Drinking Alcohol (Reprinted from Aug 2016)

This was originally a multi-part series from Aug 2016 where I explored the possibility of drinking beer and doing Low Carb.

Remember the food metabolism curve (Only Three Things in What We Eat)? That graph is only missing one thing. Alcohol.

The conventional wisdom (which seems to be repeated from Atkins) I have heard but now question is whether or not the body only burns alcohol if there are choices between alcohol and other things in the body. Alcohol is the best choice of all for the body in terms of ease of access so I wrongly concluded that the body puts off dealing with proteins, carbs and fats until the alcohol is metabolized.

The Atkins site (Q: Can I drink alcohol now following Atkins 40??) puts it this way:

The body burns alcohol for fuel when alcohol is available. So when it is burning alcohol, your body will not burn fat. This does not stop weight loss; it simply postpones it. Since the alcohol does not get stored as glycogen, you immediately get back into fat burning after the alcohol is used up.

Take careful note. They say that the body won’t burn fat but they don’t mention carbs or protein.

The truth is that the body burns all of the sources as best it can in some blended way. Some are more easily accessed than others and burn more quickly. Some are burned slower but all burn at the same time. Alcohol has it’s own curve for blood concentration (implicitly related to metabolism):

Also, Atkins can’t be right with the word “immediately” since this is such a long and smooth drop. What does make sense is that there are overlapping times when the alcohol level has reached a low enough point that the body has to start drawing energy from the stored energy sources. This isn’t a like a flipped switch at all.

Here’s some information on the interaction of Alcohol and other foods (Science here).

The concomitant ingestion of various foods with alcohol resulted in a decreased area under the blood alcohol concentration curve, a lower peak concentration and an increased time to reach peak. Michaelis-Menten kinetics indicated a decreased alcohol metabolism rate after the ingestion of carbohydrates or fats.

I think everyone who drinks realizes this (at least about carbs). If you eat food you get less drunk for both slower and longer. If you drink on an empty stomach you will get drunk faster but sober up more quickly. (PSA: Use those facts to whatever advantage you personally choose as long as you don’t drive. Find another way to stumble home than your car.)

However, that study does implicitly contradict the claim by Atkins. The study demonstrates that alcohol metabolism is reduced after the ingestion of fats. That implies to me that the body processes both at the same time. At least the dietary portion of the fat is still being burned. It’s not like the body puts the fat off into some corner and says that it won’t burn it until the alcohol is done. It does both at the same time. The alcohol acts slower but so do the other sources (Carbs, proteins and fats) just like they would in any other blended situation.

It is true that the body isn’t burning stored fat during that time, but that’s true of anything that a person eats. The body isn’t burning stored fat if it is getting enough energy from what you are digesting.

In fact the real story may be quite different. Take a look at the pathology of Alcoholic Ketoacidosis – a pretty serious condition (What Is Alcoholic Ketoacidosis?).

Cells need glucose (sugar) and insulin to function properly. Glucose comes from the food you eat, and the pancreas produces insulin. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells will not be able to use the glucose you consume for energy. To get the energy you need, your body will start to burn fat.

This is directly opposite of what Atkins says. At least for the alcoholic he has reached the point where his body is eating itself up by burning its own fat. That’s the exact goal of Atkins – to burn the body’s fat. The downside is that the blood glucose increases during that time. Note that this seems to take a lot of alcohol over an extended period of time but it does suggest that the alcohol itself does not prevent the body from burning fat.

Craft Beer

My drink of choice is craft beers. I am particularly fond of the higher octane varieties like Southern Tier’s 2X IPA. The nutritional data for that beer is:

Note that the summary below doesn’t get it right since it doesn’t include the alcohol as part of the calorie count.

This can be shown from the math:

Calories from carbs are 4 cal per gm.
Calories from protein are 4 cal per gm.
Calories from far are 9 cal per gm.
Calories from alcohol are 7 cal per gm.

So 12 ozs * .082 (percent alcohol) * 7 (cals per gram) * 28 (grams per oz) = 165 cals from alcohol. Calories from carbs are 21.4 * 4 = 85.6 cals. Cals from Protein are 2 * 3 = 8. This is 250.6, a bit more than the earlier table but close enough.

