of the prediabetes range).

My Macros

My diet consists largely of chicken, nuts and broccoli.

Chicken is a good Protein and different cuts provide different amounts of fat. Kim Chee (from Walmart refrigerated veggie section) is a good probiotic (good for stomach biome). Broccoli is a good veggie and easy to heat in a microwave bag. Finally, nuts fill in the fat numbers in a healthy way.

My Macros

My daily macros are:

My current macros are 1800 calories with 125g of Protein, 20g of Carbohydrates and 136g of Fat. Protein is a minimum. Carbs are a maximum. Fat fills up the remaining calories to meet the limit. If I go over on Protein I will go under on Fat to match. In percentages of daily calories this is 27% Protein, 5% Carbohydrates, and 68% fat.


Here is what I take daily.

Breaking Stalls

I had a long stall this year which lasted for maybe six months. I did some extended fasts which helped a little bit. I then tripped across the idea of doing Protein Sparing Modified Fasting. That broke the fast and gave me a way to make progress with the last 25 lbs that I needed to lose.

My Goals

My goals have shifted over the past 18 months. They started with hacking my Diabetes. I wanted to get off Insulin. That took two weeks.

Since then I have worked at improving my Insulin Sensitivity. For me, the main tool was Intermittent Fasting (IF). One thing that interferes with this is getting in enough Protein. I have added a Protein meal at lunch time. This hasn’t hurt my Blood Sugar numbers.

Another way of improving Insulin Sensitivity is High Intensity Training. I do CrossFit. Training with increasingly heavier weights and intensity will improve Insulin Sensitivity. I hope to keep up this training and there are plenty of goals to reach. I got my first box jump and pullup in the past month.


Intermittent Fasting – The Science (pt 2)

Here is another study (Glucose Tolerance and Skeletal Muscle Gene Expression in Response to Alternate Day Fasting).


Glucose and insulin responses to a standard meal were tested in nonobese subjects (eight men and eight women; BMI, 20 to 30 kg/m2) at baseline and after 22 days of alternate day fasting (36 hour fast). Muscle biopsies were obtained from a subset of subjects (n = 11) at baseline and on day 21 (12-hour fast).

The results were:

Glucose response to a meal was slightly impaired in women after 3 weeks of treatment (p < 0.01), but insulin response was unchanged. However, men had no change in glucose response and a significant reduction in insulin response (p < 0.03).

Some significant results:

The protocol was well tolerated, weight loss was 2.5% of initial body weight, resting metabolic rate was unchanged, and fat oxidation, as measured by the respiratory quotient, was increased.

Subjects with type 2 diabetes were excluded.

The insulin response to a meal was not influenced by alternate day fasting in women but was reduced in men (area under the curve: 207 ± 38 to 130 ± 15, p < 0.03; Figure 1B), suggesting improved insulin sensitivity.


Furthermore, the insulin response to the meal was improved in men, suggesting that insulin sensitivity may be increased and not decreased after alternate day fasting.



Nuts and Inflamation

It’s often said that nuts cause inflammation.

Here is on study (Am J Clin Nutr. 2016 Sep;104(3):722-8. doi: 10.3945/ajcn.116.134205. Epub 2016 Jul 27. Associations between nut consumption and inflammatory biomarkers. Yu Z1, Malik VS2, Keum N2, Hu FB3, Giovannucci EL3, Stampfer MJ3, Willett WC3, Fuchs CS4, Bao Y5.) concluded:

A greater intake of nuts was associated with lower amounts of a subset of inflammatory biomarkers, after adjusting for demographic, medical, dietary, and lifestyle variables. The relative concentrations (ratios) and 95% CIs comparing subjects with nut intake of ≥5 times/wk and those in the categories of never or almost never were as follows: CRP: 0.80 (0.69, 0.90), P-trend = 0.0003; and IL-6: 0.86 (0.77, 0.97), P-trend = 0.006. These associations remained significant after further adjustment for body mass index. No significant association was observed with TNFR2. Substituting 3 servings of nuts/wk for 3 servings of red meat, processed meat, eggs, or refined grains/wk was associated with significantly lower CRP (all P < 0.0001) and IL-6 (P ranges from 0.001 to 0.017).

