Status Update

I’m still alive and well. Still doing keto. Maintaining weight in the mid 160’s for about 20 months now. If I go up a bit in weight, I do PSMF. If I want to maintain weight I increase my fat intake with nuts or cheese.

My diabetes is being completely covered with diet. Good HbA1C numbers earlier this year. I’ve stopped obsessively taking my blood sugar measurements.

GNG is Context Driven

I encouraged someone in a Facebook group to increase his protein intake. Let’s call him Josh (not his real name). Josh is a Type 2 Diabetic who controls his diabetes with the low carb diet (not intermittent fasting).

Josh was afraid to increase his protein because in the past when he upped his protein his blood sugar went up the next morning.  This discouraged Josh in the past from eating a higher protein amount thinking it was making his blood sugar higher. But Josh bit the bullet and decided to try and drop his fat intake and increase his protein.

True to his past experiences, this time his blood sugar went up again but he stuck with it and saw his blood sugar fall. It took some days but it did improve. His blood sugar numbers (in the morning) on the new higher protein were 126, 147, 152, 186, 155, 160, 155, 134, 128. Those first four days would have scared me but to his credit he stuck it out.

Why the Increase in Blood Sugar?

Cahill explained this effect in his study on starvation. Here’s the chart from that study.

I’ve looked at this before in this BLOG but let’s look at it in this particular instance to try and understand why Josh’s blood sugar went up.
Josh’s numbers look a lot like the GNG values in Cahills’ curve above – they are just delayed a bit. It took at least a day or two for Josh’s glycogen to drop since he is eating three meals a day (unlike Cahill’s paper where the subjects were starved). 

Type 2 Diabetics are also really good at GNG. We produce 2x-3x the glucose from GNG than non-diabetics. That is part of why we get exaggerated responses in our blood sugars.  I think it has to due with insulin resistance in the liver. The Type 2 diabetic’s liver is Insulin Resistant meaning it doesn’t listen to the clue that rising insulin is giving that it needs to drop the production of glucose (ie, GNG). 

GNG is done in the liver until glycogen and TG stores are gone. That only happens with a sustained caloric deficit or alternately a longer fast. Cahill points out that GNG is done later in the kidneys, etc which are apparently signaled more by the presence of increased ketones. Josh reported seeing his ketone production increasing. This is as a response to a caloric deficit and the drop in glycogen and TG stores.  Ketones have to go up when glucose drops because our brains need energy.

Context, Context, Context

We diabetics get concerned about our blood sugar but we sometimes don’t understand the context (reason) that the blood sugar goes up. My goal is to better understand for myself and help explain the context to others.

What Josh has now learned is that the increase in blood sugar follows a pattern where it happens for several days then stops to drop. If he keeps this up long enough he will see it level out at a good number. The event (blood sugar going up) needs be put into the proper context (trends, what the protein is doing in the body, etc).

Increases in blood sugar can be a sign (and are in this context) of the start of a caloric deficit which leads to weight loss. The body has to do GNG to make up for the lost energy from food.

This is where the people who say GNG is demand driven are right and wrong. GNG is context driven as Cahill demonstrated clearly. The demand for GNG changes in the context of glycogen status. 

The first evidence that you are doing the right thing with blood sugar shows exactly the opposite and leads you to think you are doing the wrong thing. If you try something for three or four days and it gets worse every day it confirms your fears that it’s not good. But if it starts to turn a corner it encourages you to press on.

Cortisol is [Partly] to Blame

A part of the reason is that the first few days of a caloric deficit (or fast for that matter) increase cortisol. Your body is telling you to get up and find/eat more food. Your body could care less about whether you’ve got enough energy stores (body fat). It just knows that you need to get up and hunt down or gather in dinner. 

Cortisol and Dawn Phenomenon

Increasing cortisol is what coincidentally happens before you get up in the morning. Your body is giving you the cortisol boost to get you moving. And for a diabetic, even though their last meal was 12 hours before, their blood sugar spikes up. The blood sugar wasn’t spiking up from any particular food. It was spiking up because of the cortisol that was being produced.