How Can I Keep Drinking?

So what’s the best strategy for drinking and losing weight/lowering insulin levels? The best approach is the “cut it out approach” but let’s look at the other choices.

First. seems like it would depend upon the type of alcohol. Craft beers, like the 2X IPA, have a pretty good carb count to begin with. That’s partly why they last longer in the body than say Jack Daniel’s Whiskey. Add to that the sheer volume of downing a 12 oz beer vs a 1.5 oz shot. Eating carbs lowers the metabolism of the alcohol and craft beers would have a slower effect than liquor.

Can it be explained by alcohol amounts? A 12 0z craft beer like the 2X IPA at 8.2% alcohol and 12 ozs has about one oz of alcohol in it. Except a person drinks it over an hour instead of 5 seconds it take to down shot.

If the goal is getting drunk then a few shots are a more effective way to get there. If the goal is to enjoy a few drinks over an evening than craft beer is a good choice.

I am convinced that there’s a dual effect of drinking carbolicious drinks like Craft beer with a meal. The carbs in the beer are one effect and the carbs in the food are another and they do add together. The LC treatment says both of these are bad and just cut them out.

If the goal is decreasing Insulin Resistance then it is believed to be helpful to drop the carb consumption. Carbs increase blood glucose levels requiring a quicker insulin response from the body than other sources of food (protein and fats).

The next question is then is it better to drink Craft Beer with dinner or wait a couple of hours and then drink. Certainly delaying alcohol gives the likelihood of drinking less which means less total carbs. Drinking a craft beer every hour or so from 5-11 would mean 5-6 beers which in this case would be 21 grams of carbs per beer. Basically a pretty decent carb load over an evening.

Delaying drinking until a couple of hours then has the effect of less drinking and less carbs combined with the advantage of letting the meal start to digest. If there are carbs in the meal they are then spread out and less bunched together.

So that is what I tried yesterday with success. I started dinner at 5 and ate for a short time. I then waited till 7 and drank beer at 7, 8, and 9 PM. I went to bed at 10 AM and work up at 5 AM to a fantastic blood sugar number of 111.

One thing I have noticed is that Rye Pale Ales do not blow up my Blood Sugar levels like other IPAs (wheat based Ales) do. Not quite sure why.

The carb levels look comparable. Hard to find anything out there on the difference and I’ve never met a diabetic to share the information with. I do remember that My grandfather had a wheat allergy of some sort and could only eat Rye bread due to some unknown digestion problems.

Is there an analogy to bread? The key may lie in the glycemic index/load. According to (The Glycemic Index of Rye Bread):

One slice of rye bread has a glycemic index of 41 and a glycemic load of 5, according to the Linus Pauling Institute at Oregon State University. In contrast, one slice of white bread, made from refined grains, has a GI of 73 and a GL of 10. A high glycemic index is considered 70 or more, and low is 54 or less; a high glycemic load is 20 or more, and low is 10 or less.

So if beer is really just liquid bread and the carb/alcohol numbers are the same, then it makes sense that Rye beer has a lower glycemic index and load over other Pale Ales of similar alcohol and carb counts.

I did a completely unscientific study and measured my BG at 111 and then drank a Rye Pale Ale beer. I then waited an hour and measured my BG and got 114. When I drank the beer I did not take a bolus like I normally would have in the past. I did the same thing a beer without a bolus and an hour later measured my BG at 112. The taste in my mouth tells me that I am out of ketosis. An hour and a half later my BG was 116 and I was solidly in ketosis.

This has been a disappointing year to find Rye Pale Ale. I bought one or two 12 packs and have not seen them at all over the year. Last year I could find Rye of the Tiger and other brands in the local beer distributors but not this year.

Beer can be healthy in moderation.

Move More (reprinted from Aug 2016)

Get some aerobic activity can translate into “get off your lazy behind” to some people. I am one of them. Now if I’m more than 100 lbs overweight how easy is it for me to get more exercise? Now suppose I’m eating all three recommended meals and suffering the insulin rise that comes with those meals.