Here’s another study on the subject of nuts (Medicine (Baltimore). 2016 Nov;95(44):e5165. Impact of different types of tree nut, peanut, and soy nut consumption on serum C-reactive protein (CRP): A systematic review and meta-analysis of randomized controlled clinical trials. Mazidi M1, Rezaie P, Ferns GA, Gao HK.) concluded:

This meta-analysis suggests that nut consumption significantly decrease leptin while have no significant effect on CRP, IL6, adiponectin, IL10, and TNF-α.


Metabolism and Aging

Intuitively, we all know that our metabolism slows as we age. Did you though this has been quantified? Here’s the chart of Basal Metabolic Rates in men and women vs age:

So this, at least in part, demonstrates why it is harder at 50 to lose weight than when we are 20. For a man of 20 their BMR is about 46 and the same man (at the same size) their BMR is around 38. That’s only 82% of the age at 20. So, yes, it is harder to lose weight since you have to eat less to lose weight than you did when you were young, but it is not at all impossible.

Even if you are older, you can do it.


What if the History of Diabetes Went Wrong?

In an interesting paper the question is asked what if the history of the development of our understanding of diabetes has it wrong? The paper (J. Denis McGarry. What If Minkowski Had Been Ageusic? An Alternative Angle on Diabetes. Science, Vol. 258, No. 5083 (Oct. 30, 1992), pp. 766-770).

Despite decades of intensive investigation, the basic pathophysiological mechanisms responsible for the metabolic derangements associated with diabetes mellitus have remained elusive. Explored here is the possibility that traditional concepts in this area might have carried the wrong emphasis. It is suggested that the phenomena of insulin resistance
and hyperglycemia might be more readily understood if viewed in the context of underlying abnormalities of lipid metabolism.
Some powerful food for thought in the paper. Another paper (Arius, Energy Metabolism) summarizes the argument as:
The author considers the possibility that the hyperinsulinemia of early non-insulin—dependent diabetes is coincident with hyperamylinemia, since insulin and amylin are cosecreted. Amylin would cause an increase in plasma lactate (Cori cycle); and lactate, a better precursor than glucose for fatty acid synthesis, would indirectly promote the production of very-low-density lipoproteins (VLDL). There would follow an increased flux of triglycerides from liver to muscle (and adipose tissue) and, as proposed and elaborated on, an increase in insulin resistance and production of many of the metabolic disturbances occurring in diabetes.
 The author of the paper draws heavily on the Randle Cycle.
The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle and adipose tissue. The cycle controls fuel selection and adapts the substrate supply and demand in normal tissues. This cycle adds a nutrient-mediated fine tuning on top of the more coarse hormonal control on fuel metabolism. This adaptation to nutrient availability applies to the interaction between adipose tissue and muscle. Hormones that control adipose tissue lipolysis affect circulating concentrations of fatty acids, these in turn control the fuel selection in muscle. Mechanisms involved in the Randle Cycle include allosteric control, reversible phosphorylation and the expression of key enzymes.[5] The energy balance from meals composed of differing macronutrient composition is identical, but the glucose and fat balances that contribute to the overall energy balance change reciprocally with meal composition.
Interesting thoughts.
Fatty acids may act directly upon the pancreatic β-cell to regulate glucose-stimulated insulin secretion. This effect is biphasic. Initially fatty acids potentiate the effects of glucose. After prolonged exposure to high fatty acid concentrations this changes to an inhibition.[13] Randle suggested that the term fatty acid syndrome would be appropriate to apply to the biochemical syndrome resulting from the high concentration of fatty acids and the relationship to abnormalities of carbohydrate metabolism, including starvation, diabetes and Cushing’s syndrome.
My own weight had been in the 280 range for a long time. In the months before I was diagnosed as Type 2 Diabetic my weight dropped 50 lbs without any lifestyle changes. After I went on Metformin my weight was relatively lower for a while. When I eventually went on Insulin my weight went up 40+ lbs fairly quickly. It is well known that Insulin adds weight.
My own thought is that the Insulin is both the lock and the key. Increased levels of Insulin pushes glucose or fat into cells and decreased levels of Insulin allows fat to come out of cells. That’s why Intermittent Fasting is such a great bullet for Type 2 diabetics. It allows our fasting Insulin levels to drop. Add to that Low Carbohydrate diets and the perfect recipe for controlling Diabetes comes into play.
The problem never really was Insufficient Insulin. The problem was too much Insulin. And clearly it is a fat related problem.