Josh’s blood sugar went up because he was not getting enough calories and his body was pumping out cortisol. That’s a completely good thing in this case since it signals good things are happening. It sucks that the blood sugar goes up, but it’s completely expected for several days as Cahill shows. Stay at the caloric deficit and it will begin to drop.

GNG is Context Driven

Just because GNG is demand driven doesn’t explain the demand. The demand for GNG is produced when glycogen stores drop and ketone production hasn’t kicked in enough yet. That happens every morning in the Dawn Phenomenon.

Another way to put it is that the demand can change and it does (as Cahill put it) by the caloric deficit not being met by carbs we eat (Phase I), or glycogen stores (Phase II). Eventually the body will down-regulate the need for glucose and even GNG will drop(Phase II to Phase IV). Phase V is marked by a much higher level of ketone production which takes the place of energy from glucose.

Ketogenic Diet – Fat Adaptation

To my way of thinking, this is what is meant by fat adaptation and the ketogenic diet… Ketones being used primarily as fuel. Doesn’t come from eating a lot of dietary fat. Quite the opposite. If you eat a lot of dietary fat it will get converted to glycogen.

If you are in a caloric deficit and your glycogen stores are lowered it has implications on athletic performance. And this may be the necessary state for diabetics who are keto to be in the majority of the time in order to control their diabetes. It may be the case that we can’t control our diabetes effectively without losing performance in glycogen demanding sports (sports at higher intensities).

Easier Paths?

It would have helped if Josh had gone into this by way of Intermittent Fasting or even a two or three day fast since it would have smoothed the transition. 

The same chart can be used to help people understand why Low Carb PLUS Intermittent Fasting is an effective strategy for Diabetics.
Low Carb eliminates phase I since you are not eating carbohydrates.
Just doing Low Carb without Intermittent Fasting causes you to refill your glycogen stores every day.

An 8-12 hour cycle isn’t enough to deplete glycogen. The person stays in Phase II forever. Note that at 6-8 hours glycogen peaks and at 12 hours it’s starting to drop a bit. Glycogen has dropped quite a bit more between hours 8 and 20. 

Suppose you do a 20:4 intermittent fast (into Phase III). If you do that your glycogen stores are getting more depleted every day. It doesn’t take too many days for your glycogen stores to drop enough that you don’t refill them the next day – especially if you are Low Carb where it’s harder to refill the Glycogen stores.

That is why Intermittent Fasting works so well. But it has to be done long enough to start to downregulate GNG and upregulate ketone production. Starting at OMAD or a 20:4 margin worked for me. It’s what got me to my HbA1C of 5.2 (non-diabetic blood sugar control).

People mistakenly think that the magic of Intermittent Fasting is that you just happen to eat less calories. Maybe that’s true or maybe it isn’t but the real magic is that it depletes your glycogen stores. At some point your body has to be producing ketones. By depleting glycogen (exercise helps and hurts this BTW) you are on your way to ketone production.

Cafeteria Diet?

There’s a term, the “Cafeteria Diet” (CAF) that is used in research literature to describe a diet which is high in hyper-palatable food (described in the literature as “food regularly consumed by humans, including high‐salt, high‐fat, low‐fiber, energy dense foods such as cookies, chips, and processed meats“). These foods tend to be higher carbohydrate as well.

There are quite a few studies which looked at CAF as the explanation for Metabolic Syndrome. Here’s one of the studies (Sampey, B. P., Vanhoose, A. M., Winfield, H. M., Freemerman, A. J., Muehlbauer, M. J., Fueger, P. T., Newgard, C. B. and Makowski, L. (2011), Cafeteria Diet Is a Robust Model of Human Metabolic Syndrome With Liver and Adipose Inflammation: Comparison to High‐Fat Diet. Obesity, 19: 1109-1117). The study looked at the difference between a high fat diet and the cafeteria diet.

To investigate the obesogenic and inflammatory consequences of a cafeteria diet (CAF) compared to a lard‐based 45% HFD in rodent models, male Wistar rats were fed HFD, CAF or chow control diets for 15 weeks.

Body weight increased dramatically and remained significantly elevated in CAF‐fed rats compared to all other diets. Glucose‐ and insulin‐tolerance tests revealed that hyperinsulinemia, hyperglycemia, and glucose intolerance were exaggerated in the CAF‐fed rats compared to controls and HFD‐fed rats. 