I propose this idea for those who tell me to get more exercise. They need to strap a 120 lb weight on their back and hop on the stair machine or the elliptical. Because that’s what it is like when I get on one of those machines. My pulse rate goes up when I get up to walk to the bathroom. My guess is that my muscle mass is as much as most skinny people. How many of them can walk a mile with a 120 lb weight strapped to them?

I’ve only been on this Intermittent Fasting “diet” for about 10 days but I have a lot more energy. I can’t stay in bed long and I am awake late. I actually cleaned up my kitchen for the first time in 2 years. I cleaned out my living room and hauled a bunch of old bottles to the recycling center today (I am on a week stay-cation with the kids). Most of my house looks like I am no longer a hoarder (a joke not intended to insult those with the real condition).

When I lost 70 lbs back in 1997 I was able to do a lot of physical activity. I rode my bike and roller bladed around the neighborhood (my age at the time was upper 30’s). I long for the day when my body isn’t so pulled down by gravity that I moan to get up.

Benefits of Exercise

It is known that exercise lowers insulin resistance (Acta Med Scand Suppl. 1986;711:55-65. Effects of Exercise on Glucose Tolerance and Insulin Resistance . Brief review and some preliminary results Effects of exercise on glucose tolerance and insulin resistance. Holloszy JO, Schultz J, Kusnierkiewicz J, Hagberg JM, Ehsani AA.). From that page.

Preliminary results are presented in this paper showing that prolonged, strenuous and frequent exercise can also completely normalize GT by decreasing resistance to insulin in some patients with mild non insulin dependent diabetes mellitus (NIDDM) and in some individuals with impaired glucose tolerance (IGT).

What constitutes prolonged, strenuous and frequent exercise? The abstract continues:

The amount of exercise required to normalize GT in such patients appears to be in the range of 25 to 35 km per week of running, or a comparable amount of another form of exercise, performed on a regular basis.

That is 15-21 miles a week. I wonder how many years it would take to work up to that level if exercise? At 4 days a week, that’s running 4-5 miles a day. I am sure there are people who can and do that but really? The level of exercise it would take for a non-mild T2D to reverse their condition is pretty extreme. How many people are able to keep that up over their lifetime without some injury which stops the running?

Add to that their statement:

Exercise appears to be effective in normalizing GT only in patients who still have an adequate capacity to secrete insulin, and in whom insulin resistance is the major cause for abnormal GT.

I wonder how much my pancreas still can make? I guess I will find out as I lower my external Insulin.

Metformin and Weight Loss (From Aug 2016)

Metformin is said to do two paradoxical things at the same time:

  1. Metformin lowers insulin resistance which helps glucose to be moved from the bloodstream to the cells (The science: Reducing insulin resistance with metformin: the evidence today).
  2. Metformin used alone results in some weight loss (The science: 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study).

Here’s the paradox. If insulin is only used for pushing fat into cells then Metformin, by lowering insulin resistance should increase weight, right? What am we missing here?

One obvious answer is that insulin is the key to both pushing fat into cells as well as releasing fat from cells. Lowering insulin resistance helps take the fat from the cells and explains Metformin’s advantages. Metformin is like a key which opens the lock and allows glucose in and out of cells.

I know from my own experience that even after 5 years on the pump Metformin still helps my blood sugar levels – by roughly 20 points when taken at bedtime. Instead of waking up at 140 I wake up at 120 by taking Metformin before bed.

Metformin lowers insulin resistance. Lowering our insulin resistance both helps us take up the glucose from our blood into our cells and helps us lose weight.

Take note, I am not saying any of this to advocate for Metformin. The same study showed that Metformin can delay the onset of diabetes by as much as 10 years if given to pre-diabetics. But it is still only a delay.

Who Would Have Thought? (Repost from Aug 2016)

Who would have thought that lowering insulin use while keeping blood glucose levels stable was even possible? I don’t remember hearing that in my pump training class. They talked about how to increase insulin not decrease insulin.

Who would have thought that it would be this easy to better regulate their blood sugar levels? Skipping breakfast and lunch sounds too simple.

Why does this work?