The two diets were both high fat compared with the control diet. Both of the high fat diets resulted in increased body fat. The difference was that the CAF diet caused inflammation in white fat.

Although both high fat diets resulted in increased adiposity and hepatosteatosis, CAF‐fed rats displayed remarkable inflammation in white fat, brown fat and liver compared to HFD and controls. 

The study indicated that the CAF was a good model of Metabolic Syndrome.

In sum, the CAF provided a robust model of human metabolic syndrome compared to traditional lard‐based HFD, creating a phenotype of exaggerated obesity with glucose intolerance and inflammation. This model provides a unique platform to study the biochemical, genomic and physiological mechanisms of obesity and obesity‐related disease states that are pandemic in western civilization today.

This is interesting since the Diet Induced Obesity (DIO) models usually work in rats by feeding the rats a High Fat diet (HFD). The study concluded that the CAF diet was actually more effective at creating the Metabolic Syndrome than the High Fat Diet (HFD).

Our study has revealed that rats fed human nutrient poor foods develop severe metabolic syndrome which is more robust than the effect of traditional HFD exposure.

The power of these sorts of studies is that that were done on ad libitum fed rats. That is, they ate as much as they wanted to eat. They did not feed the rats a diet limited in any way. They simply presented the food and measured what was left to determine what the rats ate.

This can’t be blamed on sugar since the Low Fat diet contained the most sugar. It can’t simply be blamed on carbohydrates although CAF had higher carbohydrates. 

The high fat diet also had a self-regulating capacity which the CAF diet lacked. As the study noted:

…study revealed that while HFD-fed animals decreased food intake in terms of total grams to maintain caloric intake comparable to LFD and SC control, CAF-fed animals lacked this autoregulatory mechanism… CAF-fed rats were hyperphagic, eating 40% more calories/day compared to the HFD.

This may be a part of the advantage of the Low Carb High Fat diet for diabetics. To summarize:

Our study has revealed that rats fed human nutrient poor foods develop severe metabolic syndrome which is more robust than the effect of traditional HFD exposure. CAF-diet fed rats exhibited voluntary hyperphagia and grossly elevated fat intake which resulted in dramatic and rapid weight gain.

Furthermore, CAF diet feeding promoted a prediabetic condition with elevated glucose, insulin, and nonesterified fatty acids, accompanied by decreased glucose and insulin tolerance. In addition, chronically inflamed liver and adipose tissues and distorted pancreatic islet architecture were prevalent.

Glucose Response to Protein

I wrote a post a while back comparing my blood sugar response to protein compared to a non-diabetic friend’s response (Blood Sugar Responses Compared). In that n=2 study I noted that my blood sugar goes up a bit when I consume protein but my non-diabetic associate’s blood sugar goes down.

Turns out this difference has been well known for nearly a century. A while back I reviewed a paper by Conn from 1936 (Protein vs Carbs). That paper (J Clin Invest. 1936 Nov; 15(6): 665–671. THE GLYCEMIC RESPONSE TO ISOGLUCOGENIC QUANTITIES OF PROTEIN AND CARBOHYDRATE. Jerome W. Conn and L. H. Newburgh.) which compared the blood sugar response of two non-diabetics against fifteen diabetics.

Turns out there was a difference between the diabetics and the non-diabetics which matched my own n=2 results. Here’s the blood sugar response of the non-diabetics.

And here’s the blood sugar response of the diabetics.

The blood sugar of the non-diabetics dropped when lean beef was eaten. The blood sugar of the diabetics went up a small amount when lean beef was eaten. Could this be an interesting screening test for diabetics?

The OGTT (Oral Glucose Tolerance Test) is one way to determine if someone is a diabetic. They are given a large glucose drink and their blood sugar is monitored over the next couple of hours. The peak value of the diabetic above is 340 mg/dl. The peak value of the non-diabetic is around half of that at about 170 mg/dl. Clearly there’s a difference there between the diabetic and the non-diabetic.

A second difference is the time that the blood sugar takes to return to normal. In the non-diabetic they are back to their baseline at about 2 hours. The diabetic is still high four hours later.

My favorite explanations of the difference have to do with first phase insulin response being delayed in diabetics and diabetics don’t stop GNG as quickly as non-diabetics. The absolute value of the fall or rise from protein isn’t all that much compared to glucose. The point of the Conn paper was that the peak value is what matters for a diabetic. Even though half of the protein was believed to be converted to glucose

Either way, as long as I continue to have this blood sugar response to protein I still have at least one of the side-effects of diabetes.

Calories In Calories Out and Macros Ratios

An interesting study on macros ratios which compared high carbohydrates to high protein impacts (Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 2003 Feb;133(2):411-7.).

This study examined the efficacy of two weight loss diets with modified CHO/protein ratios to change body composition and blood lipids in adult women.

Women (n = 24; 45 to 56 y old) with body mass indices >26 kg/m(2) were assigned to either a CHO Group consuming a diet with a CHO/protein ratio of 3.5 (68 g protein/d) or a Protein Group with a ratio of 1.4 (125 g protein/d). Diets were isoenergetic, providing 7100 kJ/d, and similar amounts of fat ( approximately 50 g/d).

After consuming the diets for 10 wk, the CHO Group lost 6.96 +/- 1.36 kg body weight and the Protein Group lost 7.53 +/- 1.44 kg. Weight loss in the Protein Group was partitioned to a significantly higher loss of fat/lean (6.3 +/- 1.2 g/g) compared with the CHO Group (3.8 +/- 0.9).

Both groups had significant reductions in serum cholesterol ( approximately 10%), whereas the Protein Group also had significant reductions in triacylglycerols (TAG) (21%) and the ratio of TAG/HDL cholesterol (23%). Women in the CHO Group had higher insulin responses to meals and postprandial hypoglycemia, whereas women in the Protein Group reported greater satiety.

This study demonstrates that increasing the proportion of protein to carbohydrate in the diet of adult women has positive effects on body composition, blood lipids, glucose homeostasis and satiety during weight loss.

The high carbohydrate group lost 7 kg of weight but about half of the loss was lean body mass. The high protein group maintained most of their lean body mass.


ADA 2018 Standards of Care for Diabetics

The  ADA 2018 Standards of Care for Diabetics are out.

A1C targets of <7% (53 mmol/mol)

7% represents a very lax standard of care and results in an unhealthy level of blood sugar. Their own standard notes:

…further lowering of A1C from 7% to 6% [53 mmol/mol to 42 mmol/mol] is associated with further reduction in the risk of microvascular complications, although the absolute risk reductions become much smaller.

The reason they don’t use the smaller number is that the smaller number comes at the cost of too many lows. This is where the Low Carbohydrate diet comes to play since it eliminates the lows the patient can go for the lower number without risk of hypoglycemic (too low a blood sugar) events (as long as medications are adjusted down as blood sugar levels go lower). Their own words are:

Given the substantially increased risk of hypoglycemia … with polypharmacy in type 2 diabetes, the risks of lower glycemic targets outweigh the potential benefits on microvascular complications.

polypharmacy = more than one medication at the same time. The medications that they give you run a risk of dropping your blood sugar too low which is even worse than being too high.

Dietary Guidelines

The Standard of Practice has improved with respect to low carbs but still doesn’t recognize the definitive science in the area. For instance, the Standard clams:

Studies examining the ideal amount of carbohydrate intake for people with diabetes are inconclusive…

That’s just plainly false or deliberately misstated. It may be the case that to solve diabetes requires 20 grams of carbs in one person but another person can tolerate 100 grams of carbs.


…although monitoring carbohydrate intake and considering the blood glucose response to dietary carbohydrate are key for improving postprandial glucose control

This is where it gets really stupid. Monitoring something does absolutely nothing at all to state how much someone should be taking. Monitoring isn’t the answer except to determine how much carbs should be limited.

Here’s the right way to state this.

  1. Monitor carbohydrate intake using glucometer.
  2. Don’t eat foods (type or quantity) which cause your blood sugar to go up more than 10 points over 2 hours.
  3. Test all your food intake and discontinue any carbohydrate sources which cause your blood sugar to raise.

Now that would be useful advice.