We fast every day. If we ate our last meal or snack at 8 PM and eat breakfast the next day at 8 AM we’ve just done a 12 hour fast. But for insulin resistant people the Dawn Syndrome robs us of the advantage of that fast. We wake up and our numbers are higher than they should be. Increasing our pump basal amounts doesn’t help either. (In fact, if this model is right it makes it even worse).

How is extending the fast by 4-8 hours beneficial? Well, instead of stepping up from our early number (as breakfast does) we keep steadily going down in blood sugar levels. Dr Feng’s view is that there’s a transition from using stored energy in the liver to stored energy in the body’s fat cells themselves. That transition is how we lose weight and affect the insulin resistance.

A few drugs, like Metformin, can help, but not enough over a long time, We’ve got to extend our reset period and the best way to do that is through fasting.

The Shift in Thinking

The main shift in thinking was going from believing that insulin is a neutral substance which only helps to lower blood sugar. If insulin itself is the problem then treating with insulin is throwing fuel on that same fire. No wonder we keep getting sicker and sicker.

Insulin is a hormone

From this site.

Insulin is a hormone made by the pancreas that allows your body to use sugar (glucose) from carbohydrates in the food that you eat for energy or to store glucose for future use.

The same site says this.

People with type 2 diabetes do not respond well or are resistant to insulin. They may need insulin shots to help them better process sugar and to prevent long-term complications from this disease. Persons with type 2 diabetes may first be treated with oral medications, along with diet and exercise. Since type 2 diabetes is a progressive condition, the longer someone has it, the more likely they will require insulin to maintain blood sugar levels.

So let’s try and follow the conventional wisdom.

  • T2Ds don’t handle insulin well (insulin resistance)
  • T2Ds need shots to get more insulin
  • Eventually oral meds will need to be replaced with insulin in T2Ds.

That’s the best they have to offer on these sites. The problem isn’t blood sugar levels it’s our response to insulin. No real insight is given on how to improve insulin resistance. No comment on the underlying problem at all.

 

Some Thoughts on Metformin (reposted from 2016-08-09)

I think there’s some useful insight into one Oral Diabetes medication in the following originally from Aug 8, 2016.

From Wikipedia, here’s why Metformin (How Metformin Works) is a good drug for dealing with Insulin Resistance and, for me, worked well for years.

Gluconeogenesis is also a target of therapy for type 2 diabetes, such as the antidiabetic drug, metformin, which inhibits glucose formation and stimulates glucose uptake by cells.

The phrase “stimulates glucose uptake by cells” is equivalent to “helps lower insulin resistance”. From this paper (Hundal RS, Krssak M, Dufour S, et al. Mechanism by which metformin reduces glucose production in type 2 diabetes. Diabetes. 2000;49(12):2063-9), you can see why Metformin works and how it doesn’t quite work well enough in a diabetic person.

The rate of glucose production was twice as high in the diabetic subjects as in control subjects (0.70 ± 0.05 vs. 0.36 ± 0.03 mmol · m−2 · min−1, P < 0.0001). Metformin reduced that rate by 24% (to 0.53 ± 0.03 mmol · m−2 · min−1, P = 0.0009) and fasting plasma glucose concentration by 30% (to 10.8 ± 0.9 mmol/l, P = 0.0002).

So diabetics produced 2x the insulin of non-diabetics (100%) but Metformin only reduced that rate by 24%. Better than nothing but not nearly enough to make the diabetic person “normal”. And insulin resistance is a progressive disease by which the cells get better and better at not unlocking for insulin.

Going on in the paper.

The rate of gluconeogenesis was three times higher in the diabetic subjects than in the control subjects (0.59 ± 0.03 vs. 0.18 ± 0.03 mmol · m−2 · min−1) and metformin reduced that rate by 36% (to 0.38 ± 0.03 mmol · m−2 · min−1, P = 0.01). By the 2H2O method, there was a twofold increase in rates of gluconeogenesis in diabetic subjects (0.42 ± 0.04 mmol · m−2 · min−1), which decreased by 33% after metformin treatment (0.28 ± 0.03 mmol · m−2 · min−1, P = 0.0002).