The Standard of Care continues:

The role of low-carbohydrate diets in patients with diabetes remains unclear

Could it be clearer than this? My HbA1C went from 8 to 5.2 after a year and a half of Low Carb. That’s pretty darned clear, right?

The idiocy continues:

While some studies have shown modest benefits of very low–carbohydrate or ketogenic diets (less than 50-g carbohydrate per day) (78,79), this approach may only be appropriate for short-term implementation (up to 3–4 months) if desired by the patient, as there is little long-term research citing benefits or harm.

Let’s see. There’s evidence that Low Carb diets reverse diabetes. And diabetes is really bad for you. And they claim there’s no evidence of the long term benefits or harm from Low Carb diets. This begs the question – is there evidence of the damage from the alternate? Clearly, diabetes harms people long term, right?

And the definition of low carb or keto as less than 50 g of carbohydrates flies in the face of the broadly agreed on number of 20 of carbohydrates being at ketogenic levels.

Here’s where the insanity reaches a peak.

Most individuals with diabetes report a moderate intake of carbohydrate (44–46% of total calories) (51). Efforts to modify habitual eating patterns are often unsuccessful in the long term; people generally go back to their usual macronutrient distribution (51). Thus, the recommended approach is to individualize meal plans to meet caloric goals with a macronutrient distribution that is more consistent with the individual’s usual intake to increase the likelihood for long-term maintenance.

The logic is people like to eat carbs and will return to them. They lack self control so why bother telling them that low carb can be the cure for diabetes but they need to stay on the Low Carb diet FOREVER? What’s the alternative for diabetics?

How about showing the patients pictures of amputated body parts? How about taking them to a blind school where many of the patients are blind from diabetes? Why not tell them about diabetic neuropathy and the constant pins and needles that people have?

No, it’s better to give them a pill and send them out the door. Better not tell them that most of them will end up on Insulin.

Why not tell them what can happen with a Low Carb diet? Most people would love to lose weight and maybe even get below their High School Senior year weight, wouldn’t they?

Why is there ZERO support in place for people who really want to do this with Low Carb? Why are all of us on our own and being told that we shouldn’t even bother since we will fail anyway?

The next comment is somewhat useful:

As for all Americans, both children and adults with diabetes are encouraged to reduce intake of refined carbohydrates and added sugars and instead focus on carbohydrates from vegetables, legumes, fruits, dairy (milk and yogurt), and whole grains. The consumption of sugar-sweetened beverages and processed “low-fat” or “nonfat” food products with high amounts of refined grains and added sugars is strongly discouraged

If people did just those things then things would be better. But how good have people shown themselves to be at reducing refined carbohydrates? Why not just say that they need to ELIMINATE refined carbohydrates entirely? Then we can forget about compliance in reducing.

Instead the answer is to educate people to use more Insulin:

Individuals with type 1 or type 2 diabetes taking insulin at mealtime should be offered intensive and ongoing education on the need to couple insulin administration with carbohydrate intake. For people whose meal schedules or carbohydrate consumption is variable, regular counseling to help them understand the complex relationship between carbohydrate intake and insulin needs is important. In addition, education on using the insulin-to-carbohydrate ratios for meal planning can assist them with effectively modifying insulin dosing from meal to meal and improving glycemic control

Why not teach people that over dependence  on Insulin will result in Insulin Resistance and ever increasing dosage needs? Why not tell people that their ability to control their blood sugars will get worse and worse with time on Insulin? Why not tell people that every day they have high blood sugar numbers their own pancreas is dying (beta cell death) and that at some point in time they may not be able to get off Insulin ever?

I need to stop now. This is upsetting me. They really don’t care about diabetics. If they did they would tell them the truth and try to get them cured.

Give them a pill and bring in the next patient…


Branched Chain Amino Acids (BCAA) Product Review

Trying Branched Chain Amino Acids (BCAAs) for pre-workout performance boost. Product is fortified with 100 mg of caffeine so it may be interesting (a little over 1 cup of coffee worth). I normally drink a fair amount of coffee but mostly a 80% decaf/20% caffeine mix.

Product I am trying is Optimized Nutrition “ON” Amino Energy. Two scoops are 5g of Amino Acids.