It keeps getting better. A diabetic person is 3x better at gluconeogenesis but Metformin was only able to reduce that so that the diabetic person was at 2x the normal person.

And note, Metformin is about as good as it gets in that category of drug. Looks like it can help, but not solve the issues with gluconeogenesis. Something is better than nothing but don’t get lulled (like I was) into assuming all is well. If we keep filling up those protein stores than the same problem which happened to us with carbs will also happen to us with proteins.

Fatty Liver and Metformin

A randomized, double-blind, placebo-controlled trial to test whether metformin improves liver histology in patients with non-alcoholic fatty liver disease (Scand J Gastroenterol. 2009;44(7):853-60. Metformin in patients with non-alcoholic fatty liver disease: a randomized, controlled trial. Haukeland JW1, Konopski Z, Eggesbø HB, von Volkmann HL, Raschpichler G, Bjøro K, Haaland T, Løberg EM, Birkeland K.).

Forty-eight patients with biopsy-proven non-alcoholic fatty liver disease (NAFLD) were randomized to treatment with metformin (n=24) or placebo (n=24) for 6 months.

The study concluded that:

Treatment with metformin for 6 months was no better than placebo in terms of improvement in liver histology in patients with NAFLD.

Could it be because the liver is already full and can’t get fatter?

[Afterthoughts]

I still thought it was protein in the diet that was the problem with GNG. There’s some dispute in the literature about whether GNG is affected by the fat in the liver or not (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).

It looks like the final word may be in this study (Gastroenterology. 2007 Aug;133(2):496-506. Epub 2007 May 1. Relationship between hepatic/visceral fat and hepatic insulin resistance in nondiabetic and type 2 diabetic subjects. Gastaldelli A1, Cusi K, Pettiti M, Hardies J, Miyazaki Y, Berria R, Buzzigoli E, Sironi AM, Cersosimo E, Ferrannini E, Defronzo RA.). The study found that fat in the liver wasn’t the source of GNG, but visceral fat tissue.

Excess VAT primarily increases GNG flux.

Protein doesn’t turn to chocolate cake. Your Dawn Syndrome isn’t from the chicken you had last night. It’s from the cookies you ate three years ago.

Gluconeogenesis – Later Thoughts

I’ve spend time thinking about Gluconeogenesis (GNG). That’s the process where the liver creates glucose from other substrates, including Protein. Earlier on I though Protein was the culprit and was limiting my Protein intake. I don’t believe that was the problem. I believe that the problem was that my liver was overproducing glucose because it was overly fat.

And it turns out that the liver of a diabetic is particularly good at gluconeogensis. From this paper (Diabetes. 2000 Dec; 49(12): 2063–2069. Mechanism by Which Metformin Reduces Glucose Production in Type 2 Diabetes. Ripudaman S. Hundal, Martin Krssak, Sylvie Dufour, Didier Laurent, Vincent Lebon, Visvanathan Chandramouli, Silvio E. Inzucchi, William C. Schumann, Kitt F. Petersen, Bernard R. Landau, and Gerald I. Shulman) GNG is shown to be around 2x as good as a non-diabetic.

The rate of glucose production was twice as high in the diabetic subjects as in control subjects (0.70 ± 0.05 vs. 0.36 ± 0.03 mmol · m−2 · min−1, P < 0.0001).

And later in the paper:

The rate of gluconeogenesis was three times higher in the diabetic subjects than in the control subjects (0.59 ± 0.03 vs. 0.18 ± 0.03 mmol · m−2 · min−1)

 

 

Diabetes Studies

Here are Studies specifically on the effects of diets on Diabetes (particularly low carbohydrate diets).

These are studies related to diabetes in general:

 

Protein-Sparing Modified Fast (PSMF) Weight Loss Studies

Here are some of the scientific studies concerning Protein Sparing Modified Fasts (PSMF) and high protein diets.

PSMF Diets

Muscle Protein Synthesis

Studies on Protein and Diabetes

Protein as a Macronutrient and Protein Requirements

Very Low Carbohydrate Studies

This BLOG post will list Low Carbohydrate Diet Studies and will grow with time. New studies will be added to the end of this list.